[Nifedipine in hypertrophic obstructive cardiomyopathy]
Insights
Nifedipine effectively reduces outflow obstruction and increases cardiac output in patients with hypertrophic obstructive cardiomyopathy (HOCM). This calcium channel blocker also dilates coronary arteries, potentially preventing coronary spasms and angina.
Area of Science:
- Cardiology
- Pharmacology
Context:
- Hypertrophic obstructive cardiomyopathy (HOCM) is characterized by left-ventricular outflow obstruction.
- Assessing the hemodynamic effects of nifedipine in HOCM patients is crucial for understanding its therapeutic potential.
Purpose:
- To evaluate the impact of nifedipine on left-ventricular dynamics and outflow obstruction in patients with HOCM.
Summary:
- Intravenous nifedipine (3 mg) administration in 6 HOCM patients resulted in decreased mean aortic pressure and increased heart rate.
- Cardiac index significantly increased, while stroke volume index decreased. Outflow obstruction diminished, and left-ventricular end-diastolic pressure rose.
- Coronary sinus oxygen saturation increased, indicating coronary vasodilation, which may offer protection against coronary spasms and angina.
Impact:
- Nifedipine demonstrates efficacy in reducing outflow obstruction and augmenting cardiac output in HOCM.
- Coronary vasodilation induced by nifedipine may provide antianginal benefits in HOCM patients.
- The findings support nifedipine as a potential therapeutic agent for managing HOCM symptoms.
Abstract:
The effects of nifedipine on left-ventricular dynamics were assessed in 6 patients with hypertrophic obstructive cardiomyopathy (HOCM). After intravenous infusion of 3 mg nifedipine the mean aortic pressure decreased from 100 +/- 14 to 85 +/- 8 mm Hg (P less than 0.001). Heart rate increased from 70 +/- 5 to 93 +/- 5 beats per minute (P less than 0.001). This led to an increase of cardiac index from 3.0 +/- 0.5 to 3.8 +/- 0.9 l/min . m2 (P less than 0.01), whereas the stroke volume index decreased from an average of 49 +/- 11 to 42 +/- 12 ml/m2 (P less than 0.05). A marked diminution of outflow obstruction was demonstrable in 3 patients with intraventricular pressure gradients. The left-ventricular enddiastolic pressure rose from 14 +/- 3 to 18 +/- 6 mm Hg (P less than 0.02) in all patients. This effect was accompanied by a clear-cut coronary dilatation, evidenced by an increase of oxygen saturation in the coronary sinus from 29 +/- 4 to 54 +/- 9% (P less than 0.001). Thus nifedipine leads to diminished outflow obstruction and concomitant increase of cardiac output in hypertrophic cardiomyopathy. Inhibition of contraction does not seem to be compensated by peripheral effects. Coronary dilatation demonstrable in HOCM patients permits protection against coronary spasms and thus an additional antianginous effects.
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