(BQ) Part 2 book Current diagnosis & treatment cardiology presents the following contents: Supraventricular tachycardias, atrial fibrillation, conduction disorders & cardiac pacing, ventricular tachycardia, pulmonary embolic disease, sudden cardiac death, pulmonary hypertension, congenital heart disease in adults,...
ᮢ Supraventricular Tachycardias Byron K Lee, MD & Peter R Kowey, MD ESSENTIALS OF DIAGNOSIS ᮣ ᮣ Heart rate greater than 100 bpm Rhythm is supraventricular in origin ᮣ General Considerations Supraventricular tachycardias (SVTs) are rapid rhythm disturbances originating from the atria or the atrioventricular (AV) node In the absence of a bundle branch block, there is intact conduction to the ventricles via the right and left bundles leading to a narrow and normal appearing QRS Therefore, these arrhythmias are also often called narrow complex tachycardias Since many of the SVTs are episodic, many clinicians also refer to this group of arrhythmias as paroxysmal SVTs Radiofrequency ablation has become an important therapeutic option in the management of SVTs because of its ability to eliminate these arrhythmias safely Table 20–1 outlines the pharmacologic therapy for SVTs ᮣ Pathophysiology & Etiology Arrhythmias occur as a result of three main mechanisms: reentry, which is most common; enhanced or abnormal automaticity; and triggered activity Reentrant arrhythmias sustain themselves by repetitively following a revolving pathway comprising two limbs, one that takes the impulse away from, and one that carries it back to the site of origin For reentry to exist, an area of slow conduction must occur, and each limb must have a different refractory period (see the discussion on AV nodal reentrant tachycardia) In this situation, pacing (by inducing refractoriness in one limb of the circuit) can typically initiate a reentrant tachycardia Once established, pacing can also terminate the tachycardia by interfering with impulse propagation in one of the limbs 233 20 The second mechanism, automaticity, refers to spontaneous and, often, repetitive firing from a single focus, which may either be ectopic or may originate in the sinus node It should be noted that automaticity is an intrinsic property of all myocardial cells This mechanism comprises two subcategories Enhanced automaticity is defined as a focus that fires spontaneously and may originate in the sinus node, subsidiary pacemakers in the atrium including the Eustachian ridge, Bachmann bundle, coronary sinus and AV valves, the AV node, His-Purkinje system, and the ventricles Abnormal automaticity is usually secondary to a disease process causing alterations in ionic flow that produces a lower (ie, more positive) resting diastolic membrane potential Threshold potential is therefore more easily attained, thereby increasing the probability of a sustained arrhythmia The third mechanism, triggered arrhythmias, depends on oscillations in the membrane potential that closely follow an action potential In the absence of a new external electrical stimulus, these oscillations, or after-depolarizations, cause new action potentials to develop Thus, each new action potential results from the previous action potential These arrhythmias can be produced by early or late after-depolarization, depending on the timing of the first after-depolarization relative to the preceding action potential (the one that spawned the triggered activity) In early after-depolarizations, membrane repolarization is incomplete, which allows an action potential to be initiated by a subthreshold stimulus This type is often associated with electrolyte disturbance and may be the mechanism responsible for arrhythmogenesis related to the prolonged-QT syndrome and torsades de pointes caused by quinidine With delayed after-depolarization, membrane repolarization is complete, but an abnormal intracellular calcium load causes spontaneous depolarization The reason for the high calcium levels is unclear, but it can be related to inhibition of the sodium pump by drugs such as digoxin In either type of arrhythmia, the process may be repetitive and lead to a sustained tachycardia Agent Indication Intravenous Dose Oral Dose Adverse Effects Drug Interactions Class Ia Quinidine AF, AFL, AVNRT, AVRT 6–10 mg/kg over 20–30 200–400 mg q4–6h; q8h with long-acting preparations Hypotension (especially IV), ventricular proarrhythmia, GI disturbance, thrombocytopenia ↑ digitalis level ↑ warfarin effect ↑ metoprolol, propranolol, propafenone levels Procainamide AF, AFL, AVNRT, AVRT Bolus: 15 mg/kg given as 20 mg/min Infusion: 2–4 mg/min 50 mg/kg/day q3–4h; twice daily dosage with longacting preparation GI disturbance, hypotension, SLE, agranulocytosis, FUO hemolytic anemia, myasthenia gravis aggravation, ventricular proarrhythmia ↑ Procainamide level with cimetidine, quinidine, and amiodarone Flecainide AF, AFL, AT, AVNRT, AVRT N/A 50–200 mg q12h Ventricular proarrhythmia, CHF, GI disturbance CNS (dizziness, tremor, light-headedness) ↑ digitalis level ↑ flecainide level with amiodarone, cimetidine, norpace, propranolol ↓ flecainide level with smoking Propafenone AF, AFL, AVNRT, AVRT N/A 150–300 mg q8h GI disturbance, CNS (dizziness), metallic taste, CHF, first-degree AVB, IVCD, positive ANA Synergism with β-blockers Esmolol Ventricular rate control for AF, AFL, ST, AT Bolus: 500 mcg/kg over 1–2 Infusion: 50–200 mcg/kg/ N/A CHF, AVB, bradycardia, bronchospasm Propranolol Ventricular rate control for AF, AFL, ST, AT 1–5 mg at mg/min 20–320 mg/day q6h, q8h, q12h or once daily, depending on preparation CHF, AVB, bradycardia, bronchospasm Sotalol AF, AFL, AVNRT, AVRT, AT N/A 80–160 mg q12h Dyspnea, fatigue, dizziness, CHF, bradycardia, ventricular proarrhythmia, bronchospasm Synergism with Ca2+ antagonists or β-blockers Amiodarone AF, AFL, AVNRT, AVRT, AT Bolus: 150 mg over 10 Infusion: mg/min × 6h, then 0.5 mg/min 100–400 mg once daily Pulmonary toxicity, CHF, tremor, bradycardia, ↑ LFTs, corneal deposits, skin discoloration, GI intolerance, hyper-/hypothyroidism ↑ digoxin levels ↑ warfarin effect ↑ quinidine, prox/NAPA, flecainide ↑ phenytoin level Ibutilide AF, AFL mg bolus over 10 second bolus, if needed, after 10-min wait N/A Ventricular proarrhythmia, hypotension, GI disturbance Dofetilide AF, AFL N/A 125–500 mcg twice daily modified by algorithm Ventricular proarrhythmia, headache, chest pain, nausea, dizziness ᮢ Antiarrhythmic Drugs for Supraventricular Tachycardias 234 Table 20–1 Class 1c Class III Contraindicated with verapamil, cimetidine, ketoconazole, trimethoprim CHAPTER 20 Class II (IV) Class IV Diltiazem AF, AFL, AVNRT, AVRT, AT, MAT Bolus: 0.25 mg/min over then 0.35 mg/kg in 15 if needed Infusion: 5–15 mg/h 90–360 mg/day in 1–4 divided doses, depending on preparation Hypotension, bradycardia, CHF, AVB Synergism with β-blockers Verapamil AF, AFL, AVNRT, AVRT, AT, MAT 2.5–20 mg over 20 in divided doses 40–120 mg q8h; 240–360 mg once daily of long-acting preparation Hypotension, bradycardia, CHF, AVB Synergism with β-blockers Adenosine SVT diagnosis AVNRT, AVRT, AT termination mg IV rapid bolus followed by 12 mg × if needed Half dosage if administered in central line N/A Chest tightness, facial flushing, dyspnea, AVB ↑ activity by dipyridamole ↓ activity by theophylline Digoxin Ventricular rate control for AF, AFL, AT (generally not very effective in active patients) Up to 1.0 mg bolus in divided doses followed by 0.125–0.375 mg/day 0.125–0.375 mg/day in single dose GI disturbance, conduction defects, atrial/ventricular arrhythmias, headache, visual disturbances ↑ Digoxin level: amiodarone, quinidine, verapamil, indomethacin, spironolactone, alprazolam, erythromycin, tetracycline ↓ Digoxin level: antacids, cholestyramine, rifampin, neomycin ↑ Risk of digitalis toxicity with potassium depleting diuretics Class V ᮢ SUPRAVENTRICULAR TACHYCARDIAS235 AF, atrial fibrillation; AFL, atrial flutter; ANA, antinuclear antigen; AT, atrial tachycardia; AVB, atrioventricular block; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reciprocating tachycardia; CHF, congestive heart failure; CNS, central nervous system; FUO, fever of unknown origin; GI, gastrointestinal; IV, intravenous; IVCD, intraventricular conduction delay; LFT, liver function tests; MAT, multifocal atrial tachycardia; N/A, not applicable; NAPA, N-acetyl procainamide; SLE, systemic lupus erythematosus; ST, sinus tachycardia 235 ᮢ 236 CHAPTER 20 ᮣ General Diagnostic Approach Rate can also be helpful since sinus tachycardia cannot typically go over 220-age bpm and the heart rate in atrial flutter is often a multiple of 300 P wave morphology can be helpful since retrograde P waves (negative in the inferior leads: II, III, and AVF) favor AVNRT and junctional tachycardia Finally, R-P relationship refers to the distance from the R wave to the next P wave during tachycardia If this distance is longer than the P-R interval, the SVT is termed “long R-P,” whereas if this distance is short, it is termed “short R-P” (Figure 20-2) A systematic approach to interpreting the 12-lead electrocardiogram (ECG) will allow accurate determination of the type of SVT in most cases (Figure 20–1) The first step is to determine whether the rhythm is regular or irregular If it is irregular, the rhythm is likely either atrial fibrillation, atrial flutter with variable conduction, or multifocal atrial tachycardia (MAT) The appearance of the P waves will usually distinguish between these three entities In atrial fibrillation, there is chaotic atrial activity In atrial flutter, P waves are seen at rate of 240–320 bpm In MAT, there are P waves preceding each QRS complex, and there are at least three different P wave morphologies If the SVT is regular, there are several different types of SVT to consider The SVT could be sinus tachycardia, sinus node reentry, atrial flutter, atrial tachycardia, AV nodal reentrant tachycardia (AVNRT), junctional tachycardia, or atrioventricular reciprocating tachycardia (AVRT) The type of regular SVT can be usually identified by examining four aspects of the 12-lead ECG: (1) onset and termination, (2) heart rate, (3) P wave morphology, and (4) R-P relationship The onset and termination can be sudden or gradual Sinus tachycardia and junctional tachycardia typically have very gradual onset whereas the other SVTs usually start and stop more suddenly SINUS TACHYCARDIA & SINUS NODE REENTRY Sinus Tachycardia ESSENTIALS OF DIAGNOSIS ᮣ ᮣ ᮣ ᮣ Onset and termination: Gradual Heart rate: 100 to (220 – age) bpm P wave: Identical to normal sinus rhythm P wave R-P relationship: Long AF No discrete P waves SVT Irregular MAT Three or more P waves Regular AFL (with variable conduction) Flutter waves ST Onset and termination Gradual Heart rate (bpm) 100–(220 – age) Sudden Sudden Sudden Sudden JT (Accelerated AV junction rhythm) Gradual 100–160 Multiple of 300 100–180 120–200 70–120 140–250 SN reentry AFL AT AVNRT AVRT Sudden P wave Sinus Ps Sinus Ps Flutter waves Ectopic Ps Retrograde Ps Retrograde Ps Ectopic Ps R-P relationship Long R-P Long R-P Undefined Long R-P Short R-P or no P Short R-P or no P Short R-P ▲ Figure 20–1 Algorithm for distinguishing supraventricular tachycardias AF, atrial fibrillation; AFL, atrial flutter; AT, atrial tachycardia; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reciprocating tachycardia; JT, junctional tachycardia; MAT, multifocal atrial tachycardia; SN, sinus node; ST, sinus tachycardia; SVT, supraventricular tachycardia ᮢ SUPRAVENTRICULAR TACHYCARDIAS 237 ᮣ General Considerations When the sinus node fires at a rate of more than 100 bpm, the rhythm is, with one exception, considered sinus tachycardia (see section on Sinus Node Reentry) The onset and termination of sinus tachycardia is invariably gradual The range for heart rate in sinus tachycardia is 100 to (220 – age) bpm; faster rates usually imply a different cause Confirming that the tachycardic P waves are identical in morphology and axis to the normal sinus rhythm P waves is essential to the diagnosis Like normal sinus rhythm, the R-P relationship in sinus tachycardia is typically long R-P, unless the patient has a very long P-R interval seen on the baseline ECG Sinus tachycardia is usually a physiologic response, activated when the body requires a higher heart rate to meet metabolic demands or maintain blood pressure Common causes are exercise, hypotension, hypoxemia, heart failure, sepsis, fever, hyperthyroidism, fluid depletion, and blood loss The heart rate achieved is proportional to the intensity of the stimulus, but the rapidity with which the heart rate increases and decreases is a function of how quickly the stimulus is applied and withdrawn ᮣ Treatment Vagal maneuvers slow the tachycardia gradually but only while being performed; when the vagal stimulus is removed, the heart rate gradually returns to where it started Attempting to slow the heart rate pharmacologically can be detrimental because it counteracts the compensatory mechanism provided by the tachycardia Therefore, management is usually focused on treating the underlying cause of the sinus tachycardia R P Short R P R R Short Short R-P P Long P R R Long Long R-P ▲ Figure 20–2 Short R-P refers to a regular supraventricular tachycardia (SVT) where the R-P interval is shorter than the P-R interval Long R-P refers to a regular SVT where the R-P interval is longer than the P-R interval abruptly and responds to vagal maneuvers and pharmacologic interventions by terminating rather than slowing ᮣ Treatment The arrhythmia can be terminated quickly with intravenous adenosine, verapamil, or diltiazem, or via carotid massage Long-term treatment uses β-blockers and calcium channel blockers The largest reported series of patients treated with catheter ablation described success in all 10 patients No complications were reported Other smaller series described similar efficacy ATRIAL FLUTTER Sinus Node Reentry ESSENTIALS OF DIAGNOSIS ESSENTIALS OF DIAGNOSIS ᮣ ᮣ ᮣ ᮣ ᮣ Onset and termination: Sudden Heart rate: 100–160 bpm P wave: Identical to normal sinus rhythm P wave R-P relationship: Long ᮣ ᮣ ᮣ ᮣ Onset and termination: Sudden Heart rate: Usually a multiple of 300 P waves: Flutter waves at 250–340 bpm R-P relationship: Undefined due to flutter waves Prominent neck vein pulsations of about 300/min ᮣ General Considerations ᮣ General Considerations This uncommon rhythm accounts for less than 5% of SVTs It uses the sinus node or perinodal tissue as a critical part of the reentrant circuit, producing P waves identical to those seen during normal sinus rhythm The heart rate usually falls between 100 and 160 bpm Like sinus tachycardia, R-P relationship is typically long R-P Unlike sinus tachycardia, sinus node reentry is initiated by an ectopic beat rather than a physiologic stimulus and possesses the characteristics typical of a reentrant circuit It therefore begins and ends Atrial flutter is usually associated with organic heart disease and is second in frequency only to atrial fibrillation in postcoronary bypass surgery patients, with an incidence of up to 33% With a typical atrial rate of 300 bpm (range: 250–340), atrial flutter produces a “sawtooth” appearance (F waves) As is the case with atrial fibrillation (see Chapter 21), the ventricular rate depends on conduction through the AV node Unlike atrial fibrillation, the ventricular impulses are transmitted at some integer fraction of the atrial rate In rare circumstances, ᮢ 238 CHAPTER 20 1:1 conduction may occur Fixed 2:1 or 4:1 block is the usual scenario However, variable block can also occur, leading to one of the three types of irregular SVTs If flutter is suspected but F waves are not clearly visible, vagal maneuvers or pharmacologic agents, such as adenosine, can help unmask the flutter waves by enhancing the degree of AV block ᮣ Pathophysiology Atrial flutter occurs in a variety of forms; the most common is isthmus-dependent counterclockwise atrial flutter; followed by the isthmus-dependent clockwise atrial flutter; and then the atypical, nonisthmus-dependent variety The counterclockwise flutter is recognized electrocardiographically by negative F waves in leads II, III, and aVF; and positive F waves in V1 The single reentrant wavefront proceeds up the interatrial septum in a caudocranial direction, across the roof of the right atrium, down the lateral wall and across the inferior wall (Figure 20–3) Clockwise flutter, on the other hand, has positive F waves in leads II, III, and aVF; and negative F waves in lead V1 The reentrant circuit in this case moves in the reverse direction In both these types of atrial flutter, the atrial rates range between 250 and 340 bpm Right atrium Left atrium Crista terminalis Inferior vena cava Coronary sinus ᮣ Clinical Findings Symptoms attributable to atrial flutter are secondary to the ventricular response in addition to any underlying cardiac diseases Dizziness, palpitations, angina-type chest pain, dyspnea, weakness, fatigue and, occasionally, syncope may be the presenting symptoms In those patients with poor left ventricular function, overt congestive heart failure may ensue Clinical evaluation is similar to that described for atrial fibrillation (see Chapter 21), but underlying heart disease is detected more often with atrial flutter than with fibrillation ᮣ Prevention Several antiarrhythmic agents can prevent recurrences of atrial flutter It appears that both class Ia and Ic agents are effective Class III agents, such as sotalol and amiodarone, can also work very well Dofetilide, a newer class III agent, which blocks the rapid form of the delayed rectifier current, Ikr, has also been found effective in converting to and maintenance of sinus rhythm Its administration requires initiation in the hospital and a monitored setting Drugs that are contraindicated with its use include verapamil, ketoconazole, cimetidine, trimethoprim, prochlorperazine, megestrol, and hydrochlorothiazide With regard to safety, dofetilide has a proarrhythmic event rate of approximately 0.9%, which is less than the 3.3% seen in patients with congestive heart failure or the 2.5% in patients with previous ventricular tachycardia It should be emphasized that an AV nodal blocking agent should be started before initiating a class I drug If the AV node is unblocked, a type I agent could facilitate conduction of atrial flutter by improving nodal conduction or by slowing the flutter rate and paradoxically increasing the ventricular response Mitral annulus Superior vena cava Tricuspid annulus ▲ Figure 20–3 The reentry circuit of the common variety of atrial flutter (type II) The right and left atria are shown in the left anterior oblique projection The reentry circuit is confined to the right atrium and circulates in a counterclockwise direction within it (arrows) The area between the tricuspid annulus and the inferior vena cava is the critical isthmus that is targeted for ablation of this type of atrial flutter Also shown is a recording of counterclockwise atrial flutter in lead II, demonstrating the “sawtooth” pattern of flutter waves (rate, 250/min) characteristic of this type of atrial flutter (Reprinted, with permission, from Morady F N Engl J Med 1999;340:534 Copyright © 1999 Massachusetts Medical Society All rights reserved.) ᮣ Treatment A Conversion Once the diagnosis of atrial flutter is made, assessment of the patient’s status will dictate whether to perform cardioversion immediately Immediate cardioversion can be accomplished with synchronized DC cardioversion, rapid atrial pacing to interrupt the macroreentrant circuit, or intravenous infusion of an antiarrhythmic agent For DC cardioversion, as little as 25 J may be all that is required; however, at least 50 J is recommended to avoid extra shocks, and 100 J will terminate almost all episodes of atrial flutter The major drawback with DC cardioversion is the need to administer sedation Rapid atrial pacing is another method that may terminate the arrhythmia Pacing is best performed in the right atrium at a rate faster than the flutter rate, which allows the circuit to be entered by the pacing impulse If the extrinsic pacing rate exceeds the rate that can be sustained through the zone of slow conduction, the flutter wavefront can be interrupted and will no longer be present when the pacing is stopped If the patient has a pacemaker or implantable cardiac defibrillator with an atrial lead, pace termination can be done painlessly via the device An alternative method uses a swallowed transesophageal electrode Because of the interposed tissue, a high current is often necessary to capture and pace the atrium reliably, which may cause significant discomfort to the patient Of note, overdrive pacing may precipitate atrial fibrillation, which usually terminates spontaneously after several minutes Should the atrial fibrillation persist, however, it usually is easier to control the ventricular response when compared with atrial flutter Finally, rapid pharmacologic cardioversion can be considered with intravenous agents such as ibutilide Ibutilide is a unique class III antiarrhythmic agent with a rate of conversion of approximately 60% in patients with atrial flutter of less than 45 days duration Cardioversion can be expected within 30 minutes of administration The major complication with this agent is the development of torsades de pointes, which can occur in up to 12.5% of patients, with 1.7% requiring cardioversion for sustained polymorphic ventricular tachycardia These occur primarily within the first hour after administration Procainamide is another intravenous agent that can be given to pharmacologically convert atrial flutter B Rate Control In general, controlling the ventricular rate in atrial flutter is more difficult than in atrial fibrillation β-Blockers and calcium channel blockers are moderately effective in controlling the rate Digoxin is less helpful since it only weakly blocks the AV node conduction Intravenous amiodarone has been shown to be at least as efficacious as digoxin C Catheter Ablation and Other Modalities The reentrant circuit in typical atrial flutter has been successfully mapped and includes an area of slow conduction called the isthmus, which is bound by the tricuspid annulus, the inferior vena cava, and the os of the coronary sinus (Figure 20–3) Ablation in the isthmus region interrupts the reentrant circuit and has been shown to be highly efficacious (90– 100%) in permanently eliminating atrial flutter In costeffective analysis, ablation appears to be the preferred approach over cardioversion and pharmacologic prevention Non–isthmus-dependent atypical atrial flutters can be more difficult to ablate However, with current three-dimensional mapping systems (electroanatomic and noncontact high ᮢ SUPRAVENTRICULAR TACHYCARDIAS 239 resolution) even these types of atrial flutter are being ablated with high success rates If attempts to cure flutter fail, the ventricular rate can be controlled by transcatheter ablation of the AV node or His bundle With a long-standing flutter, there may be a subsequent improvement in left ventricular function D Stroke Prophylaxis Whether atrial flutter is the source of peripheral embolization and stroke is an unsettled issue because most of the published studies pool their data from patients with atrial flutter and fibrillation, and most studies are retrospective in design However, mounting evidence indicates that the risk of embolic stroke is more significant than previously thought In addition, many patients have bouts of both atrial fibrillation and flutter, thereby necessitating aspirin or anticoagulant therapy The current recommendation is to treat patients with atrial flutter just as atrial fibrillation in terms of stroke prophylaxis Calkins H et al Results of catheter ablation of typical atrial flutter Am J Cardiol 2004 Aug 15;94(4):437–42 [PMID: 15325925] Ellenbogen KA et al Efficacy of intravenous ibutilide for rapid termination of atrial fibrillation and atrial flutter: a dose dependent study J Am Coll Cardiol 1996 Jul;28(1):130–6 [PMID: 8752805] Falk RH et al Dofetilide: a new pure class III antiarrhythmic agent Am Heart J 2000 Nov;140(5):697–706 [PMID: 11054613] Feld G et al Radiofrequency catheter ablation of type atrial flutter using large-tip 8- or 10-mm electrode catheters and a high-output radiofrequency energy generator: results of a multicenter safety and efficacy study J Am Coll Cardiol 2004 Apr 21;43(8):1466–72 [PMID: 15093885] Nakagawa H et al Characterization of reentrant circuit in macroreentrant right atrial tachycardia after surgical repair of congenital heart disease: isolated channels between scars allow “focal” ablation Circulation 2001 Feb 6;103(5):699–709 [PMID: 11156882] MULTIFOCAL ATRIAL TACHYCARDIA ESSENTIALS OF DIAGNOSIS ᮣ ᮣ ᮣ Heart rate: Up to 150 bpm P waves: Three or more distinct P waves in a single lead Variable P-P, P-R, and R-R intervals ᮣ General Considerations Multifocal atrial tachycardia is an irregular SVT that constitutes less than 1% of all arrhythmias It is related to pulmonary disease in 60–85% of cases, with chronic obstructive pulmonary disease (COPD) exacerbation being the most common In addition, MAT is precipitated by respiratory failure, acute decompensated cardiac function, and infec- ᮢ 240 CHAPTER 20 tion It has also been reported to be associated with hypokalemia, hypomagnesemia, hyponatremia, pulmonary embolism, cancer, and valvular heart disease, as well occurring in the postoperative setting It occurs in children and adults Distention of the right atrium from elevated pulmonary pressures causes multiple ectopic foci to fire, with ventricular rates not usually exceeding 150 bpm Whether this rhythm is due to abnormal automaticity or triggered activity is uncertain, but the ability of verapamil to suppress the ectopic atrial activity by virtue of its calcium-channel-blocking properties supports the latter assumption Three ECG criteria must be met to diagnose MAT (Figure 20–4): (1) The presence of at least three distinct P wave morphologies recorded in the same lead (2) The absence of one dominant atrial pacemaker (3) Varying P-P, P-R, and R-R intervals Multifocal atrial tachycardia is often misdiagnosed as atrial fibrillation Although both are irregular, the former has distinct P waves with an intervening isoelectric baseline In fact, MAT may progress to atrial fibrillation ᮣ Treatment The primary treatment for MAT should be directed at the underlying disease state Oral and intravenous verapamil and several formulations of intravenous β-blockers have been effective to varying degrees in either slowing the heart rate (without terminating the rhythm) or in converting the arrhythmia to sinus rhythm Intravenous magnesium and potassium, even in patients with serum levels of these electrolytes within the normal range, convert a significant percentage of these patients to sinus rhythm Digoxin is not effective in treating this condition Moreover, treatment with digoxin may precipitate digitalis intoxication In addition, if the arrhythmia is secondary to delayed after-depolarizations, further aggravation may occur with digitalis because this drug increases delayed after-depolarizations Medications that cause atrial irritability, such as theophylline and βagonists, should be withdrawn whenever possible Application of radiofrequency energy for both AV node modification and AV node ablation with subsequent implantation of a pacemaker have been reported The numbers of patients in the studies were very small, and there are no long-term results Nevertheless, ablation of the AV junction has been shown to reduce symptomatic MAT, resulting in improved quality of life, reduced hospital admissions for recurrent symptomatic MAT, and improved left ventricular function ᮣ Prognosis Because of the severity of the precipitating underlying diseases, MAT portends a poor outcome Mortality during the hospitalization when the arrhythmia is first diagnosed is between 30% and 60%, with death being attributed to the disease state rather than the tachycardia itself In one study of patients with pulmonary disease who were admitted for acute respiratory failure, the in-hospital mortality rate for those with MAT was 87%, compared with 24% for those in a different rhythm Bradley DJ et al The clinical course of multifocal atrial tachycardia in infants and children J Am Coll Cardiol 2001 Aug;38(2):401– [PMID: 11499730] Ueng KC et al Radiofrequency catheter modification of atrioventricular junction in patients with COPD and medically refractory multifocal atrial tachycardia Chest 2000 Jan;117(1):52–9 [PMID: 10631199] ATRIAL TACHYCARDIA ESSENTIALS OF DIAGNOSIS ᮣ ᮣ ᮣ ᮣ Onset and termination: Sudden Heart rate: 100–180 bpm P wave: Distinct P waves that differ from sinus P waves R-P relationship: Long ▲ Figure 20–4 Multifocal atrial tachycardia The presence of at least three distinct P-wave morphologies, the absence of one dominant pacemaker focus, and varying P-P, R-R, and PR intervals establish the diagnosis (Reprinted, with permission, from Goldberger A, Boldberger E Clinical Electrocardiography A Simplified Approach St Louis: Mosby Year Book, 1990.) ᮣ General Considerations Atrial tachycardia originates from an ectopic site in the atrium and, therefore, the P waves are usually quite different than the sinus P waves It has been demonstrated that these arrhythmias arise from well-defined anatomic regions, including the crista terminalis, the tricuspid and mitral annuli, the right and left atrial appendage, and the region within or surrounding the pulmonary veins In situations where the P wave is identical to the sinus P wave, the SVT is usually designated to be sinus node reentry or sinus tachycardia The onset of atrial tachycardia is typically sudden; however, there can be some acceleration at the beginning, which is called the “warm-up” phase Rates can range from 100 bpm to 180 bpm The R-P relationship is usually long, unless there is a very long P-R interval, which can sometimes be appreciated on the baseline ECG The episodes may either be brief and self-terminating or chronic and persistent, eventually leading to a tachycardia-induced cardiomyopathy if left untreated Short nonsustained bursts of atrial tachycardia can be seen in 2–6% of young adults on Holter evaluations In those patients with paroxysmal sustained atrial tachycardia, there is a higher likelihood of associated organic heart disease, including coronary artery disease, valvular heart disease, congenital heart disease, and other cardiomyopathies Frequently, a transient automatic tachycardia will be present, the cause of which can usually be determined from the associated clinical setting Some of the most frequent causes include acute myocardial infarction, in which case it is seen in 4–19% of patients, electrolyte disturbances (especially hypokalemia), chronic lung disease or pulmonary infection, acute alcohol ingestion, hypoxia, and use of cardiac stimulants (theophylline, cocaine) Short, unsustained bursts of paroxysmal atrial tachycardia that last only a few seconds can be seen in adults without concomitant heart disease The form that occurs almost exclusively, and not uncommonly, in children, is a continuous tachycardia with heart rates of about 175 bpm Symptoms are severe, and congestive heart failure frequently develops as a result of a tachycardia-induced cardiomyopathy The arrhythmia may be transient in younger children, but when it persists in older children, it should be considered permanent Fortunately, if the tachycardia can be terminated, cardiac function returns to normal When it appears in adults, the continuous variety manifests milder symptoms Atrial tachycardias may have an automatic, triggered, or microreentrant mechanism Although precisely defining the basic mechanism of a particular atrial tachycardia may be difficult, understanding their basic principles may help with choosing therapy ᮣ Treatment A Pharmacologic Therapy Although there are no large-scale trials in the medical treatment of atrial tachycardias, reported data show that β-blockers ᮢ SUPRAVENTRICULAR TACHYCARDIAS 241 and calcium channel blockers are at least partially effective, particularly if the underlying mechanism of the tachycardia is abnormal automaticity or triggered activity Because of their safety profile, these drugs are usually first-line medical therapy Other antiarrhythmic drugs may be effective in treating some patients with atrial tachycardias However, there are no large-scale trials comparing the drugs or even trials comparing drugs to placebo Therefore, drug therapy is largely empiric and drug choice is determined more by side-effect profile and risk of proarrhythmia than by suspected efficacy The use of class IC antiarrhythmic drugs may be somewhat successful Flecainide and propafenone are often well tolerated in patients without structural heart disease and thus can be considered a reasonable first-line antiarrhythmic therapy Quinidine and procainamide are less well tolerated Class Ib agents are generally not effective for atrial tachycardias; however, there may be a small subset of lidocaine-sensitive atrial tachycardias in which mexilitine may be effective Sotalol may also be effective, in part because of its inherent β-blocker (class II) properties It is generally better tolerated than quinidine and may provide rate control during recurrences Nevertheless, because sotalol also has class III properties, it will prolong the QT interval and may predispose patients to torsades de pointes, similar to quinidine and procainamide Amiodarone may be effective, especially in resistant tachycardias In addition, it is the least proarrhythmic and is generally used as first-line drug therapy in patients with depressed left ventricular function Newer class III drugs, such as dofetilide, may be effective for atrial tachycardias, but there is little data about their use in atrial arrhythmias, except atrial fibrillation and atrial flutter B Ablation Ablation for atrial tachycardias has been proven safe and effective, with reported success rates between 77% and 100% It also has been shown to improve patient quality of life scores Therefore, ablation should be indicated for all symptomatic patients who have persistent symptoms despite medical therapy or intolerable side effects from medicines Furthermore, patients who are not willing to undergo medical therapy should also be considered Recently, the use of electromagnetic and noncontact mapping systems has significantly improved ablative therapy by decreasing fluoroscopic time, mapping time, and number of radiofrequency applications, thereby increasing efficacy Kalman JM et al Localization of focal atrial tachycardias–back to the future when (old) electrophysiologic first principles complement sophisticated technology J Cardiovasc Electrophysiol 2007 Jan;18(1):7–8 [PMID: 17240545] Natale A et al Ablation of right and left atrial tachycardias using a three-dimensional nonfluoroscopic mapping system Am J Cardiol 1998 Oct 15;82(8):989–92 [PMID: 9794361] Sanders P et al Characterization of focal atrial tachycardia using high-density mapping J Am Coll Cardiol 2005 Dec 6;46(11): 2088–99 [PMID: 16325047] ᮢ 242 CHAPTER 20 Scheinman MM et al The 1998 NASPE prospective catheter ablation registry Pacing Clin Electrophysiol 2000 Jun;23(6):1020–8 [PMID: 10879389] Schmitt H et al Diagnosis and ablation of focal right atrial tachycardia using a new high-resolution, non-contact mapping system Am J Cardiol 2001 Apr 15;87(8):1017–21 [PMID: 11306000] ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA ESSENTIALS OF DIAGNOSIS ᮣ Onset and termination: Sudden ᮣ Heart rate: Usually 120–200 bpm but can be faster; neck pulsations correspond to heart rate P waves: Retrograde P waves; P waves not visible in 90% of cases R-P relationship: Short, if P waves visible ᮣ ᮣ ᮣ General Considerations Atrioventricular nodal reentrant tachycardia is more common in women than in men Heart rates usually fall in the range of 120–200 bpm, although rates up to 250 bpm have been recorded Palpitations are almost universally reported A feeling of diuresis, noted with other supraventricular arrhythmias, is significantly more common in AVNRT and has been correlated with elevated right atrial pressures and elevated atrial natriuretic peptide Neck pulsations are common (Brugada phenomenon) and are secondary to simultaneous contraction of the atria and ventricles against closed mitral and tricuspid valves Dizziness and lightheadedness can occur but frank syncope is very rare Sudden death has been reported but is extremely rare Although symptoms may occur at any age, the distribution of when the tachycardia and symptoms commonly appear appears to be bimodal The initial episode may begin during the second decade of life, only to disappear and then reappear during the fourth and fifth decades of life ᮣ Pathophysiology Conduction from the right atrium to the ventricles is normally over a singular AV nodal pathway, with no route of reentry back into the atrium In persons with dual AV nodal pathways, an atrial impulse may travel antegrade from the atrium over one limb of the AV node and then back to the atrium over another limb in a retrograde fashion When only one cycle occurs, a single echo beat, in the form of a retrograde P wave, may be seen on the ECG If this echo beat can again penetrate the AV node antegrade, the cycle can perpetuate itself, leading to AVNRT It is estimated that dual AV nodal pathways exist in up to one-fourth of the population, but only a fraction of these people ever manifest a tachycardia If each limb of the circuit conducted impulses equally, echo beats and sustained AVNRT would not occur An atrial impulse traveling down both limbs at the same speed would cause each limb to be refractory when that impulse reached the bottom of the node, preventing the impulse in each limb from going back up the other Instead, the limbs have varying conduction speeds (Figure 20–5A) and refractory periods The faster conducting limb, called the β or fast pathway, has a longer refractory period, whereas the reverse is true for the second limb, called the α or slow pathway A premature atrial depolarization may initiate the tachycardia if it finds the fast pathway refractory; the premature impulse can then reach the ventricles through the slow pathway The ECG manifestation of this is a P-R interval that exceeds the baseline P-R by as much as 50–300% of its value in sinus rhythm At the same time that it enters the His– Purkinje system and the ventricles, the slow pathway impulse heads retrograde up the fast pathway, where it may block (Figure 20–5B) or continue to produce an atrial echo beat with a retrograde P wave and a short R-P interval If the slow pathway cannot propagate another impulse antegrade because of refractoriness, only a single atrial echo beat will occur (Figure 20–5C) If the slow pathway has recovered excitability, the circuit can again be entered Perpetuation of this cycle will lead to a sustained episode of AVNRT (Figure 20–5D) Ventricular ectopic beats can also initiate AVNRT by a similar mechanism Conduction up the fast pathway is usually so rapid that retrograde atrial depolarization is simultaneous or almost simultaneous with antegrade ventricular activation This causes the low-amplitude P wave to become obscured in the much higher amplitude QRS complex Therefore, the P wave is not visible 50–60% of the time In 20–30% of cases, the P wave distorts the terminal portion of the QRS causing a pseudo-S wave in the inferior leads and a pseudo-R' in lead V1, and in approximately 10% of cases the P wave distorts the initial portion of the QRS complex (Figure 20–6) Since the P wave usually occurs simultaneous to or just after the QRS, the common variety of AVNRT is a short R-P tachycardia The common type of AVNRT that is described above is also called slow–fast AVNRT “Slow-fast” refers to the antegrade and retrograde limbs of conduction during the tachycardia, respectively Distinctly more unusual, or fast–slow AVNRT, is seen in approximately 5–10% of cases Here the slow pathway has the longer refractory period, which causes it to become blocked antegrade and then to be used as the return path to the atrium In contrast, to slow-fast AVNRT, which is short R-P, fast-slow AVNRT is usually long R-P A third and even rarer variety of AVNRT is the slow–slow form in which the retrograde limb is slower than most typical slow pathways, leading to P waves midway between the QRS complexes Therefore, this type of AVNRT can be long or short R-P AVNRT, once initiated, can perpetuate itself without the participation of either the atria or ventricles Therefore, on rare occasions, the tachycardia can occur with a 2:1 block in ᮢ 560 Hypertrophic cardiomyopathies (cont.) cardiac catheterization, 169 chest radiography, 167 ECG, 167 echocardiography, 167–168, 167t, 168f diastolic function in, 165 essentials of diagnosis, 164 future prospects, 171 overview, 164 pathophysiology, 164–165 in pregnancy, 453–454 prognosis, 170–171 sudden cardiac death due to, 328–329, 328t systolic function in, 165 treatment, 169–170, 169t cardioverter defibrillation implantation, 170 chemical myectomy, 170 medical management, 169–170, 169t overview, 169, 169t pacemaker implantation, 169t, 170 surgical myectomy, 169t, 170 Hypertrophy, left ventricular, in HFpEF, 223 Hyperventilation, psychiatric disorders and, syncope vs., 324 Hypoparathyroidism, 473–474 Hypoplastic left heart, 414 Hypotension cardiogenic shock and, 76–77 orthostatic, syncope due to, 316t, 317– 318 Hypothyroidism, 468–470, 470t causes, 469, 470t clinical findings, 468–469 diagnostic studies, 469, 470t essentials of diagnosis, 468 laboratory findings, 469, 470t overview, 468 pericarditis and, 191 physical examination, 469 prognosis, 470 symptoms and signs, 468–469 treatment, 470 Hypoxia pulmonary hypertension with, 354f, 355–356 treatment, 370 syncope vs., 323 Ibutilide for atrial fibrillation, 263–264 for SVTs, 234t ICDs See Implantable cardioverter defibrillators (ICDs) Idiopathic dilated cardiomyopathy, monomorphic VT and, 304–305, 305f Idiopathic dilation of pulmonary trunk, pulmonic regurgitation due to, 135 Idiopathic left ventricular tachycardia, 307, 308f INDEX Idiopathic restrictive cardiomopathy, 173, 173t Iloprost, for PAH, 366, 368t Imaging, in acute myocardial infarction, 55 Imaging studies See specific types, e.g., Chest radiography Immune disease, infective endocarditis due to, 138 Implantable cardioverter defibrillators (ICDs) in cardiac arrest survivors management, 333–335, 335t, 336t in CHF management, 218–219, 218t components, 334 contraindications, 334–335, 336t historical background, 334 indications, 334, 336t long-term anticoagulation with, effects, 429–430 for monomorphic ventricular tachycardia, 311 in perioperative patients, management, 543–544 Impulse(s), apical, in aortic stenosis, 85 In vitro sensitivity testing, in antibiotic therapy for infective endocarditis, 147–148 Inborn errors of metabolism, restrictive cardiomyopathies due to, 173, 173t Infarction(s) myocardial acute, 51–72 See also Acute myocardial infarction defined, 52, 52t inferior, following myocardial infarction, 67 pericarditis and, 190 right ventricular after cardiogenic shock management, 80–81 cardiogenic shock due to, 75 following myocardial infarction, 69 Infective endocarditis, 137–152 causes, 137–142, 139t–141t cardiac infection, 137–138 clinical syndromes, 138–142, 139t– 141t enterococcal endocarditis, 140 extracardiac disease, 138 fungal endocarditis, 140, 140t gram-negative bacteria, 140 HIV, 141 hospital-acquired endocarditis, 142 injection drug use, 141 pacemaker endocarditis, 142 prosthetic valve endocarditis, 140– 141, 141t Staphylococcus aureus endocarditis, 139 viridans streptococcal endocarditis, 139 characteristics, 139, 139t clinical findings, 142–144, 143t abdominal, 144 cardiac, 144 fever, 143–144, 143t neurologic, 144 physical examination, 143–144, 143t skin and extremities, 144 symptoms and signs, 143, 143t congenital heart disease and, 371, 372t diagnostic criteria, 142 diagnostic studies, 144–147, 145t, 146t chest radiography, 147 detection of blood-borne infection, 144–145, 145t ECG, 148 echocardiography, 145–147, 146t serolotic testing, 145 TEE, 145–146, 146t TTE, 147 embolic events in, incidence, 426 essentials of diagnosis, 137 management, 147–152, 151t antibiotic therapy, 147–149 See also Antibiotic(s), for infective endocarditis complications, 149–150 embolism, 150 failure of antibiotic therapy, 149 mycotic aneurysm, 150 myocardial infarction, 150 pericarditis, 150 worsening valve dysfunction and heart failure, 149–150 follow-up after, 151–152 fungal endocarditis, 151 gram-negative bacteria in, 151 high-risk endocarditis, 150–151, 151t initial decisions, 147 surgery, 151, 151t overview, 137 pathophysiology, 137–142, 139t–141t in pregnancy, 452 prevention, in pregnancy, 462 pulmonic regurgitation due to, 135 treatment, long-term anticoagulation, 426 Inferior vena caval filters, for pulmonary embolic disease, 349 Infiltrative cardiomyopathy, defined, 172 Inherited arrhythmia syndromes, sudden cardiac death due to, 328t, 329–330 Inotrope(s) for acute myocardial infarction, 58t in CHF management, 212t, 213–214 Inotropic agents for cardiogenic shock after acute myocardial infarction, 78t, 79 in CHF management, 212t, 213–214 Interferon(s), cardiac toxicity from, 443t Interleukin-2, cardiac toxicity from, 443t, 444 Internal atrial defibrillator, for atrial fibrillation, 265–266 Intra-aortic balloon counterpulsation, for unstable angina, 49 Intravascular pressure, in normal pregnancy, 447, 447t Intravascular thrombi, pathogenesis, 418– 419 Intravascular volume, increased, in HFpEF, 222–223 Invasive electrophysiology studies, in syncope, 322–323 Iodide(s), for hyperthyroidism, 467t Iodine, radioactive, for hyperthyroidism, 467t, 468 Ipodate, for hyperthyroidism, 467t Irbesartan, for HFpEF, 229–230 Ischemia(s), myocardial See Myocardial ischemia Ischemia, recurrent, following myocardial infarction, 66 Ischemic heart disease, chronic, 25–37 See also Chronic ischemic heart disease Ischemic strokes, cardioembolic, 419 Isometric hand grip exercises, Isoproterenol, for cardiogenic shock after acute myocardial infarction, 79 Isosorbide dinitrate in CHF management, 212t, 214, 215 for chronic ischemic heart disease, 32t Isosorbide mononitrate, for chronic ischemic heart disease, 32t Isotope perfusion scans, in cardiac arrest survivors with structural heart disease, 332 Isradipine, for chronic ischemic heart disease, 32t Isthmus, 238f, 239 Janeway lesions, in infective endocarditis, 144 Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure, 157 Jugular venous pressure, in cardiac tamponade, 196 Jugular venous pulse, in tricuspid valve disease, 124, 125f– 127f Jugular venous waveform, in pulmonic valve disease, 135 Junctional tachycardia (accelerated AV junctional rhythm), 236f, 246 Kussmaul sign, 130 Labetalol, for hypertensive emergencies, 163t Labor and delivery, cardiovascular disease in patients during, 462–463 Laplace equation, 83 LDL goals for, in lipid disorders treatment, 17–18, 17t–19t, 19f lipid disorders and, 15, 15f Left atrial cavity, exercise training effects on, 512 Left atrial tumors, physical examination, 438 Left heart catheterization, in cardiogenic shock, 78, 78t Left ventricle, double-inlet, 414 Left ventricular aneurysm, treatment, longterm anticoagulation, 428 Left ventricular cavity, exercise training effects on, 510 Left ventricular cine-angiography, in hypertrophic cardiomyopathies, 169 Left ventricular enlargement, in HFpEF, 222–223 Left ventricular hypertrophy, in HFpEF, 223 Left ventricular mass, exercise training effects on, 512 Left ventricular thrombus, treatment, longterm anticoagulation, 427– 429 Left ventricular tumors, physical examination, 438 Left ventricular wall thickness, exercise training effects on, 510 Left-sided heart disease, pulmonary hypertension with, 354f, 355 treatment, 369–370 Left-sided heart failure, 205 Lesion(s) Janeway, in infective endocarditis, 144 obstructive valvular, severe symptomatic, in pregnancy, 448t precursor, bacteremia and, 137 Libman-Sacks endocarditis, 485 Lidocaine for acute myocardial infarction, 58t in pregnancy, 461t Lipid disorders, 14–24 apolipoproteins, 14–15, 15f, 16f clinical findings, 16–17 laboratory assessment, 17 patient history, 16 physical examination, 16–17 dietary fats and, 14 essentials of diagnosis, 14 genetics, 15 HDL and, 15, 15f LDL and, 15, 15f lipoproteins, 14–15, 15f, 16f lipoprotein(a), 15 metabolism of, 14, 16f overview, 14–15, 15f, 16f treatment, 17–24, 17t–20t, 19f, 22t diet, 20–21 exercise, 21 LDL goals, 17–18, 17t–19t, 19f lipid-lowering drugs, 21–24, 22t See also Lipid-lowering drugs for lipoprotein(a), 19–20 for low HDL, 19–20 ᮢ INDEX 561 non-HDL goals, 18–19, 20t, 21t nonpharmacologic therapy, 20–21 pharmacologic agents, 21–24, 22t See also Lipid-lowering drugs referral, 24 Lipid-lowering drugs, 21–24, 22t bile acid sequestrants, 21, 22t cholesterol absorption inhibitors, 21, 22t combination drug therapy, 23–24 fibrates, 21–22, 22t niacin, 22–23, 22t omega-3-fatty acids, 21, 22t statins, 22t, 23 Lipoma(s), 433t, 434–435 Lipoprotein(a), 15 treatment, 19–20 Lipoprotein(s), 14–15, 15f, 16f See also Lipid disorders classification, 14, 15f high-density See High-density lipoprotein low-density goals for, in lipid disorders treatment, 17–18, 17t–19t, 19f lipid disorders and, 15, 15f metabolism, 14, 16f Lithium, for hyperthyroidism, 467t LMWH See Low-molecular-weight heparin (LMWH) Loeys-Dietz syndrome, in pregnancy, 457– 458 advice against, 448t Löffler cardiomyopathy, restrictive cardiomyopathies due to, 173, 173t Lone fibrillation, 259 Long QT syndrome (LQTS) acquired, causes, 312, 313t congenital, 311–312, 312f, 313t, 314f sudden cardiac death due to, 328t, 329–330 Loop diuretics, in CHF management, 212t, 212–212 Low-density lipoprotein (LDL) goals for, in lipid disorders treatment, 17–18, 17t–19t, 19f lipid disorders and, 15, 15f Low-molecular-weight heparin (LMWH) for acute myocardial infarction, 57, 58t in long-term anticoagulation, 417 for pulmonary embolic disease, 347, 348t, 349t for unstable angina, 45t, 46 Low-output heart failure, 205 Low-pressure cardiac tamponade, 196 Lugol, for hyperthyroidism, 467t Lung(s), evaluation, Lung biopsy, in pulmonary hypertension, 362–363, 363f Lung diseases, pulmonary hypertension with, 354f, 355–356 treatment, 370 ᮢ 562 Lung scanning, radionuclide, in pulmonary embolic disease, 341, 341f Lung scintigraphy in pulmonary hypertension, 260, 262, 262f ventilation-perfusion, in pulmonary hypertension, 260, 262, 262f Lyme myocarditis, 185 Lymphoma(s), 433t, 436–437 Magnesium, for acute myocardial infarction, 58t Magnetic resonance angiography (MRA) in coarctation of aorta, 391, 392f in congenital aortic valvular disease, 375 Magnetic resonance imaging (MRI), 10 in aortic regurgitation, 102 in cardiac arrest survivors with structural heart disease, 332 in cardiac tumors, 440, 440f in chronic ischemic heart disease, 28, 29 in congenital aortic valvular disease, 375 in constrictive pericarditis, 198–199 in HFpEF, 225t, 228 in intracardiac thrombi, 420 in mitral stenosis, 109 in myocarditis, 181 in pericardial effusion, 195 in pericarditis, 488, 500 in pheochromocytoma, 475 in pregnancy, 460 in pulmonary hypertension, 362 in rheumatoid pericarditis, 493 in tetralogy of Fallot, 403 in thoracic aortic aneurysms, 524, 524f in thoracic aortic dissection, 532 in tricuspid atresia, 412 Malignancy, pericarditis related to, 190 Malignant arrhythmias, in acute myocardial infarction, 70 Marfan disease, genetics, 516, 518f Marfan syndrome in pregnancy, 457 advice against, 448t pulmonic regurgitation due to, 135 Matrix metalloproteinases (MMPs), in thoracic aortic aneurysms, 519, 520f Maze procedure, for atrial fibrillation, 266 Mechanical complications, after cardiogenic shock management, 80 Mechanical prosthetic heart valves in aortic valve replacement, 91–92 treatment, long-term anticoagulation, 426–427, 427t Mediterranean Diet, increased HDL levels due to, 21 Mesothelioma(s), 433t, 437 Metabolic disorders ECG of, syncope vs., 323 INDEX Metabolism inborn errors of, restrictive cardiomyopathies due to, 173, 173t lipoprotein, 14, 16f Metaprolol, for chronic ischemic heart disease, 32t Methimazole, for hyperthyroidism, 467, 467t Metolazone, in CHF management, 211 Metoprolol for acute myocardial infarction, 58t for heart rate control in atrial fibrillation, 261t for hyperthyroidism, 467t for syncope, 324t Metoprolol succinate, for HFpEF, 230–231 Mexiletine, in pregnancy, 461t Micturition syncope, 316t, 317 Midodrine, for syncope, 324t Minoxidil in CHF management, 214 for systemic hypertension, 158t, 161 Miodarone for maintaining sinus rhythm in atrial fibrillation, 261t, 262f in pregnancy, 461t for SVTs, 234t thyrotoxicosis due to, features, 471– 472, 471t Mitoxantrone, cardiac toxicity from, 443t Mitral aortic valve conditions, treatment, long-term anticoagulation, 426 Mitral regurgitation, 113–121 acute, 114 following myocardial infarction, 65 physical examination, 115–116 symptoms and signs, 114 causes, 113–114, 114t chronic, 113–114 physical examination, 114–115, 115f, 115t symptoms and signs, 114 clinical findings, 114–116, 115f, 115t physical examination, 114–116, 115f, 115t symptoms and signs, 114 diagnostic studies, 116–118, 117t cardiac catheterization, 118 chest radiography, 116 ECG, 116 echocardiography, 116–118, 117t differential diagnosis, 118–119 essentials of diagnosis, 113 in mixed valvular disease, physical examination, 116 overview, 113–114, 114t in pregnancy, 450 prognosis, 121 treatment, 119–121, 120t pharmacologic agents, 119 surgery, 119–121, 120t Mitral stenosis, 106–112 causes, 106, 107t clinical findings, 107–108 physical examination, 107–108 symptoms and signs, 107 diagnostic studies, 108–109 cardiac catheterization, 109 chest radiography, 108 ECG, 108 echocardiography, 108–109 MRI, 109 TEE, 108–109 essentials of diagnosis, 106 overview, 106, 107t prognosis, 112 treatment, 110–112 percutaneous mitral balloon valvotomy, 110–111 pharmacologic agents, 110 surgical, 111 Mitral valve disease ankylosing spondylitis and, 504 in pregnancy, 450 rheumatic, treatment, long-term anticoagulation, 425 Mitral valve prolapse in pregnancy, 450 treatment, long-term anticoagulation, 426 Mitral valve regurgitation, acute, following myocardial infarction, 65 Mitral valve replacement, for mitral stenosis, 111 Mixed connective tissue disease, 505–506 Mixed pulmonary hypertension, 355 M-mode echocardiography, in mitral stenosis, 108 MMPs, in thoracic aortic aneurysms, 519, 520f Mobitz II second-degree AV block, following myocardial infarction, 67 Monomorphic ventricular tachycardia, 301f, 303 in arrhythmogenic right ventricular cardiomyopathy, 305–306, 306f chronic coronary artery disease and, 302f, 304 in congenital heart disease, 306 idiopathic dilated cardiomyopathy and, 304–305, 305f management, 310–311, 310t catheter ablation, 311 immediate termination, 310 nonpharmacologic therapy, 311 pharmacologic agents, 310–311, 310t surgical ablation, 311 prevention, 310 in structural heart disease, 306–307 sudden cardiac death due to, 330 Morphine, for acute myocardial infarction, 56, 58t MRA in coarctation of aorta, 391, 392f in congenital aortic valvular disease, 375 MRI See Magnetic resonance imaging (MRI) Multifocal atrial tachycardia, 236f, 239– 240, 240f Mural thrombi, following myocardial infarction, 68–69 Murmur(s), 5–7, 6t continuous, diastolic, Graham Steell, 108 holosystolic, pansystolic, systolic, differentiation of, 6, 6t systolic ejection, in aortic stenosis, 84– 85, 85f Mycotic aneurysm, infective endocarditis due to, management, 150 Mycotic aneurysms, infective endocarditis due to, 138 Myectomy chemical, for hypertrophic cardiomyopathies, 170 surgical, for hypertrophic cardiomyopathies, 169t, 170 Myocardial biopsy, 11 Myocardial disease, ankylosing spondylitis and, 504 Myocardial imaging, during stress tests, 11 Myocardial infarction (MI) acute, 51–72 See also Acute myocardial infarction defined, 52, 52t infective endocarditis management and, 150 inferior, following myocardial infarction, 67 nonfatal, anesthesia-related, 536 pericarditis and, 190 Myocardial ischemia in acute myocardial infarction, 70 causes, 25–26 detection of, during stress tests, 10, 11t factors aggravating, 31, 31t Myocardial necrosis, in intracardiac thrombosis, 419 Myocardial perfusion imaging, in chronic ischemic heart disease, 28 Myocardial revascularization, in CHF management, 218 Myocardial tumors, symptoms and signs, 437–438, 437t Myocarditis, 179–186 causes, 180t clinical findings, 180–181 physical examination, 181 symptoms and signs, 180–181 diagnostic studies, 181–183 cardiac catheterization, 181–182 chest radiography, 181 ECG, 181 echocardiography, 181 endomyocardial biopsy, 182 MRI, 181 essentials of diagnosis, 179 giant cell, 185 histologic hallmark, 179 Lyme, 185 overview, 179 pathophysiology, 179–180 polymyositis/dermatomyositis and, 505 in pregnancy, 452 prognosis, 184 rheumatoid, 494–495 scleroderma and, 498–499 in SLE, 488–489 specific forms, 184–186 Chagas disease, 184 cytomegalovirus, 185 giant cell myocarditis, 185 HIV, 184–185 Lyme myocarditis, 185 sarcoidosis, 185–186 toxoplasmosis, 185 treatment, 183–184 Myxedema coma defined, 468 treatment, 470 Myxoma(s), 432–434, 433f, 433t Nadolol for chronic ischemic heart disease, 32t for hyperthyroidism, 467t National Cholesterol Education Program (NCEP), dietary guidelines of, 59, 482–483 Native valve endocarditis causes, 140, 140t management, valve surgery, 151, 151t Native valvular heart disease, treatment, long-term anticoagulation, 425–426 Natriuretic peptides, in CHF management, 212t, 217 Nesiritide, for acute myocardial infarction, 58t Neuralgia, syncope due to, 316t, 318 New York Heart Association (NYHA), 336 functional classes in pulmonary hypertension of, 359t on ventricular septal defects, 386, 388 Niacin, for lipid disorders, 22–23, 22t Niaspan, for lipid disorders, 23 Nicardipine for chronic ischemic heart disease, 32t for coronary artery disease, 498 Nifedipine for chronic ischemic heart disease, 32t for coronary artery disease, 498 Nisoldipine, for chronic ischemic heart disease, 32t Nitrate(s) for aortic stenosis, 88 in CHF management, 214 for chronic ischemic heart disease, 31– 32, 32t for HFpEF, 230 in pregnancy, 461t for unstable angina, 43–45, 45t ᮢ INDEX 563 Nitric oxide, in PAH, 366–367, 368t Nitroglycerin for acute myocardial infarction, 56, 58t for chronic ischemic heart disease, 31– 32, 32t Nitroprusside for acute myocardial infarction, 58t for hypertensive emergencies, 163t in pregnancy, 461t Nocturia, in CHF, 207 Node(s), Osler, in infective endocarditis, 144 Nonbacterial thrombotic endocarditis, 137 Noncapture, pacemaker, 290t, 296, 296f, 296t Nonischemic dilated cardiomyopathy, sudden cardiac death due to, 328t, 329 Non–lipid-lowering drugs, lipid effects of, 23 Nonparoxysmal junctional tachycardia, 246 Non-ST elevation myocardial infarction (NSTEMI), 38–50 See also Unstable angina on ECG, 53 laboratory findings, 42 reperfusion therapy for, 57 Noonan syndrome, pulmonic stenosis due to, 135 Norepinephrine for acute myocardial infarction, 58t for cardiogenic shock after acute myocardial infarction, 79 Normothermia, maintenance of, in perioperative risk management, 540 NSAIDs for pericarditis, 488 in periooperative patient management, 542 NSTEMI See Non-ST elevation myocardial infarction (NSTEMI) Nuclear cardiac imaging, myocardial perfusion imaging, overview, in perioperative patient evaluation, 539 radionuclide angiography, Nurses’ Health Study, 482 Nutrient(s), in TLC diet, 18, 18t Obesity, systemic hypertension and, management, 157 Obliterative cardiomyopathy, defined, 172 Obstructive sleep apnea, in HFpEF, 224 Obstructive valvular lesions, severe symptomatic, in pregnancy, 448t Octreotide, for acromegaly, 480 Oliguria, in CHF, 207 Omega-3-fatty acids (fish oil), for lipid disorders, 21, 22t Oncocytic cardiomyopathy, 433t, 435 Open commissurotomy, for mitral stenosis, 111 ᮢ 564 Open-lung biopsy, in rheumatoid pulmonary hypertension, 496 Oral anticoagulants, for mitral regurgitation, 119 Oral contraceptives, cardiac effects of, 483 Orthopnea, defined, 207 Orthostatic hypotension, syncope due to, 316t, 317–318 Osler nodes, in infective endocarditis, 144 Osteoporosis, anticoagulants and, 418 Ottawa Scoring System, 339, 339t Outflow tract ventricular tachycardia, 307– 308, 309f Oversensing, in cardiac pacing, 290t, 295– 296, 296f, 296t Oxygen, for PAH, 365 Oxygen saturation, in cardiogenic shock, 77–78 Pacemaker(s) See also Cardiac pacing atrial, wandering, 257–258 for conduction disturbances, 500 for hypertrophic cardiomyopathies, 169t, 170 long-term anticoagulation with, 429– 430 oversensing of, causes, 290t in perioperative patients, management, 543–544 Pacemaker endocarditis, 142 Pacemaker noncapture, 290t, 296, 296f, 296t Pacing See also Cardiac pacing asynchronous, 286, 287f–289f permanent, for conduction disturbances, 503 Pacing artifacts, ventricular, 294 Paclitaxel, cardiac toxicity from, 443t, 444 PAH See Pulmonary arterial hypertension (PAH) Pain chest, 1, 2t unstable angina vs., 43 gastrointestinal causes of, unstable angina vs., 43 Palpitation(s), 2, 2t Pansystolic murmur, Papillary fibroelastomas, 146, 433t, 434, 434f Paradoxical emboli, patent foramen ovale and, treatment, long-term anticoagulation, 429 Paraganglioma(s), 433t, 437 Parathyroid gland, disorders of, cardiac effects of, 472–474 Parathyroidectomy, for hyperparathyroidism, 473 Parenteral therapy, for infective endocarditis, 148 Paroxysmal nocturnal dyspnea, in CHF, 206–207 Paroxysmal supraventricular tachycardia, in pregnancy, 455 INDEX Partial anomalous pulmonary venous return, 399 Parvus et tardus pulse, 84–85 Patent ductus arteriosus, 388–390, 388f clinical findings, 389 diagnostic studies, 389 essentials of diagnosis, 388 overview, 388–389, 388f in pregnancy, 449 prognosis, 389–390 symptoms and signs, 389 treatment, 389–390 Patent foramen ovale, paradoxical emboli and, treatment, long-term anticoagulation, 429 PCI See Percutaneous coronary intervention (PCI) Peptide(s), natriuretic, in CHF management, 212t, 217 Percutaneous coronary intervention (PCI) for cardiogenic shock after acute myocardial infarction, 80 for chronic ischemic heart disease, 34 fibrinolysis vs., for acute myocardial infarction, 60, 61f Percutaneous mitral balloon valvotomy, for mitral stenosis, 110–111 Pericardial cysts, 441, 441f Pericardial diseases, 187–202 See also specific diseases, e.g., Pericarditis acute pericarditis, 192–194, 192t, 193f AIDS, 189 ankylosing spondylitis and, 504 bacterial pericarditis, 187–188 cardiac tamponade, 195–197 constrictive pericarditis, 197–201, 199f, 200f, 200t effusive-constrictive pericarditis, 201– 202 iatrogenic causes, 189 normal, 456 overview, 187 pathogenesis, 187–192, 188f connective tissue disorders, 190 Dressler syndrome, 190 drug-related, 191 hypothyroidism, 191 infectious pathogens, 187–189, 188f malignancy, 190 myocardial infarction, 190 pericardial effusion, 194–195 progressive systemic sclerosis, 190 radiation therapy–related, 189 renal failure, 191 SLE, 190 surgery-related syndromes, 189 trauma-related, 189 tuberculous pericarditis, 188–189, 188f viral pericarditis, 187 Pericardial effusion, 194–195 asymptomatic, in pregnancy, 456 clinical findings, 194 diagnostic studies, 195 essentials of diagnosis, 194 hemorrhagic, traumatic, 189 overview, 194 treatment, 195 Pericardial fluid aspirates, in pericarditis, 500 Pericardial imaging, in restrictive cardiopathies, 176 Pericardial space, pressure in, 187 Pericardial tumors physical examination, 438 symptoms and signs, 437t, 438 Pericardiectomy for pericarditis, 488 for rheumatoid pericarditis, 493 Pericardiocentesis in cardiac tumor management, 442 for pericarditis, 500 Pericarditis acute, 192–194, 192t, 193f clinical findings, 192 diagnostic studies, 192–194, 192t, 193f essentials of diagnosis, 192 overview, 192 treatment, 194 unstable angina vs., 42–43 bacterial, 187–188 constrictive, 197–201, 199f, 200f, 200t See also Constrictive pericarditis early, after heart surgery, 189 effusive-constrictive, 201–202 following myocardial infarction, 66 infective endocarditis management and, 150 polymyositis/dermatomyositis and, 505 rheumatoid, 492–493 scleroderma and, 500 in SLE, 487–488 tuberculous, 188–189, 188f viral, 187 Pericardium, anatomy and physiology, 187 Perioperative patient evaluation, 536–540 preoperative risk assessment, 536– 540, 537t, 538f–539f ACC/AHA Guidelines, 537, 538f– 539f ACP Guidelines, 537 algorithms, 536–537 cardiac complications, 539–540 exercise vs pharmacologic stress testing, 539 imaging, 539 in intermediate risk patients, 537– 539 overview, 536, 537t RCRI, 536 management, 540–544 in aortic stenosis, 543 β-blockers, 540 calcium channel blockers, 540 clonidine, 540 in deep venous thrombosis prevention, 540 in endocarditis prevention, 540–541 in heart failure, 543 ICDs, 543–544 normothermia maintenance, 540 pacemakers, 543–544 perioperative medication management, 541–542 antiarrhythmics, 542 anticoagulants, 541 aspirin, 541–542 clopidogrel, 541–542 NSAIDs, 542 prophylactic coronary revascularization, 542–543 pulmonary hypertension, 543 to reduce perioperative risk, 540– 543 in special populations, 543–544 statins, 540 vascular surgery, 543 mortality in, causes, 536 Peripartum cardiomyopathy, in pregnancy, 452–453 Peripheral blood vessels, in systemic hypertension, 156 Peripheral edema, in CHF, 208 Peripheral pulses, Permanent pacing, 286–293, 286t, 287f– 289f, 290t, 291f–295f See also Cardiac pacing, permanent pacing PET See Positron emission tomography (PET) Petechiae, in infective endocarditis, 144 Pharmacologic therapy See also specific agents and Drug(s) Pheochromocytoma, 474–476, 475t clinical findings, 474–475 diagnostic studies, 475, 475t essentials of diagnosis, 474 laboratory findings, 475, 475t overview, 474 physical examination, 475 prognosis, 476 symptoms and signs, 474–475 treatment, 475–476 Physiologic anemia during pregnancy, 446 Pindolol for chronic ischemic heart disease, 32t for syncope, 324t Plain old balloon angioplasty (POBA), for chronic ischemic heart disease, 34 Plaque, unstable, 38–40 Plasma D-dimer enzyme–linked immunosorbent assay, in pulmonary embolic disease, 339, 341 Plasmin, 60 Plethysmography, in thrombotic diseases, 490 Polymorphic ventricular tachycardia, 301f, 303–304, 311–313, 312f, 313t, 314f catecholaminergic, sudden cardiac death due to, 328t, 330 clinical findings, 311–312, 312f, 313t, 314f management, 312–313 with normal QT interval, 313, 314f overview, 311 in setting of prolonged QT interval, 311–313, 312f, 313t, 314f Polymyositis/dermatomyositis, 504–505 arrhythmias and, 505 clinical findings, 504–505 conduction disturbances and, 505 cor pulmonale and, 505 coronary arteritis and, 505 essentials of diagnosis, 504 hyperkinetic heart syndrome and, 505 myocarditis and, 505 overview, 504 pericarditis and, 505 pulmonary hypertension and, 505 valvular heart disease and, 505 Positron emission tomography (PET), 10 in cardiac arrest survivors with structural heart disease, 332 in cardiac tumors, 441 in chronic ischemic heart disease, 28, 29 rubidium, in perioperative patient evaluation, 539 Possible endocarditis, defined, 146 Postmyocardial infarction syndrome, pericarditis and, 190 Postpericardiotomy syndrome, 189 Potassium-sparing diuretics, in CHF management, 212, 212t Precursor lesion, bacteremia and, 137 Prednisone, for pericarditis, 488 Pregnancy anticoagulation during, 430–431 cardiovascular disease in, 446–463 acute myocardial infarction, risk factors, 454t adverse effects, 447, 448t causes, 447–458, 448t, 451t, 454t arrhythmias, 455–456 cardiomyopathies, 452–454 congenital heart disease, 447–450, 448t coronary artery disease, 454–455, 454t diseases of aorta, 457–458 heart blocks, 456 hypertension, 458 infective endocarditis, 452 Loeys-Dietz syndrome, 457–458 Marfan syndrome, 457 myocarditis, 452 pericardial diseases, 456 prosthetic heart valves, 450–451, 451t ᮢ INDEX 565 pulmonary hypertension, 456– 457 rheumatic heart disease, 452 valvular heart disease, 450–452, 451t clinical findings, 458–459 diagnostic difficulties, 458–459 patient history, 458 physical examination, 458, 459t symptoms and signs, 458, 459t diagnostic studies, 459–460, 459t essentials of diagnosis, 446 incidence, 446 labor and delivery period, 462–463 overview, 446 prognosis, 463 treatment, 460–463, 461t arrhythmias, 461–462, 461t heart failure, 460–461, 461t infective endocarditis, 462 pharmacologic agents, 460–462, 461t surgery, 462 thromboembolism, 461t, 462 thrombosis, 461t, 462 congenital heart disease and, management, genetic counseling, 416 normal blood volume, 446, 447t cardiac output, 446–447, 447t cardiovascular physiology, 446–447, 447t intravascular pressures and vascular resistance, 447, 447t in PAH, 365 physiologic anemia during, 446 VTE and, 338, 350 in women with prosthetic heart valves, anticoagulation prevention, 451, 451t Premature ventricular complexes (PVCs), in pregnancy, 455 Preoperative risk assessment, 536–540, 537t, 538f–539f See also Perioperative patient, evaluation, preoperative risk assessment Preparticipation physical examination, in athletes, 513–515 Pressors, for acute myocardial infarction, 58t Pressure intravascular, in normal pregnancy, 447, 447t jugular venous, in cardiac tamponade, 196 pericardial, 187 Presyncope, 1, 2t Primary hyperaldosteronism, 478 Primary hyperparathyroidism, causes, 472 Primary pulmonary hypertension, in pregnancy, 456–457 Pritikin Diet, for lipid disorders, 20 ᮢ 566 Probable endocarditis, defined, 146 Procainamide for acute myocardial infarction, 58t for atrial tachycardia, 241 for maintaining sinus rhythm in atrial fibrillation, 261t, 262f in pregnancy, 461t for SVTs, 234t Progressive systemic sclerosis, pericarditis and, 190 Prolonged QT (QTc) interval, polymorphic VT in setting of, 311–313, 312f, 313t, 314f Propafenone for atrial tachycardia, 241 for maintaining sinus rhythm in atrial fibrillation, 261t, 262f for SVTs, 234t Propantheline, for syncope, 324t Propranolol for acute myocardial infarction, 58t for chronic ischemic heart disease, 32t for heart rate control in atrial fibrillation, 261t for hyperthyroidism, 467t for SVTs, 234t Propylthiouracil, for hyperthyroidism, 467, 467t Prostacyclin, for PAH, 367, 368t Prosthetic heart valves mechanical in aortic valve replacement, 91–92 treatment, long-term anticoagulation, 426–427, 427t in pregnancy, 450–451, 451t treatment, long-term anticoagulation, 426–427, 427t Prosthetic valve endocarditis, 140–141, 141t diagnosis, 142–143 management, 150–151, 151t surgery, 150, 151t Protein(s), C-reactive, in chronic ischemic heart disease, 27 Pseudo-aneurysms, following myocardial infarction, 69 Pseudo-Cushing syndrome, 477–478 Pseudoseizure(s), psychiatric disorders and, syncope vs., 324 Psychiatric disorders with hyperventilation and pseudoseizures, syncope vs., 324 syncope due to, 316t, 318 Psychological factors, in acute myocardial infarction, 72 Pulmonary angiography in pulmonary embolic disease, 344 in pulmonary hypertension, 362 Pulmonary arterial hypertension (PAH), 352–355, 353t, 354f–357f See also Pulmonary hypertension INDEX acute decompensated right ventricular failure in, management, 365, 366f causes, 352–353, 353t described, 352, 354f diagnostic algorithm for, of American College of Chest Physicians, 363, 364f diseases associated with, 353, 353t disorders due to, 353, 355f endothelin-1 in, 366, 367f essentials of diagnosis, 352 nitric acid in, 366–367, 368t in pregnancy, 365 prevalence, 353 prognosis, 370 progression of, prognostic factors for, 369t pulmonary artery narrowing in, processes contributing to, 353, 356f survival with, 353, 355, 355f treatment, 365–369, 366f, 367f, 368t, 369f, 369t algorithm, 369f calcium channel blockers, 365 diuretics, 365 oxygen, 365 pharmacologic agents, randomized controlled trials, 365–366, 368t Pulmonary arterial systolic pressure, estimation of, 343 Pulmonary artery catheterization, in pregnancy, 460 Pulmonary atresia with intact ventricular septum, 413– 414 clinical findings, 413–414 essentials of diagnosis, 413 overview, 413 prognosis, 414 treatment, 414 with VSDs, tetralogy of Fallot and, 401– 405, 402f, 404f Pulmonary emboli, infective endocarditis due to, 138 Pulmonary embolic disease, 337–351 See also Pulmonary embolism; Venous thromboembolism (VTE) causes, 337–338, 338t thrombophilia, 337–338, 338t diagnostic studies, 339–344, 339f, 343f, 344t arterial blood gases, 339, 340t chest CT, 341–342, 342f chest radiography, 341, 341f ECG, 339 echocardiography, 343–344, 343f, 344t imaging studies, 341–344, 341f–343f, 344t nonimaging studies, 339–341, 340f plasma D-dimer enzyme–linked immunosorbent assay, 339, 341 pulmonary angiography, 344 radionuclide lung scanning, 341, 341f TEE, 343–344 troponin screening, 341 venous ultrasonography, 342–343 essentials of diagnosis, 337 overview, 337 prevention, 345–346, 345t pulmonary embolism, 338–339, 339f, 339t risk stratification, 346, 346t symptoms and signs, 338–339, 339t, 340t treatment, 346–350, 347t–349t adjunctive measures, 350 anticoagulation, 350 counseling, 350 embolectomy, 348 heparin, 346–347 inferior vena caval filters, 349 LMWH, 347, 348t, 349t thrombolysis, 347–348, 349t warfarin, 349–350 Pulmonary embolism See also Pulmonary embolic disease; Venous thromboembolism (VTE) abnormal echocardiographic findings in, 343, 344t acute, unstable angina vs., 43 clinical findings, 338–339, 339f, 339t clinical scoring systems for, 338–339, 339t deaths due to, 337 diagnostic studies, 339–344, 339f, 343f, 344t primary, causes, 337 secondary, prevalence, 337 symptoms and signs, 338–339, 339t, 340t threat to women’s health, 338 Pulmonary function testing, in pulmonary hypertension, 362 Pulmonary hypertension, 352–370 causes, 352 chronic thrombotic or embolic diseases and, 356, 370 classification, 352–358, 353t, 354f–358f functional, of World Health Organization, 365 clinical findings, 358–359, 359t physical examination, 359 symptoms and signs, 358–359, 359t defined, 352 diagnostic studies, 359–363, 359t, 360f– 363f cardiac catheterization, 362 chest radiography, 359, 360f CT, 362 ECG, 359, 359t, 360f echocardiography, 359–360, 361f exercise testing, 363 functional capacity testing, 363 lung biopsy, 362–363, 363f lung scintigraphy, 260, 262, 262f MRI, 362 pulmonary angiography, 362 pulmonary function testing, 362 vasoreactivity testing, 362 differential diagnosis, 363–365, 364f essentials of diagnosis, 352 functional classes, 359t hypoxia and, 354f, 355–356 left-sided heart disease with, 354f, 355 treatment, 369–370 lung diseases and, 354f, 355–356 treatment, 370 mixed, 355 overview, 352 PAH and, 352–355, 353t, 354f–357f pathogenesis, 352–358, 353t, 354f–358f pathophysiologic consequences, 357– 358, 358f in perioperative patients, management, 543 polymyositis/dermatomyositis and, 505 in pregnancy, 456–457 primary, in pregnancy, 456–457 prognosis, 370 rheumatoid, 496 severe, in pregnancy, 448t treatment, 365–370, 366f, 367f, 368t, 369f, 369t PAH, 365–369, 366f, 367f, 368t, 369f, 369t See also Pulmonary arterial hypertension (PAH), treatment pharmacologic agents, randomized controlled trials, 365–366, 368t Pulmonary trunk, idiopathic dilation of, pulmonic regurgitation due to, 135 Pulmonary valve stenosis, 376–379, 378f– 380f clinical findings, 377 diagnostic studies, 377–378, 378f–380f essentials of diagnosis, 376 overview, 376–377 prognosis, 378–379 symptoms and signs, 377 treatment, 378–379 Pulmonary veins, total anomalous, 414 Pulmonary venous return, partial anomalous, 399 Pulmonary ventilation-perfusion scan, in thrombotic diseases, 490 Pulmonic regurgitation cardiac auscultation in, 135 causes, 135 described, 134 pathophysiology, 134 treatment, 136 Pulmonic stenosis cardiac auscultation in, 135 causes, 135 congenital, pulmonic regurgitation due to, 135 described, 134 pathophysiology, 135 in pregnancy, 448–450 treatment, 136 Pulmonic valve disease, 134–136 diagnostic studies, 136 essentials of diagnosis, 134 pathophysiology, 134–135 physical examination, 135 in pregnancy, 450 symptoms and signs, 135 Pulmonic valve transplantation (Ross procedure), 91 Pulse(s) jugular venous, in tricuspid valve disease, 124, 125f– 127f parvus et tardus, 84–85 peripheral, Pulsus alternans, in CHF, 208 Pulsus paradoxus, in cardiac tamponade, 196 PVCs, in pregnancy, 455 QRS complex duration of, in ventricular tachycardia, 301, 302f wide, mechanism of, 300, 300f QRS complex axis, in ventricular tachycardia, 303 QRS complex tachycardia, wide See Wide QRS complex tachycardias QRS morphology, in VT, 301–303 QT interval, normal, polymorphic VT with, 313, 314f Quinidine for atrial tachycardia, 241 for maintaining sinus rhythm in atrial fibrillation, 261t, 262f in pregnancy, 461t for SVTs, 234t RAAS inhibitors, for diabetics with systemic hypertension, 159 Race, as factor in exercise training responses, 512 Radiation therapy cardiac toxicity from, 444t, 444–445 in management, 442 pericardial injury related to, 189 Radiation-induced fibrosis, restrictive cardiomyopathies due to, 173, 173t Radioactive iodine, for hyperthyroidism, 467t, 468 Radiofrequency catheter ablation, in AVRT management, 255–256, 256t complications, 256, 256t Radiofrequency modification, in slow–fast AVNRT, 243, 246 Radiography, chest See Chest radiography ᮢ INDEX 567 Radionuclide angiography, in chronic ischemic heart disease, 28, 29 in restrictive cardiomyopathies, 175 Radionuclide studies in coronary artery disease, 497–498, 498f in myocarditis, 489, 499 in pheochromocytoma, 475 in pregnancy, 460 in pulmonary embolic disease, 341, 341f in rheumatoid myocarditis, 495 Radionuclide ventriculography, in CHF, 209 Rampipril, for HFpEF, 229–230 Ranolazine, for chronic ischemic heart disease, 32t, 33–34 Rastelli procedure, 399 in congenital heart disease management, 415 Rate control for atrial fibrillation, 260, 261t for atrial flutter, 239 RCRI, in preoperative risk assessment, 536 Reactive vasoconstriction, 355 Recanalization, coronary, 55 α-Receptor blockers, for systemic hypertension, 158t, 160–161 Reentrant arrhythmias, 233 Registry of the Valvuloplasty and Angioplasty of Congenital Anomalies, 378 Regurgitation aortic, 95–105 See also Aortic regurgitation mitral, 113–121 See also Mitral regurgitation pulmonic, 134–136134 tricuspid See Tricuspid regurgitation valve, in valvular heart disease, 485 Rehabilitation, for acute myocardial infarction, 71 Remote infarction with thrombus, treatment, long-term anticoagulation, 428 Renal disease, hypertensive, 156 Renal failure, pericarditis and, 191 Renal insufficiency, systemic hypertension and, management, 161t, 162 Renin inhibitors, direct, for systemic hypertension, 161 Renin-angiotensin-aldosterone system (RAAS) inhibitors, for diabetics with systemic hypertension, 159 Reperfusion therapy, for acute myocardial infarction, 57, 59f, 60t Restrictive cardiomyopathies, 172–178 abnormalities in diastolic function in, 172–173, 176–177 causes, 173–174 classification, 173t clinical findings, 174 physical examination, 174 symptoms and signs, 174, 174t ᮢ 568 Restrictive cardiomyopathies (cont.) constrictive pericarditis vs., 177t defined, 172 diagnostic studies, 174–176 cardiac catheterization, 175–176 chest radiography, 175 CT, 176 ECG, 175 echocardiography, 175 endomyocardial biopsy, 173t, 176 pericardial imaging, 176 radionuclide angiography, 175 differential diagnosis, 176–178 essentials of diagnosis, 172 idiopathic, 173, 173t overview, 172, 173t pathophysiology, 172–173 prognosis, 178 restrictive physiology in, 173 terminology related to, 172 treatment cardiac complications, 178 for diastolic dysfunction, 176–177 thromboembolic complications, 178 underlying disease complications, 178 Restrictive physiology defined, 172 in restrictive cardiopathies, 173 Resuscitation in cardiac arrest management, complications, management, 331–332 fluid, for cardiogenic shock after acute myocardial infarction, 78– 79, 78t initial, in cardiac arrest management, 330–331 Reteplase, for acute myocardial infarction, 63 Retinoic acid, cardiac toxicity from, 443t, 444 Revascularization in cardiac arrest survivors management, 333 for cardiogenic shock after acute myocardial infarction, 80 in chronic ischemic heart disease, 34–35 coronary, prophylactic, management, in perioperative patients, 542–543 myocardial, in CHF management, 218 Revised Cardiac Risk Index (RCRI), in preoperative risk assessment, 536 Rhabdomyoma(s), 433t, 435, 436f Rheumatic fever, aortic stenosis due to, 82 Rheumatic heart disease in pregnancy, 452 pulmonic regurgitation due to, 135 Rheumatic mitral valve disease, treatment, long-term anticoagulation, 425 Rheumatic tricuspid regurgitation, 122– 123, 123t INDEX Rheumatoid arthritis, 491–497, 494f conduction disturbances, 495–496 essentials of diagnosis, 492 overview, 492 pericarditis and, 190 rheumatoid coronary artery disease, 495 rheumatoid myocarditis, 494–495 clinical findings, 494 diagnostic studies, 494–495 laboratory findings, 494 overview, 494 physical examination, 494 prognosis, 495 treatment, 495 rheumatoid pericarditis, 492–493 clinical findings, 492 diagnostic studies, 492–493 in hospitalized patients, prevalence, 492 laboratory findings, 492 overview, 492 prognosis, 493 symptoms and signs, 492 treatment, 493 rheumatoid pulmonary hypertension, 496 rheumatoid valvular heart disease, 493– 494, 494f Rheumatoid coronary artery disease, 495 Rheumatoid myocarditis, 494–495 Rheumatoid pericarditis, 492–493 See also Rheumatoid arthritis, rheumatoid pericarditis Rheumatoid pulmonary hypertension, 496 Rheumatoid valvular heart disease, rheumatoid arthritis and, 493–494, 494f Rhythm disturbances, restrictive cardiopathy management and, 178 Right atrial tumors, physical examination, 438 Right ventricle, double-inlet, 414 Right ventricular cardiomyopathy, arrhythmogenic monomorphic VT and, 305–306, 306f sudden cardiac death due to, 328t, 329 Right ventricular cavity, exercise training effects on, 512 Right ventricular infarction after cardiogenic shock management, 80–81 cardiogenic shock due to, 75 following myocardial infarction, 69 Right ventricular tumors, physical examination, 438 Right-sided heart failure, 205 Rituximab, cardiac toxicity from, 443t Ross procedure, 91 Roth spots, in infective endocarditis, 144 Rubidium positron emission tomography (PET) scanning, in perioperative patient evaluation, 539 Rupture aortic aneurysm, defined, 529–530 cardiac, following myocardial infarction, 65–66 ventricular septal, acute, following myocardial infarction, 65 Sarcoidosis, 185–186 restrictive cardiomyopathies due to, 173, 173t Sarcoma(s), 433t, 436, 436f Saturated fats, cholesterol effects of, 20–21 Saturated solution of potassium iodide (SSKI), for hyperthyroidism, 467t Scar-related ventricular tachycardia, 302f Scintigraphy lung in pulmonary hypertension, 260, 262, 262f ventilation-perfusion, in pulmonary hypertension, 260, 262, 262f in thrombotic diseases, 490 Scleroderma, 497–501, 498f, 501f arrhythmias, 499–500 conduction disturbances, 499–500 coronary artery disease, 497–498, 498f See also Coronary artery disease, scleroderma and essentials of diagnosis, 497 myocarditis, 498–499 overview, 497 pericarditis, 500 secondary scleroderma heart disease, 500–501 valvular heart disease and, 500 Sclerosis(es), progressive systemic, pericarditis and, 190 Scopolamine patch, for syncope, 324t Second heart sound, in aortic stenosis, 85 Secondary scleroderma heart disease, 500– 501 Seizure(s), syncope vs., 323 Septum, ventricular, intact, pulmonary atresia with, 413–414 Serolotic testing, in infective endocarditis, 145 Sertraline, for syncope, 324t Shock, cardiogenic, 73–81 See also Cardiogenic shock Short QT syndrome, sudden cardiac death due to, 329 Shortness of breath, in CHF, 206–207 Shunt(s), in congenital heart disease management Blalock-Taussig shunt, 415 Potts shunt, 415 systemic-to-pulmonary shunt, 415 Waterston shunt, 415 “Sick sinus syndrome.” See Sinus node dysfunction (“sick sinus syndrome”) Sildenafil, for PAH, 366, 367, 368t Single-chamber demand pacing [VVI(R), AAI(R)], 286–287, 290t Single-lead P-synchronous pacing (VDD), 287–288, 287f–288f, 291f Single-photon emission computed tomography (SPECT), in chronic ischemic heart disease, 28 Sinoatrial block, 267–268, 269f–272f Sinoatrial exit block type I, defined, 267 type II, defined, 267 Sinus arrest, defined, 267 Sinus bradycardia causes, 268, 270f defined, 267 Sinus node arrhythmia, 257 Sinus node dysfunction (“sick sinus syndrome”) diagnostic studies, 273, 275 ECG, 273 electrophysiologic studies, 273, 275 exercise testing, 275 essentials of diagnosis, 267 pathophysiology, 267–268, 269f–273f, 273t Sinus node reentry, 236f, 237 Sinus of Valsalva, aneurysms of, 400 Sinus pauses, defined, 267 Sinus tachycardia, 236–237, 236f following myocardial infarction, 67 Skin necrosis, anticoagulants and, 418 SLE See Systemic lupus erythematosus (SLE) Sleep apnea, obstructive, in HFpEF, 224 Socioeconomic factors, in systemic hypertension, 154 Sodium reduction, for systemic hypertension, 157 Sotalol in cardiac arrest survivors management, 333 for maintaining sinus rhythm in atrial fibrillation, 261t, 262f for monomorphic VT, 310–311, 310t in pregnancy, 461t for SVTs, 234t South Beach Diet, increased HDL levels due to, 21 SPECT, in chronic ischemic heart disease, 28 Spironolactone in CHF management, 212, 212t, 217 for HFpEF, 231 Splinter hemorrhages, in infective endocarditis, 144 Spondylitis, ankylosing, 501–504, 503f See also Ankylosing spondylitis Sports participation, in congenital heart disease management, 416 SSKI (saturated solution of potassium iodide), for hyperthyroidism, 467t ST elevation myocardial infarction (STEMI) anterior, following myocardial infarction, 67 ECG changes in, 53, 54f fibrinolysis for, contraindications, 57, 60t in intracardiac thrombosis, 419 PCI vs fibrinolysis for, 57, 59f reperfusion therapy for, 57 Stanford classification system, in thoracic aortic dissection, 531, 532f Staphylococcus aureus endocarditis, 139 Static exercise, 508f, 509 Static exercise training, 509–510 Statin(s) for HFpEF, 231 for lipid disorders, 22t, 23 in perioperative risk management, 540 STEMI See ST elevation myocardial infarction (STEMI) Stenosis(es) aortic, 82–94 See also Aortic stenosis mitral, 106–112 See also Mitral stenosis pulmonary valve, 376–379, 378f–380f See also Pulmonary valve stenosis pulmonic See Pulmonic stenosis tricuspid See Tricuspid stenosis Stent grafts, in thoracic aortic aneurysms management, 529 Streptokinase, for acute myocardial infarction, 62 Stress, systemic hypertension due to, management, 157 Stress cardiomyopathy, cardiogenic shock due to, 73, 74t Stress echocardiography diastolic, in HFpEF, 225t, 227 in mitral stenosis, 109 Stress tests, 10–11, 10t, 11t, 27–28 for coronary artery disease evaluation in HFpEF, 225t, 227 ECG during, 11 monitoring of, 11 exercise in aortic regurgitation, 102–103 in CHF, 209 implications for, 10, 10t myocardial imaging during, 11 myocardial ischemia detection during, methods, 10, 11t overview, 10, 10t types, 11, 11t Stroke(s) in atrial fibrillation, 422 risk factors, 423–424, 423t, 424t ischemic, cardioembolic, 419 prevention, in atrial flutter management, 239 systemic hypertension and, 156 Structural heart disease in cardiac arrest survivors evasive evaluation, 332 noninvasive evaluation, 332 VT and, 304–307, 305f, 306f monomorphic, 306–307 VT not associated with, 307–308, 307t, 308f, 309f ᮢ INDEX 569 Sudden cardiac death, 327–336 See also Cardiac arrest anesthesia-related, 536 in athletes, 513, 513t, 514f, 514t causes, 327–330, 328t ARVC, 328t, 329 bradyarrhythmias, 330 Brugada syndrome, 328t, 329–330 catecholaminergic polymorphic VT, 328t, 330 commotio cordis, 330 congenital complete heart block, 330 congenital heart disease, 328t, 329 coronary artery disease, 327–328, 328t drug-induced arrhythmias, 328t, 330 hypertrophic cardiomyopathy, 328– 329, 328t inherited arrhythmia syndromes, 328t, 329–330 monomorphic ventricular tachycardia, 330 nonischemic dilated cardiomyopathy, 328t, 329 overview, 327 short QT syndrome, 329 valvular heart disease, 328t, 329 Wolff-Parkinson-White syndrome, 330 essentials of diagnosis, 327 overview, 327 pathophysiology, 327–330, 328t persons at risk for, identification of, 335–336 risk-assessment studies, 335–336 primary prevention, 336 Sudden Cardiac Death Heart Failure Trial (SCD-HeFT), 336 Sudden death, in athletes, 513, 513t, 514f, 514t Supraventricular arrhythmias in pregnancy, 455 sudden cardiac death due to, 330 syncope due to, 316, 316t Supraventricular tachycardias (SVTs), 233– 258 See also specific types, e.g., Atrial flutter atrial flutter, 236f, 237–239, 238f atrial tachycardia, 236f, 240–242 AVNRT, 236f, 242–246, 243f–245f AVRT, 236f, 247–256, 248f–255f, 256t causes, 233 concealed bypass tracts, mechanism, 250, 254 essentials of diagnosis, 233 following myocardial infarction, 67–68 general diagnostic approach, 236, 236f, 237f junctional tachycardia (accelerated AV junctional rhythm), 236f, 246 multifocal atrial tachycardia, 236f, 239– 240, 240f overview, 233 ᮢ 570 Supraventricular tachycardias (SVTs) (cont.) paroxysmal, in pregnancy, 455 pathophysiology, 233 sinus node arrhythmia, 257 sinus node reentry, 236f, 237 treatment antiarrhythmic drugs, 234t–235t catheter ablation, 239 conversion, 238–239 rate control, 239 stroke prophylaxis, 239 wandering atrial pacemaker, 257–258 wide QRS complex tachycardias, differentiation among, 256– 257, 257f, 258f Supraventricular tachycardias (SVTS), following myocardial infarction, 67–68 Surgical ablation for AVRT, 256 in cardiac arrest survivors management, 334 for monomorphic ventricular tachycardia, 311 Surgical myectomy, for hypertrophic cardiomyopathies, 169t, 170 SVTs See Supraventricular tachycardias (SVTs) Syncope, 1, 2t, 315–326 causes, 315–318, 316t AV block, 315–316, 316t blood flow obstruction, 315, 316t bradyarrhythmias, 315–316, 316t cardiac, 315–316, 316t carotid sinus hypersensitivity, 316t, 317 electrical disturbances, 315–316, 316t neuralgia, 316t, 318 neurocardiogenic, 316–317, 316t, 319f orthostatic hypotension, 316t, 317– 318 psychiatric disorders, 316t, 318 supraventricular arrhythmias, 316, 316t tachyarrhythmias, 316, 316t Torsades de pointes, 316, 316t VT, 316, 316t clinical findings, 318, 320 deglutition, 316t, 317 diagnostic approach to, 320f diagnostic studies, 320–323, 320f, 322f ambulatory monitoring, 321, 322f ECG, 320–321 echocardiography, 321 exercise stress tests, 321 head-up tilt-table testing, 322 invasive electrophysiology studies, 322–323 transcranial Doppler ultrasonography, 322 differential diagnosis, 323–324 effort, aortic stenosis and, 83 INDEX essentials of diagnosis, 315 micturition, 316t, 317 overview, 315 pathophysiology, 315–318, 316t prognosis, 325–326 situational, 316t, 317 treatment, 324–325, 324t electrophysiologic therapies, 325 nonpharmacologic therapy, 324 overview, 324 pharmacologic agents, 324–325, 324t tussive, 316t, 317 vasovagal, 316–317, 316t, 319f Syncope of unknown cause, 318 Systematic exercise training, effects of, 509– 510 Systemic arterial pressure, Systemic emboli, infective endocarditis due to, 138 Systemic hypertension, 153–163 See also Hypertension, systemic Systemic lupus erythematosus (SLE), 484– 491 cardiac arrhythmias in, 491 cardiomyopathy in, 488–489 conduction disturbances in, 491 coronary artery disease with, 490–491 clinical findings, 490 diagnostic studies, 490–491 overview, 490 symptoms and signs, 490 treatment, 491 essentials of diagnosis, 484 myocarditis, 488–489 clinical findings, 489 diagnostic studies, 489 overview, 488–489 symptoms and signs, 489 treatment, 489 overview, 484 pericarditis and, 190 pericarditis in, 487–488 clinical findings, 488 diagnostic studies, 488 laboratory findings, 488 overview, 487 symptoms and signs, 488 treatment, 488 prognosis, 491 thrombotic diseases with, 489–490 clinical findings, 489–490 diagnostic studies, 490 laboratory findings, 490 overview, 489 symptoms and signs, 489–490 treatment, 490 tricuspid valve disease due to, 123 valvular heart disease with, 485–487, 486f, 487f clinical findings, 485–487 diagnostic studies, 487 Libman-Sacks endocarditis, 485 overview, 485 physical examination, 486–487 symptoms and signs, 485–486 treatment, 487 valve regurgitation, 485 valve thickening, 485, 486f, 487t valve vegetations, 485 Systemic venous hypertension, in CHF, 208 Systemic-to-pulmonary shunts, in congenital heart disease management, 415 Systolic ejection murmur, in aortic stenosis, 84–85, 85f Systolic function, in hypertrophic cardiomyopathies, 165 Systolic heart failure, 205–206, 206t Systolic murmurs, differentiation of, 6, 6t TAAD1 locus, 518 Tachyarrhythmia(s), syncope due to, 316, 316t Tachycardia(s) atrial, 236f, 240–242 See also Atrial tachycardia atrioventricular nodal reentrant, 236f, 242–246, 243f–245f See also Atrioventricular nodal reentrant tachycardia (AVNRT) atrioventricular reciprocating, 236f, 247–256, 248f–255f, 256t junctional, 236f, 246 multifocal atrial, 236f, 239–240, 240f nonparoxysmal junctional, 246 sinus, 236–237, 236f following myocardial infarction, 67 supraventricular, 233–258 See also Supraventricular tachycardias (SVTs) ventricular, 299–314 See also Ventricular tachycardia wide QRS complex See Wide QRS complex tachycardias Tako-tsubo cardiomyopathy, cardiogenic shock due to, 73, 74t TEE See Transesophageal echocardiography (TEE) Temporary pacing, 284–286, 285t transvenous, 285–286 Tenecteplase, for acute myocardial infarction, 63 Tetralogy of Fallot anatomy, 402f anomalies associated with, 402 clinical findings, 403 diagnostic studies, 403 essentials of diagnosis, 401–402 laboratory findings, 403 overview, 402, 402f in pregnancy, 449 prognosis, 403, 405 pulmonary atresia with VSDs and, 401– 405, 402f, 404f pulmonic regurgitation due to, 135 pulmonic stenosis due to, 135 symptoms and signs, 403 treatment, 403, 405 Theophylline, for syncope, 324t Therapeutic lifestyle changes (TLC), steps in, model of, 18, 19f Therapeutic lifestyle changes (TLC) diet, nutrient composition of, 18, 18t Thiazide(s), in CHF management, 211, 212t Thionamide(s), for hyperthyroidism, 467t Third heart sound, Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel (ATP) III), 17 Thoracic aorta dissection or rupture, 520–524, 522f– 524f, 523t growth rate, 520 Thoracic Aortic Aneurysm and Dissection locus, 518 Thoracic aortic aneurysms, 516–529 asymptomatic, surgical intervention, size criteria for, 523, 523t causes, 516–519, 518f–521f clinical findings, 520–524, 522f–524f, 523t Crawford classification, 516, 517f diagnostic studies, 524–525, 524f essentials of diagnosis, 516 “hinge points” in, 521, 522f Marfan disease and, 516, 518f matrix metalloproteinases in, 519, 520f natural history, 520–524, 522f–524f, 523t overview, 516, 529–531, 530f, 531f patterns, 516, 517f physical examination, 524 symptoms and signs, 524 treatment, 525–529, 526f, 526t, 527f specific clinical scenarios and issues, 528–529 stent grafts, 529 surgery contraindications, 526 indications, 526, 526f risks associated with, 525–526, 526t techniques, 526–527, 527f types, 516, 517f Thoracic aortic dissection, 529–535 anatomic classification, 531, 532f clinical findings, 531 diagnostic studies, 531–532 differential diagnosis, 532–533 essentials of diagnosis, 529 prognosis, 535, 535f symptoms and signs, 531 terminology related to, 529–531, 530f, 531f treatment, 533–534, 533f, 534f pharmacologic agents, 533–534, 533f surgery, 534, 534f Three-dimensional echocardiography, in mitral stenosis, 108 Three-dimensional imaging modalities, in thoracic aortic dissection, 532 Thrombocytopenia, anticoagulants and, 418 Thromboembolic disease, in pregnancy, 457 Thromboembolism in pregnancy, treatment, 461t, 462 restrictive cardiomyopathies management and, 178 venous See Venous thromboembolism (VTE) Thrombolysis, for pulmonary embolic disease, 347–348, 349t Thrombolytic drugs, for unstable angina, 45t, 47 Thrombophilia, VTE due to, 337–338, 338t Thrombosis(es), 40 in pregnancy, treatment, 461t, 462 venous, deep, prevention, in perioperative risk management, 540 Thrombotic diseases chronic, pulmonary hypertension due to, 356, 370 in SLE, 489–490 Thrombotic endocarditis, nonbacterial, 137 Thrombus(i) embolization of, 419–420 intravascular, pathogenesis, 418–419 left ventricular, treatment, long-term anticoagulation, 427–429 mural, following myocardial infarction, 68–69 remote infarction with, treatment, long-term anticoagulation, 428 Thyroid gland cardiovascular drugs effects on, 471, 471t disorders of, cardiac effects of, 464–472 See also specific disorders function of, heart disease effects on, 471 Thyroid hormone, cardiovascular system effects of, 464 Thyrotoxicosis, amiodarone-induced, features, 471–472, 471t TIAs, 1, 2t Ticlopidine, for unstable angina, 46 Tirofiban, for acute myocardial infarction, 58t Tissue Doppler imaging, Tissue plasminogen activator (t-PA), for acute myocardial infarction, 62–63 TLC diet, nutrient composition of, 18, 18t Torsades de pointes, syncope due to, 316, 316t Total anomalous pulmonary veins, 414 ᮢ INDEX 571 Toxic disorders, ECG of, Toxoplasmosis, 185 Transaminitis, bosentan and, 366 Transcranial Doppler ultrasonography, in syncope, 322 Transcutaneous pacing, 284–285, 285t Transesophageal echocardiography (TEE), 8–9 for atrial fibrillation, 264 false results, causes, 146t in infective endocarditis, 145–146, 146t in intracardiac thrombi, 420, 421f, 422f in mitral stenosis, 108–109 in pregnancy, 459 in pulmonary embolic disease, 343–344 in thoracic aortic dissection, 532 in thrombotic diseases, 490 Trans-fats, 21 Transient arterial occlusion, in dynamic auscultation, Transient CNS deficits, 1, 2t Transient ischemic attacks (TIAs), 1, 2t Transmyocardial pacing, 284 Transplantation cardiac in cardiac tumor management, 442– 443 in CHF management, 219, 219t pulmonic valve, 91 Transposition of great arteries, 409–411, 410f anatomy, 410f clinical findings, 410 congenitally corrected, 396–399, 397f– 399f See also Congenitally corrected transposition of great arteries diagnostic studies, 410 essentials of diagnosis, 409 overview, 409–410 prognosis, 410–411 symptoms and signs, 410 treatment, 410–411 Transthoracic color-flow Doppler echocardiography in rheumatoid valvular heart disease, 493 in valvular heart disease, 487 Transthoracic echocardiography (TTE) in infective endocarditis, 147 in rheumatoid valvular heart disease, 493 in valvular heart disease, 487 Trastuzumab, cardiac toxicity from, 443t, 444 Trauma, pericardial diseases related to, 189 Traumatic hemorrhagic pericardial effusions, 189 Treadmill exercise testing, in sinus node dysfunction (“sick sinus syndrome”), 275 Treprostinil, for PAH, 368, 368t Tricuspid aortic valve degeneration, aortic stenosis due to, 82 ᮢ 572 Tricuspid atresia, 411–412, 412f, 413f clinical findings, 411 diagnostic studies, 411–412, 413f essentials of diagnosis, 411 overview, 411, 412f prognosis, 412 symptoms and signs, 411 treatment, 412 Tricuspid regurgitation cardiac auscultation in, 124–125, 127f cardiac catheterization in, 130, 132f catheter-induced, 123–124 described, 122, 123t echocardiography in, 128, 130 functional, 122, 123t jugular venous pulse in, 124, 125f–127f rheumatic, 122–123, 123t tricuspid valve disease due to 123t, 124 Tricuspid stenosis cardiac auscultation in, 125 cardiac catheterization in, 130, 132f described, 122, 123t echocardiography in, 130, 131f jugular venous pulse in, 124, 127f tricuspid valve disease due to, 122–124, 123t, Tricuspid valve disease, 122–134 causes, 122–124, 123t, 135 diagnostic studies, 125–133, 128f–132f cardiac catheterization, 130, 132f chest radiography, 126 ECG, 126, 128f echocardiography, 126–130, 129f– 131f essentials of diagnosis, 122 overview, 122, 134 pathophysiology, 122–124, 123t physical examination, 124–125, 125f– 127f in pregnancy, 450 prognosis, 134, 136 symptoms and signs, 124–125, 125f–127f treatment, 133, 136 medical, 133 postoperative, 134 surgery, 133 Tricuspid valve endocarditis diagnosis, 143 tricuspid valve disease due to, 123 Tricuspid valve prolapse, tricuspid valve disease due to, 123 Triggered arrhythmias, 233 Tropical endocardial fibrosis, restrictive cardiomyopathies due to, 173, 173t Troponin(s) mortality associated with, 55, 56f screening for, in pulmonary embolic disease, 341 Truncus arteriosus, 414 Trypanosomiasis, American, 184 TTE See Transthoracic echocardiography (TTE) INDEX Tuberculous pericarditis, 188–189, 188f Tumor(s) atrial left, physical examination, 438 right, physical examination, 438 carcinoid cardiac effects of, 480–481 tricuspid valve disease due to, 123 cardiac, 432–445 See also specific types clinical findings, 437–438, 437t diagnostic studies, 438–441, 439f, 440f CT, 439–440 echocardiography, 438–439, 439f MRI, 440, 440f PET, 441 differential diagnosis, 441, 441f, 442f essentials of diagnosis, 432 metastatic, 432, 433t prognosis, 443 overview, 432–437, 433f–436f, 433t physical examination, 438 primary, 432–437, 433f–436f, 433t benign, 432–435, 433f–436f, 433t fibromas, 433t, 435, 435f hamartomas, 433t, 435 hemangiomas, 433t, 435 lipomas, 433t, 434–435 myxomas, 432–434, 433f, 433t papillary fibroelastomas, 433t, 434, 434f rhabdomyomas, 433t, 435, 436f malignant, 433t, 436–437, 436f lymphomas, 433t, 436–437 mesotheliomas, 433t, 437 paragangliomas, 433t, 437 sarcomas, 433t, 436, 436f prognosis, 443 prognosis, 443 symptoms and signs, 437–438, 437t treatment, 441–445, 443t, 444t cardiac transplantation, 442–443 oncologic, cardiac toxicities from, 443–445, 443t, 444t pericardiocentesis, 442 pharmacologic agents, 441–442 radiation, 442 surgery, 442 Tumor necrosis factor-α receptor inhibitors, for rheumatoid valvular heart disease, 493–494 Tussive syncope, 316t, 317 2007 American College of Physicians (ACP) guidelines, in pulmonary embolic disease, 347 Two-dimensional echocardiography, in mitral stenosis, 108 Ultrasonography transcranial Doppler, in syncope, 322 venous Doppler, in pulmonary embolic disease, 342–343 in pulmonary embolic disease, 342– 343 Undersensing, in cardiac pacing, 290t, 293– 294, 295f Unfractionated heparin (UFH) for acute myocardial infarction, 57, 58t in long-term anticoagulation, 417 for pulmonary embolic disease, 346– 347, 347t for unstable angina, 45t, 46 Unipolar pacing, 290 Unstable angina, 38–50 See also Unstable angina/non-ST elevation myocardial infarction (USA/ NSTEMI) acute aortic dissection vs., 42 acute myocardial infarction vs., 42 acute pericariditis vs., 42–43 acute pulmonary embolism vs., 43 background, 38 chest pain vs., 43 clinical findings, 40–41, 40t physical examination, 41 symptoms and signs, 40–41, 40t clinical spectrum, 38 diagnostic studies, 41–42 angiography, 41–42 ECG, 41 holter monitoring, 41 noninvasive tests, 42 differential diagnosis, 42–43 essentials of diagnosis, 38 gastrointestinal pathologies vs., 43 obstruction in, 40 overview, 38 pathophysiology, 38–40, 39f prognosis, 50, 50t treatment, 43–50, 44f, 45t, 47t antiplatelet/anticoagulant therapy, 45–47, 45t β-blockers, 45t, 47 CABG surgery, 49 calcium channel blockers, 45t, 47–48 catheter-based, 49 definitive, 49–50 general meausres, 43 initial, 43–49, 44f, 45t, 47t intra-aortic balloon counterpulsation, 49 nitrates, 43–45, 45t thrombolytic drugs, 45t, 47 Unstable angina/non-ST elevation myocardial infarction (USA/ NSTEMI), 38–50 See also Unstable angina incidence, 38 long-term risk reduction in patients with, ABCDE approach for, 50, 50t treatment, risk stratification in, 44f Unstable plaque, 38–40 Upstroke, carotid, in aortic stenosis, 84–85, 85f Urokinase, for acute myocardial infarction, 62 Vagal maneuvers for AVNRT, 243 for AVRT, 254 Vagotonic AV block, 277, 284t VALODD trial, 229 Valsalva maneuver, hemodynamic response to, in CHF, 208 syncope and, 316t, 317 VALsartan In Diastolic Dysfunction (VALODD) trial, 229 Valve(s), heart See also specific types bioprosthetic, long-term anticoagulation and, 427, 427t prosthetic See Prosthetic heart valves Valve regurgitation, in valvular heart disease, 485 Valve thickening, in valvular heart disease, 485, 486f, 487t Valve vegetations, in valvular heart disease, 485 Valvular heart disease native, treatment, long-term anticoagulation, 425–426 in pericarditis, 500 polymyositis/dermatomyositis and, 505 in pregnancy, 450–452, 451t rheumatoid, rheumatoid arthritis and, 493–494, 494f in SLE, 485–487, 486f, 487f See also Systemic lupus erythematosus (SLE), valvular heart disease with sudden cardiac death due to, 328t, 329 valve vegetations in, 485 Valvular lesions, obstructive, severe symptomatic, in pregnancy, 448t Valvular tumors, symptoms and signs, 437t, 438 Valvuloplasty, aortic balloon, for aortic stenosis, 88–89 Vascular disease, extracranial, syncope vs., 323–324 Vascular resistance, in normal pregnancy, 447, 447t Vascular surgery patients, management of perioperative patient, 543 Vasoactive drugs, in CHF management, 212t, 214–215 Vasoconstriction, 40 reactive, 355 Vasodilator(s) for acute myocardial infarction, 58t for aortic stenosis, 88 for cardiogenic shock after acute myocardial infarction, 78t, 79 in CHF management, 212t, 214–215 for mitral regurgitation, 119 peripheral, for systemic hypertension, 158t, 161 Vasopressin receptor antagonists, in CHF management, 212t, 213 Vasopressor(s), for cardiogenic shock after acute myocardial infarction, 78t, 79 Vasoreactivity testing, in pulmonary hypertension, 362 Vasovagal near-syncope spell, ambulator monitor reading during, 316, 318, 319f Vasovagal syncope, syncope due to, 316– 317, 316t, 319f Vegetarian diets, for lipid disorders, 20 Vegetation(s), 137–138 growth of, 137–138 metastatic, 138 valve, in valvular heart disease, 485 Venogram, in thrombotic diseases, 490 Venous hypertension, systemic, in CHF, 208 Venous pulse, jugular, Venous thromboembolism (VTE) See also Pulmonary embolic disease; Pulmonary embolism defined, 337 hospitalizations due to, 337 in pregnancy, 338, 350 risk factors, thrombophilia, 337–338, 338t Venous thrombosis, deep, prevention, in perioperative risk management, 540 Venous ultrasonography Doppler, in pulmonary embolic disease, 342–343 in pulmonary embolic disease, 342–343 Ventilation-oxygenation, for cardiogenic shock after acute myocardial infarction, 78, 78t Ventilation-perfusion lung scintigraphy, in pulmonary hypertension, 260, 262, 262f Ventricle(s) left, double-inlet, 414 right, double-inlet, 414 Ventricular aneurysmectomy, in CHF management, 218 Ventricular arrhythmias following myocardial infarction, 68 in pregnancy, 455 restrictive cardiopathy management and, 178 Ventricular cardiomyopathy, right, arrhythmogenic, monomorphic VT and, 305–306, 306f Ventricular defibrillators, for atrial fibrillation, 265–266 Ventricular function, in acute myocardial infarction, 70 Ventricular pacing artifacts, 294 Ventricular septal defects (VSDs), 384–388, 385f, 387f clinical studies, 385–386 diagnostic studies, 386, 387f essentials of diagnosis, 384 ᮢ INDEX 573 overview, 384–385 in pregnancy, 448 prognosis, 386, 388 pulmonary atresia with, tetralogy of Fallot and, 401–405, 402f, 404f See also Tetralogy of Fallot symptoms and signs, 385–386 treatment, 386, 388 Ventricular septal rupture, acute, following myocardial infarction, 65 Ventricular septum, intact, pulmonary atresia with, 413–414 Ventricular tachycardia (VT), 299–314 annular, 308 AV relationship in, 301, 301f, 302f classifications, 301f, 303–304, 304t clinical manifestations, 299 defined, 455 diagnostic issues, 299–301, 300f approach to patient with wide QRS complex tachycardia, 300– 301, 300f misdiagnosis, 299 underdiagnosis, 299 diagnostic studies, 308–310 essentials of diagnosis, 299 fascicular, 307, 308f idiopathic left, 307, 308f magnitude, 299 management, in monomorphic VT, 310–311, 310t See also Monomorphic ventricular tachycardia, management monomorphic See Monomorphic ventricular tachycardia not associated with structural heart disease, 307–308, 307t, 308f, 309f outflow tract, 307–308, 309f overview, 299 polymorphic, 301f, 303–304, 311–313, 312f, 313t, 314f See also Polymorphic ventricular tachycardia in pregnancy, 455–456 prognosis, 313–314 QRS complex axis in, 303 QRS complex duration in, 301, 302f QRS morphology in, 301–303 scar-related, 302f structural heart disease and, 304–307, 305f, 306f syncope due to, 316, 316t Ventricular thrombus, left, treatment, longterm anticoagulation, 427– 429 Ventricular tumors left, physical examination, 438 right, physical examination, 438 Ventricular-arterial coupling, abnormal, in HFpEF, 223 Ventriculography, radionuclide, in CHF, 209 ᮢ 574 Verapamil for chronic ischemic heart disease, 32t, 33 for heart rate control in atrial fibrillation, 261t in perioperative risk management, 540 for SVTs, 235t Vinca alkaloids, cardiac toxicity from, 443t Viral pericarditis, 187 Viridans streptococcal endocarditis, 139 Vitamin K antagonists, oral, in long-term anticoagulation, 417–418 VOO, AOO, DOO, 286, 287f–289f VSDs See Ventricular septal defects (VSDs) VT See Ventricular tachycardia (VT) VTE See Venous thromboembolism (VTE) Wall motion abnormalities, assessment, in chronic ischemic heart disease, 28 Wandering atrial pacemaker, 257–258 INDEX Warfarin management, in perioperative patients, 541 during pregnancy, 430, 461t for pulmonary embolic disease, 349–350 reversal of, 349 for rheumatic mitral valve disease, 427 Waterston shunt, in congenital heart disease management, 415 Waveform, jugular venous, in pulmonic valve disease, 135 Weakness, in CHF, 207 Wenckebach AV block, 276 Wenckebach period, 276 Wide QRS complex tachycardias diagnostic approach to, 300–301, 300f differentiation among, 256–257, 257f, 258f patient history, 303 physical examination, 303 12-lead ECG in, 303, 303t Wolff-Parkinson-White syndrome See also Atrioventricular reciprocating tachycardia (AVRT) atrial fibrillation in, 264, 265f bypass tracts and, in AVRT, 236f, 247– 256, 248f–255f, 256t defined, 247 Ebstein anomaly and, 394, 395f in pregnancy, 455 sudden cardiac death due to, 330 treatment, radiofrequency catheter ablation, 255 World Health Organization functional classes in pulmonary hypertension of, 359t functional classification of pulmonary hypertension of, 365 in pulmonary hypertension classification, 352 on restrictive cardiomyopathy definition, 172 ... Pacing Clin Electrophysiol 20 07 Jan;30(1):85– 92 [PMID: 1 724 1 320 ] Kothari S et al Atriofascicular pathways: where to ablate? Pacing Clin Electrophysiol 20 06 Nov ;29 (11): 122 6–33 [PMID: 17100675] DIFFERENTIATION... Europace 20 06 Dec;8( 12) :1 022 –6 [PMID: 17101 629 ] Skanes AC et al Cryothermal ablation of the slow pathway for the elimination of atrioventricular nodal reentrant tachycardia Circulation 20 00 Dec 5;1 02( 23) :28 56–60... Electrophysiol 20 02 Aug;13(8):831–4 [PMID: 122 127 08] JUNCTIONAL TACHYCARDIA (ACCELERATED AV JUNCTIONAL RHYTHM) ESSENTIALS OF DIAGNOSIS ᮣ ᮣ ᮣ ᮣ Onset and termination: Gradual Heart rate: 70– 120 bpm P