Evidence-based Cardiology – part 8 pps

(11·0%) (RR 0·66, 95% CI 0·53–0·81, P ϭ0·0009). There were fewer sudden deaths in the metoprolol CR/XL group than in the placebo group (79 v 132; RR 0·59, P ϭ0·0002) and fewer deaths from worsening heart failure (30 v 58; RR 0·51, P ϭ0·0023). 197 In the BEST trial the effects of the non-selective ␤ blocker bucindolol was compared with placebo in 2708 patients with CHF in NYHA class III–IV. 207 Bucindolol was initiated with 3mg 2ϫ/day and titrated up over 6–8 weeks to 50–100mg 2ϫ/day. The study was prematurely terminated by the safety committee. Mortality was reduced from 447 deaths to 409 deaths (RR 0·91, 95% CI 0·88–1·02, P ϭ0·12). In a subgroup analysis there was a heterogeneous response among groups analyzed. Patients with NYHA class IV or ejection fraction below 20% did not appear to benefit. Furthermore, in a subgroup of African-Americans there was a 17% excess mortality suggesting a lack of benefit among these patients. However, these were post hoc analyses and not prespecified end points. The recently reported COPERNICUS trial was performed in 2289 patients with symptomatic chronic heart failure with symptoms at rest or at minimal exertion. 198 Carvedilol was initiated with 3·125mg ϫ2/day and titrated to 25 mg ϫ2/day. There was a significant reduction in all-cause mortality from 190 (18·5% per patient-year) to 130 (11·4%) with a hazard ratio of 0·65 (95% CI 0·52–0·81); P ϭ0·0001. The effect was consistent among a number of prespecified subgroups. In a post hoc subgroup analysis of patients in the MERIT-HF study with similar characteristics as the patients in the COPERNICUS trial, with an EF of Ͻ0·25 and NYHA class III–IV, there was a comparable reduction in all-cause mortality (45 [11%] v 72 [18%] deaths; hazard ratio 0·61, 95% CI 0·11–0·58, P ϭ0·0086). 208 All three large ␤ blocker studies (CIBIS-II, MERIT-HF, COPERNICUS) had been stopped early because of clear evidence of benefit and therefore resulted in limited long-term experience with this treatment. Nevertheless, these trials have extended the documentation for survival benefit with ␤ adrenergic blockers to more than 15000 patients. Overall experience from these trials is that treatment has been possible to initiate with high tolerability during the titration phase. As the BEST trial showed somewhat different results than the other three trials and also compared with the meta- analysis by Doughty et al 209 there is a suggestion that these agents differ in their effect. Several smaller trials have been published comparing metoprolol and carvedilol. A recent crossover study suggested that there are differences with respect to receptor effects, while long-term clinical effects were comparable. 210 This is further explored in the COMET trial where carvedilol and metoprolol are compared in 3042 patients. The trial finishes its follow up in October 2002, and results are expected by the end of 2002. The effects of ␤ blockers in the elderly are currently being studied in the SENIORS trial where nebivalol is being compared with placebo in patients above 70 years of age and with chronic heart failure. In the situation of heart failure secondary to acute myocardial infarction, there are data from several older large post myocardial infarction trials that ␤ blockers would be beneficial also when symptoms of heart failure are pres- ent. 173–175 These findings were first tested prospectively in the CAPRICORN study, in which carvedilol or placebo was given to 1959 patients with a recent myocardial infarction and signs of left ventricular dysfunction (EF Յ40%). 211 There was no effect on the primary end point mortality or cardiovascular hospitalization (hazard ratio 0·92, 95% CI 0·80–1·07), but there was a statistically significant reduction in all-cause mortality, 166 (15%) versus 151 (12%) deaths (hazard ratio 0·77, 95% CI 0·60–0·98, P ϭ0·03). The risk reduction was of similar magnitude as previous post myocardial infarction trials with ␤ blockers. Documented value of ␤ blockers Proven indication: always acceptable ● To improve long-term survival in patients with mild to severe heart failure ● To improve cardiac function and symptoms in patients with symptomatic chronic heart failure, already on conventional treatment with ACE inhibitors (or an ARB), diuretics or digitalis ● To improve outcome in patients with acute myocardial infarction and left ventricular dysfunction with or without symptomatic heart failure ● Symptomatic treatment of patients with heart failure who do not tolerate ACE inhibitors Acceptable indication but of uncertain efficacy and may be controversial ● Symptomatic heart failure from diastolic dysfunction Not proven: potentially harmful (contraindicated) ● Acute decompensated heart failure ● CHF with pronounced hypotension and/or bradycardia Clinical perspective Drug titration and intolerance Due to initial negative inotropic effects, treatment with ␤ blockers requires a slow titration procedure. Parallel to myocardial recovery, ␤ blocker dosages can usually safely be increased. It has been noticed that patients with simulta- neous marked hypotension and tachycardia, expressing severe decompensation, may not tolerate ␤ blockers. Nevertheless, figures of intolerance have been low in randomized trials, comparable to those of ACE inhibitors. Starting doses with different ␤ blockers have been: bisoprolol 1·25mg/day; carvedilol 3·125–6.25mg 2ϫ/day; metoprolol Grade C Grade C Grade A Evidence-based Cardiology 670 12.5–25mg/day. Doses are increased every 1–2 weeks, when doses are doubled, until maintenance doses of full conventional ␤ blockade are achieved. Although a reduction in heart rate probably is important, it has not been possible to adequately identify responders from non-responders to ␤ blocker therapy. In cases with significant obstructive pulmonary disease, ␤ blockers should be used with caution, and a selective ␤ blocker would be preferred. Central nervous system modulators Moxonidine Reduction of the sympathetic nervous system activity can also be achieved by stimulating receptors within the central nervous system. Studies in this area has been performed with clonidine 212 and moxonidine. Moxonidine has been documented in several phase II and III trials. In a study over 12 weeks in 97 patients, Swedberg and coworkers demonstrated a significant attenuation of plasma norepinephrine levels. 213 With a sustained release preparation of moxonidine, a more prolonged and effective reduction of plasma norepinephrine was obtained in 265 subjects. 214 The reduction was 40–50%, achieved within 3 weeks from initiation. However, in a large phase III trial with moxonidine sustained release (MOXCON) an early increase in death rate and adverse events in the moxonidine SR group led to pre- mature termination of the trial because of safety concerns after 1934 patients had been entered. Final analysis revealed 54 deaths (5·5%) in the moxonidine SR group and 32 deaths (3·1%) in the placebo group. Survival curves revealed a significantly (P ϭ 0·005) worse outcome in the moxonidine SR group. Hospitalization for heart failure, acute myocardial infarction, and adverse events were also more frequent in the moxonidine SR group. 215 This trial terminated the efforts to explore whether CNS inhibition of adrenergic activation could be an alternative to ␤ adrenergic blockade in heart failure. Antiarrhythmic drugs in heart failure Although progressive pump dysfunction is a common cause of death in heart failure, sudden death is probably the most common reason, and has been considered responsible in 25–50% of all deaths. 216–219 Besides a few cases of primary asystole, the majority of sudden deaths are due to ventricular arrhythmias. 220 The issue of antiarrhythmic therapy in heart failure patients has therefore been of major interest. Internal car- dioversion defibrillators are now used for prevention of sudden death from ventricular arrhythmias, and the use of these therapeutic devices is dealt with elsewhere in this book. Most antiarrhythmics cause a depression of left ventricular function. Although frequent and complex ventricular arrhythmias may be predictive of sudden death, left ventricular dysfunction is a more powerful predictor. 221 Furthermore, these drugs may have a proarrhythmic effect, especially in cases of left ventricular dysfunction. In the CAST study the efficacy of antiarrhythmic drugs in patients with left ventricular dysfunction after myocardial infarction and with complex ventricular arrhythmias was evaluated. Patients who responded with attenuation of arrhythmias after drug testing were randomized to encainide, flecainide, or moricizine. The results showed an increase in mortality in patients treated with these agents. 222 Amiodarone is a class III antiarrhythmic drug with no or little negative inotropic effect. Previous promising smaller trials encour- aged larger trials, such as the GESICA study. In this study, 516 patients with heart failure on conventional treatment were randomized to open label amiodarone treatment (n ϭ 260) or conventional treatment (n ϭ 256). Both sudden deaths and deaths due to heart failure were reduced, comprising in total 87 deaths in patients on amiodorone and 106 in the placebo group (P ϭ 0·02). 223 However, these results were not reproduced in another study in patients with CHF and asymptomatic ventricular arrhythmias. 224 In this study 674 patients were investigated, but amiodarone treatment was not associated with reduction of overall mortality or mortality from sudden death. Two other parallel studies have recently been finished, in which amiodarone was used in patients with a recent myocardial infarction and left ventricular dysfunction. 225,226 In addition, patients in the CAMIAT study had complex ventricular arrhythmias. Although all-cause mortality was not significantly lower in the treatment groups, both studies showed a reduction in arrhythmic deaths. A meta-analysis of 13 amiodarone trials demonstrated a significant reduction in total mortality (10·9 v 12.3% per year; OR 0·87 [95% CI 0·78–0·99], P ϭ 0·03) and in arrhythmic deaths (4·0 v 5·7% per year; OR 0·71 [95% CI 0·59–0·85], P ϭ 0·0003). 227,228 Sotalol, a ␤ blocker with class III antiarrhythmic proper- ties, has not been found to reduce deaths from ventricular arrhythmias. On the contrary, a study with the non-␤ blocker isoform d-sotalol in postmyocardial patients had to be terminated in advance because of an increased mortality in the sotalol group. 229 ACE inhibitors reduce the risk of progressive heart failure deaths. The possibility of ACE inhibitors to affect arrhythmias has been reviewed. 230 In some of the heart failure trials there has also been a reduction in the rate of sudden deaths. 78,231 However, these findings were not confirmed in the SOLVD trial. 232 The most impressive effects on sudden deaths have been found in the large survival studies with ␤ blockers. Consistent effects were found with all three agents, bisoprolol, metoprolol, and carvedilol. 196–198 Management of overt heart failure 671 Documented value of antiarrhythmic therapy in heart failure Proven indication: always acceptable ● ␤ Adrenergic blockade in patients with congestive heart failure Acceptable indication but of uncertain efficacy and may be controversial ● Prevention of arrhythmic deaths in patients with ventricular arrhythmias Not proven: potentially harmful (contraindicated) ● Class I antiarrhythmic drugs in patients with asymptomatic ventricular arrhythmias and heart failure ● Class III antiarrhythmic drugs, besides amiodarone Mechanical devices and pacing Different kinds of left ventricular mechanical assist devices (LVADs) have been studied for several years and they have been in clinical use since at least early 1990s. 233 Long-term effects have been unclear. A randomized trial has been presented in this context. In REMATCH (Randomized Evaluation of Mechanical Assistance for the Treatment of Grade A Grade B Grade A Evidence-based Cardiology 672 Table 46.1 Key recommendations Aim of treatment Class of drug Level of evidence Symptomatic improvement of congestion, improvement of exercise capacity Diuretics Reduction of mortality in mild to moderate heart failure Angiotensin converting enzyme inhibitors ␤ Adrenergic blockers Reduction of mortality in severe heart failure Angiotensin converting enzyme inhibitors ␤ Adrenergic blockers Spironolactone Reduction of mortality in patients not tolerating an ACE inhibitor Angiotensin-II receptor 1 blockers Reduction of morbidity and symptoms in mild–severe heart failure Angiotensin converting enzyme inhibitors ␤ Adrenergic blockers Angiotensin-II receptor 1 blockers Spironolactone Digitalis Short-term improvement of symptoms in patients with severe CHF. Non-digitalis Bridging towards more definitive surgical treatment, such inotropic drugs as cardiac transplantation Prevention of arrhythmic deaths in patients with symptomatic Amiodarone ventricular arrhythmias Bridging towards heart transplantation in terminal heart failure Left ventricular assist device Grade B Grade B Grade A Grade A Grade A Grade A Grade A Grade A Grade B Grade A Grade A Grade A Grade A Grade A Grade A Congestive Heart failure), 129 patients with advanced heart failure in NYHA class IV were randomized to optimal medical management or LVAD (HeartMate). 234 No patient was eligible for heart transplantation. The objectives were to assess effects on survival and quality of life. The mean age was 67 years and the average ejection fraction 17%. Kaplan–Meier survival analysis showed a reduction of 48% in the risk of death from any cause in the group that received left ventricular assist devices as compared with the medical therapy group (RR 0.52, 95% CI 0.34–0.78, P ϭ 0.001). The rates of survival at 1 year were 52% in the device group and 25% in the medical therapy group (P ϭ 0.002), and the rates at 2 years were 23% and 8% (P ϭ 0.09), respectively. The frequency of serious adverse events in the device group was 2.35 times (95% CI 1·86–2.95) that in the medical therapy group, with a predominance of infection, bleeding, and malfunction of the device. The quality of life was significantly improved at 1 year in the device group assessed as SF-36 and Beck Depression Inventory. There was also a non-significant improvement in Minnesota Living with Heart Failure. The study shows that LVADs can prolong life and improve quality of life in severe heart failure. The treatment effect is limited in time and there was no significant improvement after 2 years. The important question is to evaluate the cost effectiveness of this expensive therapy in relation to other treatments. The published information suggests that the treatment costs were considerable. There are several surgical approaches to heart failure including revascularization, left ventricular reconstruction, cardiomyoplasty and mitral valvular repair. However, the clinical studies have not been controlled, and yet the partial left ventricular ventriculotomy (Batista) and cardiomyoplasty have even been classified as not recommended. Besides conventional indication for antibradycardia pacing, other pacing modalities have been tried for patients with CHF. A dual chamber pacing with shortening of the atrioventricular conduction has been investigated in a small series. More recently, so called resynchronization therapy using pacing of both the right and the left ventricles has been introduced. There are promising results from smaller studies showing improved left ventricular function and symptomatology. 237–239 Larger randomized studies are now in progress testing this concept on clinical outcomes. Concluding remarks In the treatment of CHF there are two main classes of drugs – ACE inhibitors and ␤ blockers – with solid and consistent documentation for reduction of morbidity and mortality. Furthermore, spironolactone has recently been accepted by the scientific community to be of value in this respect. The ARBs have not sufficient documentation to be placed on an equal status with ACE inhibitors. However, the ARBs are widely accepted as a substitute when patients are not tolerating an ACE inhibitor (Table 46.1). The concept of neurohormonal blockade is also evaluated in studies on endothelin receptor blockers and vasopeptidase inhibitors. Some of these trials are imminent. The development of devices and surgical methods are today somewhat more uncertain. References 1.Ribner B, Plucinski DA, Hsieh AM et al. Acute effects of digoxin on total systemic vascular resistance in congestive heart failure due to dilated cardiomyopathy. Am J Cardiol 1985;56:896. 2.Gheorghiade M, St Clair J, St Clair C, Beller GA. Hemodynamic effects of intravenous digoxin in patients with severe heart failure initially treated with diuretics and vasodilators. J Am Coll Cardiol 1987;9:849. 3.Cohn K, Selzer A, Kersh ES et al. Variability of hemodynamic response to acute digitalization in chronic cardiac failure due to cardiomyopathy and coronary artery disease. Am J Cardiol 1975;31:461. Grade C Grade B 4.Braunwald E. Effects of digitalis on the normal and the failing heart. J Am Coll Cardiol 1985;5:51A. 5.Ferguson DW, Berg WJ, Sanders JS et al. Sympathoinhibitory responses to digitalis glycosides in heart failure patients. Circulation 1989;80:65–77. 6.Ferguson DW. Baroreflex-mediated circulatory control in human heart failure. Heart Failure 1990;6:3. 7.Goldsmith SR, Simon AB, Miller E. Effect of digitalis on norepinephrine kinetics in congestive heart failure. J Am Coll Cardiol 1992;20:858–63. 8.Dobbs SN, Kenyon WI, Dobbs RJ. Maintenance digoxin after an episode of heart failure. Placebo controlled trial in outpatients. BMJ 1977;1:749. 9.Fleg L, Gottlieb SH, Lakatta EG. Is digoxin really important in compensated heart failure? Am J Med 1982;73:244. 10.Taggart AJ, Johnston GD, McDevitt DG. Digoxin withdrawal after cardiac failure in patients with sinus rhythm. J Cardiovasc Pharmacol 1983;5:229. 11.Lee DCS, Johnston RA, Bingham JB et al. Heart failure in outpatients. A randomized trial of digoxin versus placebo. N Engl J Med 1982;306:699. 12.Guyatt GH, Sullivan MJJ, Fallen EL et al. A controlled trial of digoxin in congestive heart failure. Am J Cardiol 1988; 61:371. 13.Haerer W, Bauer U, Hetzel M, Fehske J. Long-term effects of digoxin and diuretics in congestive heart failure. Results of a placebo-controlled randomized double-blind study. Circulation 1988;78:53. 14.The Captopril-Digoxin Multicenter Research Group. Comparative effects of therapy with captopril and digoxin in patients with mild moderate heart failure. JAMA 1988; 259:539–44. 15.German and Austrian Xamoterol Study Group. Double-blind placebo-controlled comparison of digoxin and xamoterol in chronic heart failure. Lancet 1988;i:489. 16.DiBianco R, Shabetai R, Kostuk W et al. A comparison of oral milrinone, digoxin, and their combination in the treatment of patients with chronic heart failure. N Engl J Med 1989;320: 677–83. 17.Uretsky BF, Young JB, Shahidi FE et al. Randomized study assessing the effect of digoxin withdrawal in patients with mild to moderate chronic congestive heart failure: results of the PROVED Trial. J Am Coll Cardiol 1993;22:955–62. 18.Packer M, Gheorghiade M, Young JB et al. Withdrawal of digoxin from patients with chronic heart failure treated with angiotensin-converting enzyme inhibitors. N Engl J Med 1993;329:1–7. 19.Perry G, Brown E, Thornton R et al. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med 1997;336:525–33. 20.Stason WR, Cannon PJ, Heinemann HO, Laragh JH. Furosemide: a clinical evaluation of diuretic action. Circulation 1966;34:910–20. 21.Cody RJ, Ljungman S, Covit AB et al. Regulation of glomerular filtration rate in chronic congestive heart failure patients. Kidney Int 1988;34:361–7. 22.Francis GS, Goldsmith SR, Levine TB, Olivari MT, Cohn JN. The neurohumoral axis in congestive heart failure. Ann Intern Med 1984;101:370–7. Management of overt heart failure 673 23.Lal S, Murtagw JG, Pollock AM, Fletcher E, Binnion PF. Acute hemodynamic effects of furosemide in patients with normal and raised left atrial pressures. Br Heart J 1969;31: 711–17. 24.Stampfer M, Epstein SE, Beiser D, Braunwald E. Haemodynamic effects of diuresis at rest and during intense uprights exercise in patients with impaired cardiac function. Circulation 1968;37:900–11. 25.Magrini F, Niarchos AP. Hemodynamic effects of massive peripheral edema. Am Heart J 1983;105:90–4. 26.Francis GS, Siegel RM, Goldsmith SR et al. Acute vasocon- strictor response to intravenous furosemide in patients with chronic congestive heart failure. Ann Intern Med 1985; 103:1–6. 27.Dikshit K, Vyden JK, Forrester JS et al. Renal and extrarenal hemodynamic effects of furosemide in congestive heart failure after myocardial infarction. N Engl J Med 1973;288: 1087–90. 28.Nelson GIC, Ahuja RC, Silke B, Taylor SH. Haemodynamic effects of furosemide and its influence on repetitive rapid volume loading in acute myocardial infarction. Eur Heart J 1983;4:706–11. 29.Verma SP, Silke B, Reynolds G et al. Immediate effects of bumetanide on systemic haemodynamics and left ventricular volume in acute and chronic heart failure. Br J Clin Pharmacol 1987;24:21–32. 30.Ramirez A, Abelman WH. Haemodynamic effects of diuresis by ethacrynic acid. Ann Intern Med 1968;121:320–7. 31.Valette H, Hebert JL, Apoil E. Acute haemodynamic effects of a single intravenous dose of piretanide in congestive heart failure. Eur J Clin Pharmacol 1983;24:163–7. 32.Fiehring H, Achhammer I. Influence of 10mg torasemide iv and 20mg furosemide iv on the intracardiac pressures in patients with heart failure at rest and during exercise. Prog Pharmacol Clin Pharmacol 1990;8:87–104. 33.Mackay IG, Muir AL, Watson ML. Contribution of prostaglandins to the systemic and renal vascular response to frusemide in normal man. Br J Clin Pharmacol 1984;17: 513–19. 34.Ikram H, Chan W, Espiner EA, Nicholls ME. Haemodynamic and humoral responses to acute and chronic frusemide therapy in congestive heart failure. Clin Sci 1980;59:443–9. 35.Haerer W, Bauer U, Sultan N. Acute and chronic effects of a diuretic monotherapy with piretanide in congestive heart failure – a placebo controlled trial. Cardiovasc Drugs Ther 1990;4:515–22. 36.Podszus T, Piesche L. Effect of torasemide on pulmonary and cardiac haemodynamics after oral treatment of chronic heart failure. Prog Pharmacol Clin Pharmacol 1990;8:157–66. 37.Cheitlin MD, Byrd R, Benowitz N. Amiloride improves haemodynamics in patients with chronic congestive heart failure treated with chronic digoxin and diuretics. Cardiovasc Drugs Ther 1991;5:719–26. 38.Francis GS, Benedict C, Johnstone DE et al. Comparison of neuroendocrine activation in patients with left ventricular dysfunction with and without congestive heart failure. Circulation 1990;82:1724–9. 39.Bayliss J, Norell M, Canepa-Anson R, Sutton G, Poole-Wilson P. Untreated heart failure: clinical and neuroendocrine effects of introducing diuretics. Br Heart J 1987;57:17–22. 40.Achhammer I. Long-term efficacy and tolerance of torasemide in congestive heart failure. Prog Pharmacol Clin Pharmacol 1990;8:127–36. 41.Dusing R, Piesche L. Second-line therapy of congestive heart failure with torasemide. Prog Pharmacol Clin Pharmacol 1990;8:105–20. 42.Odemuyiwa O, Gilmartin J, Kenny D, Hall RJC. Captopril and the diuretic requirements in moderate and severe chronic heart failure. Eur Heart J 1989;10:586. 43.Anand IS, Kalra GS, Ferrari R et al. Enalapril as initial and sole treatment in severe chronic heart failure with sodium retention. Int J Cardiol 1990;28:341. 44.Richardson A, Bayliss J, Scriven AJ et al. Double-blind comparison of captopril alone against furosemide plus amiloride in mild heart failure. Lancet 1987;ii:709. 45.Cody RJ, Kubo SH, Pickworth KK. Diuretic treatment for the sodium retention of congestive heart failure. Arch Intern Med 1994;154:1905–14. 46.Laragh JH. Hormones in the pathogenesis of congestive heart failure: vasopressin, aldosterone, angiotensin II. Circulation 1962;25:1015–23. 47.Swedberg K, Eneroth P, Kjekshus J, Wilhelmsen L, for the CONSENSUS trial study group. Hormones regulating cardiovascular function in patients with severe congestive heart failure and their relation to mortality. Circulation 1990;82:1730–6. 48.Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium. Fibrosis and renin-angiotensin-aldosterone system. Circulation 1991;83:1849–65. 49.Young M, Fullerton M, Dilley R, Funder J. Mineralocorticoids, hypertension, and cardiac fibrosis. J Clin Invest 1994;93: 2578–83. 50.Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A et al. The effect of spironolactone on morbidity and mortality in patients with severe failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999;341: 709–17. 51.Eichna LW, Sobel BJ, Kessler RH. Hemodynamic and renal effects produced in congestive heart failure by the intravenous administration of a ganglionic blocking agent. Trans Assoc Am Phys 1956;69:207–13. 52.Burch GE. Evidence for increased venous tone in chronic heart failure. Arch Intern Med 1956;98:750–66. 53.Zelis R, Mason DT, Braunwald E. A comparison of the effects of vasodilator stimuli on peripheral resistance vessels in normal subjects and in patients with congestive heart failure. J Clin Invest 1968;47:960–70. 54.Majid PA, Sharma B, Taylor SH. Phentolamine for vasodilator treatment of severe heart failure. Lancet 1971;ii:719–24. 55.Franciosa JA, Guiha NH, Limas CJ, Rodriguera E, Cohn JN. Improved left ventricular function during nitroprusside infusion in acute myocardial infarction. Lancet 1972;i:650–4. 56.Cohn JN, Franciosa JA. Vasodilator therapy of cardiac failure. N Engl J Med 1977;297:27–31. 57.Tsai SC, Adamik R, Manganiello VC, Moss J. Effects of nitroprusside and nitroglycerin on cGMP content and PGI2 formation in aorta and vena cava. Biochem Pharmacol 1989; 38:61–5. 58.Lavine SJ, Campbell CA, Held AC, Johnson V. Effect of nitroglycerin-induced reduction of left ventricular filling pressure Evidence-based Cardiology 674 on diastolic filling in acute dilated heart failure. J Am Coll Cardiol 1989;14:233–41. 59.Mason DT, Braunwald E. The effects of nitroglycerin and amyl nitrate on arteriolar and venous tone in the human forearm. Circulation 1965;32:755–65. 60.Armstrong PW, Armstrong JA, Marks GS. Pharmacokinetic- hemodynamic studies of intravenous nitroglycerin in congestive heart failure. Circulation 1980;62:160–6. 61.Leier CV, Bambach D, Thompson MJ et al. Central and regional hemodynamic effects of intravenous isosorbide dinitrate, nitroglycerin, and nitroprusside in patients with congestive heart failure. Am J Cardiol 1981;48:1115–23. 62.Flaherty JT, Reid PR, Kelly DT et al. Intravenous nitroglycerin in acute myocardial infarction. Circulation 1975;51:132–9. 63.Ludbrook PR, Byrne JD, Kurnik PB, McKnight RC. Influence of reduction of preload and afterload by nitroglycerin on left ventricular diastolic pressure-volume relation and relaxation in man. Circulation 1977;56:937–43. 64.DeMarco T, Chatterjee K, Rouleau JL, Parmley WW. Abnormal coronary hemodynamics and myocardial energetics in patients with chronic heart failure caused by ischemic heart disease and dilated cardiomyopathy. Am Heart J 1988; 115:809–15. 65.Unverferth DV, Magorien RD, Lewis RP, Leier CV. The role of subendocardial ischemia in perpetuating myocardial failure in patients with nonischemic congestive cardiomyopathy. Am Heart J 1983;105:176–9. 66.Chiariello M, Gold HK, Leinbach RC, David MA, Maroko PR. Comparison between the effects of nitroprusside and nitroglycerin on ischemic injury during acute myocardial infarction. Circulation 1976;54:766–73. 67.Stevenson LW, Dracup KA, Tillisch JH. Efficacy of medical therapy tailored for severe congestive heart failure in patients transferred for urgent cardiac transplantation. Am J Cardiol 1989;63:461–4. 68.Chatterjee K, Ports TA, Brundage BH et al. Oral hydralazine in chronic heart failure: sustained beneficial hemodynamic effects. Ann Intern Med 1980;92:600–4. 69.Franciosa JA, Nordstrom LA, Cohn JN. Nitrate therapy for congestive heart failure. JAMA 1978;240:443–6. 70.Miller RR, Awan NA, Maxwell KS, Mason DT. Sustained reduction of cardiac impedance and preload in congestive heart failure with the antihypertensive vasodilator prazosin. N Engl J Med 1977;297:303–7. 71.Franciosa JA, Jordan RA, Wilen MM, Leddy CL. Minoxidil in patients with chronic left heart failure: contrasting hemodynamic and clinical effects in a controlled trial. Circulation 1984;70:63–8. 72.Leier CV, Desch CE, Magorien RD et al. Positive inotropic effects of hydralazine in human subjects. Comparison with prazosin in the setting of congestive heart failure. Am J Cardiol 1980;46:1039–44. 73.Rouleau JL, Chatterjee K, Benge W, Parmley WW, Hiramatsu B. Alterations in left ventricular function and coronary hemodynamics with captopril, hydralazine, and prazosin in chronic ischemic heart failure, a comparative study. Circulation 1982;65:671–8. 74.Daly P, Rouleau JL, Cousineau D, Burgess JH, Chatterjee K. Effects of captopril and a combination of hydralazine and isosorbide dinitrate on myocardial sympathetic tone in patients with severe congestive heart failure. Br Heart J 1986; 56:152–7. 75.Magorien RD, Unverferth DV, Brown GP, Leier CV. Dobutamine and hydralazine. Comparative influences of positive inotropy and vasodilation on coronary blood flow and myocardial energetics in nonischemic congestive heart failure. J Am Coll Cardiol 1983;1:499–505. 76.Massie B, Chatterjee K, Werner J et al. Hemodynamic advan- tage of combined administration of hydralazine orally and nitrates nonparenterally in the vasodilator therapy of chronic heart failure. Am J Cardiol 1977;40:794–801. 77.Packer M, Meller J, Medina N, Yushak M, Gorlin R. Provocation of myocardial ischemia events during initiation of vasodilator therapy for severe chronic heart failure. Clinical and hemodynamic evaluation of 52 consecutive patients with ischemic cardiomyopathy. Am J Cardiol 1981;48:939–46. 78.Cohn JN, Johnson G, Ziesche S et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med 1991;325:303–10. 79.Elkayam U, Amin J, Mehra A et al. A prospective, randomized, double-blind, crossover study to compare the efficacy and safety of chronic nifedipine therapy with that of isosorbide dinitrate and their combination in the treatment of chronic congestive heart failure. Circulation 1990;82:1954–61. 80.Danish Study Group on Verapamil in Myocardial Infarction. Secondary prevention with verapamil after myocardial infarction. Am J Cardiol 1990;66:331–401. 81.Iida K, Matsuda M, Ajisaka R et al. Effects of nifedipine on left ventricular systolic and diastolic function in patients with ischemic heart disease. Japan Heart J 1987;28:495–506. 82.Barjon JN, Rouleau JL, Bichet D, Juneau C, De Champlain J. Chronic renal and neurohumoral effects of the calcium-entry blocker nisoldipine in patients with congestive heart failure. J Am Coll Cardiol 1987;9:622–30. 83.Gheorghiade M, Hall V, Goldberg D, Levine TB, Goldstein S. Long-term clinical and neurohormonal effects of nicardipine in patients with severe heart failure on maintenance therapy with angiotensin converting enzyme inhibitors. J Am Coll Cardiol 1991;17:274A. 84.Dunselman PHJM, Kuntze CEE, Van Bruggen A et al. Efficacy of felodipine in congestive heart failure. Eur Heart J 1989;10: 354–64. 85.Cohn JN, Archibald DG, Ziesche S et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure. N Engl J Med 1986;314:1547–52. 86.Cohn JN, Ziesche SM, Smith R et al. Effect of the calcium antagonist felodipine has supplementary vasodilator therapy in patients with chronic heart failure treated with enalapril: V-HeFT III. Circulation 1997;96:856–63. 87.Packer M, O’Connor CM, Ghali JK et al. Effect of amlodipine on morbidity and mortality in severe chronic heart failure. N Engl J Med 1996;335:1107–14. 88.Thackray S, Witte K, Clark AL, Cleland JG. Clinical trials update: OPTIME-CHF, PRAISE-2, ALL-HAT. Eur J Heart Fail 2000;2:209–12. 89.Packer M, Rouleau J, Swedberg K et al. Effect of flosequinan on survival in chronic heart failure. Circulation 1993;88:301. Management of overt heart failure 675 90.McKenna WJ, Swedberg K, Zannad F et al. Experience of chronic intravenous epoprostenol infusion in end-stage cardiac failure:results of FIRST. Eur Heart J 1994;15:I-36. 91.Sharpe DN, Murphy J, Coxon R, Hannan SF. Enalapril in patients with chronic heart failure: a placebo-controlled, randomized, double-blind study. Circulation 1984;70:271–8. 92.DiCarlo L, Chatterjee K, Parmley WW et al. Enalapril A new angiotensin converting inhibitor in chronic heart failure:acute and chronic hemodynamic evaluations. J Am Coll Cardiol 1983;2:865–71. 93.Packer M, Medina N, Yushak M, Lee WH. Usefulness of plasma renin activity in predicting haemodynamic and clinical responses and survival during long term converting enzyme inhibition in severe chronic heart failure. Experience in 100 consecutive patients. Br Heart J 1985;54:298–304. 94.The Consensus Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure. N Engl J Med 1987;316:1429–35. 95.Sharpe N, Murphy J, Heather S, Hannan S. Treatment of patients with symptomless left ventricular dysfunction after myocardial infarction. Lancet 1988;i:255–9. 96.Pfeffer JM, Pfeffer MA. Angiotensin converting enzyme inhibition and ventricular remodeling in heart failure. Am J Med 1988;84:37–44. 97.Swedberg K, Eneroth P, Kjekshus J, Wilhelmsen L for the CONSENSUS Trial Study Group. Hormones regulating cardiovascular function in patients with severe congestive heart failure and their relation to mortality. Circulation 1990;82: 1730–6. 98.Packer M. The neurohormonal hypothesis: a theory to explain the mechanism of disease progression in heart failure. J Am Coll Cardiol 1992;20:248–54. 99.The SOLVD Investigators. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med 1992;327:685–91. 100.Rogers WJ, Johnstone DE, Yusuf S et al. Quality of life among 5025 patients with left ventricular dysfunction randomized between placebo and enalapril: the studies of left ventricular dysfunction. J Am Coll Cardiol 1994;23:393–400. 101.Pfeffer MA, Braunwald E, Moyé LA et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 1992;327:669–77. 102.Kober L, Torp-Pedersen C, Carlsen JE et al. A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 1995;333:1670–6. 103.The Acute Infarction Ramipril Efficacy (AIRE) Study Investigators. Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. Lancet 1993;342:821–8. 104.Packer M, Poole-Wilson PA, Armstrong PW et al. Comparative effects of low and high doses of the angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure. ATLAS Study Group. Circulation 1999; 100:2312–18. 105.Flather MD, Yusuf S, Kober L et al. Long-term ACE-inhibitor therapy in patients with heart failure or left-ventricular dysfunction: a systematic overview of data from individual patients. ACE-Inhibitor Myocardial Infarction Collaborative Group. Lancet 2000;355:1575–81. 106.Narang R, Swedberg K, Cleland JG. What is the ideal study design for evaluation of treatment for heart failure? Insights from trials assessing the effect of ACE inhibitors on exercise capacity. Eur Heart J 1996;17:120–34. 107.Garg R, Yusuf S. Overview of randomized trials of angiotensin- converting enzyme inhibitors on mortality and morbidity in patients with heart failure. JAMA 1995;273: 1450–6. 108.Yusuf S, Pepine CJ, Garces C et al. Effect of enalapril on myocardial infarction and unstable angina in patients with low ejection fractions. Lancet 1992;340:1173–8. 109.Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 2000;342:145–53. 110.Paul SD, Kuntz KM, Eagle KA, Weinstein MC. Costs and effectiveness of angiotensin converting enzyme inhibition in patients with congestive heart failure. Arch Intern Med 1994;154:1143–9. 111.Tsevat J, Duke D, Goldman L et al. Cost effectiveness of captopril therapy after myocardial infarction. J Am Coll Cardiol 1995;26:914–19. 112.Martinez C, Ball SG. Cost effectiveness of ramipril therapy for patients with clinical evidence of heart failure after acute myocardial infarction. Br J Clin Pract 1995;78(Suppl.): 26–32. 113.McMurray J, Davie A. The pharmacoeconomics of ACE inhibitors in chronic heart failure. Pharmacoeconomics 1996;9:188–97. 114.Dickstein K, Chang P, Willenheimer et al. Comparison of the effects of losartan and enalapril on clinical status and exercise performance in patients with moderate or severe chronic heart failure. J Am Coll Cardiol 1995;26:438–45. 115.Pitt B, Segal R, Martinez FA et al. Randomised trial of losartan versus captopril in patients over 65 with heart failure (Evaluation of losartan in the elderly study, ELITE). Lancet 1997;349:747–52. 116.Pitt B, Poole-Wilson PA, Segal R et al. Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure: randomised trial – the Losartan Heart Failure Survival Study ELITE II. Lancet 2000;355:1582–7. 117.McKelvie RS, Yusuf S, Pericak D et al. Comparison of can- desartan, enalapril, and their combination in congestive heart failure: randomized evaluation of strategies for left ventricular dysfunction (RESOLVD) pilot study. The RESOLVD Pilot Study Investigators. Circulation 1999;100:1056–64. 118.Feldman AM. Classification of positive inotropic agents. J Am Coll Cardiol 1993;22:1233–7. 119.Smith JH, Oriol A, Morch J et al. Hemodynamic studies in cardiogenic shock. Treatment with isoproterenol and metaraminol. Circulation 1967;35:1084–91. 120.Tuttle RR, Mills J. Dobutamine. Development of a new cate- cholamine to selectively increase cardiac contractility. Circ Res 1975;36:185–96. 121.Meyer SL, Curry GC, Donsky MS et al. Influence of dobutamine on hemodynamics and coronary blood flow in patients Evidence-based Cardiology 676 with and without coronary artery disease. Am J Cardiol 1976;38:103–8. 122.Akhtar N, Midulic E, Cohn JN, Chaudry MH. Hemodynamic effect of dobutamine in patients with severe heart failure. Am J Cardiol 1975;36:202–5. 123.Leier CV, Webel J, Buch CA. The cardiovascular effects of the continuous infusion of dobutamine in patients with severe cardiac failure. Circulation 1977;56:468–72. 124.Pozen RG, DiBianco R, Katz RJ et al. Myocardial metabolic and hemodynamic effects of dobutamine in heart failure complicating coronary artery disease. Circulation 1981;63: 1279–85. 125.Leier CV, Unverferth DV, Kates RE. The relationship between plasma dobutamine concentrations and cardiovascular responses in cardiac failure. Am J Med 1979;66:238–42. 126.Colucci WS, Denniss AR, Leatherman GF. Intracoronary infusion of dobutamine to patients with and without severe congestive heart failure. J Clin Invest 1988;81:1103–10. 127.Bristow MR, Port JD, Hershberger RE, Gilbert EM, Feldman AM. The ␤-adrenergic receptor-adenylate cyclase complex as a target for therapeutic intervention in heart failure. Eur Heart J 1989;10:45–54. 128.Unverferth DV, Blanford M, Kates RE, Leier VI. Tolerance to dobutamine after a 72-hour continuous infusion. Am J Med 1980;69:262–6. 129.Applefeld MM, Newman KA, Grove WR et al. Intermittent continuous outpatient dobutamine infusion in the management of congestive heart failure. Am J Cardiol 1983;51: 455–8. 130.Dies F, Krell MJ, Whitlow P et al. Intermittent dobutamine in ambulatory outpatients with chronic cardiac failure. Circulation 1986;74:II-38–II-38. 131.Goldberg LI. Cardiovascular and renal actions of dopamine. Potential clinical application. Pharmacol Rev 1972;241: 1–29. 132.Goldberg LI, Volkman PH, Kohli JD. A comparison of the vascular dopamine receptor with other dopamine receptors. Annu Rev Pharmacol Toxicol 1978;18:57–79. 133.Rajfer SI, Goldberg LI. Dopamine in the treatment of heart failure. Eur Heart J 1982;3:103–6. 134.Lockhandwala MF, Barrett RJ. Cardiovascular dopamine receptors. Physiological pharmaceutical and therapeutic impli- cations. J Auton Pharmacol 1982;2:189–215. 135.Caponetto S, Terrachini V, Canale C et al. Long-term treatment of congestive heart failure with oral ibopamine: effects of rhythm disorders and neurohormonal alterations. Cardiology 1990;77:43–8. 136.Itoh H, Taniguchi K, Tsajibayashi R, Koike A, Sato Y. Hemodynamic effects and pharmacokinetics of long-term therapy with ibopamine in patients with chronic heart failure. Cardiology 1992;80:356–60. 137.van Veldhuisen DJ, Man in’t Veld AJ, Dunselman PHJM et al. Double-blind placebo-controlled study of ibopamine and digoxin in patients with mild to moderate heart failure: results of the Dutch Ibopamine Multicenter Trial (DIMT). J Am Coll Cardiol 1993;22:1564–73. 138.Hampton JR, van Veldhuisen DJ, Kleber FX et al. Randomised study of effect of ibopamine on survival in patients with advanced severe heart failure. Lancet 1997;349:971–7. 139.The Xamoterol in Severe Heart Failure Study Group. Xamoterol in severe heart failure. Lancet 1990;336:1–6. 140.Alousi AA, Farah AE, Lesher GY, Opalka CJJ. Cardiotonic activity of amrinone-WIN 40680 [5-amino-3,4Јbipyridin- 6(1H)-one]. Circ Res 1979;45:666–77. 141.Millard RW, Dube G, Grupp G et al. Direct vasodilator and positive inotropic actions of amrinone. J Mol Cell Cardiol 1980;12:647–52. 142.Firth B, Ratner AV, Grassman ED et al. Assessment of the inotropic and vasodilator effects of amrinone versus isoproterenol. Am J Cardiol 1984;54:1331–6. 143.Rettig GF, Schieffer HJ. Acute effects of intravenous milrinone in heart failure. Eur Heart J 1989;10:39–43. 144.Baim DS, McDowell AV, Cherniles J et al. Evaluation of a new bipyridine inotropic agent – milrinone – in patients with severe congestive heart failure. N Engl J Med 1983;309:748–56. 145.Klocke RK, Mager G, Kux A et al. Effects of a twenty-four hour milrinone infusion in patients with severe heart failure and cardiogenic shock as a function of the hemodynamic initial condition. Am Heart J 1991;121:1965–73. 146.Kinney EL, Ballard JO, Carlin B, Zelis R. Amrinone-mediated thrombocytopenia. Scand J Haematol 1983;31:376–80. 147.Cowley AJ, Stainer K, Fullwood L, Muller AF, Hampton JR. Effects of enoximone in patients with heart failure uncon- trolled by captopril and diuretics. Int J Cardiol 1990;28: S45–S53. 148.Bristow MR, Renlund DG, Gilbert EM, O’Connell JB. Enoximone in severe heart failure: clinical results and effects on ␤-adrenergic receptors. Int J Cardiol 1990;28:S21. 149.Herrmann HC, Ruddy TD, Dec GW et al. Diastolic function in patients with severe heart failure: comparison of the effects of enoximone and nitroprusside. Circulation 1987; 75:1214–21. 150.Gage J, Rutman H, Lucido D, LeJemtel TH. Additive effects of dobutamine and amrinone on myocardial contractility and ventricular performance in patients with severe heart failure. Circulation 1986;74:367–73. 151.Uretsky BF, Lawless CE, Verbalis JG et al. Combined therapy with dobutamine and amrinone in severe heart failure. Chest 1987;92:657–62. 152.Anderson JL. Hemodynamic and clinical benefits with intravenous milrinone in severe chronic heart failure. Results of a multicenter study in the United States. Am Heart J 1991; 121:1956–64. 153.Packer M, Carver JR, Rodeheffer RJ et al. Effect of oral milrinone on mortality in severe chronic heart failure. N Engl J Med 1991;325:1468–75. 154.Uretsky BF, Jessup M, Konstam MA et al. Multicenter trial of oral enoximone in patients with moderate to moderately severe congestive heart failure. Circulation 1990;82:774–80. 155.DiBianco R, Shebetai R, Silverman BD et al. Oral amrinone for the treatment of chronic congestive heart failure. Results of a multicenter randomized double-blind and placebo-controlled withdrawal study. J Am Coll Cardiol 1984;4:855–66. 156.Hagemeijer F. Calcium sensitization with pimobendan. Pharmacology, haemodynamic improvement, and sudden death in patients with chronic congestive heart failure. Eur Heart J 1993;14:551–66. Management of overt heart failure 677 157.Fujino K, Sperelakis N, Solaro RJ. Sensitization of dog and guinea pig heart myofilaments to calcium activation and the inotropic effect of pimobendan. Comparison with milrinone. Circ Res 1988;63:911–22. 158.Böhm M, Morano I, Pieske B et al. Contribution of cAMP-phosphodiesterase inhibition and sensitization of the conctractile proteins for calcium to the inotropic effects of pimobendan in the failing human heart. Circ Res 1991;68: 689–701. 159.Katz SD, Kubo SH, Jessup M et al. A multicenter, randomized, double-blind, placebo-controlled trial of pimobendan, a new cardiotonic and vasodilator agent, in patients with severe congestive heart failure. Am Heart J 1992;123: 95–103. 160.Kubo SH, Gollub S, Bourge R et al. Beneficial effects of pimobendan on exercise tolerance and quality of life in patients with heart failure. Circulation 1992;85:942–9. 161.Just H, Hjalmarson Å, Remme WJ et al. pimobendan in congestive heart failure. Results of the PICO trial. Circulation 1995;92:722. 162.Schwartz A, Wallick ET, Lee SW et al. Studies on the mechanism of action of 3,4-dihydro-6-4-(3,4-dimethoxybenzoyl)- 1-piperazinyl-2(1H)-quinolinone (OPC-8212), a new positive inotropic drug. Arzneimittelforschung 1984;34:384–9. 163.Yamashita S, Hosokawa T, Kojima M et al. In vitro and in vivo studies of 3,4-dihydro-6-[4-(3,4-dimethoxybenzoyl)- 1-piperazinyl]-2(1H)-quinolinone on myocardial oxygen con- sumption in dogs with ischemic heart failure. Japan Circ J 1986;50:659–66. 164.Matsumori A, Shioi T, Yamada T, Matsui S, Sasayama S. Vesnarinone, a new inotropic agent, inhibits cytokine produc- tion by stimulated human blood from patients with heart failure. Circulation 1994;89:955–8. 165.Feldman AM, Bristow MR, Parmley WW et al. Effects of vesnarinone on morbidity and mortality in patients with heart failure. N Engl J Med 1993;329:149–55. 166.Otsuka America, PNC. Letter to VEST Investigators, 29 July 1996. 167.Nieminen MS, Akkila J, Hasenfuss G, Kleber FX, Lehtonen LA, Mitrovic V et al. Hemodynamic and neurohumoral effects of continuous infusion of levosimendan in patients with congestive heart failure. J Am Coll Cardiol 2000;36: 1903–12. 168.Slawsky MT, Colucci WS, Gottlieb SS et al. Acute hemodynamic and clinical effects of levosimendan in patients with severe heart failure. Study Investigators. Circulation 2000; 102:2222–7. 169.Swedberg K, Waagstein F, Hjalmarson Å, Wallentin I. Prolongation of survival in congestive cardiomyopathy by beta-receptor blockade. Lancet 1979;i:1375–6. 170.Waagstein F, Hjalmarson Å, Varnauskas E, Wallentin I. Effect of chronic beta-adrenergic receptor blockade in congestive cardiomyopathy. Br Heart J 1975;37:1022–36. 171.Sloand EM, Thompson BT. Propranolol-induced pulmonary edema and shock in a patient with pheochromocytoma. Arch Intern Med 1984;144:173–4. 172.Greenblatt DJ, Koch-Weser J. Adverse reactions to propranolol in hospitalized patients. Am Heart J 1973;86: 478–84. 173.Herlitz J, Hjalmarson Å, Holmberg S et al. Development of congestive heart failure after treatment with metoprolol in acute myocardial infarction. Br Heart J 1984;51:539–44. 174.Chadda K, Goldstein S, Byington R, Curb JD. Effect of propranolol after acute myocardial infarction in patients with congestive heart failure. Circulation 1986;73:503–10. 175.Olsson G, Rehnqvist N. Effect of metoprolol in postinfarction patients with increased heart size. Eur Heart J 1986;7: 468–74. 176.Gilbert EM, Anderson JL, Deitchman D et al. Long-term ␤-blocker vasodilator therapy improves cardiac function in idiopathic dilated cardiomyopathy: a double-blind, randomized study of bucindolol versus placebo. Am J Med 1990;88: 223–9. 177.DasGupta P, Lahiri A. Can intravenous beta blockade predict long-term haemodynamic benefit in chronic congestive heart failure secondary to ischaemic heart disease? Clin Invest 1992;70:S98–S104. 178.Andersson B, Lomsky M, Waagstein F. The link between acute haemodynamic adrenergic beta-blockade and long-term effects in patients with heart failure. Eur Heart J 1993;14: 1375–85. 179.Haber HL, Simek CL, Gimple LW et al. Why do patients with congestive heart failure tolerate the initiation of beta-blocker therapy. Circulation 1993;88:1610–19. 180.Andersson B, Caidahl K, Di Lenarda A et al. Changes in early and late diastolic filling patterns induced by long-term adrenergic beta-blockade in patients with idiopathic dilated cardiomyopathy. Circulation 1996;94:673–82. 181.Woodley SL, Gilbert EM, Anderson JL et al. ␤-blockade with bucindolol in heart failure caused by ischemic versus idiopathic dilated cardiomyopathy. Circulation 1991;84:2426–41. 182.Eichhorn EJ, Bedotto JB, Malloy CR et al. Effect of ␤-adrenergic blockade on myocardial function and energetics in congestive heart failure. Circulation 1990;82:473–83. 183.Bristow MR, O’Connell JB, Gilbert EM et al. Dose-response of chronic ␤-blocker treatment in heart failure from either idiopathic dilated or ischemic cardiomyopathy. Circulation 1994;89:1632–42. 184.Eichhorn EJ, Heesch CM, Risser RC, Marcoux L, Hatfield B. Predictors of systolic and diastolic improvement in patients with dilated cardiomyopathy treated with metoprolol. J Am Coll Cardiol 1995;25:154–62. 185.Metra M, Nardi M, Giubbini R, Cas LC. Effects of short- and long-term carvedilol administration on rest and exercise hemodynamic vaiables, exercise capacity and clinical condi- tions in patients with idiopathic dilated cardiomyopathy. J Am Coll Cardiol 1995;24:1678–87. 186.Hall SA, Cigarroa CG, Marcoux L et al. Time course of improvement in left ventricular function, mass and geometry in patients with congestive heart failure treated with beta- adrenergic blockade. J Am Coll Cardiol 1995;25:1154–61. 187.Australia-New Zealand Heart Failure Research Collaborative Group. Effects of carvedilol, a vasodilator-␤-blocker, in patients with congestive heart failure due to ischemic heart disease. Circulation 1995;92:212–18. 188.Groenning BA, Nilsson JC, Sondergaard L, Fritz-Hansen T, Larsson HB, Hildebrandt PR. Antiremodeling effects on the left ventricle during beta-blockade with metoprolol in the Evidence-based Cardiology 678 [...]... Cardiol 1993;71: 98 2–6 57.Brown CA, O’Connell JB Myocarditis and idiopathic dilated cardiomyopathy Am J Med 1995;99:30 9–1 4 58. Codd MB, Sugrue DD, Gersh BJ, Melton LJ Epidemiology of idiopathic dilated and hypertrophic cardiomyopathy Circulation 1 989 ;80 :56 4–7 2 59.Felker GM, Hu W, Hare JM The spectrum of dilated cardiomyopathy The Johns Hopkins experience with 1,2 78 patients Medicine 1999; 78: 27 0 8 3 60.McDonagh... cardiomyopathy in women versus men Am J Cardiol 1993;72: 58 0–5 67.Pearson GD, Veille J, Rahimtoola S et al Peripartum cardiomyopathy National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) Workshop Recommendations and Review JAMA 2000; 282 3:1 18 3 8 68. Lampert MB, Lang RM Peripartum cardiomyopathy Am Heart J 1995;130 :86 0–7 0 69.Grogan M, Redfield MM, Bailey KR et al Long-term... myocarditis in peripartum cardiomyopathy Am J Cardiol 1994;74:47 4–7 73.Felker GM, Jaeger CJ, Klodas E et al Myocarditis and longterm survival in peripartum cardiomyopathy Am Heart J 2000;140: 78 5–9 1 74.Pearl W Familial occurrence of peripartum cardiomyopathy Am Heart J 1995;129:42 1–2 75.Witlin AG, Mabie WC, Sibai BM Peripartum cardiomyopathy: an ominous diagnosis Am J Obstet Gynecol 1997;176: 18 2 8 76.Elkayam... 1992;20: 8 5–9 80 .Costanzo-Nordin MR, O’Connell JB, Subramanian R, Robinson JA, Scanlon PJ Myocarditis confirmed by biopsy presenting as acute myocardial infarction Br Heart J 1 985 ; 53:2 5–9 81 .Hufnagel G, Pankuweit S, Richter A et al The European Study of Epidemiology and Treatment of Cardiac Inflammatory Diseases (ESETCID) Herz 2000;25:27 9 8 5 82 .Aretz HT Myocarditis: the Dallas Criteria Human Pathol 1 987 ; 18: 61 9–2 4... by endomyocardial biopsy N Engl J Med 1 983 ;310:1 2–1 8 16.Godman GC, Bunting H, Melnick JL The histopathology of Coxsackie virus infection in mice 1 Morphologic observations with four different viral types Am J Pathol 1952; 28: 22 3–4 5 17.Woodruff JF Viral myocarditis Am J Pathol 1 980 ;101: 42 7–7 9 18. Olsen EGJ Endomyocardial biopsy Br Heart J 19 78; 40:9 5 8 19.Wolfgram LJ, Beisel KW, Herskowitz A, Rose NR... dysfunction after recent and remote myocardial infarction Lancet 1996; 3 48: 7–1 2 230.Pahor M, Gambassi G, Carbonin P Antiarrhythmic effects of ACE inhibitors A matter of faith or reality? Cardiovasc Res 1994; 28: 7–1 2 231.Newman TJ, Maskin CS, Dennick LG et al Effects of captopril on survival in patients with heart failure Am J Med 1 988 ;84 :14 0–4 680 232.The SOLVD investigators Effect of enalapril on survival in... 2002 (in press) 215.Jones CG, Cleland JGF Meeting report – the LIDO, HOPE, MOXCON and WASH studies Eur J Heart Fail 1999;1: 42 5–3 1 216.Kannel WB, Plehn JF, Cupples LA Cardiac failure and sudden death in the Framingham study Am Heart J 1 988 ;115: 86 9–7 5 217.Kjekshus J Arrhythmias and mortality in congestive heart failure Am J Cardiol 1990;64:42I–48I 2 18. Andersson B, Waagstein F Spectrum and outcome of congestive... dilated cardiomyopathy J Am Coll Cardiol 1995; 26 :8 0–4 70.Lampert MB, Weinert L, Hibbard J et al Contractile reserve in patients with peripartum cardiomyopathy and recovered left ventricular function Am J Obstet Gynecol 1997;176: 18 9–9 5 71.Midei MG, DeMent SH, Feldman AM, Hutchins GM, Baughman KL Peripartum myocarditis and cardiomyopathy Circulation 1990 ;81 :92 2 8 72.Rizeq MN, Rickenbacher PR, Fowler MB, Billingham... 1992 ;89 :132 0–4 23.Alvarez FL, Neu N, Rose NR, Craig SW, Beisel KW Heartspecific autoantibodies induced by Coxsackie virus B3: identification of heart autoantigens Clin Immunol Immunopathol 1 987 ;43:12 9–3 9 24.Neu N, Beisel KW, Traystman MD, Rose NR, Craig SW Autoantibodies specific for the cardiac myosin isoform are found in mice susceptible to Coxsackie B3-induced myocarditis J Immunol 1 987 ;1 38: 2 48 8 9 2... naturally processed protein J Immunol 1996;157: 23 9–4 6 26.Limas CJ, Goldenberg IF, Limas C Autoantibodies against beta-adrenoreceptors in human dilated cardiomyopathy Circ Res 1 989 ;64:9 7–1 03 27.Schultheiss HP, Schulze K, Huhl U, Ulrich G, Klingenberg M The ADP/ATP carrier as a mitochondrial autoantigen – facts and perspectives Ann NY Acad Sci 1 986 ; 488 :4 4–6 4 28. Wolff PG, Kühl U, Schultheiss HP Laminin distribution . after myocardial infarction. Lancet 1 988 ;i:25 5–9 . 96.Pfeffer JM, Pfeffer MA. Angiotensin converting enzyme inhibition and ventricular remodeling in heart failure. Am J Med 1 988 ;84 :3 7–4 4. 97.Swedberg K, Eneroth. Am J Cardiol 1 983 ;51: 45 5 8 . 130.Dies F, Krell MJ, Whitlow P et al. Intermittent dobutamine in ambulatory outpatients with chronic cardiac failure. Circulation 1 986 ;74:II- 38 II- 38. 131.Goldberg. antibodies to cytoskeletal elements – for example, laminin, 28 myosin, 38 actin, tropomyosin, 30 and Evidence-based Cardiology 684 other sarcolemmal epitopes 31 – and immunization with cardiac

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