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[Hemodynamic and coronary effects of intravenous verapamil in coronary insufficiency]
Insights
Verapamil reduces myocardial oxygen consumption by dilating arteries and decreasing heart contractility. This calcium channel blocker improves the heart
Area of Science:
- Cardiovascular Pharmacology
- Clinical Hemodynamics
- Myocardial Metabolism
Context:
- Chronic coronary insufficiency patients require effective treatments.
- Intravenous Verapamil's effects on coronary and systemic hemodynamics are not fully understood.
- Assessing Verapamil's impact on myocardial oxygen supply-demand balance is crucial.
Purpose:
- To investigate the coronary and hemodynamic effects of intravenous Verapamil in patients with chronic coronary insufficiency.
- To evaluate Verapamil's influence on myocardial oxygen consumption and lactate extraction.
- To determine the mechanisms behind Verapamil's effects on cardiac function.
Summary:
- Verapamil administration led to decreased left ventricular end-diastolic pressure and myocardial oxygen consumption.
- Cardiac output and total systemic resistance remained unchanged, while dP/dt max increased less significantly post-Verapamil.
- Coronary artery vasodilation and reduced coronary arterio-venous oxygen difference contributed to decreased myocardial oxygen consumption.
Impact:
- Verapamil demonstrates negative inotropic and arterial vasodilator effects, reducing myocardial oxygen demand.
- The drug favorably impacts myocardial energy equilibrium, evidenced by increased lactate extraction coefficient during pacing.
- Findings support Verapamil's therapeutic potential in managing chronic coronary insufficiency.
Abstract:
Verapamil inhibits calcium influx through the slow calcium canals. The coronary an haemodynamic effects of intravenous Verapamil were studied in 8 patients with chronic coronary insufficiency documented by coronary arteriography. The following measurements were made in spontaneous rhythm and during atrial pacing under basal conditions and 10 minutes after intravenous Verapamil (0.10 to 0.17 mg/kg) relayed with a continuous infusion of 5 x 10(-3) mg/Kg/mn: heart rate, cardiac output, left ventricularr pressure (Millar 5 F micromanometer), femoral artery pressure, coronary sinus flow by continuous thermodilution, oxygen and lactate concentrations in arterial and arterio-venous oxygen difference, and index of myocardial oxygen consumption and the coefficient of lactate extraction were then calculated. The coronary and haemodynamic effects of atrial pacing were similar before and after Verapamil at a given rate. Left ventricula end diastolic pressure decreased, cardiac output and total systemic resistance were unchanged, dP/dt max increased but to a lesser degree after Verapamil (P less than 0.05). Coronary arterio-venous oxygen difference decreased after Verapamil. The coronary and haemodynamic effects of Verapamil were similar in spontaneous rhythm and during atrial pacing. In spontaneous rhythm, the heart rate and left ventricular end diastolic pressure increased. In spontaneous and paced rhythm, femoral artery pressure, total systemic resistance and dP/dt max decreased. Cardiac output remained the same. Myocardial oxygen consumption decreased mainly because of a reduced coronary arterio-venous oxygen difference and because of unchanged coronary flow in spontaneous rhythm oxygen consumption seems to have a favourable effect on the myocardial energy equilibrium as shown by the increased coefficient of lactate extraction during atrial pacing after Verapamil. This study shows the negative inotropic and arterial vasodilator effects of Verapamil to be responsible for the reduced myocardial oxygen consumption. It also caused coronary artery vasodilation.