Hemodynamic Effects Of Captopril Research Articles

Aspirin Inhibits the Acute Arterial and Venous Vasodilator Response to Captopril in Patients with Chronic Heart Failure

The potentially beneficial hemodynamic effects of angiotensin-converting enzyme (ACE) inhibitors in heart failure may relate, in part, to their ability to increase the production of vasodilator prostanoids. Low dose aspirin is commonly prescribed in CHF and may attenuate the vasodilator effects of ACE inhibitors. We sought to determine the effects of low dose aspirin on the peripheral hemodynamic effects of captopril in patients with chronic heart failure (CHF). Nine patients with chronic heart failure were randomized in a placebo controlled, cross over study, to 75 mg of aspirin daily or placebo. After 7 days treatment the response to 25 mg of captopril was evaluated over 180 min using venous occlusion plethysmography. Forearm blood flow (FBF) and forearm venous capacitance (FVC) were measured. Mean arterial pressure and heart rate did not change. After placebo, FBF increased in response to captopril (+18%, 95%CI 24.2, 11.8), a response inhibited by aspirin (-1.4%, 2.9, -5.7), p < 0.005. After placebo, FVC increased in response to captopril (+7.6%, 9.8, 5.4), which was also inhibited by aspirin (+2.0%, 4.6, -0.6), aspirin vs. placebo, p = 0.02). In patients with chronic heart failure even low dose aspirin inhibits both the acute arterial and venous dilator responses to captopril. This action of aspirin may reduce the long-term clinical benefits of ACE inhibitors.

Vantaggio della terapia combinata con captopril e nitrati nell&amp;middot;insuff icienza cardiaca congestizia grave

We compared the acute hemodynamic effects of captopril and nitrates in 11 patients with severe congestive heart failure and grade IV cardiac disability. Pressures were measured using a Swan-Ganz catheter system; cardiac output and stroke index were measured by thermodilution, and left-ventricular (LV) volumes and ejection fraction were calculated simultaneously with the hemodynamic measurements from radionuclide ventriculography. Measurements were made in each of 4 treatment states: control, sublingual isosorbide dinitrate (ISDN; 5 and 15 mg), oral captopril (50-200 mg daily) and during combined therapy with captopril and ISDN. Captopril produced a fall in mean arterial pressure (p < 0.01) from 81 +/- 14 to 72 +/- 13 mm Hg and a rise in stroke index from 30 +/- 5 to 35 +/- 91/min/m2 (p < 0.05), while LV ejection fraction increased from 18 +/- 5 to 21 +/- 7% (p < 0.05). ISDN reduced mean arterial, pulmonary arterial, right-atrial and wedge pressure. The combination of captopril and ISDN produced a greater fall in mean arterial pressure, a further rise in ejection fraction to 22 +/- 8% (p < 0.05), a fall in systemic (p < 0.05) and pulmonary vascular resistance (p < 0.01) and a rise in cardiac (p < 0.01) and stroke work index (p < 0.01), while the beneficial effects of ISDN on right-atrial, pulmonary arterial and wedge pressure were again achieved. LV contractility, assessed from end-systolic stress-shortening relations, was essentially unaltered or decreased very slightly. The study showed that combined therapy with captopril and nitrates produced acute hemodynamic benefits superior to those achieved by treatment with captopril or nitrates alone.

Angiotensin-converting enzyme inhibitors: More different than alike?: Focus on cardiac performance

Development of an increased systemic vascular resistance and the concomitant increase in blood pressure are associated with significant changes in left ventricular structure and function. The plasma and tissue renin-angiotensin systems play an important, but variable, role in the regulation of blood pressure and systemic vascular resistance in normotensive and hypertensive patients. Non-angiotensin-mediated effects of angiotensin-converting enzyme (ACE) inhibitors and/or differential tissue specificities may result in a variable hemodynamic response to individual therapies. Using first-pass radionuclide cineangiography, the hemodynamic effects of captopril, lisinopril, and fosinopril were compared. Fosinopril induced a greater reduction in systemic vascular resistance than did equipotent hypotensive doses of captopril or lisinopril and was associated with an increase in cardiac output, left ventricular peak ejection rate, and left ventricular peak filling rate. Along with previously accumulated data, these results suggest that structural differences among ACE inhibitors may result in unique physiologic effects. Fosinopril appears to have a cardiotropic effect that causes improved left ventricular diastolic performance; this effect is unique among currently available ACE inhibitors. The clinical significance of the unique profiles of individual ACE inhibitors awaits assessment via comparative clinical investigations.

Hemodynamic effects of captopril and isosorbide mononitrate started early in acute myocardial infarction: A randomized placebo-controlled study

Objectives. The aim of this study was to study the hemodynamic effects of orally administered captopril and isosorbide mononitrate in suspected acute myocardial infarction.Background. Early treatment with converting enzyme inhibitors and nitrates in acute myocardial infarction may limit infarct expansion and prevent left ventricular dilation.Methods. In a double-blind study, 81 patients were randomized within 36 h of the onset of symptoms of suspected acute myocardial infarction to 1 month of oral captopril (6.25 mg initial dose, followed 2 h later by 12.5 mg and continuing with 12.5 mg three times daily), isosorbide mononitrate (initial dose 20 mg followed by 20 mg three times daily) or matching placebo. The effects of treatment on changes from baseline in mean arterial blood pressure, heart rate, stroke volume, cardiac output and systemic vascular resistance were assessed noninvasively using Doppler echocardiography 1 h after the first dose, 1 week after infarction and at 6 weeks (that is, 2 weeks after the scheduled end of trial treatment).Results. One hour after the start of treatment, blood pressure was reduced by ≈10% with both captopril and isosorbide mono-nitrate, but this difference did not persist at 1 week. Captopril was associated with a significant increase in cardiac output compared with placebo of 13 ± 3% at 1 h (p < 0.01), 23 ± 5% at 1 week (p < 0.001) and 22 ± 6% (p < 0.05) at 6 weeks (2 weeks after the end of trial treatment). This increase in cardiac output with captopril was mainly due to a substantial and sustained increase in stroke volume, although there was also a small increase in heart rate at 1 week. Both captopril and isosorbide mononitrate reduced systemic vascular resistance within 1 h of the start of treatment, but only the effect of captopril was sustained (perhaps because the three-times daily nitrate regimen induced tolerance). Study treatment was well tolerated, and the incidence of withdrawal of study treatment for hypotension was not significantly different from that with placebo.Conclusions. This study indicates that the hemodynamic effects of both captopril and isosorbide mononitrate are well tolerated in the acute phase of myocardial infarction and that captopril favorably influences cardiac function.

The relationship between diuretic dose, and the haemodynamic response to captopril in patients with cardiac failure.

The effect of diuretic dose on the haemodynamic response to captopril was assessed in nine patients with chronic cardiac failure. Each patient was given an intravenous dose of captopril while maintained on (a) a low dose diuretic regime, and (b) a high dose diuretic regime. Activity of the renin angiotensin aldosterone system, as assessed by plasma concentrations of these hormones, was greater when patients were receiving the higher dose diuretic regime. The magnitude of haemodynamic response produced by intravenous captopril was greater when the patients were maintained on the high dose diuretic regime, although no significant correlation was found between resting plasma renin activity and resting plasma angiotensin II concentration and the change produced by captopril in any haemodynamic response on either diuretic regime. An increased dosage of loop diuretic potentiates the haemodynamic effects of captopril in patients with cardiac failure. Reduction of diuretic dose prior to introduction of captopril may protect against severe first dose hypotension.

Naloxone reversal of hypotension due to captopril overdose

The hemodynamic effects of captopril and other angiotensin-converting enzyme inhibitors may be mediated by the endogenous opioid system. The opioid antagonist naloxone has been shown to block or reverse the hypotensive actions of captopril. We report a case of an intentional captopril overdose, manifested by marked hypotension, that resolved promptly with the administration of naloxone. To our knowledge, this is the first reported case of captopril-induced hypotension treated with naloxone. Our experience demonstrates a possible role of naloxone in the reversal of hypotension resulting from captopril.

Regional Haemodynamic Effects of Captopril, Enalaprilat and Lisinopril in Conscious Water-Replete and Water-Deprived Brattleboro Rats

1. The regional haemodynamic effects of intravenous bolus doses of captopril, enalaprilat and lisinopril were assessed in conscious Brattleboro (i.e. vasopressin-deficient) rats, chronically instrumented with miniaturized pulsed Doppler probes and intravascular catheters. 2. Responses to incremental doses of each drug (spanning the median effective dose for the inhibition of the pressor response to angiotensin I) were examined in both water-replete and water-deprived states. 3. In the water-replete state, the haemodynamic profiles of captopril, enalaprilat and lisinopril were generally similar, with incremental doses causing rises in mesenteric and renal flow and, to a lesser extent, hindquarters flow. There were small tachycardias and only slight falls in mean blood pressure. 4. In the water-deprived state, the effects of all three drugs were greatly enhanced; tachycardic and hypotensive effects occurred together with increases in mesenteric, renal and hindquarters flows. However, for renal flow and renal vascular conductance the effectiveness of the drugs decreased in the order enalaprilat greater than captopril greater than lisinopril, whereas for mesenteric flow and mesenteric vascular conductance the order was captopril greater than enalaprilat greater than lisinopril. 5. Since marked haemodynamic actions were seen with doses one-tenth of the median effective dose for the inhibition of the pressor effect of angiotensin I, it is likely these effects were due to inhibition of angiotensin-converting enzyme, although not necessarily to inhibition of angiotensin II production.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial natriuretic peptide in congestive heart failure: Postural changes and reset with chronic captopril therapy

The response of atrial natriuretic peptide (ANP) to standing and the acute and chronic administration of the vasodilator, captopril, were examined in 15 patients with chronic congestive heart failure. In the supine position, ANP was increased (361 ± 202 pg/ml); however, only a loose correlation existed between atrial pressures and ANP (right atrial vs ANP, r = 0.03, p = N.S., and pulmonary capillary wedge pressures vs ANP, r = 0.4, p = N.S.). Standing and acute captopril therapy decreased atrial pressures and ANP but did not significantly improve the correlation between atrial pressures and ANP. With chronic captopril therapy, atrial pressures remained decreased; however, ANP had returned to control values (370 ± 254 pg/ml vs 361 ± 202 pg/ml) and failed to decrease with standing (370 ± 259 pg/ml lying vs 351 ± 194 pg/ml standing). These changes in ANP (with chronic captopril therapy) persisted even once the hemodynamic effects of captopril had dissipated (3 hours post dose). This study indicates that in patients with severe chronic congestive heart failure (1) only a poor correlation exists between ANP and atrial pressures and (2) with chronic captopril therapy ANP increases to higher levels for a given atrial pressure and fails to decrease with standing despite a decrease in atrial pressures.

Haemodynamic Effects of Captopril in Acute Left Ventricular Failure Complicating Myocardial Infarction

Activation of the renin-angiotensin system in acute myocardial infarction may have important haemodynamic consequences. The effects of captopril were assessed in nine patients with acute left ventricular failure complicating myocardial infarction. Plasma angiotensin II was elevated at 16.8 (3.6) pmol/l (mean [SE]) including high levels in three of four patients in the absence of any previous therapy, including diuretics. Repeated low doses of captopril were administered to reduce pulmonary capillary wedge pressure less than 14 mm Hg or to a maximum total dose of 25 mg. Right atrial pressure fell from 12.4 (0.9) to 9.4 (0.7) mm Hg p less than 0.001, pulmonary arterial pressure from 32.7 (3) to 26.4 (2.2) p = 0.01, and pulmonary capillary wedge pressure from 25.7 (2.9) to 19.9 (2.2) p = 0.01. Despite a fall in systemic vascular resistance from 1,540 (110) to 1,330 (76) dyn/s/cm5, and mean arterial pressure from 84.8 (3.9) to 76.7 (2.7) p = 0.001, changes in cardiac output were small: 3.8 (0.3) to 4.2 (0.3) NS. Angiotensin II fell in all patients even after only 3.125 mg to a mean of 3.6 (1.0). These improvements occurred whether basal angiotensin II was elevated or normal, and in the presence or absence of diuretic therapy. At 24 hours, seven patients received captopril in the maximum titrated dose of the previous day. Haemodynamic changes at one hour were of similar magnitude to those during incremental dosing. These results suggest that reduction of angiotensin II exerts beneficial haemodynamic effects in heart failure complicating acute myocardial infarction.

Haemodynamic and neurohumoral response to exercise in patients with congestive heart failure treated with captopril.

The contribution of the renin-angiotensin system to the cardiovascular response to exercise was studied in 12 patients with congestive heart failure. The haemodynamic effects of captopril were measured at rest and during supine bicycle exercise. After captopril administration, resting systemic vascular resistance fell by 26.6% and mean blood pressure by 16.7% and cardiac index increased by 19.7%. During exercise, captopril decreased systemic vascular resistance by 25.6% and mean blood pressure by 8.2% and increased cardiac index by 24.4%. Pulmonary wedge pressure fell by 25% at rest but was not altered by captopril during exercise. Pretreatment plasma renin activity increased from 13.4(16.0) ng/ml/hr (10.3(12.3) mmol/l/hr) at rest to 20.0(27.8) ng/ml/hr (15.4(21.4) mmol/l/hr) during exercise. Pretreatment plasma noradrenaline concentration increased from 659(433) pg/ml (39(25.6) nmol/l) at rest to 2622(1486) pg/ml during exercise (155(88) nmol/l). Captopril favourably alters systemic vascular resistance and cardiac index during exercise in patients with congestive heart failure. This may reflect inhibition of the increased activity of the renin-angiotensin system during exercise in these patients and a subsequent reduction in systemic vasoconstriction.

Hemodynamic effects of captopril in one-kidney, one clip hypertensive rabbits.

Hemodynamic effects of captopril were examined in chronic one-kidney, one clip renal hypertensive rabbits and normotensive controls either in normal sodium or in sodium depletion. The mean arterial pressure (MAP) of hypertensive and normotensive rabbits in sodium depletion did not differ from that in normal sodium, while plasma renin activity (PRA) was elevated by sodium depletion. The cardiac output of sodium depleted groups decreased slightly. The increase in total peripheral resistance was greater in hypertensive than in normotensive groups. The MAP in all groups was decreased by acute administration of captopril irrespective of sodium intake. The decrease in MAP in the sodium-depleted hypertensive group was correlated with the control values of PRA, but no correlation was observed in other groups. Captopril significantly reduced the cardiac output of the sodium-depleted hypertensive group, but not of the other groups. These results show that: (1) the lowering effect of captopril on arterial pressure is not mediated only by blocking of the renin-angiotensin system, and (2) the decrease in cardiac output with captopril in sodium depleted hypertensive rabbits is an important factor in the reduction in the arterial pressure.

9 Mechanisms Influencing the Haemodynamic Effects of Captopril in Man

9 Mechanisms Influencing the Haemodynamic Effects of Captopril in Man

Quantitative differences in the hemodynamic effects of captopril and nitroprusside in severe chronic heart failure

The hemodynamic effects of oral captopril and intravenous nitroprusside were compared in 15 patients with severe chronic congestive heart failure. At doses of both drugs titrated so as to produce similar decreases in systemic vascular resistance in each patient, nitroprusside produced substantially greater increases in cardiac index (+0.67 versus +0.31 liters/min/m2, p less than 0.01) but smaller decreases in mean arterial pressure (-18.4 versus -11.0 mm Hg, p less than 0.01) than did captopril. This finding was due to a significant decrease in heart rate with captopril (-7 beats/min, p less than 0.01) which was not seen with nitroprusside, since changes in stroke volume index with both drugs were similar. Nitroprusside produced a decrease in pulmonary arteriolar resistance quantitatively similar to the decrease in systemic vascular resistance, but the decrease in pulmonary arteriolar resistance with captopril was not significant. Despite similar decreases in systemic resistance, captopril produced a greater decrease in left ventricular filling pressure (-10.2 versus -6.9 mm Hg, p less than 0.01) but a smaller decrease in mean right atrial pressure (-3.1 versus -5.3 mm Hg, p less than 0.01) than did nitroprusside. Thus, captopril has actions independent of its systemic vasodilator effects which account for the quantitative differences observed in its hemodynamic responses compared with those of nitroprusside in patients with severe chronic heart failure. These differences support experimental evidence that angiotensin, in addition to its direct systemic arterial vasoconstrictor actions, exerts positive chronotropic effects and alters ventricular compliance but has minimal direct effects on the limb venous circulation and on the pulmonary vasculature.

Complementary combined captopril and terbutaline therapy in severe chronic congestive heart failure

The hemodynamic effects of captopril (CPT) alone and in combination with the beta-adrenergic receptor agonist terbutaline (TBT) were evaluated in 10 patients with severe chronic congestive heart failure (CHF). The heart rate remained unchanged, while CPT lowered mean systemic blood pressure from 86 to 64 mm Hg ( p < 0.001) and decreased left ventricular filling pressure markedly from 27 to 19 mm Hg ( p < 0.001). The addition of TBT produced no further change in these variables ( p > 0.05). Simultaneously, CPT augmented cardiac index (Cl) from 2.1 to 2.9 L/min/m 2 ( p < 0.01) and stroke index (Sl) from 27 to 37 ml/beat/m 2 ( p < 0.001). Concomitant CPT-TBT further raised Cl to 3.2 L/min/m 2 and Sl to 40 ml/beat/m 2 (both p < 0.001). Further, the CPT-effected decline in total systemic vascular resistance from 1577 to 841 dynes · sec · cm −5 ( p < 0.001) was not reduced additionally by CPT-TBT combination ( p > 0.05). These results indicate that both CPT and TBT markedly augment cardiac function in CHF. Moreover, the salutary effects of the systemic vasodilator appear additive to the beneficial actions of the beta-adrenergic receptor agonist, thereby providing substantial augmentation of the function of the failing heart.

Hemodynamic effects of captopril in chronic heart failure: Efficacy of low-dose treatment and comparison with prazosin

The acute hemodynamic effects and long-term therapeutic actions of low doses of the oral angiotensin-converting enzyme (ACE) inhibitor captopril (CPT) were evaluated in 18 patients with severe chronic congestive heart failure (CHF). Increasing doses of 1, 2.5, 6.25, 12.5, and 25 mg of CPT were given at 2-hour intervals. Increased stroke volume index (SVI) and reduced mean pulmonary capillary wedge (PCW) pressure occurred at 1 hour ( p < 0.05) with an associated decline of blood pressure. Maximal hemodynamic improvement for the group was seen at 6 and 7 hours following the 6.25 and 12.5 mg doses when SVI was elevated 35% and mean PCW pressure decreased 40% from control. CPT in doses of 12.5 to 50 mg every 8 hours was continued long term in these 18 CHF patients. Four patients died, and one was noncompliant; drug therapy was withdrawn in two patients with symptomatic hypertension and in one patient who experienced an alteration in taste. The remaining 10 patients showed significant improvement in symptoms and treadmill exercise duration at 3 months after CPT therapy was started. Moreover, repeat hemodynamic measurements were similar to optimal measurements obtained during the initial study. In a further study, the acute hemodynamic and hormonal effects of sequentially randomized 5 mg prazosin and 25 mg CPT were compared in 10 CHF patients. While both drugs reduced PCW pressure and vascular resistance, CPT effects were greater. Further, CPT alone effected a small rise in cardiac index and minor decline in heart rate, and CPT diminished aldosterone levels and increased plasma renin activity while prazosin did not.

Hemodynamic effects of captopril in pulmonary hypertension of collagen vascular disease

Captopril 12.5 to 50 mg as a single dose was given to six patients with pulmonary hypertension secondary to collagen vascular disease. Total pulmonary resistance was decreased in four patients from 19% to 39%, but mean pulmonary artery pressure (63 ± 15 mm Hg) was not decreased, probably because of the concurrent increase in cardiac output from 21% to 52% (2 p < 0.05). The systemic arterial pressure was slightly decreased due to the decrease in total systemic resistance. Control plasma renin activity ranged from 0.15 to 16 ng/ml/hr and was increased during captopril from 19% to 356%. These results, although preliminary, suggest that captopril may be beneficial in certain patients with pulmonary hypertension secondary to collagen vascular disease.

Hemodynamic effects of captopril in patients with severe chronic heart failure

The hemodynamic effects of captopril (SQ 14225), an oral inhibitor of angiotensin-converting enzyme, were measured in 10 patients with severe chronic heart failure poorly controlled by digitalis and diuretics. After administration of a 25 mg dose, the cardiac index increased from 1.82 ± 0.14 to 2.28 ± 0.30 liters/min/m 2 (p < 0.05) while pulmonary capillary wedge pressure decreased from 22.7 ± 2.0 to 14.7 ± 4.7 mm Hg (p < 0.05). Mean blood pressure and systemic vascular resistance decreased from 85.7 ± 6.7 to 71.2 ± 12.0 mm Hg (p < 0.001) and from 1,909 ± 246 to 1,362 ± 347 dynes-s-cm 5 (p < 0.001), respectively. Heart rate did not change significantly. There was an inverse relation between maximal augmentation in cardiac index and maximal reduction in pulmonary capillary wedge pressure (r = −0.82, p < 0.01). While most patients demonstrated a constant hemodynamic benefit after repeated administration of captopril, some exhibited a triphasic response with attenuation of effects after the second dose and restoration of effects after the third dose. These hemodynamic benefits were observed in patients with stable chronic heart failure whose plasma renin activity was within normal range (1.1 to 7.3 ng/ml/hour).

Hemodynamic effects of captopril in essential hypertension, renovascular hypertension and cardiac failure: Correlations with short- and long-term effects on plasma renin

The hemodynamic effects of captopril were investigated in 22 patients with essential hypertension, 22 with hypertension and renal artery stenosis and 14 with refractory chronic heart failure. The effects of a first dose of captopril, 50 mg orally, were observed for 2 hours, and the effects of repeated doses, 450 mg/day in combination with mild dietary sodium restriction, for at least 4 weeks. Short-term captopril treatment caused similar reductions in blood pressure in the three patient groups, that is, 21 ± 3 mm Hg in essential hypertension, 29 ± 6 mm Hg in renovascular hypertension and 21 ± 2 mm Hg in heart failure (mean ± standard error of the mean) despite large differences in pretreatment plasma renin. Heart rate and cardiac output did not change in hypertensive patients, and cardiac filling pressures decreased. The changes in right atrial pressure, pulmonary artery pressure and pulmonary capillary wedge pressure in essential hypertension and in renovascular hypertension did not differ. Heart rate decreased and cardiac output increased in heart failure, whereas cardiac filling pressures decreased. Blood pressure responses to long-term captopril therapy in essential and in renovascular hypertension were similar and, as with short-term treatment, changes in blood pressure were largely determined by changes in peripheral resistance. Several measurements of extracellular fluid volume showed no evidence of fluid retention by the kidneys. Short-term but not long-term blood pressure responses were correlated with pretreatment plasma renin (percent change in mean arterial pressure, short-term, versus log renin, r = 0.47, p < 0.001, n = 14). Both short- and long-term responses of total peripheral resistance were correlated with plasma renin (percent change in resistance, short-term versus log renin, r = 0.64, p < 0.001, n = 40; percent change in resistance, long-term versus log renin, r = 0.56, p < 0.001, n = 31). The correlations were weak and probably not important for clinical practice. These data indicate that other factors besides circulating renin are important in captopril's hypotensive effect. The favorable hemodynamic effects of converting enzyme inhibition warrant further consideration of this principle of therapy in the clinical management of most forms of hypertension and also in the treatment of chronic heart failure.

Captopril in congestive heart failure.

British Journal of Clinical PharmacologyVolume 14, Issue S2 p. 193S-199S Free Access Captopril in congestive heart failure. G Liebau, G LiebauSearch for more papers by this authorAJ Riegger, AJ RieggerSearch for more papers by this authorP Schanzenbacher, P SchanzenbacherSearch for more papers by this authorH Steilner, H SteilnerSearch for more papers by this authorS Oehrlein, S OehrleinSearch for more papers by this author G Liebau, G LiebauSearch for more papers by this authorAJ Riegger, AJ RieggerSearch for more papers by this authorP Schanzenbacher, P SchanzenbacherSearch for more papers by this authorH Steilner, H SteilnerSearch for more papers by this authorS Oehrlein, S OehrleinSearch for more papers by this author First published: April 1982 https://doi.org/10.1111/j.1365-2125.1982.tb02077.xCitations: 7AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat References COHN, J.N. (1981). Physiological basis of vasodilator therapy for heart failure. Am. J. Med., 71, 135– 139. COLUCCI, W.S., WILLIAMS, G.H., ALEXANDER, R.W. & BRAUNWALD, E. (1981). Mechanisms and implications of vasodilator tolerance in the treatment of congestive heart failure. Am. J. Med., 71, 89– 99. GREENBERG, B.H., DeMOTS, H., MURPHY, E. & RAHIMTOOLA, S.H. (1982). Arterial dilators in mitral regurgitation: Effects on rest and exercise haemodynamics and long-term clinical follow up. Circulation, 65, 181– 187. FORD, L.E. (1980). Effect of afterload reduction on myocardial energetics. Circ. Res., 46, 161– 166. HOCKINGS, B.E., COPE, G.D., CLARKE, G.M. & TAYLOR, R.R. (1980). Comparison of vasodilator drug prazosin with digoxin in aortic regurgitation. Br. Heart J., 43, 550– 555. IKRAM, H., MASLOWSKI, A.H. & NICHOLLS, G.M. (1981). Haemodynamic effects of dobutamine in patients with congestive heart failure receiving captopril. Br. Heart J., 46, 528– 530. LIEBAU, G. (1982). Captopril in congestive heart failure. Klin. Wschr., 60, 107– 113. LIEBAU, G., RIEGGER, A.J.G. & STEILNER, H. (1981). Haemodynamic effects of captopril in patients with congestive heart failure and hypertension. In: Recent advances in hypertension therapy: captopril. pp. 76– 86, Amsterdam, Excerpta Medica. Citing Literature Volume14, IssueS2April 1982Pages 193S-199S ReferencesRelatedInformation

Immediate effects of captopril in acute left ventricular failure secondary to myocardial infarction.

In eight patients with acute left ventricular failure secondary to myocardial infarction the haemodynamic effects of captopril (25 mg), an orally active converting enzyme inhibitor, were measured. Haemodynamic modifications were maximal at 60 min and lasted for 2-3 h. Pulmonary wedge pressure fell from 23.5 +/- 4.9 (mean +/- SD) to 16.8 +/- 4.7 mmHg (P less than 0.01), cardiac output rose from 3.24 +/- 1 to 4.05 +/- 0.91 1/min (P less than 0.01). Systemic vascular resistance decreased from 27.34 +/- 3.81 to 17.52 +/- 1.65 mmHg min l-1 (P less than 0.01). Mean arterial pressure fell from 89.6 +/- 13.9 to 75.7 +/- 16.3 mmHg (P less than 0.001) while heart rate was not significantly modified. Six patients who had high pretreatment plasma renin activity values responded by a decrease in ventricular filling pressure and/or an increase in cardiac output. One patient with normal initial plasma renin activity value showed similar haemodynamic effects. THese data suggest that in the short term captopril is a vasodilator with both arterial and venous effects and improves cardiac function in acute left ventricular failure secondary to myocardial infarction.