Diastolic Heart Failure – part 10 ppsx

21. Pericarditis and Cardiomyopathy 319 Doppler imaging. It can also be assessed by fl ow propagation velocity with color M-mode, but its accuracy is reduced in a heart with a small cavity as in hypertrophic or restrictive cardiomyopathy. Early diastolic longitudinal velocity of the mitral annulus has been found to correlate with the tau. Although it changes with exercise and preload in healthy hearts, it is less likely affected by exercise and preload when the heart is abnormal or reduced by myocardial process. Therefore, E′ or Ea is almost always reduced in restrictive cardiomyopathy even when left atrial pressure is markedly elevated. 2,19 However, in constrictive pericarditis myocardial relaxation is relatively well preserved. In addition, lateral expansion of the heart during diastole is reduced by constricting pericardium and ventricular fi lling depends more on the aug- menting longitudinal motion of the heart. There- fore, unless there is concomitant myocardial damage near the septal mitral annulus, Ea velocity is not reduced and even increases progressively with worsening of a constrictive process. 14–16 There is very little overlap of Ea between myocardial disease and pericardial disease, Ea being >7 cm/s in the latter, which is again paradoxical to Ea in restrictive cardiomyopathy. 16 Therefore, mitral infl ow tissue Doppler velocity of the mitral annulus in constrictive pericarditis may appear similar to that in healthy individuals, but two- dimensional imaging and hepatic vein Doppler velocities cannot be confused between normal individuals and constrictive pericarditis. In pericardial constriction, cardiac catheterization shows the “dip and plateau” or “square root” confi guration, 20 but a similar pattern is also seen in restrictive cardiomyopathy. 21 The ventricular interdependence and dissociation between intrathoracic and intracardiac pressures characteristic for constriction can also be demonstrated by cardiac catheterization, as described later in this chapter. Normal or mildly elevated brain natriuretic peptide in patients with heart failure and normal ejection fraction also suggests constriction. 2 It appears that brain natriuretic peptide is usually lower in patients with idiopathic constrictive pericarditis than in patients with previous cardiac surgery or radiation. Because brain natriuretic peptide is not specifi c for constrictive pericarditis, defi nitive establishment of the diagnosis of constriction requires further hemodynamic confi rmation by echocardiography or cardiac catheterization. Treatment The treatment for chronic pericardial constriction is complete pericardiectomy. Although medical management transiently ameliorates some of the symptoms, it is not considered defi nitive therapy. Steroids and other immunosuppressive agents have no role in the management of chronic pericardial constriction. In the early period of pericardial constriction (within 3 months of onset), steroids may be of benefi t or spontaneous resolution of constrictive physiology may occur (see discussion of transient constriction). In high dosages over a protracted period of chronic constrictive pericarditis, steroids may be benefi cial with partial resolution of symptoms and mild improvement in constrictive physiology. The benefi ts are transient and the added burden of protracted steroid usage increases comorbidity by the time the patient presents for defi nitive surgical resection of the pericardium, further underscor- ing the need for an early and accurate diagnosis. Chronic pericardial constriction is an inexorable and progressive choking of the intrapericardial structures, resulting in edema, ascites, effusions, hepatic engorgement, low cardiac output, cardiac cachexia, and eventual death. Complete pericardiectomy entails removal of the entire pericardium from the anterior and inferior surfaces of the right ventricle; the anterior, lateral, and diaphragmatic surfaces of the left ventricle; and superiorly the root of the great vessels. Occasionally visceral pericardiectomy is necessary for lowering intracardiac pressure and improving symptoms, and constriction due to visceral pericardium should be suspected in the absence of restrictive cardiomyopathy in a patient who gains transient or incomplete relief from complete parietal pericardial resection. 22 Effusive-Constrictive Pericarditis Effusive-constrictive pericarditis is an interesting condition representing a unique clinical situation of combined pericardial effusion and constrictive pericarditis. Usually, a patient presents initially with pericardial effusion and clinical/hemodynamic evidence of increased fi lling pressures or 320 F. Mookadam and J.K. Oh tamponade/constriction. 23,24 Constrictive hemodynamics persists even after removal or disap- pearance of pericardial effusion and decreased intrapericardial pressure. In some patients, the underlying constrictive pericarditis requires pericardiectomy. In other patients, constrictive pericarditis is due to reversible infl ammation of the pericardium related to the same cause as pericardial effusion and may resolve spontaneously or after treatment with antiinfl ammatory agent(s). The latter condition has been termed transient constrictive pericarditis. 23,25 Transient Constrictive Pericarditis About 7%–10% of patients with acute pericarditis have a transient constrictive phase. 24 These patients usually have a moderate amount of pericardial effusion, and, as the pericardial effusion disappears, the pericardium remains infl amed, thickened, and noncompliant, resulting in constrictive hemodynamics. The patient presents with dyspnea, peripheral edema, increased jugular venous pressure, and, sometimes, ascites, as in patients with chronic constrictive pericarditis. This transient constrictive phase may last 2–3 months before it gradually resolves either spontaneously or with treatment with antiinfl ammatory agents. When hemodynamics and fi ndings typical of constriction develop in patients with acute pericarditis, initial treatment is indomethacin (Indocin) for 2–3 weeks and, if there is no response, steroids for 2 months (60 mg daily × 1 week, then tapered over 6–8 weeks) after ensuring that the pericarditis is not caused by bacteria. Increased pericardial thickness usually returns to normal thickness promptly (within 1–2 weeks), and the patient’s constrictive hemodynamics resolves. All causes of chronic constrictive pericarditis except for radiation treatment have also been identifi ed in transient constrictive pericarditis. 25 It is possible that constrictive pericarditis is curable during the initial phase (less than 3 months) of the disease, and it may be worthwhile treating patients with constrictive pericarditis antiinfl ammatory agents (nonsteroidal and/or steroid) if the onset of constriction is recent. Doppler and invasive cardiac hemodynamic studies of transient constrictive pericarditis are the same as those for chronic constriction. Mag- netic resonance imaging may be able to identify transient constrictive pericarditis by detecting infl ammation as opposed to fi brosis of the pericardium and demonstrate normalization of increased pericardial thickness after medical treatment (Figure 21.11). 26 FIGURE 21.11. Case of transient pericarditis. (Left) Baseline computed tomography scan of the chest shows generalized thickening of the pericardium and a large left pleural effusion. (Right) Repeated computed tomography scan of the chest 1 week later shows marked decrease in the pericardial thickness and no pleural effusion. 21. Pericarditis and Cardiomyopathy 321 Restrictive Cardiomyopathy Restrictive heart disease is characterized by impaired ventricular fi lling because of a relatively stiff and fi brosed myocardium with relatively preserved systolic function. 27–30 In restrictive cardiomyopathy, compliance is impaired because of a primary myocyte fi brosis or is secondary to infi l- trative disorders such as amyloid or mucopoly- saccharide 31–34 Similarly, in endomyocardial fi brosis, the impaired diastolic fi lling is due to a fi brosed and thickened endocardium. In the absence of an identifi able cause of restrictive cardiomyopathy, it is considered a primary form of the disease. This may be familial or idiopathic and can occur in children or adults. 30,34,35 The familial form may be associated with heart block and skeletal myopathy as well as skeletal deformities. 35 Restrictive cardiomyopathy secondary to identifi able infi ltrative or storage processes can be seen in cardiac amyloidosis, hypereosinophilic syndrome, Fabry’s disease, and endocardial fi bro- elastosis. 36–38 Less common etiologies of restrictive cardiomyopathy are drug (e.g., hydroxychloro- quine) and radiation therapy. 38 In general, both left and right ventricles are involved in the disease process but clinical presentation of failure of either the left or the right ventricle may predomi- nate or may present with biventricular congestive heart failure. In all of the restrictive cardiomyopathies, various stages of diastolic dysfunction may be present, depending on the extent and duration of the infi ltrative process. Pathophysiology Restrictive cardiomyopathy results from a primary etiology or is secondary to an infi ltrative process with hemodynamic effects closely resembling those of pericardial constriction. In almost all myopathies, myocardial relaxation is reduced. 2 As myocardial relaxation commences in early diastole, the decline in ventricular pressure during the isovolumic relaxation period is slowed, but left atrial pressure is elevated in symptomatic patients. The combination of reduced myocardial relaxation and increased fi lling pressure results in pre- dominant early diastolic fi lling. Because of a rapid rise in early diastolic pressure, a “dip and plateau” or “square root” confi guration of the LV pressure tracing during early diastole can be seen. Com- pared with constriction, the LV end-diastolic pressures frequently exceed the right ventricular pressure by 5 mm Hg or more. This may be a dis- cerning feature distinguishing restrictive cardiomyopathy from pericardial constriction in which diastolic pressure equalization occurs with differ- ences less than 5 mm Hg between the left and right ventricular fi lling pressures. 21,39 The plateau of the right ventricular diastolic pressure is at least one- third the peak of the right ventricular systolic pressure in patients with constriction compared with restrictive cardiomyopathy in which it is lower. However, there is a large overlap in these hemodynamic values between the two conditions. 21 More specifi c hemodynamic features should be looked for during cardiac catheterization to distinguish constriction from restriction as discussed later in this chapter. Diagnosis The clinical presentation can be very similar to that of pericardial constriction; however, the extracardiac manifestations may provide a clue to the diagnosis. A family history of cardiac disease is more likely to favor primary restrictive cardiomyopathy. The electrocardiogram is variable with normal, low (infi ltration), or increased voltages (Fabry’s disease); heart block is not uncommon. Chest radiography is generally not helpful in distinguishing constriction from restriction unless a calcifi ed pericardium is present. Two-dimensional echocardiography is helpful in identifying specifi c etiologies of restrictive cardiomyopathy as well as differentiating this from pericardial constriction as described earlier (Figure 21.12). Ventricular septal motion is usually abnormal in constriction because of increased ventricular interdependence but does not have respiratory fl uctuation in restrictive cardiomyopathy. Left ventricular size is relatively normal, and the atria are enlarged. The presence of thickened walls with paradoxically normal or low voltages noted on electrocardiography suggests amyloid infi ltration. The typical “sparkly” or “granular” appearance noted in the literature is less specifi c with newer harmonic imaging on echocardio- 322 F. Mookadam and J.K. Oh graphic equipment. Extracardiac manifestations of the underlying disease or other two-dimensional features such as apical thrombus with peripheral eosinophilia help make the diagnosis of hypereosinophilic syndrome (Figure 21.13). In Doppler studies, there is no ventricular interdependence. Hepatic vein Doppler imaging demonstrates diastolic fl ow reversal with inspiration in symptomatic patients with restrictive cardiomyopathy (see Figure 21.8B). FIGURE 21.12. Typical apical four-chamber view of primary restrictive cardiomyopathy. Ventricular dimensions are normal, but both atria are markedly enlarged, as well as the pulmonary vein (arrow). LA, left atrium; RA, right atrium. FIGURE 21.13. Apical four-chamber view of hypereosinophilic syndrome involving the heart. Both apices are filled with eosino- philic thrombus (arrows). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. The other differentiating features on echocardiography in restrictive cardiomyopathy are the absence of respiratory variation in cardiac hemodynamics across the left and right atrioventricular valves and the reduced Ea velocity of the mitral annulus (Figure 21.14). Color M-mode echocardiography demonstrated a reduced propagation velocity of mitral infl ow in restrictive cardiomyopathy, whereas it is relatively normal in constriction. 14–16 If LV cavity size is small, it is, however, 21. Pericarditis and Cardiomyopathy 323 possible to have falsely normal mitral infl ow propagation velocity. Because color propagation velocity as determined by color M-mode and tissue Doppler imaging of the mitral annulus provide similar information, color-M mode does not appear to have increased diagnostic value. Cardiac amyloid is the most common of the secondary restrictive cardiomyopathies. It is rec- ognized by the presence of extra cardiac amyloid (renal, carpal tunnel syndrome, etc.). Cardiac involvement in amyloidosis portends a poor prognosis. 40,41 Regardless of the type of amyloid (primary, secondary to myeloma, senile, or due to chronic infl ammatory conditions), the cardiac fi ndings are essentially the same. Cardiac amyloid is characterized by increased left and right ventricular wall thickness, although normal wall thickness cannot exclude the diagnosis of small pericardial effusion and multivalvular mild regur- gitation due to amyloid infi ltration of the valve. There may be LV outfl ow obstruction with systolic anterior motion of the mitral valve. 42 A B F IGURE 21.14. (A) Characteristic Doppler findings in constrictive pericarditis: mitral inflow velocity (upper left), color M-mode image of mitral inflow with normal propagation velocity and respiratory variation of E velocity (upper right), hepatic vein velocity with diastolic flow reversal with expiration (lower left), and tissue Doppler velocity of the mitral annulus showing increased early diastolic velocity with respiratory variation (lower right). (B) Mitral inflow velocity (left) and tissue Doppler recording (right) of restrictive cardiomyopathy. Mitral inflow velocity has characteristic restrictive inflow with increased E velocity and a short deceleration time. Early diastolic mitral annulus velocity (arrow, 2 cm/s) is markedly reduced. 324 F. Mookadam and J.K. Oh Restrictive diastolic function is noted when advanced in the presentation. Idiopathic hypereosinophilic syndrome is defi ned as an elevated eosinophil count exceeding 1,500/µL for at least 6 months and absence of an underlying cause for the eosinophilia. 43 Cardiac involvement has three stages: asymp- tomatic necrotic stage, intracavitary thrombi stage, and the fi nal fi brotic stage with endomyocardial fi brosis and damage to the atrioventricular valve. Echocardiographic fi ndings usually demonstrate apical obliteration by thrombus, atrial enlargement, diastolic dysfunction, and relatively preserved systolic function. 44 Atrioventricular valve involvement is common. Computed tomography and magnetic resonance imaging in restrictive cardiomyopathy have a limited role, as wall thickness and the morphology of the atria and ventricles can be assessed by echocardiography. Treatment The prognosis for restrictive cardiomyopathy is heterogeneous and depends on the underlying etiology. However, even in the same etiologic cat- egory, prognosis differs and depends on extracardiac involvement in part or on the extent of myocardial involvement in a particular patient. The pattern of diastolic dysfunction also has a prognostic implication within the same disease class. 40 Treatment essentially is directed at symptomatic relief, which lowers systemic venous overload and pulmonary venous congestion. Diuretics should be used with the cognition that excess may worsen cardiac output and precipitate fatigue and hypotension. Digoxin should not be used in amyloid heart disease or in a restrictive cardiomyopathy that exhibits relative bradycar- dia or elements of heart block. The most curative therapy is cardiac transplantation. New Invasive Hemodynamic Features to Differentiate Constriction From Restriction Despite the different pathophysiologic mechanisms of constrictive pericarditis and restrictive cardiomyopathy, they share many similar invasive hemodynamic fi ndings. Both have increased atrial pressures and equalization of end-diastolic pressures, although the equalization is more common in constrictive pericarditis. The dip and plateau pattern seen in ventricular diastolic pressure tracings have classically been associated with constriction. This fi nding refl ects rapid early diastolic fi lling of the ventricles, followed by an abrupt cessation of fi lling in mid and late diastole. This pattern is also found in restrictive cardiomyopathy and is the result of the noncompliant myocardium limiting mid and late diastolic fi lling. As in noninvasive evaluation, one must use respiratory variation in ventricular fi lling to differentiate between constriction and restriction during cardiac catheterization. The dissociation between intrathoracic and intracardiac pressures in constriction causes a respiratory variation in pressure difference between pulmonary capillary wedge pressure and LV diastolic pressure (see Figure 21.6) Therefore, there is less fi lling of the LV and the LV systolic pressure decreases with inspiration, while fi lling increases in the right ventricle resulting in an increase in right ventricular systolic pressure. With expiration, LV fi lling increases, which raises LV systolic pressure, and right ventricular fi lling decreases, resulting in a lower right ventricular systolic pressure. This reciprocal diastolic fi lling in the left and right ventricles causes a discordant systolic pressure change between them in constriction. 39 Because this respiratory differential fi lling originates from the left side of the heart, the LV pressure will decrease at an early phase of inspiration and the right ventricular systolic pressure increases toward the end of inspiration (Figure 21.15). In restrictive cardiomyopathy, however, hemodynamic changes are the result of the stiff ventricular myocardium. The intrathoracic pressures are transmitted to the myocardium, and the pressure gradient between the pulmonary capillary wedge pressure and the LV diastolic pressure remains constant throughout the respiratory cycle. Simultaneous pressure measurement of the left and right ventricles will be concordant throughout the respiratory cycle so that with inspiration the decrease in intrathoracic pressure causes a decrease in LV and right ventricular systolic pressures equally. Therefore, the unique hemodynamic features of constriction, interventricular interaction, variation in ventricu- 21. Pericarditis and Cardiomyopathy 325 lar fi lling with respiration, and discordant systolic pressure change in the right and left ventricles need to be demonstrated to diagnose constrictive pericarditis. Endomyocardial Biopsy An endomyocardial biopsy procedure may be performed for patients expected to have restrictive cardiomyopathy. The biopsy is usually done to exclude a specifi c heart muscle disease such as amyloid or sarcoidosis. Biopsy tissue may show idiopathic restrictive cardiomyopathy that demonstrates nonspecifi c fi brosis with increased collagen deposition and myocellular hypertrophy without necrosis or disarray. The diagnostic yield is low and rarely useful in distinguishing restrictive cardiomyopathy from constrictive pericarditis. Conclusion The differentiation of pericardial constriction from restrictive cardiomyopathy remains a diagnostic challenge for clinicians. For patients pre- senting with symptoms of congestive heart failure and a normal ejection fraction for whom a diagnosis of pericardial constriction or restrictive cardiomyopathy is under consideration, the dis- tinction is of paramount importance because management and prognosis hinge on an accurate diagnosis. Noninvasive testing is increasingly benefi cial with detailed echocardiographic exami- nations including a complete Doppler study with FIGURE 21.15. Simultaneous left ventricular (LV) and right ventricular (RV) pressure tracings from restrictive cardiomyopathy and constrictive pericarditis. In both conditions, there is equalization of ventricular end-diastolic pressures and “square root” sign (or “dip and plateau”). However, in restrictive cardiomyopathy there was a concordant change in the LV and RV systolic pressures with respiration, whereas there was a discordant pressure change in the LV and RV systolic pressures with respiration in constrictive pericarditis. EXP, expiration; INSP, inspiration. 326 F. Mookadam and J.K. Oh respirometer to assess respirophasic changes of intracardiac hemodynamics and tissue Doppler imaging. Computed tomography and magnetic resonance imaging are useful to demonstrate increased pericardial thickness and/or characteristic ventricular septal motion for constriction. However, normal pericardial thickness alone cannot exclude the diagnosis of constrictive pericarditis. Hemodynamic cardiac catheterization may still be necessary to help make a diagnosis when the diagnosis is still uncertain after a comprehensive noninvasive evaluation. Occasionally exploratory thoracotomy may be necessary for a defi nitive diagnosis when all noninvasive, catheterization, and biopsy procedures fail to provide a diagnosis and yet constriction or restriction still remains under consideration. References 1. Senni M, Rodeheffer R, Tribouilloy C, et al. Use of echocardiography in the management of congestive heart failure in the community. J Am Coll Cardiol 1999;33:164–170. 2. Oh J, Hatle L, Tajik A, Little W. Diastolic heart failure can be diagnosed by comprehensive two- dimensional and Doppler echocardiography. J Am Coll Cardiol 2006;47(3):500–506. 3. Leya F, Arab D, Joyal D, et al. The effi cacy of brain natriuretic peptide levels in differentiating constrictive pericarditis from restrictive cardiomyopathy. J Am Coll Cardiol 2005;45:1900–1902. 4. Ling L, Oh J, Schaff H, et al. Constrictive pericarditis in the modern era. Evolving clinical spectrum and impact on outcome after pericardiectomy. Cir- culation 1999;100:1380–1306. 5. 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Smiseth and Michał Tendera 329 Definition and Epidemiology of Diastolic Heart Failure Congestive heart failure is a clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to eject or fi ll with blood. The main symptoms are dyspnea and fatigue, which limit exercise capacity, and there is fl uid retention and elevated fi lling pressures, which can lead to pulmonary vascular congestion or peripheral edema. In addition, there is typically cardiac dilatation and reduced left ventricular (LV) systolic function. Over the past two decades this concept has been challenged because a number of studies confi rm that up to 50% of patients with congestive heart failure have normal LV ejection fraction (LVEF; Chapter 14), and this entity has been widely referred to as diastolic heart failure (DHF). Table 22.1 summarizes the key issues of DHF. Patients with acute heart failure and pulmonary edema may also have a normal LVEF. 1 As reviewed in Chapter 1, a preserved EF in DHF merely indi- cates that global LV performance is maintained by activation of compensatory mechanisms. Many patients with normal EF appear to have mild systolic dysfunction, as indicated by reduced systolic atrioventricular plane displacement. 2 Further- more, most patients with SHF have impairment of diastolic function. Therefore, DHF and SHF should not be considered as entirely different disease entities. In DHF, however, the pathophysiology is dominated by abnormal LV diastolic properties, whereas loss of contractile force domi- nates in SHF. Diastolic heart failure with a normal EF is relatively uncommon in younger patients but increases in importance in the elderly. Because LV systolic function may not be entirely normal in DHF, and because most patients with SHF have diastolic dysfunction, a different termi- nology has been proposed. Rather than DHF, one may use the terms heart failure with preserved ejection fraction or heart failure with normal ejection fraction (HFNEF). Similarly, SHF may be called heart failure with reduced ejection fraction (HFREF). The reason why this nomenclature may be preferred is that it makes no a priori assump- tions about pathophysiology. On the other hand, HFNEF may confuse the issue because this termi- nology puts too much emphasis on EF, which is a suboptimal measure of LV function. Furthermore, HFNEF by defi nition also includes conditions such as mitral stenosis, cardiac tamponade, constrictive pericarditis, and cor pulmonale, which do not represent LV myocardial dysfunction. Therefore, neither of the terms is perfect, and at present both are in use. Patients with SHF and DHF have similar symptoms and signs, and therefore clinical history and physical examination do not differentiate between the two conditions. The diagnosis of DHF requires measurement of LV systolic function, and this is done most often with echocardiography. Invasive LV angiography or other imaging techniques may be used as well. Somewhat different cut-off values for normal or mildly reduced LVEF have been used in the literature. In the recent report from the European Study Group on Diastolic Heart Failure 3 and in the National Heart, Lung and [...]... 5–9 Diastolic heart failure (DHF), 3, 9–1 5, 14, 22 acute heart failure and, 235 aging and, 20 6–2 07, 33 1–3 32 anemia and, 210 atrial fibrillation and, 207, 20 9–2 10 CAD and, 210 cardiac output with, 126 cardiovascular congestion in, 2 2–2 3 chronic heart failure and, 1 1–1 5 concentric hypertrophy and, 122 decompensated, 181 definition of, 121, 32 9–3 30 diabetes and, 207, 210, 336 diagnosis of, 14 9–1 60, 17 5–1 83,... Myocardial relaxation, 2 1–3 6, 24 determinants of, 2 7–3 0 load and, 27 time course of, 2 7–3 0 Myocardial stiffness, 34, 14 3–1 45 cardiomyocytes and, 3 0–3 1 Myocardial stretch, 25 4–2 57 Myocardial tagging, 166 Myocardial velocities, 9 9–1 12 assessment of, 9 9–1 00 diastolic deformation indexes, 11 1–1 12 diastolic dysfunction and, 10 7–1 08 interpretation of, 10 6–1 07 parameters of, 10 0–1 06 Myocarditis, 166 Myocytes... ventilation, 4 9–5 0 344 Heart transplantation, 233 Helsinki Aging Study, 215 Hemochromatosis, 231 Hemodynamic pump, 9–1 0 failure of, 1 1–1 2 Hepatic disease, 313 Hepatic vein velocities, 15 3–1 56 HF See Heart failure HFNEF See Heart failure with normal ejection fraction HFPEF See Heart failure with preserved ejection fraction HFREF See Heart failure with reduced ejection fraction Hong-Kong Diastolic Heart Failure. .. Myocardial stiffness; Ventricular stiffness with DHF, 77 diastolic myocardial, 14 3–1 45 end -diastolic, 2 1–3 6 of LA, 6 0–6 1, 63 of LV, 142 muscle, 14 3–1 45 Strain, 100 , 170 atrial, 6 1–6 2 D and, 103 imaging and, 102 systolic, 112, 229 Strain rate, 6 1–6 2, 100 , 103 , 11 1–1 12, 229 diastolic, 112 imaging and, 102 Stress-induced tachycardia, 54 Stress-strain relation, 14 3–1 45 Stroke volume (SV), 9, 34, 64, 166 with DHF,... dysfunction, 15 6–1 58 Growth factors, 31 Guanosine monophosphatedependent protein kinase, 32 Guidelines for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology, 182 H HCM See Hypertrophic cardiomyopathy Heart failure (HF) See also Chronic heart failure; Congestive heart failure; Diastolic heart failure; Systolic heart failure ACE-I for, 22 3–2 27 combined diastolic and... 22 7–2 28 Catecholamines, 7 3–7 4 Catheterization, 207 in constrictive pericarditis, 319 Cavity size, 2 5–2 6 Chamber compliance, 89 CHARM See Candesartan in Heart Failure- Assessment of Reduction in Mortality and Morbidity CHF See Congestive heart failure Chronic heart failure DHF and, 1 1–1 5 phenotypes of, 1 3–1 5 progression of, 1 1–1 3 treatment of, 22 3–2 34 Chronic obstructive pulmonary disease (COPD), 21 0–2 11... 17 5–1 83 neurohormones and, 7 1–7 7 obesity and, 20 6–2 07 prevalence of, 20 6–2 09 prognosis in, 21 3–2 19, 336 renal dysfunction and, 21 0–2 11 respiratory diseases and, 210 vs SHF, 11 9–1 31 with SHF, 18 1–1 82 smoking and, 210 stiffness with, 77 stroke volume with, 126 symptoms of, 129 treatment of, 22 3–2 36, 336 trials of, 224 valvular heart disease and, 336 women and, 209 Diastolic myocardial stiffness, 14 3–1 45... abnormalities in patients with “isolated” diastolic heart failure and diastolic dysfunction Circulation 2002 ;105 :119 5– 1201 3 Paulus WJ, et al How to diagnose diastolic heart failure A consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction By the Heart Failure and Echocardiography Associations of the European Society of Cardiology Eur Heart J Advance Access published... myocardial stiffness, 14 3–1 45 Diastolic pressure-volume DHF and, 26 horizontal position of, 25 SHF and, 26 slope of, 2 5–2 7 vertical position of, 2 4–2 5 Diastolic relaxation, 29 Diastolic suction, 24, 82, 87 Diastolic velocities, 10 8–1 09 DIG See Digitalis Investigation Group Digitalis, 23 0–2 31 Digitalis Investigation Group (DIG), 21 3–2 14, 21 6–2 17, 224, 23 0–2 31 Digoxin, 23 0–2 31 amyloidosis and, 324 Dilated... 17 5–1 83, 332 diastolic pressure-volume and, 26 echocardiography for, 14 9–1 60 EF with, 125 epidemiology of, 20 5–2 11 etiology of, 33 0–3 31 fibronectin and, 31 hospital admissions for, 21 8–2 19 hyperlipidemia and, 210 hypertension and, 18 0–1 81, 207, 209 invasive evaluation of, 13 7–1 45 key issues with, 330 Index LV and, 12 1–1 26 LVEF and, 20 5–2 11, 21 3–2 19 measurement of, 12 9–1 30 mortality with, 21 3–2 14 natriuretic . W. Diastolic dysfunction in congestive heart failure. N Engl J Med 1991;325:155 7–1 564. 28. European Study Group on Diastolic Heart Failure. How to diagnose diastolic heart failure. Eur Heart. failure. Eur Heart J 1998;1998(19):99 0–1 003. 29. Kabbani S. Diastolic heart failure. How to diagnose diastolic heart failure. Eur Heart J 2000;18:50 1–5 09. 30. Ammash N, Seward J, Bailey K,. dysfunction. Etiology of Diastolic Heart Failure Diastolic heart failure is not a specifi c disease, and it is therefore important to search for underlying disorders. Diastolic heart failure is associated

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