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Original Article Effect of Vasodilator Therapy on Mortality in Chronic Congestive Heart Failure Jay N. Cohn, M.D., Donald G.

Archibald, M.Phil., Susan Ziesche, R.N., Joseph A. Franciosa, M.D., W. Eugene Harston, M.D., Felix E. Tristani, M.D., W. Bruce Dunkman, M.D., William Jacobs, M.D., Gary S. Francis, M.D., Kathleen H.

Flohr, M.D., Steven Goldman, M.D., Frederick R. Cobb, M.D., Pravin M. Shah, M.D., Robert Saunders, M.D., Ross D. Fletcher, M.D., Henry S. Loeb, M.D., Vincent C. Hughes, M.D., and Bonnie Baker, M.D.

N Engl J Med 1986; 314:1547-1552 DOI: 10.1056/NEJM42404. Abstract To evaluate the effects of vasodilator therapy on mortality among patients with chronic congestive heart failure, we randomly assigned 642 men with impaired cardiac function and reduced exercise tolerance who were taking digoxin and a diuretic to receive additional double-blind treatment with placebo, prazosin (20 mg per day), or the combination of hydralazine (300 mg per day) and isosorbide dinitrate (160 mg per day).

Follow-up averaged 2.3 years (range, 6 months to 5.7 years). Mortality over the entire follow-up period was lower in the group that received hydralazine and isosorbide dinitrate than in the placebo group. This difference was of borderline statistical significance.

For mortality by two years, a major end point specified in the protocol, the risk reduction among patients treated with both hydralazine and isosorbide dinitrate was 34 percent (P. THE demonstration of a favorable hemodynamic response to vasodilator drugs in patients with congestive heart failure has led to the wide use of these agents to supplement digitalis and diuretics in the treatment of symptomatic patients. Symptoms and exercise tolerance have been the major therapeutic end points of most previous trials, but the effect of vasodilator drugs on mortality has not been adequately examined. In 1980, a Veterans Administration Cooperative Study was initiated to determine whether two widely employed vasodilator regimens could alter life expectancy. In a double-blind trial, men with stable chronic congestive heart failure undergoing conventional treatment with digoxin and diuretics were assigned randomly to receive additional treatment with prazosin, both hydralazine and isosorbide dinitrate, or placebo. The concept to be tested was that peripheral vasoconstriction not only contributes to hemodynamic derangement and symptoms in heart failure but also may contribute to progressive deterioration of left ventricular function and premature death.

A total of 642 patients were entered into the trial, and all were followed for at least six months until the end of the follow-up period (December 15, 1985). In addition to information on mortality, the follow-up data consisted of a variety of sequential measurements, including radionuclide ejection fraction, quantitative exercise tolerance, echocardiography, Holter monitoring, and global assessment of functional status. This report emphasizes the analysis of mortality, the primary end point. Methods Patients with chronic congestive heart failure were recruited in 11 participating Veterans Administration hospitals. Recruitment was limited to men between the ages of 18 and 75. Eligibility for the trial was based on evidence of cardiac dilatation (cardiothoracic ratio >0.55 on chest x-ray film or a left ventricular internal diameter in diastole >2.7 cm per square meter on echocardiography) or left ventricular functional impairment (radionuclide ejection fraction 0.7 ng per milliliter) and to optimize the fluid balance.

Clinical evaluations and exercise-tolerance tests on two consecutive visits (separated by two weeks) had to reveal clinical and exercise stability before randomization could take place. The patients enrolled in the study continued to receive the optimal dose of digoxin and diuretic and also received one of three study regimens in double-blind fashion. One group was given placebo tablets and placebo capsules that were to be taken four times daily. A second group took 2.5-mg prazosin capsules and placebo tablets four times daily. The third group was given 37.5 mg of hydralazine in matching capsules and 20 mg of isosorbide dinitrate in matching tablets that were to be taken four times daily. In all groups, therapy began with one capsule and one tablet four times daily. In the absence of side effects, this dose was increased two weeks later to two capsules and two tablets four times daily.

If side effects that were thought to be drug-related occurred, the dose could be reduced to half a tablet four times daily or to one capsule twice daily. If the dose was reduced, an attempt was made to reinstitute the full doses at a later date. The patients were stratified according to whether they had coronary artery disease. The diagnosis of coronary disease was based on a documented history of previous myocardial infarction, typical angina pectoris, and coronary stenoses >75 percent of the diameter of the lumen on angiography. In the absence of one or more of these signs, the patient was assigned to the group without coronary artery disease. Optimal power for the comparison of each treatment to placebo would have been achieved with 20 percent more patients in the placebo group than in the group that received the vasodilator therapy.

Randomization was carried out in each stratification group at each center in blocks of seven, with three patients randomly assigned to receive placebo and two patients assigned to receive each of the vasodilator regimens. This ratio was used because it allowed a reasonable block size and it provided nearly optimal power for comparisons between each active treatment and placebo and nearly optimal power for a possible comparison between all the active treatments together and placebo. The patients' drug kits were identical in appearance and were labeled with a coded number. When assigning a patient to a treatment group, an investigator called the coordinating center to learn which coded number would be given to that patient.

In order to limit dropouts, rigid criteria were established for 'treatment failures.' Physicians in the study were advised to hospitalize patients with worsening symptoms and, if appropriate, to use temporary intravenous vasodilator or inotropic interventions for stabilization. The physicians were also advised to give these patients the study medications again on discharge. At least two such intervention experiences were generally required, along with objective evidence of deterioration, before the study medications were discontinued and replaced with known therapy. The initial goal of a sample size of 720 patients was chosen to provide a power of 84 percent if either treatment reduced the annual mortality rate to 33 percent below that in the placebo group. All statistical tests were two-tailed.

The method of O'Brien and Fleming, with four assessments for possible early stopping, was used to monitor the trial., With this procedure, comparisons of the treatments with respect to survival at the end of a trial can be considered statistically significant (P2.04 is attained. The study investigators had no knowledge of the results of the interim analyses of safety and efficacy; these aspects of the trial were monitored by the operations committee. The distribution of base-line variables in each treatment group was compared with that in the placebo group by means of either the chi-square test or the t-test. The primary analysis included all study patients and all deaths in their randomized treatment group, according to the intention-to-treat principle. The cumulative mortality curves were calculated with the life-table approach by means of the actuarial method.

To compare the treatment groups with respect to survival, the Cox life-table regression model was used when adjustments were made for base-line variables. For unadjusted comparisons, two standard tests, the log-rank test and the generalized Wilcoxon test, were used; the calculations were done with BMDP statistical software. Results Patient recruitment began in March 1980 and ended on June 15, 1985; 642 patients were entered into the study (273 in the placebo group, 183 in the prazosin group, and 186 in the hydralazine–isosorbide dinitrate group). Follow-up ended (without early stopping) on December 15, 1985. Of the 642 patients in the study, 284 (44.2 percent) had coronary disease and 358 (55.8 percent) had heart failure unrelated to coronary disease.

The distribution of base-line variables was remarkably similar in the three treatment groups. The only apparent imbalance was a slightly but significantly (P = 0.03) higher cardiothoracic ratio and a slightly (P = 0.05) lower exercise tolerance in the group treated with prazosin ( Table 1 Base-Line Data in the Three Treatment Groups. The reasons for permanent discontinuation of the study drugs were side effects, clinical deterioration, a nonfatal cardiac event, or patient decision.

Excluding the discontinuations that took place within one month before death, one or both types of placebo were discontinued in 47 patients (17 percent) in the group receiving placebo ( Table 2 Permanent Discontinuation of Study Drugs. Prazosin was discontinued in 43 patients (23 percent). In the hydralazine–isosorbide dinitrate group, 31 patients (17 percent) stopped taking both drugs, whereas 10 additional patients discontinued hydralazine only and 19 discontinued isosorbide dinitrate only. In other patients, the drug dosage was reduced to relieve side effects. Six months after randomization, 83 percent of the patients in the placebo group were prescribed full doses of placebo, 75 percent of those in the prazosin group were prescribed full doses of prazosin, and 55 percent of those in the hydralazine–isosorbide dinitrate group were prescribed full doses of both those drugs. The average prescribed doses were as follows: prazosin, 18.6 mg per day; hydralazine, 270 mg per day; and isosorbide dinitrate, 136 mg per day.

More than 85 percent of the prescribed tablets were taken in each treatment group. The mean follow-up period was 2.3 years (range, 6 months to 5.7 years). Persistent attempts were made to determine the survival status of all patients at the end of the study. Only four patients remained lost to follow-up: two in the placebo group, one in the prazosin group, and one in the hydralazine–nitrate group.

During the follow-up period, there were 120 deaths in the placebo group (44.0 percent), 91 deaths in the prazosin group (49.7 percent), and 72 deaths in the hydralazine–nitrate group (38.7 percent). Among the patients with chronic heart failure who died, it was difficult to exclude the heart condition as a contributing factor to death — even when other serious diseases were present. Therefore, this analysis has been confined to mortality from all causes. The investigators classified 45 percent of the deaths as 'sudden.' Life-table analysis that was based on intention to treat and that included all deaths revealed no difference between the prazosin and placebo groups ( Figure 1 Cumulative Mortality from the Time of Randomization in the Three Treatment Groups. A reduction in mortality over the entire follow-up period was observed in the hydralazine–nitrate group, as compared with the placebo group (P = 0.093 on the log-rank test and P = 0.046 on the generalized Wilcoxon test, which gives more weight to treatment differences occurring in the earlier part of the mortality curves and less weight to the latter part of the curves, where the numbers are smaller).

The Wilcoxon statistic was not quite significant at the P = 0.05 level after adjustments were made for multiple tests over time for possible early stopping. At one year, the cumulative mortality rate in the group treated with hydralazine–nitrate (12.1 percent) was 38 percent lower than that in the placebo group (19.5 percent; Table 3 Cumulative Mortality Rates at Each Anniversary of Randomization in the Placebo and Hydralazine–Isosorbide Dinitrate (Hyd–Iso) Groups. The absolute difference in mortality rates between these two groups increased during three years and then began to diminish. Since it was anticipated that any positive treatment effect might wane after two years, the cumulative mortality at two years had been specified in the study protocol as a major end point to be considered (after consideration of overall mortality). For the first two-year period, the Cox life-table regression model yielded an estimate of a cumulative reduction in mortality risk of 34 percent in the hydralazine–nitrate group, as compared with the placebo group (P.

Discussion The rationale for vasodilator therapy for heart failure is evidence that vasoconstriction in the systemic arterial and venous beds raises impedance to left ventricular ejection and shifts blood centrally from the venous capacitance vessels. The result of these circulatory effects is increased preload and afterload that adversely affect left ventricular performance and contribute to the low cardiac output and venous congestion that characterize heart failure. Studies of the hemodynamic effects of sodium nitroprusside have revealed that the relaxing effect of the drug on the arteries and veins could produce a profoundly favorable effect on left ventricular performance.

Subsequent studies indicated that orally administered prazosin or hydralazine, given in combination with nitrates, could produce a similar hemodynamic effect.,, Short-term trials with these agents have produced various results. In some studies, symptoms and exercise tolerance, as well as measures of left ventricular function, have improved. In others, however, no evidence of efficacy has been observed., None of these studies have been large enough to evaluate the influence of these drugs on mortality. We found that mortality among the patients treated with hydralazine–nitrate was reduced in comparison with patients in the placebo group, by 38 percent at the end of one year, by 25 percent at two years, and by 23 percent at three years. For the entire follow-up period, the reduction in mortality in the hydralazine–nitrate group, as analyzed by a variety of statistical methods, was at the borderline of statistical significance (P∼0.05). Cumulative mortality up to two years, a prespecified end point of the study, was significantly reduced in the hydralazine–nitrate group (P.

Supported by the Cooperative Studies Program of the Medical Research Service, Veterans Administration Central Office, Washington, D.C. *The Veterans Administration Study Group consisted of the following: Chairman's Office: Study Chairman, Jay N. Cohn, M.D.; and Study Coordinator, Susan Ziesche, R.N. Participants: VA Medical Centers, participating investigators, nurses, and technicians: Cincinnati — Kathleen Flohr, M.D., Janice Clarke, M.D. (past), Dollie Hessler, R.N., Rosemarie Wood, R.N., and Judy Schaffer, R.N.; Durham, N.C.—Frederick R. Cobb, M.D., Michael Higgenbotham, M.D., Eugenia Wilson, R.N., and Jeanne Watkinson, R.N.; Hines, Ill. — William Jacobs, M.D., Henry S.

Loeb, M.D., and Ann Henrick, R.N.; Little Rock, Ark. Franciosa, M.D., Bonnie Baker, M.D., Penny Casebolt, R.N., and Mary Wilen, L.P.N.; Los Angeles — Pravin M.

Shah, M.D., Maylene Wong, M.D., and Jill James; Milwaukee — Felix E. Tristani, M.D., Vincent C. Hughes, M.D., Sandra Laedtke, R.N., and Grace Daniels, L.P.N.; Minneapolis — Gary S. Francis, M.D., Susan M. Ziesche, R.N., Janet A. Nelson, R.N., Therese Noel, R.N., and Linda Schlasuer, R.N. (past); Nashville — W.

Gene Harston, M.D., Barbara H. Smith, R.N., and Lisa Manning, R.N.; Philadelphia — W. Bruce Dunkman, M.D., Cheryl Leddy, M.D. (past), Richard A. Jones, R.N., Janice Van Wart, R.N., Peggy Arment, R.N., and Sherrie Stiffler, R.N.; Tuscon, Ariz. — Steven Goldman, M.D., David Hager.

(past), Julie Brandt, R.N., Lucretia Nelson, R.N., and Ray Holcombe, R.N.; and Washington, D.C. — Robert Saunders, M.D., Mark Wish, M.D., and Joseph Orndorff, R.N.

Executive Committee: Jay N. Cohn, M.D., Chairman, Donald G. Archibald, M.Phil., Joseph A. Franciosa, M.D., Gary Francis, M.D., Pravin Shah, M.D., Ross Fletcher, M.D., Susan Ziesche, R.N., and Clair Haakenson, R.Ph., M.S. (ad hoc member). Biostatistics and Research Data Processing: West Haven Cooperative.

Studies Program Coordinating Center: Chief — Yick-Kwong Chan, Ph.D.; Study Biostatistician — Donald G. Archibald, M.Phil.; Programmers — Mary Anne Hope, M.S., and Chinyu Lee, M.S. (past); Statistical Assistants — Raymond Kilstrom, M.B.A., Arnold Pfenninger, M.S.

(past), and Katherine Newvine (past); and Computer Assistants — Stella Marcinauskis, Velma Williams, and Rosann Botte (past). Central Electrocardiographic Laboratory: Director — Ross Fletcher, M.D., Washington, D.C, VA Medical Center. Central Echocardiographic Laboratory: Director — Pravin Shah, M.D., Wadsworth VA Medical Center.

Cooperative Studies Program Clinical Research Pharmacy Coordinating Center (Albuquerque, N.M.): Chief — Michael Sather, R, Ph., M.S.; Clinical Research Pharmacist — Clair Haakenson, R.Ph., M.S.; and Pharmacy Technician — Roy Fetter. Operations Committee: Chairman — Richard Gorlin, M.D.; William Parmley, M.D., Leon Goldberg, M.D., Genell Knatterud, Ph.D., David Shand, M.D. (past), and Yick-Kwong Chan, Ph.D. Human Rights Committee: Chairman — Graham S. Gibbard, Ph.D.; Barbara Kathe, R.S.M., Ph.D., Mary Joan Cook, R.S.M., Ph.D., Richard C. Feldman, Esq., Jane S. Rasmussen, M.D., Wesley M.

Vietzke, M.D., Vincent Marenna, Mable J. Draper, R.Ph., Walter W. Powell, Ph.D., and Sheila Wellington; Alternates — Paul J. DiMaggio, Ph.D., Jack Evans, Esq., and James M. Solomon, M.D.

Cooperative Studies Program Central Administration (VA Central Office, Washington, D.C): Chief — Daniel Deykin, M.D., and James A. Hagans, M.D., Ph.D. (past); and Staff Assistant — Ping C Huang, Ph.D. References • 1 Guiha NH, Cohn JN, Mikulic E, Franciosa JA, Limas CJ.. Treatment of refractory heart failure with infusion of nitroprusside. N Engl J Med 1974; 291:587–92. • 2 Cohn JN, Franciosa JA.. Vasodilator therapy of cardiac failure.

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