Hemodynamic and hormonal responses during captopril therapy for heart failure: Acute, chronic and withdrawal studies

Nicholls, M. Gary; Ikram, Hamid; Espiner, Eric A.; Maslowski, A H; Scandrett, M.S.; Penman, Teresa

doi:10.1016/0002-9149(82)90367-8

Cited by 47 publications

(14 citation statements)

References 22 publications

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“…1980a;Nicholls et al 1982). The present data are confirmatory since angiotensin I1 correlated closely with concomitant aldosterone levels in our patients.…”

Section: Discussionsupporting

confidence: 88%

Stability and Inter‐relationships of Hormone, Haemodynamic and Electrolyte Levels in Heart Failure in Man

Fitzpatrick

Nicholls

Ikram

et al. 1985

Clin Exp Pharma Physio

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Relationships between clinical status, haemodynamic measurements, hormone and biochemical indices, and maintenance diuretic dose in patients with chronic cardiac failure, are not clear. This study assessed such relationships and their stability under standardized conditions in 21 hospitalized patients. The daily maintenance dose of frusemide correlated closely and in a positive fashion with plasma levels of renin activity, angiotensin II and aldosterone (P less than 0.001), and to a lesser extent with plasma noradrenaline. Although there was some overlap, patients most incapacitated by their heart failure had the highest circulating levels of renin activity, angiotensin II, aldosterone and noradrenaline. Plasma aldosterone correlated closely with concomitant angiotensin II levels (r = 0.70, P less than 0.001) but not with its other secretagogues ACTH (as reflected by plasma cortisol) or plasma potassium. Close positive correlations between angiotensin II and plasma levels of urea and creatinine (P less than 0.01) were observed. Both renin and angiotensin II showed positive relationships with right heart pressures, but were inversely related to cardiac index and arterial pressure. These results show close relationships between clinical and haemodynamic indices on one hand, and hormones on the other. The renin-angiotensin system appears to be the primary regulator of aldosterone under these conditions, and its activity relates closely to haemodynamic measurements and to the degree of azotaemia.

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“…1980a;Nicholls et al 1982). The present data are confirmatory since angiotensin I1 correlated closely with concomitant aldosterone levels in our patients.…”

Section: Discussionsupporting

confidence: 88%

Stability and Inter‐relationships of Hormone, Haemodynamic and Electrolyte Levels in Heart Failure in Man

Fitzpatrick

Nicholls

Ikram

et al. 1985

Clin Exp Pharma Physio

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“…Our results are compatible with those re ported by others [11][12][13][14]. The observed de crease in systemic venous and PCW pres sures are more difficult to explain.…”

Section: Discussionsupporting

confidence: 92%

“…The decrease in heart rate from 83.4 to 70.8 bpm observed by us and others, is most likely due to reflex sympathetic withdrawal follow ing captopril [11], All patients experienced very impressive subjective improvement, associated with documented improvement in the hemody namic parameters. It has been postulated that endogenous opiates and endorphines take part in the mechanisms causing this sub jective improvement [14].…”

Section: Discussionmentioning

confidence: 99%

Captopril in Refractory Heart Failure: Clinical and Hemodynamic Observations

Abinader¹,

Sharif²,

Rosenfeld³

et al. 1983

Cardiology

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10 patients suffering from refractory heart failure were treated with an oral angiotensin converting enzyme inhibitor captopril. The etiology of heart failure in 9 patients was related to ischemic heart disease, and to valvular heart disease in 1 patient. All patients experienced subjective improvement and feeling of well-being. The functional capacity improved to class II-IIB. Serial chest X-ray films showed improvement in pulmonary congestion. The time course of the hemodynamic effect appeared to 0.5–1.5 h after intake, and tended to disappear about 6 h later. The optimal dose of the drug achieving maximal hemodynamic benefit without excessive hypotension was 50 mg. Some of the patients exhibited a triphasic response. The cardiac index increased from 1.99 ± 0.1 to 2.69 ± 0.151/min/m (p < 0.001), while pulmonary capillary wedge pressure decreased from 25.3 ± 5.86 to 13.67 ± 4.14 mm Hg (p < 0.001). Mean peripheral arterial blood pressure decreased from 90.06 ± 3.7 to 71.4 ± 2.7 mm Hg. The total peripheral resistance decreased from 1,942 ± 169 to 1,170 ± 109 dyn × s × cm^-5. The total pulmonary resistance decreased from 272.6 ± 42.9 to 142.34 ± 13.76 dyn × s × cm^-5. Heart rate decreased from 83.4 ± 10.9 to 70.8 ± 10.14 bpm (p < 0.01). During a 6-month follow-up period the beneficial clinical effects of captopril were sustained, without late vasodilator tolerance. 1 death, unrelated to captopril, occurred. 2 patients developed transient rash, and 1 experienced transient dysgeusia.

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“…There was a reduction of systemic resistance and an increase in cardiac output, stroke volume, and stroke work index. In left ventricular failure decreasing systemic vascular resistance to improve cardiac performance is the basis for the use of vasodilator therapy (Chatterjee & Parmley, 1977 Nicholls et al (1982) we found that on withdrawal of captopril there was little rebound haemodynamic deterioration or worsening of left ventricular function. During treatment neither anginal attacks not extension of myocardial ischaemia occurred.…”

Section: Discussionmentioning

confidence: 89%

Beneficial effects of captopril in left ventricular failure in patients with myocardial infarction.

Bounhoure¹,

Kayanakis²,

Jm³

et al. 1982

Brit J Clinical Pharma

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1 Ten patients with acute myocardial infarction and left ventricular failure were studied. Acute myocardial infarction was anterolateral in eight patients, posterolateral in one, and anteroseptal in one. Three patients were grade II, 4 grade III, and 3 grade IV of Killip's classification. None presented with arterial hypertension but mean values of plasma renin activity and serum aldosterone were 20.7 ng/ml/h and 13.5 ng/100 ml. Haemodynamic measurements were performed by using a flow-directed catheter. Cardiac output was determined in triplicate by thermo-dilution (Edwards computer). Classic haemodynamic measurements included: heart rate, cardiac index, stroke volume index, stroke work index, blood pressure, right atrial pressure, pulmonary vascular resistance, systemic vascular resistance, and pulmonary diastolic blood pressure. Curves of ventricular function correlating stroke work index and pulmonary diastolic blood pressure were constructed. Haemodynamic changes after drug therapy were tested for significance using the paired t test. All patients received heparin, oxygen, and an intravenous infusion of isosorbide dinitrate. 2 Haemodynamic measurements were repeated at 30 min intervals and after isosorbide infusion until values returned to normal. The infusion was then discontinued and pressures returned to control values. At this time, oral captopril was administered, the first dose being 12.5 mg. Subsequent doses of 12.5 mg up to 50 mg were given if systolic blood pressure remained above 100 mm Hg and pulmonary diastolic pressure greater than 18 mm Hg. When the most effective oral dose was determined it was administered at six hourly intervals. This therapy resulted in an improvement of functional class, with a reduction in Killip's grade from class III to 1.7 (mean value). Heart rate, mean atrial pressure, and pulmonary diastolic pressure decreased by 10%, 32% and 41%. Cardiac index increased from 2.4 + 0.8 I/min/m2 to 2.8 (p < 0.02) and stroke volume index increased by 37.2%. Pulmonary vascular resistance decreased by 22.14% (p < 0.001) and the product of heart rate x blood pressure decreased by 33.6% (p <0.001).3 Haemodynamic effects of oral captopril treatment were beneficial in left ventricular failure and acute myocardial infarction without immediate side effects. In acute left ventricular failure the renin angiotensin system was appreciably stimulated. All ten patients who were treated for a mean of 6.5 days showed a significant subjective, clinical, and haemodynamic improvement. After discharge from the coronary care unit anterolateral infarctions produced by ventricular fibrillation resulted in four deaths. 4 These data suggest that captopril may be an effective therapy in acute myocardial infarction with left ventricular failure and that it is more effective than other vasodilators. Nevertheless, more patients need to be studied for a longer period before definite conclusions can be drawn.

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Hemodynamic and hormonal responses during captopril therapy for heart failure: Acute, chronic and withdrawal studies

Cited by 47 publications

References 22 publications

Stability and Inter‐relationships of Hormone, Haemodynamic and Electrolyte Levels in Heart Failure in Man

Stability and Inter‐relationships of Hormone, Haemodynamic and Electrolyte Levels in Heart Failure in Man

Captopril in Refractory Heart Failure: Clinical and Hemodynamic Observations

Beneficial effects of captopril in left ventricular failure in patients with myocardial infarction.

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