Ebook Challenging concepts in cardiovascular medicine - A case based approach with expert commentary: Part 2

(BQ) Part 2 the book Challenging concepts in cardiovascular medicine - A case based approach with expert commentary presents the following contents: Heart rhythm disturbances, adult congenital heart disease, general cardiovascular medicine.

16 Paroxysmal atrial fibrillation Shouvik Haldar Expert commentary Professor John Camm Case history A 55-year-old man was referred to cardiology outpatients by his general practitioner (GP) with a 2-month history of intermittent palpitations He was taking ramipril for hypertension and had no other relevant medical history He drank 30 units of alcohol per week and was a lifelong non-smoker There was no significant family history He described four recent episodes of self-terminating palpitations They were of sudden onset, occurring both at rest and during mild exertion, and had each lasted between 15 and 60 minutes The first episode had occurred after he had returned from a party, having consumed a significant amount of alcohol The others had occurred whilst at work On each occasion, he had felt his heart pounding fast and chaotically and during the more prolonged attacks, he had felt dizzy and breathless Clinical examination revealed a regular pulse of 75 beats per minute (bpm) with a blood pressure (BP) of 145/80 mmHg He had normal heart sounds with no signs of cardiac failure His 12-lead electrocardiogram (ECG) confirmed a normal sinus rhythm with a normal electrical axis Transthoracic echocardiography (TTE) confirmed a normal cardiac structure and function with a mildly dilated left atrial size of 40 mm (normal 27–38 mm) Exercise stress testing did not induce any arrhythmias and was negative for ischaemia Routine blood tests, including thyroid function, were normal At this stage, there was a high clinical suspicion of paroxysmal atrial fibrillation (PAF) However, in the absence of ECG evidence to confirm this diagnosis, treatment was not commenced He was advised to reduce his alcohol and caffeine intake and an outpatient 7-day event recorder was requested with subsequent follow-up arranged By the time of his 6-week follow-up, he had had a further two symptomatic episodes Neither of these had occurred during his 7-day event recorder which had not documented any arrhythmias Fortunately, the patient had attended Accident & Emergency (A&E) with a symptomatic episode Despite spontaneously reverting to sinus rhythm, an initial ECG had captured fast AF In view of his history, the A&E specialist had given him a copy of the ECG, which he had been instructed to bring along to his follow-up appointment (Figure 16.1) Now with firm evidence of PAF, treatment options were discussed at his outpatient review Although his paroxysms were fairly infrequent, the patient was highly symptomatic from them With no evidence of structural heart abnormalities or ischaemic heart disease, a class I AAD in the form of flecainide 300 mg was initiated as a pillin-the-pocket strategy The CHADS2 criteria (Table 16.1) were used to stratify the patient’s thromboembolic risk which duly scored the patient at ‘1’ This gave the patient a ‘moderate risk’ of thromboembolism and the patient was commenced on aspirin 75 mg once daily Expert comment Treatment with an anti-arrhythmic drug (AAD) should not be readily considered without a definitive ECG diagnosis However, if you have tried and failed to get a recording, it may be reasonable to try a beta-blocker Expert comment It is a good idea to give the patient a letter requesting A&E to an ECG as soon as the patient turns up complaining of an arrhythmia A&E can then be asked to give a copy to the patient and fax a copy to the physician If involving the GP, you should first check that they have an ECG machine and again give the patient a letter for the GP practice Expert comment With a CHADS2 score of 1, current guidelines allow the doctor/patient to choose aspirin or warfarin However, the evidence base for aspirin is relatively poor Expert comment A ‘pill-in-the-pocket’ strategy should really be tested in A&E or Coronary Care Unit (CCU) before patients can be discharged to take the medication themselves in the community 166 Challenging concepts in cardiovascular medicine Clinical tip Diagnosis of arrhythmias with regard to temporal relation A thorough history and clinical evaluation is essential in diagnosing arrhythmias, but tools such as ambulatory ECG monitors can be invaluable In those with frequent (daily) symptoms, a Holter monitor can continuously record and save data for up to 48 hours Patients are encouraged to keep an event diary, allowing the correlation of symptoms with ECG recordings Patients with infrequent symptoms require loop event recorders that can continuously record data, with information stored only upon activation by the patient Once activated, they are programmed to capture the preceding and subsequent two minutes of data Compared to Holter monitors, event recorders can be used for longer periods, have a higher yield in diagnosing arrhythmias, and have been proven to be more cost-effective and efficacious for the evaluation of palpitations [1] If prolonged external ambulatory event monitors fail to document an arrhythmia, an implantable loop recorder (e.g Reveal™ device) can be used This device is implanted subcutaneously and has a battery life of up to two years It continuously scans for arrhythmias and automatically stores tachycardia or bradycardia events for future analysis, in addition to information when activated by the patient Figure 16.1 ECG on arrival to Accident & Emergency (courtesy of Jonas de Jong) Learning point Aetiology of atrial fibrillation AF is a complex re-entrant arrhythmia based on the coexistence of multiple wavelets of electrical activity within the atria The exact aetiology remains unclear, but multiple mechanisms have been implicated in the genesis of AF These include ectopic activity in the form of pulmonary and nonpulmonary vein triggers, susceptible atrial substrates (e.g atrial tissue that perpetuates AF secondary to structural or electrical remodelling, fibrosis or gap junction mutations), and areas with excessive autonomic activity Of these, the pulmonary vein foci, which represent muscular ‘sleeves’ of atrial myocardium that extend into the pulmonary veins, have been shown to exhibit the majority of ectopic activity, leading to the triggering of AF [2] Table 16.1 Adapted CHADS2 scheme for the assessment of stroke risk in patients with (non-valvular) AF [3] CHADS2 risk factor Points Congestive heart failure Hypertension (systolic >160 mmHg) Age > 75 years Diabetes Prior stroke or TIA 1 1 Total CHADS2 score Risk of stroke Annual stroke rate (%) Antithrombotic therapy indicated 2–6 Low Moderate High 1.9 2.8 4.0–18.2 Aspirin Warfarin or aspirin Warfarin Learning point How to reduce the risk of stroke in atrial fibrillation The most feared complication of AF is stroke secondary to thromboembolism As the prevalence of AF increases with an ageing population, prophylaxis against thromboembolism remains the fundamental issue in the therapeutic management of AF In practice, the risk of stroke is increased four- to five-fold in non-valvular AF This is regardless of whether patients have paroxysmal or more prolonged bouts of AF, i.e persistent or permanent Prophylaxis with antiplatelet agents or oral anticoagulants is determined by a patient’s risk of thromboembolism Well-validated and simple risk stratification models, such as the CHADS2 (Table 16.1) and the NICE thromboprophylaxis guideline schemes, are commonly used to aid decision-making [4] Both of these schemes classify patients into low-risk, moderate-risk, and high-risk categories continued 167 Case 16 Paroxysmal atrial fibrillation Low-risk patients are managed with aspirin (75–300 mg daily) Those at moderate risk can be treated with either aspirin or warfarin The majority of patients fall into this intermediate category with the decision to anticoagulate based on risk-benefit assessments and a patient’s preference rather than robust data Patients at high risk should be anticoagulated with warfarin, aiming for a target INR of 2–3 Combination therapy with aspirin and clopidogrel should only be used in patients whose risk warrants warfarin for thromboprophylaxis, but who are unable to tolerate it The CHADS2 score does have its limitations as it does not take into account all risk factors for stroke Many patients fall into the moderate-risk category where data exist to show that these patients may well benefit more from warfarin than aspirin A more risk factor-orientated approach in stroke risk stratification is the CHA2DS2-VASc score which refines the score by considering additional factors (refer to Case 3, Table 3.1), thus providing a more accurate assessment of thromboembolism risk The left atrial appendage (LAA) is the origin for a large proportion of thromboemboli Early surgical efforts to obliterate this structure proved favourable in reducing the risk of thromboembolism and current guidelines recommend routine surgical excision of the LAA, in addition to mitral valve surgery to reduce the risk of stroke [5-8] In those who warrant oral anticoagulation, but have contraindications, a new approach, based on this principle, has evolved Closing the LAA with a percutaneous device (Figure 16.2) appears to be a promising alternative, with encouraging results in a recent study using the Watchman® device [9] Clinical tip National Institute of Health and Clinical Excellence (NICE) guidelines for the ‘pill-in-the-pocket’ strategy [4] In patients with PAF, relatively infrequent (100 mmHg and a resting heart rate above 70 bpm; Able to understand how and when to take the medication In those with PAF, either rhythm control or rate control may be used as the initial strategy However, there are minimal clinical data on which is the better approach This is due to the fact that only 25% of patients involved in the major clinical trials comparing rhythm control vs rate control had PAF Interestingly, those who were highly symptomatic were also excluded from the trials Generally speaking, in PAF, rhythm control to reduce the number and length of paroxysms should be the initial approach If this fails having tried the different AADs available, then a rate control strategy to control the ventricular response is acceptable Of course, the option of a more interventional approach remains and is dealt with later in the text 168 Challenging concepts in cardiovascular medicine Learning point How to maintain sinus rhythm post-cardioversion Expert comment Class I agents can only be used in patients without significant underlying heart disease Oral sotalol may cause cardioversion Intravenous sotalol may also be effective although it is not widely used Intravenous amiodarone is highly effective, but it may take 24 hours or more to achieve cardioversion Expert comment The administration of adenosine in these circumstances highlights the fact that adenosine does not slow atrial flutter frequency; if anything, it tends to accelerate the arrhythmia Despite the fact that the direct effects of adenosine are transient, adenosine may also cause atrial flutter to degenerate into atrial fibrillation which may then persist The majority of drugs used for pharmacological cardioversion are also used to maintain sinus rhythm Amiodarone has consistently been shown to be the most effective, but chronic use is limited due to its extensive side effect profile [12-14] Standard beta-blockers offer an attractive combination of modest efficacy and limited adverse effects Therefore, they are recommended as first-line in the prevention of PAF, followed by class I agents [4,15] Sotalol is equally as effective as amiodarone in converting AF into sinus rhythm [12] It is also effective in the maintenance of sinus rhythm [16] Its class III action requires doses above 80 mg twice daily and the ECG should be checked after dose adjustments to look for possible QT interval prolongation Although this is part of its therapeutic effect, when the QTc is >500 ms, the dose should be cut back Sotalol should be avoided in those with significant conduction disease (second- or third-degree atrioventricular block [AVB]), significant left ventricular dysfunction, and renal impairment due to the risk of QT prolongation and pro-arrhythmia Two months later, the patient re-presented to the A&E department Having taken a dose of flecainide for an episode of his palpitations, he experienced a sudden acceleration in his heart rate, rendering him very symptomatic He was found to be haemodynamically stable with a narrow complex tachycardia (NCT) and a ventricular rate of 240 bpm He was given mg of intravenous adenosine which transiently revealed atrial flutter waves at a rate of 240 bpm before reverting back to the tachycardia At this point, a cardiology consult was requested The specialist diagnosed atrial flutter with 1:1 AV conduction He administered mg of intravenous verapamil to the patient which achieved 2:1 AV block and slowed the flutter rate down to 150 bpm One hour later, the arrhythmia terminated and the patient was back in sinus rhythm Prior to discharge, the cardiology team reviewed his medical therapy As his symptoms were becoming increasingly distressing, it was felt that the ‘pill-in-the-pocket’ approach was no longer appropriate He was switched to regular flecainide, with the addition of betablockers to prevent accelerated AV conduction in the event of further atrial flutter Three months later, the patient was reviewed in outpatients As a result of increasing lethargy and daytime somnolence, he had stopped taking beta-blockers and his GP had prescribed diltiazem as an alternative with continued flecainide Unfortunately, Clinical tip Class IC anti-arrhythmic drugs and co-prescribing an atrioventricular nodal blocking agent ● ● ● Class IC AADs (flecainide, propafenone, and quinidine) are sodium channel blockers and when used in atrial flutter, can slow the rate of the arrhythmia Therefore, having administered these agents, a narrow complex atrial flutter at 300 bpm with 2:1 AV conduction at 150 bpm may paradoxically convert to a faster NCT at 200–250 bpm This is because the atrial flutter rate may slow enough to allow the AV node to conduct in a 1:1 fashion [17] It is also important to note that the faster ventricular response may occasionally result in a wider QRS morphology because of enhanced sodium channel blockade at these rates The resulting broad complex tachycardia created may be mistaken for ventricular tachycardia [18] In a haemodynamically stable patient where this is suspected, intravenous adenosine is a safe way to establish the diagnosis; if flutter is confirmed, acute rate control with an intravenous calcium channel blocker or beta-blocker should be commenced immediately In either circumstance, the resultant accelerated ventricular response may lead to haemodynamic instability and needs to be treated accordingly Importantly, this effect can also occur in AF as these drugs can ‘organize’ AF into atrial flutter, as in this case Therefore, experts advocate co-prescribing an AV nodal blocking agent with class I AADs in atrial arrhythmias to prevent accelerated ventricular responses 169 Case 16 Paroxysmal atrial fibrillation despite combination therapy, his symptoms remained refractory Although not keen on invasive procedures, the patient was keen for symptomatic relief and agreed to discuss the option of catheter ablation with an electrophysiologist Learning point Catheter ablation for atrial fibrillation explained Early catheter-based attempts to cure AF focussed on replicating the surgical Cox–Maze procedure Linear lesions via radiofrequency catheter ablation were made to isolate parts of the atria, thus preventing the propagation of AF This technique gave credence to the concept of susceptible atrial substrates [19] It was during these procedures in 1998 when Haissaguerre et al discovered that ectopic pulmonary vein foci played a significant role in the initiation of AF [2] Subsequent ablation procedures were aimed at pulmonary vein isolation (PVI) to eliminate the triggering of AF These procedures produced encouraging results, so much so that PVI has gone on to become the cornerstone of all current AF ablation techniques (Figure 16.3) Expert comment Young patients often find beta-blocker therapy very debilitating, especially when trying to prevent an occasional AF recurrence The alternative agents to protect the ventricles from a rapid rate in PAF are nondihydropyridine calcium antagonists (verapamil or diltiazem), but digoxin should not be used in this setting since it may encourage recurrence of the arrhythmia The procedure is generally done under general anaesthetic preceded by on-table transoesophageal echocardiography to exclude LAA thrombus After transvenous femoral access, the left atrium is entered by means of trans-septal puncture Mapping and ablation is performed in the region of the pulmonary vein antrum to isolate the veins electrically from the atrium In more refractory cases, additional procedures may be required to check and ensure successful PVI and/or map and ablate additional susceptible atrial substrates [20] PAF is predominantly a trigger-dependent phenomenon (particularly in recent onset cases), unlike persistent or permanent AF where electrical and structural remodelling has had time to alter the atrial substrate Ablation techniques reflect these differences with PVI enough to ‘cure’ most patients with PAF whereas persistent or permanent AF requires PVI plus additional substrate modification (as mentioned above) This may entail additional linear lesions in the left atrium and/or targeting areas of abnormal electrical activity in either atrium (complex fractionated electrograms) to eliminate arrhythmogenic areas that maintain AF propagation [21] Success rates in PAF patients are as high as 80 to 90% (1-year follow-up data) whereas in persistent/ permanent AF, it is in the region of 50 to 70% (mean follow-up data of