Original Article
Effect of Oral Milrinone on Mortality in Severe Chronic Heart Failure
N Engl J Med 1991; 325:1468-1475November 21, 1991
- Abstract
- Abstract
Background.
Milrinone, a phosphodiesterase inhibitor, enhances cardiac contractility by increasing intracellular levels of cyclic AMP, but the long-term effect of this type of positive inotropic agent on the survival of patients with chronic heart failure has not been determined.
Methods.
We randomly assigned 1088 patients with severe chronic heart failure (New York Heart Association class III or IV) and advanced left ventricular dysfunction to double-blind treatment with 40 mg of oral milrinone daily (561 patients) or placebo (527 patients). In addition, all patients received conventional therapy with digoxin, diuretics, and a converting-enzyme inhibitor throughout the trial. The median period of follow-up was 6.1 months (range, 1 day to 20 months).
Results.
As compared with placebo, milrinone therapy was associated with a 28 percent increase in mortality from all causes (95 percent confidence interval, 1 to 61 percent; P = 0.038) and a 34 percent increase in cardiovascular mortality (95 percent confidence interval, 6 to 69 percent; P = 0.016). The adverse effect of milrinone was greatest in patients with the most severe symptoms (New York Heart Association class IV), who had a 53 percent increase in mortality (95 percent confidence interval, 13 to 107 percent; P = 0.006). Milrinone did not have a beneficial effect on the survival of any subgroup. Patients treated with milrinone had more hospitalizations (44 vs. 39 percent, P = 0.041 ), were withdrawn from double-blind therapy more frequently (12.7 vs. 8.7 percent, P = 0.041), and had serious adverse cardiovascular reactions, including hypotension (P = 0.006) and syncope (P = 0.002), more often than the patients given placebo.
Conclusions.
Our findings indicate that despite its beneficial hemodynamic actions, long-term therapy with oral milrinone increases the morbidity and mortality of patients with severe chronic heart failure. The mechanism by which the drug exerts its deleterious effects is unknown. (N Engl J Med 1991;325:1468–.)
Media in This Article
Figure 1
Kaplan–Meier Analysis Showing Cumulative Rates of Survival in Patients with Chronic Heart Failure Treated with Milrinone or Placebo.Figure 2
Kaplan–Meier Analysis Showing Cumulative Rates of Survival in Patients with Class IV Heart Failure, According to Treatment Group.Article Activity
- Article
BECAUSE cardiac contractility is impaired in patients with chronic heart failure, many drugs have been developed to enhance the inotropic state of the failing heart.1 Some drugs increase the concentration of intracellular sodium, either by stimulating the activity of the sodium channel (sodium-channel agonists) or by inhibiting the activity of sodium/potassium—transporting ATPase (digitalis glycosides). Other positive inotropic agents increase the concentration of intracellular cyclic AMP, either by promoting its synthesis (beta-adrenergic agonists) or by retarding its degradation (phosphodiesterase inhibitors). The use of cyclic AMP—enhancing agents has been viewed as a particularly rational approach to the treatment of chronic heart failure, since the production of cyclic AMP is deficient in failing human hearts, especially those of patients in the terminal stages of the disease.2 , 3
Despite the theoretical appeal of cyclic AMP—enhancing positive inotropic agents, there has been considerable uncertainty about the long-term efficacy and safety of these drugs in patients with chronic heart failure.1 , 4 Beta-adrenergic agonists and phosphodiesterase inhibitors have not generally had favorable effects on symptoms and exercise tolerance in placebo-controlled trials,5 6 7 8 9 10 11 12 even though many of these drugs produce immediate and long-term hemodynamic benefits.13 14 15 Furthermore, uncontrolled and controlled studies have suggested that cyclic AMP—enhancing agents may accelerate the progression of the underlying disease and provoke the development of serious ventricular arrhythmias.4 , 9 , 16 , 17 These observations have led physicians to fear that the prolonged use of beta-adrenergic agonists and phosphodiesterase inhibitors may shorten the survival of patients with chronic heart failure.4 , 18 , 19 An increase in mortality has been reported in small studies carried out with the partial beta-adrenergic agonist xamoterol7 and with the phosphodiesterase inhibitors enoximone and imazodan.10 , 11
However, previous efforts to evaluate the effect of positive inotropic agents on the survival of patients with chronic heart failure have had three major limitations. First, most trials have been carried out in patients with mild-to-moderate symptoms, but the patients who are most likely to require and receive a new drug for heart failure are those with severe symptoms.19 Second, most trials have been conducted in patients who were not taking converting-enzyme inhibitors.18 Yet, converting-enzyme inhibitors have now emerged as standard therapy for heart failure (especially in patients with advanced disability),20 and blockade of the renin—angiotensin system may favorably modify the hemodynamic and hormonal actions of positive inotropic agents.15 , 21 Third, all previous trials have been designed to evaluate the effects of new drugs on symptoms and exercise tolerance. None have had the statistical power to measure the influence of therapy with a positive inotropic agent on mortality.9 10 11 These three limitations have raised the possibility that unfavorable conclusions4 5 6 7 8 9 10 11 about the utility of positive inotropic agents (based on the results of small clinical trials) may have been unwarranted. Additional uncertainties have been introduced by the favorable results of controlled studies carried out in an experimental model of heart failure in rats, which showed that the phosphodiesterase inhibitor milrinone attenuated the progression of ventricular enlargement after an acute myocardial injury22 and prolonged survival.23 These experimental studies with milrinone were particularly encouraging, since similar results were observed in the same model when the animals were given captopril and enalapril,23 24 25 and these results correctly predicted the subsequent demonstration of the beneficial effects of the two converting-enzyme inhibitors in patients.20 , 26 , 27
To clarify the discordant findings of experimental and clinical studies with milrinone, we conducted the Prospective Randomized Milrinone Survival Evaluation (PROMISE). The primary objective of this trial was to determine the effect of milrinone on the mortality of patients with severe chronic heart failure who remained symptomatic despite conventional therapy.
Methods
The study was performed under the auspices of a Committee of Investigators (which designed the study), a Clinical Coordinating Center (which made day-to-day policy decisions), a Biostatistics Center (which analyzed the data), and a Data and Safety Monitoring Board (which consisted of nonparticipating physicians who reviewed the unblinded results of the study every four to six months). Participating investigators had no knowledge of the results of the interim analyses. All four groups functioned independently of the sponsor of the study (Sterling Research Group).
Study Design
Patients with chronic heart failure whose symptoms remained severe despite conventional therapy were enrolled at 119 centers in the United States and Canada. Heart failure was defined as the presence of dyspnea or fatigue at rest or on exertion in association with a left ventricular ejection fraction ≤35 percent, as assessed by radionuclide ventriculography. All patients had had symptoms of New York Heart Association functional class III or IV for at least three months (including symptoms at rest within two weeks) and had been receiving treatment with digoxin, diuretics, and a converting-enzyme inhibitor for at least four weeks. Treatment with nitrates, hydralazine, prazosin, and other vasodilator drugs was allowed but (in contrast to the use of converting-enzyme inhibitors) was not mandated. Patients were excluded from participation in the study if they had heart failure due to obstructive valvular disease, active myocarditis, hypertrophic or amyloid cardiomyopathy, uncorrected thyroid disease, or a malfunctioning artificial heart valve. Patients were also excluded if they had any of the following: a history of a serious symptomatic ventricular arrhythmia; severe, frequent, or exercise-limiting angina pectoris; a myocardial infarction within the previous three months; severe primary pulmonary, renal, or hepatic disease; a systolic blood pressure below 85 mm Hg; or a serum potassium concentration below 3.5 mmol per liter. In addition, patients who required therapy with beta-adrenergic blockers, calcium-channel blockers, disopyramide, flecainide, encainide, levodopa, dopamine, or dobutamine were not permitted to enter the study.
Before randomization, the clinical status of each patient was assessed; vital signs were recorded; cardiac size and function were determined (by chest radiography and radionuclide ventriculography, respectively); cardiac arrhythmias were quantified (during a 24-hour ambulatory recording); and blood was collected for the measurement of serum electrolytes and serum digoxin and the evaluation of renal function. Patients were then randomly assigned in a double-blind fashion to receive either milrinone (10 mg orally four times daily) or matching placebo, in addition to digoxin, diuretics, and a converting-enzyme inhibitor (captopril or enalapril). Randomization was stratified according to the pretreatment left ventricular ejection fraction. The clinical status of each patient was reevaluated every one to three months. The doses of milrinone could be decreased to 5.0 or 7.5 mg four times daily (if side effects occurred that were thought to be drug-related) or could be increased to 12.5 or 15.0 mg four times daily (if the patient had an unsatisfactory clinical response to the drug). The doses of all cardioactive drugs (including digoxin, diuretics, and the convertingenzyme inhibitor) could be adjusted at the discretion of the investigator. If the patient's condition deteriorated during the study, the investigator could prescribe any treatment that was clinically indicated; however, patients were not permitted to receive open-label milrinone.
The protocol was approved by the institutional review boards at all participating centers, and before undergoing any study procedures each patient gave written informed consent.
Statistical Analysis
The principal end point of the study was mortality due to all causes. Secondary end points included cardiovascular mortality, the number of hospitalizations, the addition of vasodilators because of worsening heart failure, symptoms, and adverse reactions. In addition to evaluation of these end points in the trial as a whole, the effect of milrinone on survival was assessed in specific subgroups defined by the following 10 prognostically important variables recorded before randomization: left ventricular ejection fraction, cause of heart failure, New York Heart Association functional class, serum sodium concentration, serum creatinine concentration, age, sex, presence or absence of angina, cardiothoracic ratio, and presence or absence of ventricular tachycardia. The first three of these subgroup analyses were planned prospectively in the original protocol or at the first meeting of the Data and Safety Monitoring Board.
The study was designed to have a power of 90 percent (two-tailed) to detect a difference of 25 percent in mortality between the two treatment groups. Since it was recognized that any estimate of mortality made before the study might be inaccurate, it was planned that the trial should continue until 190 patients receiving placebo had died (as determined by the Data and Safety Monitoring Board). To protect against increasing the rate of false positive errors due to interim analyses, we used the Lan—DeMets procedure,28 with an O'Brien—Fleming type of boundary,29 which requires only the expected number of deaths to be specified in advance.
The base-line characteristics of the two treatment groups were compared by the t-test (for continuous variables) and the chi-square statistic (for noncontinuous variables). Cumulative survival curves were constructed by Kaplan–Meier survivorship methods,30 and differences between the curves were tested for significance by both the log-rank statistic and a Cox proportional-hazards regression model.31 The survival analyses included all randomized patients, and all deaths were recorded according to the treatment group to which the patient had originally been assigned (intention-to-treat principle). Differences between the treatment groups in events after randomization were analyzed by the t-test or chi-square test, as appropriate. For comparisons with ordinal-response data or outcomes not normally distributed, nonparametric rank statistical methods were used (such as the Wilcoxon two-sample rank-sum test).
Results
The trial began on January 24, 1989, and was stopped by the sponsor on the recommendation of the Data and Safety Monitoring Board on October 4, 1990, five months before its scheduled completion. The decision to stop the study was based on the finding of an adverse effect of milrinone on the survival of patients with chronic heart failure.
When the trial was stopped, 1088 patients were enrolled: 561 patients were assigned to treatment with milrinone, and 527 to treatment with placebo. The two groups were similar in all their pretreatment characteristics (Table 1Table 1
Base-Line Hemodynamic and Clinical Characteristics of the Patients, According to Treatment Group.*). After randomization, patients received an average daily dose (±SE) of 37±1 mg of milrinone or 38 ±1 mg of placebo. These doses were maintained at similar levels throughout the follow-up period. Compliance with the prescribed study medication (assessed by pill counts) averaged more than 90 percent at all visits for both treatment groups. The duration of follow-up ranged from 1 day to 20 months (median, 6.1 months); 554 patients were followed for at least 6 months, and no patient was lost to follow-up.Mortality
During the course of the study, there were 168 deaths (30 percent) in the group assigned to treatment with milrinone and 127 deaths (24 percent) in the group assigned to placebo. Curves for cumulative survival (intention-to-treat analysis) are shown in Figure 1Figure 1
Kaplan–Meier Analysis Showing Cumulative Rates of Survival in Patients with Chronic Heart Failure Treated with Milrinone or Placebo.. According to the log-rank test, milrinone treatment was associated with a 28 percent increase in mortality due to all causes (95 percent confidence interval, 1 to 61 percent; nominal P = 0.038; after adjustment for early stopping, P = 0.060). The log hazard ratio remained constant during the course of the study, indicating that the increased mortality risk associated with milrinone therapy did not vary significantly as a function of time.Of the 295 patients who died during the study, 284 (96 percent) died of cardiovascular causes (165 in the milrinone group and 119 in the placebo group). According to the log-rank test, milrinone treatment was associated with a 34 percent increase in cardiovascular mortality (95 percent confidence interval, 6 to 69 percent; nominal P = 0.016; after adjustment for early stopping, P = 0.037).
Outcome in Subgroups
To determine whether milrinone had a beneficial effect on survival in a subgroup of patients with chronic heart failure, the effect of treatment on mortality was examined in subgroups defined by the following 10 variables recorded before randomization: left ventricular ejection fraction, cause of heart failure, functional class, serum sodium concentration, serum creatinine concentration, age, sex, presence or absence of angina, cardiothoracic ratio, and presence or absence of ventricular tachycardia. Milrinone exerted an adverse effect in all these subgroups; no significant beneficial effect of treatment on survival was observed in any subgroup (Table 2Table 2
Effect of Long-Term Milrinone Therapy on Survival, According to Prognostically Important Variables.). It is noteworthy that milrinone increased mortality significantly in three particular subgroups of patients: those with class IV symptoms, those with a low serum sodium concentration, and those with a markedly increased cardiothoracic ratio.Patients with New York Heart Association class IV heart failure (most severe symptoms) are of particular interest, since this subgroup represents the patients most likely to receive a new drug for heart failure. Cumulative-survival curves for this subgroup are shown in Figure 2Figure 2
Kaplan–Meier Analysis Showing Cumulative Rates of Survival in Patients with Class IV Heart Failure, According to Treatment Group.. According to the log-rank test, milrinone therapy was associated with a 53 percent increase in mortality in this subgroup (95 percent confidence interval, 13 to 107 percent; P = 0.006). However, the magnitude of the effect of milrinone on patients with class IV symptoms was not significantly different from that on patients with class III symptoms (P = 0.10). In general, the effect of milrinone in the subgroups defined by the presence of any of the 10 base-line covariates (Table 2) was similar to the effect of the drug in the subgroups defined by the absence of these base-line characteristics.Functional Capacity
When all patients were considered together, there was no evidence of a favorable effect of milrinone on symptoms or functional capacity. The two treatment groups did not differ in the number of patients who had an improvement in functional class after two months of therapy (34 percent receiving milrinone vs. 31 percent receiving placebo), the number who had worsening heart failure as an adverse reaction (30 percent vs. 29 percent), the number who reported functional deterioration during the study (5 percent vs. 6 percent), or the number who required the addition of vasodilators for worsening heart failure (5 percent vs. 6 percent). Patients in the milrinone group were hospitalized more frequently than those in the placebo group (44 percent vs. 39 percent; P = 0.041); most hospitalizations were for cardiovascular events.
Adverse Reactions
Patients in the milrinone group were permanently withdrawn from double-blind therapy more frequently and earlier than those in the placebo group (P = 0.041) (Fig. 3Figure 3
Kaplan–Meier Analysis Showing Cumulative Rates of Withdrawal from Double-Blind Therapy, According to Treatment Group.). The study drug was discontinued in 71 patients (12.7 percent) treated with milrinone but in only 46 patients (8.7 percent) given placebo. The reasons for discontinuation are shown in Table 3Table 3
Reasons for Permanent Discontinuation of Study Drugs.. The difference between the two treatment groups in the rate of withdrawal was related in large part to the higher frequency of adverse reactions in the patients treated with milrinone. When all side effects were considered (whether or not they resulted in the discontinuation of double-blind therapy), adverse events were significantly more frequent among patients receiving milrinone than among those receiving placebo (P = 0.006). Selected adverse reactions are listed in Table 4Table 4
Incidence of Selected Adverse Reactions in the Treatment Groups.. The following reactions were significantly more frequent in the milrinone group: headache (P = 0.005), diarrhea (P = 0.007), blurred vision (P = 0.001), hypotension (P = 0.006), palpitations (P = 0.017), and syncope (P = 0.002).Discussion
Our findings indicate that long-term treatment with oral milrinone has a deleterious effect on the survival of patients with severe chronic heart failure. Milrinone therapy was associated with a 28 percent increase in mortality due to all causes and a 34 percent increase in cardiovascular mortality in patients with advanced left ventricular dysfunction whose symptoms remained severe despite conventional therapy. Milrinone adversely affected survival in all subgroups of patients; no subgroup had a significant beneficial effect of treatment on survival. In addition, milrinone failed to improve functional capacity or reduce the risk of worsening heart failure. Instead, long-term treatment with the drug was associated with an increased frequency of hospitalizations and an increased risk of serious adverse cardiovascular reactions. These unfavorable effects of oral milrinone therapy led the Data and Safety Monitoring Board to recommend to the sponsor that the study be stopped before its scheduled completion.
The results of the present trial are consistent with the findings of previous clinical studies carried out with cyclic AMP—enhancing agents in patients with chronic heart failure. Two earlier placebo-controlled trials of beta-adrenergic agonists (intravenous dobutamine32 and oral xamoterol7) and three previous placebo-controlled studies of phosphodiesterase inhibitors (milrinone,9 enoximone,10 and imazodan11) reported that treatment with these drugs was associated with an increase in mortality. Interpretation of these studies, however, was complicated by the facts that the number of fatal events was small,7 , 9 10 11 the two treatment groups were imbalanced before randomization,9 withdrawal of the study medication was encouraged,9 , 10 patients were permitted to cross over between one treatment group and the other,11 , 32 and the drugs tested exerted circulatory effects (in addition to increasing cardiac contractility) that may have led to an adverse outcome.7 All these deficiencies were avoided in the design of the present study, yet the conclusions were similar: Treatment with milrinone increased the risk of death.
This unfavorable clinical experience contrasts markedly with the results of experimental studies in animals, which showed that milrinone improves cardiac performance and survival.22 , 23 In a model of heart failure in rats, milrinone attenuated the magnitude of ventricular enlargement22 and reduced the risk of death23 to an extent similar to that achieved with converting-enzyme inhibitors.23 24 25 However, studies of the effects of milrinone in rats may not accurately predict the effects of the drug in patients, since milrinone does not inhibit phosphodiesterase, elevate cyclic AMP levels, or exert positive inotropic effects in hearts of rats.33 The drug acts only as a vasodilator in these animals and thus may prolong life as do other vasodilators.20 , 23 , 34 In contrast, along with its vasodilating actions, milrinone does inhibit phosphodiesterase, elevate cyclic AMP levels, and exert positive inotropic effects in the hearts of patients.2 , 35 These observations suggest that the effects of milrinone on myocardial levels of cyclic AMP may be responsible for the drug's adverse effects on the survival of patients with heart failure.
The precise mechanism by which long-term treatment with milrinone increases mortality in patients with chronic heart failure remains unknown. In experimental studies, drug-induced increases in the intracellular concentration of cyclic AMP have been shown to be directly toxic to myocardial cells and to enhance electrophysiologic mechanisms that lead to rhythm disturbances.36 37 38 39 In clinical studies, treatment with cyclic AMP—enhancing drugs has been associated with acceleration of disease progression and the development of serious ventricular arrhythmias 9 , 10 , 16 , 17 The Possibility that milrinone may exert important proarrhythmic effects is supported by the results of the present trial, in which symptoms commonly caused by serious ventricular arrhythmias (hypotension, blurred vision, and syncope) occurred more frequently in the milrinone-treated patients. However, these symptoms could also have been produced by the vasodilating effects of milrinone, which (when combined with those of a converting-enzyme inhibitor) could lead to marked declines in blood pressure.3 , 35 Further analysis of serial hemodynamic and electrocardiographic measurements carried out in the present trial, together with an elucidation of the mode of death in the patients, may shed light on the mechanism of the adverse effect of milrinone.
Can the results of the present study be generalized to other positive inotropic agents? The present trial was designed to evaluate the effects of a single dosing regimen of milrinone in patients with severe symptoms and advanced left ventricular dysfunction who were also receiving digoxin, diuretics, and converting-enzyme inhibitors. Consequently, it is possible that data from our study may not necessarily be applicable to the use of milrinone or other drugs with positive inotropic effects, when given in different doses to patients with less severe symptoms who may be treated with different concurrent medications. Yet, the results with milrinone in the present trial are strikingly similar to the findings of many small placebo-controlled studies, in which various doses of several cyclic AMP—enhancing agents (e.g., prenalterol, enoximone, imazodan, and vesnarinone) were administered to patients with less severe symptoms, usually in the absence of therapy with a converting-enzyme inhibitor.7 , 9 10 11 , 18 , 32 The results of these small controlled studies with beta-adrenergic agonists and phosphodiesterase inhibitors,18 when combined with the findings of the present large trial, suggest that increased mortality may be a general effect of agents that enhance the myocardial concentration of cyclic AMP in the failing heart.
In conclusion, despite its favorable hemodynamic effects,14 long-term therapy with oral milrinone increases morbidity and mortality among patients with severe chronic heart failure, without producing important clinical benefits. The finding that milrinone was ineffective in ameliorating the symptoms of heart failure suggests that we should no longer view the impairment of cyclic AMP production in the failing heart2 as a biochemical deficiency to be remedied. On the contrary, our observation that milrinone was harmful supports the hypothesis that the decline in the production of myocardial cyclic AMP has an adaptive role in chronic heart failure,40 , 41 perhaps through attenuation of the primary mechanism by which high levels of endogenous catecholamines exert toxic effects on the heart.37 , 42
Supported by a grant from Sterling Research Group, Malvem, Pa.
*Members of the PROMISE Study Research Group are listed in the Appendix.
Source Information
From the Divisions of Cardiology, Mount Sinai School of Medicine, New York (M.P., M.L.K., J.A.S.); Jeanes—St. Agnes Hospital, Philadelphia (J.R.C.); Mayo School of Medicine, Rochester, Minn. (R.J.R.); Florida Heart Group, Orlando (R.J.I.); Washington Adventist Hospital, Takoma Park, Md. (R.D.); Winthrop University Hospital, Mineola, N.Y. (S.M.Z.); Medical University of South Carolina, Charleston (G.H.H.); University of California at Davis, Sacramento (W.J.B.); University of Southern California School of Medicine, Los Angeles (U.E.); State University of New York at Stony Brook and Veterans Affairs Medical Center, Northport, N.Y. (G.I.M.); the Sterling Research Group, Malvern, Pa. (J.S., P.K.T.); and the Biostatistics Center, University of Wisconsin, Madison (D.L.D.). Address reprint requests to Dr. Packer at the Center for Heart Failure Research, Mount Sinai School of Medicine, 1 Gustave Levy P1., New York, NY 10029.
Appendix
The study organization of the Prospective Randomized Milrinone Survival Evaluation comprised the following persons: Study Chairman: M. Packer; Study Coordinator: J.A. Sollano; Data and Safety Monitoring Board: R.J. Cody (chair), L.D. Fisher, S. Goldstein, D.G. Julian, P.D. Kligfield, and W.T. Friedewald; Biostatistics Center (University of Wisconsin, Madison): D.L. DeMets (director), S.A. Anderson, and T.M. Franke; Clinical Coordinating Center (Mount Sinai School of Medicine, New York): M. Packer (director), J.A. Sollano, D. Ahern, and J. Maravel; Study Operations/Monitoring Center (Sterling Research Group, Chesterbrook, Pa.): J. Shannon (director), P.K. Tandon, R.J. Schwarz, J.A. Novak, C. Biddlecome, J.M. Grabicki, J. Malatesta, and M. Todd; Steering Committee: M. Packer (chair), J.R. Benotti, J.H. Chesebro, U. Elkayam, G.S. Francis, M.L. Hess, B.M. Massie, and D.M. Mancini; Mortality Committee: G.S. Francis (chair), J. Abrams, F.R. Cobb, EJ. Eichhorn, T.D. Giles, and F.R. Kahl; Ancillary Trials Committee: J.H. Chesebro (co-chair), R.J. Rodeheffer (co-chair), R.H. Falk, P.E. Fenster, G.I. Mallis, G.W. Moe, J.G. Shanes, and R.C. Touchon; Holter Committee: B.M. Massie (chair), L.A. Brookfield, G.H. Hendrix, M.L. Kukin, J.F. Moran, P.J. Podrid, and P. Somani; Nursing Research Committee: J.L. Bazell (co-chair), D. Nauman (co-chair); D. Ahern, L. Gorkin, E.M. Handberg, J. Vasquez-Johnson, and J.A. Sollano.
The following are the participating centers and principal investigators of the study: Albany, N.Y.: Albany Medical College, S.A. Fein. Albuquerque, N.M.: University of New Mexico, J. Abrams; Lovelace Medical Center, C.K. Jutila. Atlanta: M. Sabom; Atlanta Cardiology Group, B.R. Williams, Jr.; Emory University School of Medicine, R.C. Schlant. Baltimore: Metropolitan Medical Associates, D.A. Goldscher. Beverly Hills, Calif.: Brotman Medical Center and University of California, R.P. Karlsberg. Boston: Boston University School of Medicine, R.H. Falk; Tufts University School of Medicine, J.E. Udelson. Bridgeport, Conn.: St. Vincent's Medical Center, EJ. Kosinski. Chalmette, La.: BJ. Iteld. Charleston, S.C.: Medical University of South Carolina, G.H. Hendrix. Charlotte, N.C.: Bennett Cardiac Center, W.T. Bennett; Mecklenburg Cardiovascular Consultants, D.E. Wise. Chicago: Rush Medical School, M.H. Davidson; Michael Reese Hospital and Medical Center, M.A. Silver. Cincinnati: Christ Hospital, D.J. Kereiakes. Cleveland: Cleveland Clinic Foundation, F.M. Fouad-Tarazi. Dallas: University of Texas Southwestern and Dallas Veterans Affairs Medical Centers, EJ. Eichhorn; Doctors Hospital, B. Hillert. Denver: Rocky Mountain Heart Research Associates, N. Vijay. Derby, Conn.: Griffin Hospital, K.V. Schwartz. Des Moines, la.: Iowa Heart Center, WJ. Wickemeyer. Detroit: Woodland Medical Center, E. Malinowski. Durham, N.C.: Duke University School of Medicine, F.R. Cobb. Fort Wayne, Ind.: Fort Wayne Cardiology, K.J. Kelly. Fremont, Calif.: C.J. Carlson. Gainesville, Fla.: University of Florida College of Medicine, CJ. Pepine. Grand Rapids, Mich.: Blodgett Memorial Medical Center, W.F. LaPenna. Halifax, N.S., Canada: Victoria General Hospital, D.E. Johnstone. Hanover, N.H.: Dartmouth Medical School, J.F. Plehn. Houston: St. Luke's Episcopal Hospital, E.K. Massin. Huntington, W.V.: Marshall University School of Medicine, R.C. Touchon. Indianapolis: C.M. Orr; Krannert Institute of Cardiology, Indiana School of Medicine, and Indianapolis Veterans Affairs Medical Center, T.J. Ryan. Iowa City, la.: University of Iowa College of Medicine, D.W. Ferguson. Jacksonville, Fla.: Riverside Clinic, G.A. Anderson; University of Florida Health Science Center at Jacksonville, A.B. Miller; Mayo Clinic, R.E. Safford; Jacksonville Cardiovascular Clinic, P.J. Bannon. Kingston, Ont., Canada: Kingston General Hospital, J.O. Parker. Lajolla, Calif.: Medical Arts Center, D.L. Costello; Scripps Clinic, G.P. Curtis. Lakeland, Fla.: Watson Clinic, K.F. Browne. Las Vegas: Cardiology Consultants of Nevada, C.A. Rhodes. Lexington, Ky.: University of Kentucky Medical Center, M.R. Berk. Little Rock, Ark.: Cardiology Consultants, S.W. Hutchins. Los Angeles: Century Park Research Associates, M.C. Levy; Hospital of the Good Samaritan, R.V. Matthews; UCLA School of Medicine, L.W. Stevenson; University of Southern California School of Medicine, U. Elkayam. Madison, Wis.: University of Wisconsin Medical School, C. VanderArk. Marrero, La.: Cardiology Center, D.M. Cassidy. Maywood, Ill.: Loyola University Medical Center, J.F. Moran. Melbourne, Fla.: Melbourne Cardiac Center, M.F. Lesser. Melrose Park, Ill.: Gottlieb Hospital, J.G. Shanes. Metairie, La.: C.A. DeAbate. Miami: Miami Heart Institute, M.A. Canosa-Terris. Mineola, N.Y.: Cardiovascular Medical Associates, M. Goodman; Winthrop University Hospital, S.M. Zeldis. Minneapolis: University of Minnesota School of Medicine, G.S. Francis and G.L. Pierpont; Minneapolis Heart Institute, I.F. Goldenberg; Fairview Southdale—Ridge Hospital, W.T. Hession. National City, Calif.: Heart Center of San Diego, J.A. Robinson. New Orleans: Tulane University School of Medicine, T.D. Giles. New York: Mount Sinai School of Medicine, M.L. Kukin; Columbia College of Physicians and Surgeons, G.W. Neuberg; S.A. Siegel. Norfolk, Va.: Cardiology Consultants, J.P. Parker. Oklahoma City: University of Oklahoma College of Medicine, U. Thadani. Orange, Calif.: University of California Irvine Medical Center, B. Allen. Orange, N.J.: S.K. Agarwal. Orlando, Fla.: Florida Heart Group, R.J. Ivanhoe and LJ. Acierno. Park Ridge, Ill.: Lutheran General Hospital, R.P. Sorkin. Pensacola, Fla.: Medical Center Clinic, M.C. Branco. Petoskey, Mich.: Burns Clinic Medical Center, H.J. Willens. Philadelphia: Jeanes—St. Agnes Hospital, J.R. Carver; Temple University School of Medicine, M. Jessup; University of Pennsylvania School of Medicine, D.M. Mancini; Philadelphia Heart Institute, J. David Ogilby; Albert Einstein Medical Center, J.H. Wertheimer. Portland, Oreg.: Oregon Health Sciences University School of Medicine, B.H. Greenberg. Poughkeepsie, N.Y.: Hudson Valley Cardiovascular Associates, R. Fiore. Redondo Beach, Calif.: B.Jackson. Reno, Nev.: Sierra Nevada Cardiology Associates, D.A. Spring. Richmond, Va.: Medical College of Virginia, R.J. Quigg. Rochester, Minn.: Mayo School of Medicine, J.H. Chesebro and R.J. Rodeheffer. Rochester, N.Y.: University of Rochester School of Medicine, P.J. Fitzpatrick. Sacramento, Calif.: University of California at Davis, W.J. Bommer. San Antonio, Tex.: Methodist Hospital, V.A. Covin. San Diego, Calif.: University of California at San Diego, R. Shabetai. San Francisco: Veterans Affairs Medical Center and University of California, San Francisco, B.M. Massie. Sarasota, Fla.: Sarasota Memorial Hospital, M.J. Frey. Savannah, Ga.: Memorial Medical Center, L.S. Goodman. Scottsdale, Ariz.: Mayo Clinic, R.S. Ruzich. Seattle: South Seattle Consulting Physicians, D.W. Gottlieb; Seattle Heart Clinic, R.J. Wescott; Virginia Mason Medical Center, J. Holmes. Sellersville, Pa.: Buxmont Cardiology, M.M. Greenspan. Spokane, Wash.: Deaconess—Sacred Heart Medical Center, M.A. DeWood. Springfield, Ill.: Prairie Cardiovascular Center—St. John's Hospital, R.C. Woodruff, III. St. Louis: St. Louis University School of Medicine, L.W. Miller. St. Paul, Minn.: St. Paul—Ramsey Medical Center, J.W. McBride. Staten Island, N.Y.: St. Vincent's Medical Center of Richmond, D.A. Bloomfield. Stony Brook, N.Y.: State University of New York at Stony Brook and Veterans Affairs Medical Center (Northport, N.Y.), G.I. Mallis and E.A. Brown, Jr. Takoma Park, Md.: Washington Adventist Hospital, R. DiBianco. Toledo, Ohio: Medical College of Ohio, P. Somani. Toronto: Sunnybrook Health Sciences Center, R. Baigre; St. Michael's Hospital, University of Toronto, G.W. Moe. Tucker, Ga.: North Atlanta Cardiology Group, W. Sear. Tucson, Ariz.: University of Arizona College of Medicine, P.E. Fenster. Valhalla, N.Y.: New York Medical College, R. Kay. Vero Beach, Fla.: Doctors Clinic, A. Glaser. Wichita, Kans.: The Goyle Clinic, K.K. Goyle; Galichia Medical Group, J.P. Galichia. Winchester, Va.: Selma Medical Associates, J.C. Laidlaw. Winston-Salem, N.C.: Bowman Gray School of Medicine, F.R. Kahl. Worcester, Mass.: University of Massachusetts Medical Center, J.R. Benotti.
- References
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