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Biomedical subjects

J L Halperin

Publications and source records attributed to J L Halperin.

64 records · Page 4Linked to original sources
PubMed1982

Determinants of clinical response and survival in patients with congestive heart failure treated with captopril.

The efficacy of chronic ambulatory captopril (CPT) therapy was evaluated over an 18-month period in 36 patients with refractory chronic congestive heart failure (CHF) by cardiac catheterization, treadmill exercise, nuclear scintigraphy, echocardiography, and symptomatology. Clinical improvement to New York Heart Association functional class I or class II was observed in 63% of the patients (20 of 32) after 2 months of treatment; this amelioration of CHF symptoms was sustained in 63% of the patients (10 of 16) at 18 months. Exercise tolerance increased in 64% of the patients (16 of 25) at early follow-up and in 79% (11 of 14) at late follow-up. Univariate analysis revealed that the pre- and post-CPT stroke work indices (SWI) and the post-CPT cardiac index related to favorable long-term clinical response. Fourteen CHF patients (39%) died during the 18-month follow-up. Univariate analysis revealed that the pretreatment SWI, right atrial pressure, plasma norepinephrine concentration, and echocardiographic shortening fraction were significant predictors of mortality. Multivariate analysis indicated that the SWI was the principal determinant of survival: the 18-month cumulative survival rate for CHF patients with a SWI less than 32 gm . m/m2 was 44% compared to 88% when the SWI was greater than 32 gm . m/m2. Thus, CPT results in sustained symptomatic and functional improvements in patients with advanced CHF, but the mortality remains high and is primarily related to the severity of cardiac dysfunction.

Acute Kidney Injury↗
PubMed1982

Coronary hemodynamic effects of angiotensin inhibition by captopril and teprotide in patients with congestive heart failure.

The coronary hemodynamic effects of vasodilator therapy with angiotensin-converting enzyme inhibitors (captopril and teprotide) were studied in 11 patients with ischemic heart disease and severe congestive heart failure (CHF). Over 2 hours, systemic vascular resistance was reduced from 2,408 +/- 240 to 1,715 +/- 170 dynes . s . cm-5 (p less than 0.001), and cardiac output improved 18%, resulting in lower arterial pressure (101 +/- 8 to 86 +/- 5 mm Hg, p less than 0.001) and left ventricular filling pressure (30 +/- 2 to 21 +/- 2 mm Hg, p less than 0.001). Coronary sinus thermodilution blood flow paralleled perfusion pressure but did not significantly vary overall (160 +/- 20 to 133 +/- 12 ml/min, difference not significant [NS]). Coronary vascular resistance was unchanged. Although the left ventricular stroke work index rose slightly (37.7 +/- 8.8 to 41.3 +/- 7.9 g l m/m2, p less than 0.05), there was no change in the coronary arteriovenous oxygen content difference (10.8 +/- 1.0 to 10.4 +/- 1.0 ml/10 ml, NS) or calculated myocardial oxygen consumption (16.4 +/- 1.9 to 13.9 /- 1.6 ml/min, NS). The heart rate-systolic blood pressure product declined significantly during this period (8,824 +/- 703 to 7,087 +/- 514 beats . mm Hg, p less than 0.02); this relief of cardiac effort was a function of the pretreatment plasma renin activity. A derived index of external myocardial efficiency improved 37% (19 +/- 3 to 26 +/- 6, p less than 0.05), reflecting greater left ventricular work without increased oxygen demand. Enhancement of myocardial performance after converting enzyme inhibition appears dependent on reduction of angiotensin-mediated ventricular afterload and preload. The lack of coronary vasomotor effects in patients with advanced ischemic cardiomyopathy may reflect limited coronary vascular reserve. Improvement of heart failure in these patients developed without evidence of myocardial ischemia, since balance was maintained between oxygen supply and demand.

Aged↗
PubMed1982

The effect of angiotensin converting enzyme inhibition of coronary blood flow and hemodynamics in patients without coronary artery disease.

We examined the role of the renin-angiotensin system in the regulation of systemic and coronary vascular tone by studying the effect of converting enzyme inhibition by teprotide on systemic and coronary hemodynamic parameters in 14 normal patients undergoing routine cardiac catheterization. Serial hemodynamic measurements were made before and up to 30 minutes after 1 mg/kg of intravenous teprotide. A significant rise in cardiac index and stroke volume index occurred with a fall in systemic vascular resistance. The increase in cardiac index was related to the level of resting plasma renin activity. Blood pressure, pulmonary artery and left ventricular end-diastolic pressures remained unchanged. Coronary sinus thermodilution blood flow also showed no significant change; however, some patients demonstrated dramatic increase in flow. The change in blood flow was highly correlated with the resting plasma renin activity (r = 0.939 P less than 0.001). The change in coronary vascular resistance and myocardial oxygen consumption were likewise related to the resting plasma renin level. Converting enzyme inhibition produces significant systemic hemodynamic changes in normal patients which implies that the renin-angiotensin system is important in normal cardiovascular homeostasis. The direct relationship between plasma renin activity and coronary blood flow suggests that the renin-angiotensin system may play an important role in coronary vasomotor regulation.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1982

Peripheral arterial and venous responses to acetylstrophanthidin in patients with acute myocardial infarction.

The peripheral arterial and venous responses to rapidly active acetylstrophanthidin (rather than the much slower digitalis) were studied in patients with acute myocardial infarction without congestive heart failure. In eight control patients placebo did not change mean blood pressure (BP), calf blood flow (CBF), calf vascular resistance (CVR), or calf venous volume (CVV). Seventeen patients received 10 mg IV acetylstrophanthidin. In these patients BP increased 5.3%, CBF decreased 18.2%, and CVR increased 29.2%. Venous capacitance was not changed. Acetylstrophanthidin induced no significant change in cardiac output, systemic vascular, resistance, pulmonary capillary wedge pressure, or right atrial pressure. In patients with acute myocardial infarction not complicated by congestive heart failure, digitalis may promote limb vasoconstriction and increase blood pressure, but it does not adversely affect cardiac function.

Electrocardiography↗
PubMed1982

Regional circulatory response to converting-enzyme inhibition in congestive heart failure.

1 To determine the distribution of flow, the regional haemodynamic response to 100 mg of captopril was determined in 36 patients with refractory cardiac heart failure. Measurements included forearm blood flow by venous occlusion plethysmography (eight patients), splanchnic blood flow by indocyanine green clearance (10 patients), and coronary blood flow by thermodilution (12 patients). 2 Cardiac index significantly rose in one hour (1.9 +/- 0.1 to 2.2 +/- 0.1 1/m/m2, p less than 0.01) while forearm blood flow rose slightly (2.9 +/- 0.8 to 3.2 +/- 0.3 ml/100 ml/min). Renal blood flow rose significantly by 30% (344 +/- 48 to 533 +/- 82 ml/min, p less than 0.02). Despite a fall in rate pressure product (8.8 +/- 0.7 to 7.1 +/- 0.5 mm Hg bt x 10(3), p less than 0.02), coronary blood flow did not significantly change (160 +/- 20 to 133 +/- 12 ml/min), indicating an improved supply-demand relationship. 3 External myocardial efficiency improved (19 +/- 3 to 26 +/- 6%, p less than 0.05). Coronary blood flow is unaffected and converting-enzyme inhibitor improves myocardial efficiency. This strategic reduction in vascular impedence distinguishes converting-enzyme inhibitors as a unique class of vasodilators in the treatment of coronary heart failure.

Aged↗
PubMed1981

Angiotensin inhibition in severe heart failure: acute central and limb hemodynamic effects of captopril with observations on sustained oral therapy.

The systemic, pulmonary, and limb circulatory responses to the angiotensin-converting enzyme inhibitor, captopril, were determined in 10 patients with severe, chronic heart failure. Immediate effects include sustained reductions in arterial pressure and pulmonary capillary wedge pressure and improvement in cardiac output, as reported with other vasodilator drugs. Calf vascular resistance did not change despite substantial lowering of total systemic vascular resistance, indicating that arteriolar dilatation occurred on a selective basis. Transient reduction in mean right atrial pressure paralleled slight calf venodilatation, but effects upon the resistance vasculature predominated. Plasma renin activity and norepinephrine concentrations increased after therapy in the acute phase as plasma aldosterone levels consistently fell. During maintenance oral treatment over 7 to 15 months (median, 11.5 months), patients displayed symptomatic benefit, improved functional capacity, and greater exercise tolerance. No major adverse reactions developed. These findings suggest that angiotensin converting enzyme inhibition with captopril in congestive heart failure patients improved cardiocirculatory function through selective arteriolar dilatation. The reordering of regional blood flow which appears to result from release of angiotensin-mediated vasoconstriction, as well as the suppression of aldosterone, may underlie the prolonged benefit observed in these patients. This oral vasodilator appears to represent an effective adjunct for the treatment of advanced, chronic heart failure refractory to conventional measures.

Administration, Oral↗
PubMed1981

Acute regional circulatory and renal hemodynamic effects of converting-enzyme inhibition in patients with congestive heart failure.

The acute effects of the angiotensin converting-enzyme inhibitor captopril on regional blood flow, renal hemodynamics and sodium excretion were studied in 12 patients with severe congestive heart failure. Converting-enzyme inhibition decreased systemic vascular resistance by 27% and increased cardiac index by 16%. Estimated hepatic blood flow decreased 17%, but renal blood flow increased 60%. The ratio of renal-systemic blood flow increased from 0.10 +/- 0.01 to 0.14 +/- 0.02 (p = 0.031). Although renal plasma flow increased from 202.8 +/- 28.8 to 323.7 +/- 42.7 ml/min (p less than 0.008), the glomerular filtration rate did not change significantly from the mean pretreatment value of 82.1 +/- 12.3 ml/min. The filtration fraction decreased from 41.3 +/- 3.8% to 33.4 +/- 4.5% (p = 0.050), while urinary sodium excretion doubled, from 34.5 +/- 9.6 to 68.2 +/- 19.6 muEq/min. The plasma renin activity increased from 12.6 +/- 5.0 to 29.9 +/- 8.4 ng/ml/hr (p = 0.030) as plasma aldosterone concentration decreased from 30.5 +/- 6.5 to 11.3 4/- 1.2 ng/dl (p = 0.010) and norepinephrine concentrations decreased from 774 +/- 105 to 618 +/- 85 pg/ml (p = 0.020). We conclude that converting-enzyme inhibition reverses renal vasoconstriction in congestive heart failure and redistributes regional blood flow. The natriuresis may be mediated by one or more of the following: improved renal plasma flow, reduction in filtration fraction, suppression of hyperaldosteronism, and lowering of circulatory catecholamine concentrations.

Acute Disease↗