[Effects of diltiazem on cardiac and coronary circulation, at rest and during rapid auricular electric stimulation]
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Rapid atrial pacing in patients with coronary artery disease increased myocardial oxygen demand. Diltiazem, a calcium channel blocker, mitigated these effects, improving cardiac performance and oxygen supply.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Chronic coronary artery disease poses significant risks to cardiac performance.
- Understanding the impact of interventions on myocardial oxygen balance is crucial.
Purpose of the Study:
- To investigate the effects of rapid atrial pacing and diltiazem on cardiac function and blood flow in patients with coronary artery disease.
- To assess diltiazem's ability to counteract adverse effects of pacing.
Main Methods:
- Studied 20 patients with chronic coronary artery disease.
- Administered rapid atrial pacing and intravenous diltiazem (20 mg/kg).
- Monitored cardiac performance, systemic and coronary blood flow, and myocardial oxygen consumption.
Main Results:
- Rapid atrial pacing increased coronary flow, oxygen consumption, and left ventricular end-diastolic pressure, while decreasing coronary resistance.
- Diltiazem reduced femoral arterial pressure, coronary arteriovenous difference, and oxygen consumption, increasing lactate difference.
- Diltiazem counteracted negative pacing effects on lactate balance and reduced ventricular end-diastolic volume.
Conclusions:
- Diltiazem effectively opposed undesirable effects of rapid atrial pacing on myocardial lactate balance.
- Diltiazem's benefits may stem from reduced myocardial oxygen demand (less ventricular strain) and increased supply (vasodilation), not solely hemodynamic changes.
Abstract:
The effects on cardiac performance and systemic and coronary blood flow of rapid atrial pacing alone and associated with an intravenous infusion of a slow calcium channel inhibitor, diltiazem, at a dose of 20 mg/kg were studied in 20 patients with chronic coronary artery disease. Atrial pacing increased coronary flow and myocardial oxygen consumption: it decreased coronary arterial resistance and the coronary arteriovenous difference in lactates. Left ventricular end diastolic pressure rose significantly compared to the basal state in the period following pacing. The administration of diltiazem was associated with a significant fall of femoral arterial pressure, of coronary arteriovenous difference and myocardial consumption of oxygen, and an increase in the coronary arteriovenous difference in lactate. Left ventricular end diastolic pressure did not differ significantly from the basal values recorded after terminating atrial pacing. Left ventricular end diastolic volume decreased. Diltiazem opposed or cancelled the undesirable effects of rapid atrial pacing with respect to coronary arteriovenous difference in lactate content. The beneficial action of diltiazem does not seem to be closely related to its hemodynamic effects. It could be related to a reduction in myocardial oxygen demands due to a decrease in systolic ventricular strain and the specific metabolic effects of the drug, and also to an increase in myocardial oxygen supply due to the reduction in left ventricular end diastolic stress and the coronary vasodilation caused by the drug.