Cardiovascular effects of prenalterol on rest and exercise haemodynamics in patients with chronic congestive cardiac failure.

?The cardiovascular effects of the cardioselective beta, agonist prenalterol have been studied in nine patients with severe chronic congestive cardiac failure and in six patients with left ventricular dysfunction resulting from previous myocardial infarction. In the patients with cardiac failure intravenous prenalterol in a dosage of 1.5 microgram/kg bodyweight increased the cardiac index from 1.8 +/- 0.1 to 21.+/- 0.1 1/min per m2 and the left ventricular ejection fraction from 22 +/- 3 to 28 +/- 3%. There was a modest but significant increase in heart rate from 76 +/- 3 to 87 +/- 4 beats/min. Systemic vascular resistance fell from 2285 +/- 51 to 2041 +/- 534 dynes s-1 cm-5. On exercise, the left ventricular filling pressure fell from 33 +/- 6 to 26 +/- 3 and both cardiac index and stroke index increased by 13% and 16%, respectively. There was no significant change in heart rate or systemic blood pressure. In the patients with left ventricular dysfunction, coronary sinus blood flow increased from 107 +/- 11 to 133 +/- 12 ml/min but the increase in myocardial oxygen consumption was small and not significant (11.6 +/- 1.2 and 14.5 +/- 1.9 ml/min). In all patients there was no evidence that prenalterol was arrhythmogenic.     

Acute and chronic effects of nicardipine on rest and exercise haemodynamics in post-myocardial infarction patients with latent cardiac failure

The acute and chronic haemodynamic effects of nicardipine werestudied, at rest and during exercise, in 10 post-myocardialinfarction patients with latent cardiac failure and no signsof residual my ocardial ischaemia. Intravenous administrationof nicardipine (5 mg over 10 min) was associated with a significantincrease in cardiac index and significant reductions in meanpulmonary artery pressure, mean pulmonary wedge pressure, totalpulmonary resistance and systemic vascular resistance underconditions of rest and peak exercise. After 3 weeks of oraltreatment (20 mg three times daily) cardiac index did not change,but the improvements in mean pulmonary artery pressure, meanpulmonary wedge pressure and total pulmonary resistance weresustained at rest and during exercise, at the same workloadattained prior to medication. Chronic treatment with nicardi–pinesignificantly increased exercise tolerance, while mean pulmonaryartery pressure, mean pulmonary wedge pressure and total pulmonaryresistance were maintained below the control values. It is concludedthat nicardipine improves both rest and exercise cardiac performancein post–myocardial infarction patients with latent cardiacfailure, thus avoiding the risk of pulmonary congestion.     

A dose response study with oral prenalterol in patients with chronic congestive cardiac failure

Prenalterol is an orally active cardioselective beta agonist, with a long half-life. Previous studies have confirmed its inotropic activity following intravenous infusion in patients with heart failure. It has little chronotropic activity and no significant arrhythmogenicity. We have studied the response to sustained-release oral prenalterol given over four weeks at doses of 20, 40, 100, and 200 mg daily in 10 patients with New York Heart Association class II and III heart failure due to ischemic heart disease. All were in sinus rhythm and already receiving diuretics and digoxin. The drug was well tolerated and without side effects. Nine patients showed a dose-related improvement in their exercise tolerance as measured on the treadmill, up to a dose of 100 mg daily, with a significant increase in estimated oxygen uptake. There was a dose-related reduction in maximum heart rate, systolic blood pressure, and rate-pressure product during exercise, which is suggestive of a reduction in myocardial oxygen consumption. We conclude that prenalterol improves exercise tolerance without any significant cardiovascular or other side effects, and produces a clinically relevant and sustained improvement in patients with chronic heart failure. M-mode echocardiographic measurements of left ventricular dimension and function at rest did not show any change during the study.     

Haemodynamic effects of isosorbide dinitrate in patients with congestive cardiac failure at rest and during submaximal supine exercise.

Eight patients with chronic congestive cardiac failure secondary to ischaemic heart disease performed submaximal supine exercise before and after 5 mg sublingual isosorbide dinitrate (ISDN) at the time of cardiac catheterisation. Exercise before ISDN produced a poor response in left ventricular performance. After ISDN this response was significantly improved. Compared with the control exercise period cardiac index (CI) increased from mean 2.9 to 3.5 l/mn/m2 (p = less than 0.0025), stroke volume index (SVI) from mean 24 to 29 ml/m2 (p = less than 0.0005) and left ventricular stroke work index (LVSWI) from mean 22 to 28 g-m/m2 (p = less than 0.0025). Although ISDN reduced LVEDP significantly at rest, there were associated small but significant falls in CI, SVI and LVSWI. The improvement in exercise cardiac index was related to the ejection fraction, or the ejection fraction of the contractile section where a left ventricular aneurysm was present. ISDN may be effective in improving exercise tolerance in ambulant patients with chronic congestive cardiac failure.     

Long-term hemodynamic effects of prenalterol in patients with severe congestive heart failure

In a controlled, randomized, double-blind study we investigated the long-term effects of the beta 1-adrenoceptor agonist prenalterol in 16 patients with severe congestive heart failure (NYHA class III or IV). Previous to and 1 week, 3 months, and 6 months after continuous oral intake of 40 to 120 mg prenalterol a day, catheterization of the right heart combined with an ergometer test was carried out; M mode and two dimensional echocardiograms as well as systolic time intervals were also recorded. With prenalterol the heart rate increased within 1 week from 81 +/- 7 to 90 +/- 7 beats/min (mean +/- SD) (p less than .05) and remained increased after 3 months (93 +/- 9 beats/min, p less than .01) and 6 months (91 +/- 6 beats/min, p less than .05). After 1 week the cardiac index rose from 2.7 +/- 0.7 to 3.3 +/- 0.7 l/min/m2 (p less than .01), and after 3 and 6 months it fell again to 3.0 +/- 0.9 l/min/m2 and 2.9 +/- 0.7 l/min/m2, respectively. In the ergometer test the improvement in performance was not significant. The mean velocity of circumferential fiber shortening initially increased from 0.58 +/- 0.20 to 0.79 +/- 0.28 circumferences/sec (p less than .01), but dropped after 3 months to 0.62 +/- 0.31 circumferences/sec. The ejection fraction determined from the two-dimensional echocardiogram rose after 1 week from 20 +/- 10 to 27 +/- 12% (p less than .05), but decreased again after 3 months (23 +/- 11%) and 6 months (20 +/- 10%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of alinidine (ST 567) at rest and during exercise in patients with chronic congestive heart failure

Selective inhibition of sinus node function offers the possibility to decrease heart rate and reduce myocardial oxygen consumption in patients with impaired cardiac function, if myocardial contractility is not further attenuated. To study the influence of a specific sinus node inhibitor on myocardial function, alinidine was given to 10 patients with chronic congestive heart failure and stable sinus rhythm. Radionuclide ventriculography was used to monitor left ventricular function at rest and during a standardized exercise protocol. After a bolus injection of 45 mg of alinidine followed by infusion of 10 mg/hr, radionuclide studies were repeated 1.5 and 3 hours later. The results show that left ventricular ejection fraction, stroke volume, and end-diastolic volume index were essentially unchanged, whereas cardiac index decreased by 10% at rest and during exercise. Heart rate decreased markedly by 14% at rest and by 13% during exercise. Systolic blood pressure was reduced by 6% at rest and by 14% during exercise. As a result of the marked decrease of these two parameters, a pronounced effect was seen on rate-pressure product with a 19% decrease at rest and a 24% decrease during exercise. No significant side effects were observed. Alinidine might be given to patients with chronic congestive heart failure and sinus rhythm in doses up to 45 mg without exerting a clinically relevant negative inotropic effect. Therefore it may represent an alternative to other drugs when a decrease in heart rate is desired to reduce myocardial oxygen consumption.     

Effect of nicardipine on rest and exercise hemodynamics in chronic congestive heart failure

The hemodynamic response to vasodilation induced by the new calcium channel antagonist nicardipine was studied in 10 patients with severe, chronic congestive heart failure. Rest and exercise hemodynamics were evaluated in the baseline state and after 1 week of oral nicardipine therapy (30 mg 3 times daily). In addition, respiratory gas exchange and arteriovenous oxygen difference were measured to assess changes in oxygen utilization. The responses of the sympathetic nervous system were evaluated by measuring plasma norepinephrine concentrations at rest and during maximal exercise. At rest, nicardipine administration was associated with significant reductions in mean systemic arterial pressure, systemic vascular resistance, pulmonary artery wedge pressure and pulmonary arterial pressure, and significant increases in cardiac index and stroke volume index. These effects were maintained during exercise. In contrast to findings with other calcium channel antagonists, no negative inotropic effect of nicardipine was identified. Nicardipine administration was associated with reduction of arteriovenous oxygen difference. Nicardipine had no effect on plasma norepinephrine concentrations, suggesting absence of reflex sympathetic nervous activation. Thus, nicardipine-mediated vasodilation leads to significant improvements in both rest and exercise cardiac performance.     

Characterization of lymphocyte beta-adrenergic receptors at rest and during exercise in ambulatory patients with chronic congestive heart failure

To investigate beta-adrenergic receptor dysfunction in congestive heart failure (CHF), the density of lymphocyte beta receptors and adenylate cyclase activity was measured at rest and at peak exercise in 30 patients with CHF and 7 age-matched control subjects. At rest, patients with CHF had reduced beta-receptor density (normals 33 +/- 2; CHF 21 +/- 2 fmol/mg protein; p less than 0.01) and isoproterenol-stimulated adenylate cyclase activity (normals 50 +/- 9; CHF 28 +/- 4 pmol/mg protein/min; p less than 0.05). Sodium fluoride-stimulated adenylate cyclase activity was also reduced (normals 98 +/- 17; CHF 48 +/- 12 pmol/mg protein/min; p less than 0.01). In the patients with CHF, there was no significant correlation between receptor density and peak exercise VO2, ejection fraction or resting plasma catecholamines. In the normal subjects, maximal exercise increased beta-receptor density by 100% (rest 33 +/- 2; exercise 67 +/- 7 fmol/mg protein) and isoproterenol-stimulated adenylate cyclase activity by 66% (rest 50 +/- 9; exercise 83 +/- 18 pmol/mg protein/min (both p less than 0.01]. In contrast, patients with CHF exhibited only a 58% increase in beta-receptor density (rest 20 +/- 3; exercise 32 +/- 6 fmol/mg protein; p less than 0.01) and no significant change in isoproterenol-stimulated adenylate cyclase activity (rest 27 +/- 5; exercise 24 +/- 5 pmol/mg protein/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Improvement in exercise haemodynamics by isosorbide dinitrate in patients with severe congestive cardiac failure secondary to ischaemic heart disease.

Seven patients with severe chronic congestive cardiac failure secondary to ischaemic heart disease performed submaximal supine exercise before and after 5 mg sublingual isosorbide dinitrate at the time of cardiac catheterisation. Exercise before isosorbide dinitrate produced a poor response in left ventricular performance. After isosorbide dinitrate this response was significantly improved. Compared with the control exercise period, cardiac index increased from mean 2.6 to 3.1 1/min per m2 (P less than 0.0025), stroke volume index from mean 22 to 27 ml/m2 (P less than 0.0025), and left ventricular stroke work index from mean 21 to 30 g m/m2 (P less than 0.01). Mean left ventricular filling pressure fell from 37 to 26 mmHg (P less than 0.01). Although isosorbide dinitrate reduced left ventricular filling pressure at rest from mean 26 to 17 mmHg (P less than 0.005), there was no significant change in mean cardiac index or stroke volume index, while left ventricular stroke work index decreased from mean 29 to 22 g m/m2 (P less than 0.05). Isosorbide dinitrate effectively reduces left ventricular filling pressure in the resting patient with congestive cardiac failure but produces a more comprehensive improvement in left ventricular performance during exercise.     

Regulatory peptides in the plasma of patients with chronic cardiac failure at rest and during exercise.

The levels of several regulatory peptides were measured in peripheral plasma samples from individuals with chronic cardiac failure (CCF) and matched controls in both the resting state and during a short period of maximal exercise. Basal levels of noradrenaline (NA; 705 +/- 114 vs 195 +/- 54 ng.l-1; mean +/- SEM; P < 0.05), plasma renin activity (PRA; 12.9 +/- 2.9 vs 2.1 +/- 0.3 ng AI ml-1.h-1; P < 0.05) and aldosterone (ALDO; 325 +/- 49 vs 87 +/- 8 ng.l-1; P < 0.05) were all raised in the patients with CCF, and increased further with exercise. Basal circulating levels of atrial natriuretic peptide (ANP) were also significantly higher in the CCF group compared to controls (136 +/- 35 vs 27 +/- 5 ng.l-1; P < 0.01), but the response to exercise was attenuated, so that at peak exercise, no significant difference was observed. Basal circulating levels of gastrin-releasing peptide (GRP) (29 +/- 4 vs 40 +/- 4 ng.l-1; P < 0.05) and secretin (13 +/- 1 vs 32 +/- 4 ng.l-1; P < 0.05) were significantly lower in the CCF group when compared to controls and there was no significant change in the levels of either peptide with exercise. Levels of neurokinin A (NKA), neuropeptide Y (NPY) and neurotensin (NT) were somewhat higher in patients, but the differences were not significant, and there were no changes during exercise. There were also no significant differences in the levels of vasoactive intestinal peptide (VIP), glucose-dependent insulinotropic polypeptide (GIP), insulin or glucagon in either experimental group both before and during exercise. We have therefore identified different circulating levels of certain regulatory peptides in patients with CCF, but the significance of these remains unclear.     

Haemodynamic effects of hydralazine at rest and during exercise in patients with chronic heart failure.

The administration of vasodilator drugs has been shown to have beneficial effects at rest in patients with acute or chronic heart failure. To determine the efficacy of hydralazine during exercise, 10 severely symptomatic patients with chronic left ventricular failure from diffuse coronary disease or cardiomyopathy were studied at rest and during upright exercise on a bicycle ergometer. All patients were already receiving optimal treatment with digitalis and diuretics. At rest treatment with hydralazine resulted in a fall in both mean arterial and pulmonary wedge pressure. There was a 50 per cent reduction in systemic vascular resistance compared with pretreatment measurements and there was an equally impressive increase in stroke volume index. During exertion the changes noted at rest were sustained though occurred to a lesser degree; thus there was a 20 per cent fall in arterial resistance and a 20 per cent rise in stroke volume index compared with control. These findings show that hydralazine administration not only results in a beneficial effect on cardiac function at rest but that this effect is maintained during upright exercise in patients with impaired left ventricular function, thus providing further support for its use in the long-term management of such patients.     

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)     

Acute effects of beta 1 agonism with prenalterol on catecholamine circulating levels in patients with congestive heart failure

The effects of a single intravenous infusion of prenalterol, a beta 1 selective agonist, on haemodynamics (echocardiography) and venous plasma catecholamine concentration were studied in 8 patients with severe congestive heart failure. In these patients, age-adjusted plasma norepinephrine (NE) and epinephrine (E) levels before prenalterol infusion were higher compared to values found in 10 control healthy subjects (both P less than 0.01). In heart failure patients, circulating NE levels were not dissimilar in 2 samples drawn 60 and 0 minutes before commencing prenalterol infusion (772.0 +/- 131 ng/l [mean +/- SD] and 775.5 +/- 130.0 ng/l respectively). Prenalterol induced a significant improvement in the cardiac index, stroke index, ejection fraction and velocity of circumferential fiber shortening, associated with a moderate but significant decrease in peripheral vascular resistance. All these changes persisted for 60 minutes after the end of infusion. Circulating NE levels were 604.0 +/- 125 ng/l at 60 min. after start of infusion (P less than 0.01 vs pre-infusion levels) and 526.1 +/- 108 ng/l at 60 min. after the end of infusion (P less than 0.01 vs pre-infusion levels). Plasma E showed a slight decrease, which did not attain statistical significance. Heart rate and diastolic blood pressure remained unchanged during and after infusion, while systolic blood pressure increased by 10-15 mmHg during and after infusion. We conclude that a single 1-hour prenalterol infusion in patients with severe congestive heart failure induces an haemodynamic improvement associated with a reduction of previously elevated circulating NE levels. This reduction could indicate a lowering in the intensity of the afferent stimulus for the reflex sympathetic overactivity.     

Hemodynamic effects of intravenous prenalterol in patients on long-term digoxin therapy for congestive heart failure

The hemodynamic effects of a new beta-1-adrenoceptor agonist,prenalterol, were studied in 12 patients with regurgitant valvedisease and/or ischemic heart disease (prenalterol group). Fiveother patients were randomized to a control group and studiedin the same way except that saline was administered insteadof prenalterol. All patients were on long-term digoxin therapy.Heart rate, stroke volume, cardiac output, arteriovenous oxygendifference, pressures in the right atrium, pulmonary arteryand left ventricle were determined both at rest and during recumbentexercise before and after administration of 50 µg prenalterol/kgbody weight, or of saline. Prenalterol caused a significant increase in heart rate andcardiac output and a significant reduction in arteriovenousoxygen difference, in left ventricular filling pressure andin right atrial pressure both at rest and during exercise. Asignificant increase of stroke volume was seen only during exercise.In the placebo group, no significant hemodynamic changes wererecorded. No adverse effects were observed. Thus, prenalterol seems to have beneficial hemodynamic effects,additive to those of digitalis. The drug is potentially usefulin the treatment of heart failure, but further studies on thespecific mechanism of action and the long-term effects are warranted.     

Piroximone, dobutamine and nitroprusside: comparative effects on haemodynamics in patients with congestive heart failure

Four intravenous doses of piroximone, an imidazolone derivative, were administered to 12 patients with congestive heart failure to produce a four-point dose-response curve. The haemodynamic effects were compared with those of dobutamine and nitroprusside, the substances being given sequentially and in randomized order. Piroximone and dobutamine significantly and similarly increased cardiac index (CI) and stroke volume index (SVI). Nitroprusside produced no such effect. By contrast, piroximone and nitroprusside significantly and similarly decreased mean pulmonary artery pressure (MPAP), pulmonary capillary wedge pressure (PCWP), right atrial pressure (RAP) and pulmonary vascular resistance (PVR), while such changes were not seen following dobutamine. Direct comparisons between the agents were made at doses that lowered systemic vascular resistance (SVR) to the same extent. The major difference between dobutamine and piroximone was an apparent additional vasodilator activity displayed by piroximone as demonstrated by a significantly greater decrease in MPAP, PCWP and RAP for a matched reduction in SVR and a similar increase in CI. The major difference between nitroprusside and piroximone was the significantly higher increase in CI and SVI elicited by piroximone for a matched reduction in SVR and a similar decrease in PCWP and RAP. The changes in loading conditions being equivalent, the higher increase in CI is likely to be accounted for by a direct inotropic activity.     

Effects of metoprolol on rest and exercise cardiac function and plasma catecholamines in chronic congestive heart failure secondary to ischemic or idiopathic cardiomyopathy

To define the effects of 2 months of metoprolol therapy on cardiac function, aerobic performance and sympathetic nervous system activity, metoprolol (75 to 100 mg/day) was administered to 10 patients with chronic congestive heart failure (CHF). Metoprolol was discontinued in 2 patients because of worsening CHF. In the remaining 8 patients, peak oxygen uptake increased significantly (14.8 +/- 3.0 to 16.1 +/- 2.5 ml/kg/min, p less than 0.05) as did the oxygen pulse (9.0 +/- 2.2 to 12.6 +/- 1.8 ml/beat, p less than 0.02). Resting heart rate (87 +/- 18 to 62 +/- 9 beats/min, p less than 0.05) and peak exercise heart rate (133 +/- 13 to 105 +/- 30 beats/min, p less than 0.02) were both reduced. Mean resting ejection fraction increased from 0.15 +/- 0.06 to 0.25 +/- 0.11 and peak exercise ejection fraction also tended to increase (0.19 +/- 0.11 to 0.28 +/- 0.15, difference not significant). Both resting plasma norepinephrine (613 +/- 706 to 303 +/- 142 pg/ml, p less than 0.05) and epinephrine (71 +/- 50 to 40 +/- 21 pg/ml, p less than 0.05) were reduced. Circulating lymphocyte beta-adrenergic receptor number was unchanged (1,334 +/- 292 to 1,344 +/- 456 receptors/cell, difference not significant). It is concluded that metoprolol therapy is associated with improvements in rest and exercise ventricular performance and maximal aerobic capacity. These improvements are associated with a decline in resting sympathetic nervous system activity.     

卡维地洛对充血性心力衰竭患者心功能的影响

目的　探讨卡维地洛对充血性心力衰竭患者心功能的影响。　方法　充血性心力衰竭患者 6 2例(其中扩张性心肌病心力衰竭患者 15例 ,缺血性心脏病心力衰竭患者 4 7例 ) ,左室射血分数 (LVEF)≤ 4 0 % ,心功能(NYHA)Ⅱ～Ⅳ级 ,常规治疗 (洋地黄 ,利尿剂 ,ACEI)基础上随机分为卡维地洛试验组和安慰剂对照组。应用心脏彩色超声仪测定治疗前及治疗后 1个月 ,3个月左室结构和功能指标的变化。观察卡维地洛治疗三个月后对心功能的影响。　结果　卡维地洛平均用量为 2 1 1mg d± 9 6mg d。经过 3个月治疗 ,试验组症状和心功能改善 ,与对照组比较左室射血分数上升 (P <0 0 0 2 ) ,左室收缩末容积下降 (P <0 0 5 ) ;左室舒张末容积与对照组比较虽无统计学差异但与治疗前比较亦明显下降 (P <0 0 5 )。　结论　在洋地黄、利尿剂、ACEI的治疗基础上 ,应用卡维地洛能显著改善充血性心力衰竭患者的心功能 ,改善心室结构 ,且疗效与应用剂量无关。     

Haemodynamic and cardiac metabolic effects of the new {beta}1 agonist prenalterol in patients with cardiac failure

Prenalterol, a ß₁ selective agonist, exerts a positiveinotropic action in animal studies as well as in human volunteersand is effective when administered orally. To assess its immediatehaemodynamic and myocardial metabolic effects, we studied theresponse to prenalterol (50 and 100 µg kg^–1 givenintravenously by cardiac catheterization) in 15 patients withcongestive heart failure secondary to coronary artery diseaseor non-ischaemic cardiomyopathy. At peak effect, cardiac indexincreased from 2.6 ± 0.5 to 3.2 ± 0.81 min^–1m² (mean ± S.D.) (P <0.001); peak rate of left ventricularpressure development rose from 963 ± 242 to 1335 ±411 mmHg s^–1 (P < 0.001); left ventriuclar end-diastolicpressure fell from 25 ± 6 to 17 ± 7 mgHg (P <0.001);coronary sinus blood flow increased from 113 ± 39 to148 ± 55 ml min^–1 (P <0.01); myocardial oxygenconsumption was augmented from 12.7 ± 3.9 to 16.4 ±5.8 ml min^–1 (P < 0.001); and heart rate increasedslightly (from 76 ± 12 to 86 ± 14 beats min^–1;(P <0.05)). No significant changes occurred in left ventricularsystolic pressure, stroke volume index, myocardial lactate extractionrate and myocardial arteriovenous oxygen difference, and nopatients developed angina, ECG changes or ventricular arrhythmias.Infusion of prenalterol effectively improved haemodynamic functionand cardiac metabolism in cardiomyopathy. Therefore this agentdeserves further investigation to evaluate its possible rolefor the long-term therapy of patients with chronic heart failure.