Cardiac Performance In Patients Research Articles

Long-term (3-month) effects of a new beta-blocker (nebivolol) on cardiac performance in dilated cardiomyopathy

Objectives. This study examined the long-term (3-month) effects of nebivolol, a new beta-adrenergic blocking agent, on cardiac performance in patients with dilated cardiomyopathy.Background. Several beta-blocking drugs have been reported to have a beneficial hemodynamic effect in patients with dilated cardiomyopathy, but few data obtained in a placebo-controlled randomized study have addressed the mechanisms of improvement.Methods. Twenty-four patients with dilated idiopathic (n = 22) or ischemic (n = 2) cardiomyopathy (ejection fraction 0.15 to 0.40) in stable New York Heart Association functional class II or III were entered into a double-blind randomized trial of nebivolol, a new, potent, selective beta1-antagonist. Exercise time, invasive hemodynamic data (12- and 24-h monitoring) and variables of left ventricular function were examined at baseline and after 3 months of orally administered nebivolol (1 to 5 mg/day, n = 11) or placebo (n = 13).Results. Heart rate decreased (group mean 85 to 71 beats/min vs. 87 to 87 beats/min with placebo) and stroke volume increased significantly (group mean 43 to 55 ml vs. 42 to 43 ml) with nebivolol; decreases in systemic resistance, systemic arterial pressure, wedge pressure and pulmonary artery pressure were not significantly different from those with placebo. Similar hemodynamic results were obtained in the catheterization laboratory. Analysis of high fidelity measurements of left ventricular pressure showed a decrease in left ventricular end-diastolic pressure in the nebivolol group (group mean 21 to 15 vs. 24 to 20 mm Hg with placebo) but no change in the maximal rate of pressure development or in two variables of left ventricular relaxation (maximal negative rate of change of left ventricular pressure [dP/dtmax]and the time constant tau). Left ventricular mass decreased (p = 0.04). Despite a decrease in heart rate with nebivolol, there was a slight decrease in left ventricular end-diastolic volume (p = NS). End-systolic volume tended to decrease (p = 0.07) despite no reduction in end-systolic stress. The net result was a significant increase in ejection fraction (group mean 0.23 to 0.33 vs. 0.21 to 0.23 with placebo), presumably as a result of an increase in contractile performance. This effect was corroborated by an increase in a relatively load-independent variable of myocardial performance.Conclusions. Nebivolol improved stroke volume, ejection fraction and left ventricular end-diastolic pressure, not through a measurable reduction in afterload or a lusitropic effect, but by improving systolic contractile performance.

Atrioventricular pacing in congenital heart disease

We have attempted to optimize cardiac performance in patients with congenital heart disease requiring artificial pacing by using pacemakers capable of both sensing and pacing both the atrium and the ventricle (DDD). We reviewed our results with 88 patients receiving DDD devices to determine the safety and dependability of these devices in children. Age ranged from 1 hour to 25 years. Endocardial leads were used in 68 patients, whereas epicardial leads were used in 20 patients. Previous cardiac procedures had been done in 30 patients. There were nine deaths but none due to pacemaker malfunction. Endocardial leads functioned better than epicardial leads. Ninety-eight percent of patients with endocardial leads and 62% of patients with epicardial leads were maintained in the DDD mode. Complications were infrequent and all were corrected without long-term sequelae. The DDD mode may offer considerable benefits to children who require artificial pacing. Our data allow us to conclude that most children can be paced safely and dependably in the DDD mode.

Systemic and coronary hemodynamic effects of bepridil in patients with depressed left ventricular function

To assess the effects of oral bepridil therapy (10–14 days) on cardiac performance and myocardial energetics in the presence of depressed left ventricular function, systemic and coronary hemodynamic effects and neurohumoral effects were evaluated in 7 patients with coronary artery disease and reduced ejection fraction at control, submaximal, and maximal pacing rates during atrial pacing stress. After bepridil therapy, arterial, right atrial, and left ventricular filling pressures as well as systemic vascular resistance and left ventricular stroke work index did not change, suggesting no deleterious effects of bepridil on cardiac performance in patients with reduced ejection fraction. Rate-pressure product, myocardial oxygen consumption, coronary sinus blood flow, myocardial lactate extraction, and catecholamine balance remained unchanged. Development of angina during pacing showed a variable response to bepridil. We conclude that despite its potential negative inotropic effect, bepridil does not exert deleterious effects on hemodynamics or left ventricular performance. The mechanism for its beneficial antianginal effect may be due to favorable redistribution of myocardial blood flow to ischemic zones; no clear effect on anginal threshold or sympathetic tone could be demonstrated in these patients.

Therapeutic effect of oral dipyridamole on myocardial perfusion and cardiac performance in patients with hypertrophic cardiomyopathy

Recent studies have indicated that myocardial ischemia could occur and could play an important role in the pathophysiology of patients with hypertrophic cardiomyopathy (HCM). We therefore investigated whether or not dipyridamole—a selective coronary vasodilating agent-could favorably modify myocardial perfusion and the clinical manifestations in 20 patients with HCM (19 nonobstructive and one mildly obstructive) with an average age of 50 years. Oral dipyridamole, 150 mg/day for 2 weeks, prevented reversible perfusion defects initially observed in six patients on baseline exercise thallium-201 ( 201TI) scintigraphy and significantly increased the 201TI clearance (40 ± 13% to 44 ± 12%), while one patient developed new reversible perfusion defects. There were significant increases in echocardiographic fractional shortening and treadmill exercise time and reductions in cardiac size and supraventricular arrhythmias with dipyridamole therapy. These observations suggest that coronary vasodilation with dipyridamole may improve myocardial perfusion and cardiac function in patients with HCM.

Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: A pilot study

purpose: To test the hypothesis that long-term furosemide therapy in patients with congestive heart failure (CHF) is associated with clinically significant thiamine deficiency via urinary loss. design: (1) Biochemical evaluation of thiamine status in hospitalized patients with CHF treated with long-term furosemide and in age-matched control patients. (2) Uncontrolled trial of the effect of intravenous thiamine on cardiac performance in a subset of six patients with CHF. setting: General medical ward of a teaching community hospital. patients: Twenty-three patients with chronic CHF receiving furosemide, and 16 age-matched control patients without heart failure and not taking diuretics. Daily furosemide doses were 80 to 240 mg, and duration of furosemide therapy was 3 to 14 months. Patients with identifiable causes of inadequate thiamine intake, absorption, or utilization or increased metabolic requirements were excluded. intervention: A 7-day course of intravenous thiamine, 100 mg twice daily, in six consenting patients with CHF. results: A high thiamine pyrophosphate effect (TPPE), indicating thiamine deficiency, was found in 21 of 23 furosemide-treated patients and in two of 16 controls (p < 0.001). The mean (± SE) TPPE (normal: 0% to 15%) in furosemide-treated and control patients was 27.7 ± 2.5% and 7.1 ± 1.6%, respectively (p <0.001). Despite the high TPPE, the mean (± SE) urinary thiamine excretion in the furosemide-treated patients (n = 18) was inappropriately high (defined as greater than 130 μg/g creatinine), 410 ± 95 μg/g creatinine, even in comparison with that in the controls (n = 14): 236 ± 69 μg/g creatinine. In six patients treated with intravenous thiamine, the elevated TPPE decreased to normal, from a mean (± SE) of 27.0 ± 3.8% to 4.5 ± 1.3% (p <0.001), indicating normal thiamine utilization capacity. Left ventricular ejection fraction increased in four of five of these patients studied by echocardiography. conclusion: These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements.

Evaluation of Cardiac Function with Radionuclide Angiography in Hypertension

Alterations of left ventricular systolic and diastolic function at rest and during exercise have been described in the first stages of coronary artery disease, hypertrophic cardiomyopathy and essential hypertension. Ab~ormalities in the systolic response to exercise are common in patients with hypertension, and can be caused by diastolic changes that have been reported as very early indications of this disease. Widespread prescribing of ,,-blockers for the treatment of hypertension must take into account that these drugs usually depress cardiac function and therefore aggravate the systolic performance, which is already impaired. For this reason, a new class of ,,-blockers (hybrid drugs with vasodilator properties) that may be devoid of these effects is now under intensive investigation. One of these novel drugs, nebivolol, was used to assess modifications of the cardiac performance in patients with hypertension, using radionuclide angiography (RNA).

Is atrial activation beneficial in heart transplant recipients?

Because of the distortion of alrial morphology that occurs during cardiac allograft transplantation in humans, the beneficial effects of properly sequenced atrial and ventricular activation are unclear in these patients. To evaluate the atrial contribution to ventricular pump performance in heart transplant recipients, arterial pressure and cardiac output during pacing from either chamber were measured in nine patients 10 ± 1 days after transplantation.Systolic, diastolic and mean systemic arterial pressures were significantly higher during atrial pacing compared with ventricular pacing: 143 ± 23 versus 125 ± 20 mm Hg, 73 ± 15 versus 66 ± 14 mm Hg and 94 ± 17 versus 84 ± 16 mm Hg, respectively (p < 0.05 for all). In addition, cardiac output decreased from 5.5 ± 1.4 to 4.6 ± 1.5 liters/min (p < 0.005) for atrial versus ventricular pacing.Thus, there is a significant atrial contribution to cardiac performance in patients after heart transplantation. This may have clinical implications in those patients who later require a permanent pacemaker.

Clinical and hemodynamic correlates of sympathetic nerve activity in normal humans and patients with heart failure: Evidence from direct micronenrographic recordings

To characterize the neural excitatory state of heart failure, simultaneous measurements of efferent sympathetic nerve activity to muscle (by microneurography) and rest hemodynamics were obtained in 10 normal subjects (age 25 ± 2 years, mean ± SEM) and 29 patients with heart failure (age 49 ± 2 years; New York Heart Association functional class II to IV; left ventricular ejection fraction 21 ± 1%; cardiac index = 2.16 ± 0.13 liters/min per m2; pulmonary capillary wedge pressure 23 ± 2 mm Hg). Sympathetic nerve activity was significantly higher in the patients with heart failure (54.7 ± 4.5 bursts/min) than in normal subjects (16.7 ± 2.2 bursts/min, p < 0.001).Multiple linear regression analyses indicated that sympathetic activity in these human subjects was most strongly and inversely correlated with left ventricular stroke work index (r = −0.86, p < 0.0001) and stroke volume index (r = −0.85, p < 0.0001). There was a strong positive correlation between sympathetic nerve activity and pulmonary artery diastolic (r = 0.82, p < 0.0001) and mean (r = 0.81, p < 0.0001) pressures. Similar correlations were seen when patients with heart failure were analyzed separately. There was no significant correlation between sympathetic nerve activity and mean arterial pressure, left ventricular ejection fraction (by radionuclide ventriculography), cardiac chamber size (by echocardiography) or arterial oxygen tension in the patients with heart failure.Direct measurements of sympathetic nerve activity correlated closely with plasma norepinephrine (r = 0.72, p < 0.0001) in patients with heart failure. Thus, sympathetic nerve activity at rest parallels impairment of cardiac performance in patients with heart failure.

Circadian Variation of Cardiac Performance in Coronary Heart Disease

To study the circadian variation of cardiac performance in patients with coronary heart disease, three exercise tests on a bicycle crgometer were performed during the active part of the day (10 a.m., 2 p.m. and 6 p.m.), recording ST-segment depression and pulmonary capillary wedge pressure. Ten male patients with angiographically documented coronary heart disease underwent bicycle ergometry during placebo and during nitrate therapy (placebo controlled, double-blind crossover 2 × 20 mg IS-5-MN and 1 × 120 mg ISDN sustained release). During placebo as well as during nitrate therapy there was a gradual decrease of cardiac performance during the day, documented by the increase in ST-depression and pulmonary capillary wedge pressure at equal work loads. High nitrate concns led to a significant reduction of both ST-depression and preload with a marked circadian-phase dependency of cardiovascular effects.

Circadian Variation of Cardiac Performance in Coronary Heart Disease

To study the circadian variation of cardiac performance in patients with coronary heart disease, three exercise tests on a bicycle ergometer were performed during the active part of the day (10 a.m., 2 p.m. and 6 p.m.), recording ST-segment depression and pulmonary capillary wedge pressure. Ten male patients with angiographically documented coronary heart disease underwent bicycle ergometry during placebo and during nitrate therapy (placebo controlled, double-blind crossover 2 x 20 mg IS-5-MN and 1 x 120 mg ISDN sustained release). During placebo as well as during nitrate therapy there was a gradual decrease of cardiac performance during the day, documented by the increase in ST-depression and pulmonary capillary wedge pressure at equal work loads. High nitrate concns led to a significant reduction of both ST-depression and preload with a marked circadian-phase dependency of cardiovascular effects.

Clinical relevance of long-term therapy with levodopa and orally active dopamine analogues in patients with chronic congestive heart failure

Beneficial effects of long-term treatment with dopamine analogues in patients with congestive heart failure may result from their vasodilating properties, in particular from renal artery vasodilation. Oral application of levodopa results in increased dopamine plasma levels and can improve cardiac performance and renal function in patients with congestive heart failure. A daily levodopa dosage of at least 4 g appears to a prerequisite for long-term response to the drug. Because of frequent side effects including nausea, vomiting, and dyskinesia at this dosage, the clinical usefulness of levodopa seems to be limited to a minority of patients. Ventricular arrhythmias have been shown to increase significantly during long-term levodopa therapy, probably due to stimulation of myocardial beta receptors. Increased ventricular arrhythmias or significant central nervous side effects have not been observed after administration of ibopamine and fenoldopam, which are orally active analogues of dopamine. Both agents exhibit potent arterial vasodilating properties and have been shown to increase cardiac performance in patients with congestive heart failure after short-term administration. The long-term beneficial effects of ibopamine and fenoldopam in the treatment of congestive heart failure have not yet been clarified. However, available results are encouraging and warrant further clinical evaluation of these agents, as well as the development of new analogues of dopamine, in particular of potent vascular dopamine agonists.

Correlations Between the Cardiovascular Effects of Pimobendan and Plasma Concentrations of the Parent Compound and of Its Major Active Metabolite, UD-CG 212 CL, in Patients with Congestive Heart Failure

Pimobendan was administered orally (10 mg single dose on day 1, then 5 mg twice daily for 4 weeks) to nine patients with chronic heart failure undergoing hemodynamic monitoring. The time course of changes in plasma concentrations of pimobendan and of its major active metabolite. UD-CG 212 CL. was similar on days 1.2. and 28. Pimobendan plasma levels peaked 1.5–2.0 h after drug intake; plasma concentrations of UD-CG 212 CL reached a maxiμm 1 h later; the terminal half-life of pimobendan in plasma varied between 1.44 ± 0.94 h on day 1 and 1.19 ± 0.36 h on day 2. Initially, cardiovascular variables changed with increasing plasma drug levels and reached a maxiμm 4 h after pimobendan intake: later, we found no correlation between plasma concentrations and hemodynamic effects. A steady state of hemodynamic improvement was achieved after 4 weeks of maintenance therapy with pimobendan. Baseline pulmonary capillary wedge pressure dropped from 16 ± 7 mm Hg on day 1 to 5 ± 3 mm Hg at noon on day 28 (–69%: p < 0.001), and baseline cardiac index increased from 2.2 ± 0.5 L/min/m2 on day 1 to 2.7 ± 0.9 L/min/m2 on day 28 ( + 23% p < 0.01). Pimobendan is a long-acting drug that effectively improves cardiac performance in patients with chronic congestive heart failure

Correlations Between the Cardiovascular Effects of Pimobendan and Plasma Concentrations of the Parent Compound and of Its Major Active Metabolite, UD-CG 212 CL, in Patients with Congestive Heart Failure

Pimobendan was administered orally (10 mg single dose on day 1, then 5 mg twice daily for 4 weeks) to nine patients with chronic heart failure undergoing hemodynamic monitoring. The time course of changes in plasma concentrations of pimobendan and of its major active metabolite. UD-CG 212 CL, was similar on days 1, 2, and 28. Pimobendan plasma levels peaked 1.5-2.0 h after drug intake: plasma concentrations of UD-CG 212 CL reached a maximum 1 h later; the terminal half-life of pimobendan in plasma varied between 1.44 +/- 0.94 h on day 1 and 1.19 +/- 0.36 h on day 2. Initially, cardiovascular variables changed with increasing plasma drug levels and reached a maximum 4 h after pimobendan intake; later, we found no correlation between plasma concentrations and hemodynamic effects. A steady state of hemodynamic improvement was achieved after 4 weeks of maintenance therapy with pimobendan. Baseline pulmonary capillary wedge pressure dropped from 16 +/- 7 mm Hg on day 1 to 5 +/- 3 mm Hg at noon on day 28 (-69%; p less than 0.001), and baseline cardiac index increased from 2.2 +/- 0.5 L/min/m2 on day 1 to 2.7 +/- 0.9 L/min/m2 on day 28 (+23%; p less than 0.01). Pimobendan is a long-acting drug that effectively improves cardiac performance in patients with chronic congestive heart failure.

Cardiovascular effects of berberine in patients with severe congestive heart failure.

Berberine, an alkaloid of the protoberberine family, has been shown to have strong positive inotropic and peripheral resistance-lowering effects in dogs with and without heart failure. To determine the acute cardiovascular effects of berberine in humans, 12 patients with refractory congestive heart failure were studied before and during berberine intravenous infusion at rates of 0.02 and 0.2 mg/kg per min for 30 minutes. The lower infusion dose produced no significant circulatory changes, apart from a reduction in heart rate (14%). The 0.2 mg/kg per min dose elicited several significant changes: (a) Decreases in systemic (48%, p less than 0.01) and pulmonary vascular resistance (41%, p less than 0.01), and in right atrium (28%, p less than 0.05) and left ventricular end-diastolic pressures (32%, p less than 0.01). (b) Increases in cardiac index (45%, p less than 0.01), stroke index (45%, p less than 0.01), and LV ejection fraction measured by contrast angiography (56%, p less than 0.01). (c) Increases in hemodynamic and echocardiographic indices of LV performance: peak measured velocity of shortening (45%, p less than 0.01), peak shortening velocity at zero load (41%, p less than 0.01), rate of development of pressure at developed isovolumic pressure of 40 mmHg (20%, p less than 0.01), percent fractional shortening (50%, p less than 0.01), and the mean velocity of circumferential fiber shortening (54%, p less than 0.01). (d) Decrease of arteriovenous oxygen difference (28%, p less than 0.05) with no changes in total body oxygen uptake, arterial oxygen tension, or hemoglobin dissociation properties.(ABSTRACT TRUNCATED AT 250 WORDS)

Converting enzyme inhibition and heart failure

Angiotensin converting enzyme inhibitors are known to improve cardiac performance in patients with severe heart failure, and are probably safer and more effective than other vasodilators. Less is known about their effects in mild and moderate heart failure. Results at one year are presented about an ongoing double-blind, placebo-controlled parallel-group study on 94 outpatients in New York Heart Association functional class II and III. After a three-week period during which appropriate doses of digoxin were administered and a stable response to exercise was obtained, diuretic therapy was withdrawn if in use and captopril or placebo treatment was assigned randomly. The assessment of patients was performed by symptom history, clinical examination, New York Heart Association functional class, chest radiograph, 12-lead electrocardiogram, 24-hour Holter monitoring, M-mode echocardiography, and bicycle exercise at the time of random selection and at specified times during a two-year follow-up. Preliminary data after one year suggest that patients receiving placebo may have a greater tendency to need diuretics and may improve New York Heart Association functional class less often than those receiving captopril. No statistically significant treatment differences were found for the noninvasive test results. Detailed analysis suggests that treatment with an angiotensin converting enzyme inhibitor may be more advantageous than that with placebo for some groups of patients. Investigations are under way to determine which patients might benefit most from angiotensin converting enzyme inhibitors.

Plasma Cobalt and Cardiac Performance in Patients with End-Stage Renal Disease

Plasma Cobalt and Cardiac Performance in Patients with End-Stage Renal Disease

Vasodilators as first-line therapy for congestive heart failure: A comparative hemodynamic study of hydralazine, digoxin, and their combination

Although digitalis and vasodilators both enhance cardiac performance in patients with congestive heart failure, their relative efficacy is unknown. Accordingly, the acute hemodynamic effects of intravenous hydraiazine (0.15 mg/kg), digoxin (1.0 mg), and the hydralazine-digoxin combination were evaluated in 14 normotensive heart failure patients at sitting rest, nine of whom were also studied during submaximal upright bicycle exercise. Hemodynamic responses at rest and exercise were similar. Cardiac output and stroke volume rose with both agents, the increase in cardiac output with hydralazine exceeding that with digoxin at rest. Left and right ventricular filling pressures declined equally. Systemic arterial mean pressure and total systemic vascular resistance fell with hydralazine, while, with digoxin, systemic arterial mean pressure increased and total systemic vascular resistance was unchanged. The hydralazine-digoxin combination produced increases in cardiac output and stroke volume that were greater than with either drug alone, and that equalled the sum of the drugs' individual effects; reductions in ventricular filling pressures were similar to the single-drug interventions. Thus, hydralazine is at least as effective as digoxin in improving cardiac function over the short term. Vasodilators may constitute an acceptable alternative to digitalis as initial therapy for congestive heart faillure, except where a reduction in systemic arterial pressure is potentially deleterious. Use of combined treatment produces greater increases in cardiac output than with either drug alone, but requires risking the toxicities of two agents.

Improved Cardiac Performance by Salbutamol, a Selective β2-Agonist, in Chronic Cor Pulmonale

The effects of salbutamol, a relative specific beta 2-agonist, on hemodynamics and arterial blood oxygenation, were studied in 12 patients with chronic cor pulmonale. The studies were done during heart catheterization at rest (n = 12) and during arm bicycle exercise (n = 7) before and during salbutamol infusion of 0.2 microgram/kg/min. At rest, salbutamol significantly increased cardiac index on average by 31%, stroke volume index by 11%, and heart rate by 12 beats/min. Mean pulmonary artery pressure was not changed by salbutamol, whereas a small reduction in mean arterial pressure was observed. The vascular resistance was reduced by 15% in pulmonary and 24% in systemic circulation. Similar hemodynamic changes by salbutamol were observed during exercise. Arterial oxygen tension and saturation were not changed by salbutamol, but a significant rise in mixed venous oxygen saturation and oxygen delivery were observed both at rest and during exercise. Thus, salbutamol infusion improves the cardiac performance in patients with chronic cor pulmonale through a chronotropic effect combined with vasodilation in both the systemic and pulmonary circulation and thereby increased stroke volume. No deleterious effects on arterial blood oxygenation by salbutamol infusion were observed.

Static exercise with congestive heart failure and the response to vasodilating drugs

The hemodynamic response to static exercise in 28 patients with congestive heart failure (CHF) was compared with that in 8 control subjects. Static handgrip exercise at 50% of the maximal voluntary contraction was performed to fatigue. In patients with CHF, pulmonary arterial wedge pressure increased from 20 +/- 18 to 31 +/- 10 mm Hg (p less than 0.001) (mean +/- standard deviation) and systemic vascular resistance increased from 1,730 +/- 454 to 2,151 +/- 724 dynes s cm-5 (p less than 0.001). Although cardiac index did not change significantly, stroke volume index and stroke work index decreased from 24 +/- 6 to 20 +/- 6 ml/m2 (p less than 0.001) and 28 +/- 11 to 25 +/- 12 g-m/s2 (p less than 0.05), respectively. In control subjects, pulmonary arterial wedge pressure did not change significantly; cardiac index increased from 3.6 +/- 0.3 to 4.0 +/- 0.4 liters/min/m2 (p less than 0.05) and systemic vascular resistance increased slightly, from 1,011 +/- 186 to 1,106 +/- 180 dynes s cm-5 (p less than 0.05). The effects of arterial dilation with hydralazine on the response to static exercise were assessed in 10 of the patients with CHF. Compared with predrug exercise, cardiac index increased 68% (p less than 0.01), stroke volume index increased 76% (p less than 0.01) and systemic vascular resistance decreased 47% (p less than 0.01) after administration of hydralazine. Thus, static exercise can have adverse effects on cardiac performance in patients with CHF.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Eating on Cardiac Performance in Congestive Heart Failure

We assessed the effects of ingestion of a meal on cardiac performance in patients with chronic severe congestive heart failure. A group of 32 patients underwent right heart catheterization on the day prior to study. Patients then fasted overnight (12 hours). In the morning, baseline hemodynamic measurements were obtained on all patients; then 11 patients (group 1) consumed a liquid meal of 317 kcal, and 21 patients (group 2) received a placebo medication and continued fasting. Hemodynamic measurements were then obtained at intervals over two hours. Significant changes were seen in group 1 only. Cardiac index increased 22 percent, stroke work index increased 14 percent, pulmonary arterial wedge pressure decreased 20 percent, and systemic vascular resistance decreased 22 percent in group 1. This study demonstrates an important effect of ingestion of a meal on cardiac performance in patients with heart failure. To avoid overestimating the beneficial effects of therapy, eating must be carefully controlled when assessing the effects of various therapies in these patients.