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[Acute hemodynamic effects of the vasodilator beta blocker carvedilol in heart failure]
A Buchwald1, C Unterberg, R van der Does
1Abteilung Kardiologie und Pulmonologie, Universitätsklinik Göttingen.
Insights
Intravenous carvedilol did not show an acute vasodilating effect in heart failure patients. The drug did not decrease blood pressure or peripheral resistance, contrary to expectations for vasodilation.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Carvedilol, a beta-blocker, is known to induce vasodilation in coronary artery disease patients.
- Heart failure is often associated with altered hemodynamics and reduced cardiac function.
Purpose of the Study:
- To investigate the acute vasodilating effect of intravenous carvedilol in patients with heart failure.
- To assess the impact of carvedilol on hemodynamic parameters during exercise in heart failure.
Main Methods:
- A double-blind, randomized, placebo-controlled, cross-over study.
- Inclusion of patients with coronary artery disease and dilated cardiomyopathy (ejection fraction < 40%).
- Measurement of rate-pressure-product, heart rate, blood pressure, and total peripheral resistance via Swan-Ganz catheterization and supine ergometry.
Main Results:
- Intravenous carvedilol (5 mg) did not significantly alter blood pressure compared to placebo.
- Heart rate was lower at rest and during exercise with carvedilol.
- Total peripheral resistance during exercise was higher with carvedilol, particularly in the coronary artery disease group.
Conclusions:
- Acute intravenous administration of carvedilol does not demonstrate a vasodilating effect in patients with heart failure.
- The observed effects on heart rate and peripheral resistance suggest a different hemodynamic profile than anticipated vasodilation.
Abstract:
The beta-blocker carvedilol has been shown to induce vasodilation in patients with coronary artery disease. In a double-blind, randomized, placebo-controlled cross-over study, we looked for the acute vasodilating effect after i.v. administration in patients with heart failure. In 10 patients with coronary artery disease and six patients with dilated cardiomyopathy, all with an ejection fraction lower than 40%, the rate-pressure-product during supine ergometry and Swan-Ganz-catheterization rose to a significantly smaller extent after 5 mg carvedilol i.v. compared to placebo. This was mainly due to a lower heart rate at rest and during exercise, while blood pressure was not changed compared to placebo. Calculated total peripheral resistance during exercise after carvedilol was higher--significantly so in the CAD-group--than after placebo. These results show that in patients with heart failure, an acute vasodilating effect of i.v. carvedilol is not detectable.
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