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[Acute hemodynamic and coronary effects of captopril in chronic cardiac failure]
Insights
Captopril significantly improves cardiac function in patients with severe heart failure by reducing blood pressure and improving blood flow. This ACE inhibitor enhances cardiac output and reduces the heart
Area of Science:
- Cardiology
- Pharmacology
Context:
- Chronic severe heart failure (NYHA Class III-IV) impacts cardiac hemodynamics.
- Patients included primary cardiomyopathy and ischemic heart disease.
Purpose:
- To evaluate the acute effects of captopril on hemodynamics, coronary flow, and myocardial metabolism in severe heart failure patients.
Summary:
- A single 50-100 mg dose of captopril acutely improved cardiac index and systolic index.
- Captopril reduced afterload (mean aortic pressure, systemic arterial resistance) and preload (left ventricular end-diastolic pressure).
- No significant changes in myocardial contractility (V.max) were observed.
Impact:
- Captopril demonstrates potent acute hemodynamic benefits in severe heart failure.
- Findings support captopril's role in managing patients with advanced cardiac dysfunction.
Abstract:
The acute effects of captopril on haemodynamics, coronary flow and myocardial metabolism were studied in 12 patients with chronic severe cardiac failure (primary cardiomyopathy: 10 cases; ischaemic: 2 cases) in functional Classes III or IV of the NYHA. All patients were male and their average age was 51.3 +/- 14.1 years (range 27 to 68 years). Measurements were carried out under basal conditions and 90 minutes after a single dose of 50 mg (5 cases) or 100 mg (7 cases) of captopril. Captopril administration leads to an increase in cardiac index from 2.05 +/- 0.32 to 2.34 +/- 0.35 l/min/m2 (p less than 0.05) and a greater increase in systolic index from 23.9 +/- 6.7 to 29.8 +/- 6.9 ml/syst/m2 (p less than 0.01), because the heart rate decreased slightly (p less than 0.05). These changes were the result of a decrease in afterload: mean aortic pressure fell from 85 +/- 11.8 to 68 +/- 19.6 mmHg (p less than 0.01) and systemic arterial resistance fell from 2 886 +/- 745 to 2 010 +/- 610 dynes/cm-5/sec/m-2 (p less than 0.01). Captopril also led to a fall in venous tone, i.e. pre-load: left ventricular end diastolic pressure fell from 26.9 +/- 6.1 to 20.8 +/- 6.6 mmHg: p less than 0.01. There was no change in contractility as shown by the absence of variation of the V.max (0.92 +/- 0.18 under basal conditions, and 0.90 +/- 0.15 after 90 minutes).(ABSTRACT TRUNCATED AT 250 WORDS)