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Effects of verapamil on coronary hemodynamic function and vasomobility relative to its mechanism of antianginal
Insights
Intravenous verapamil moderately dilates systemic and coronary vessels in patients with coronary artery disease. While it reduces vascular resistance, it offers milder dilation of large coronary arteries compared to nitroglycerin.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Coronary artery disease (CAD) involves narrowed or blocked arteries, impacting blood flow to the heart.
- Understanding the effects of vasodilators on coronary and systemic hemodynamics is crucial for managing CAD.
Purpose of the Study:
- To investigate the impact of intravenous verapamil on systemic and coronary hemodynamic function in patients with CAD.
- To assess verapamil's effect on coronary artery dilation and compare it with nitroglycerin.
Main Methods:
- 12 patients with CAD underwent cardiac catheterization.
- Verapamil was administered via bolus and infusion.
- Systemic and coronary hemodynamics were measured using thermodilution.
- Coronary angiography with computer-assisted analysis assessed vessel caliber and stenosis.
- Comparison with sublingual nitroglycerin was performed in 8 patients.
Main Results:
- Verapamil reduced mean arterial pressure, systemic vascular resistance, and stroke work index.
- Coronary vascular resistance decreased, with a non-significant increase in coronary sinus blood flow.
- Verapamil caused significant dilation in 50% of normal and diseased coronary segments, reducing stenosis resistance by 14%.
- Nitroglycerin induced greater coronary dilation and a 28% reduction in stenosis resistance.
Conclusions:
- Verapamil moderately dilates systemic and coronary small resistance vessels without increasing myocardial oxygen demand.
- Verapamil also mildly dilates large coronary arteries in both normal and diseased segments.
- Verapamil's dilation of large coronary arteries is less potent than that of nitroglycerin.
Abstract:
The effect of intravenous verapamil on systemic and coronary hemodynamic function was studied at cardiac catheterization in 12 patients with coronary artery disease. Verapamil was administered as a 2-minute bolus (0.145 mg/kg) followed by an infusion (0.005 mg/kg/min). Cardiac output and coronary sinus blood flow were measured by thermodilution techniques. Caliber of the large coronary arteries and of diseased segments was determined from the coronary angiogram using a computer-assisted method. Verapamil reduced mean arterial pressure 14% (p less than 0.001), systemic vascular resistance 21% (p less than 0.01), and stroke work index 16% (p less than 0.001). Coronary vascular resistance decreased 24% (p less than 0.01) with a small increase in coronary sinus blood flow (+13%, difference not significant [NS]). Myocardial oxygen consumption determined in 5 patients showed no significant change with verapamil. Luminal area in 39 coronary lesions was measured in the "normal" portion of the diseased segment and at its maximal constriction, and an estimate of flow resistance in the stenosis was computed. Overall, 50% of "normal" and of diseased coronary segments dilated significantly with verapamil. Stenosis dilation resulted in an average 14% reduction (p less than 0.01) in estimated flow resistance. In 8 patients, the luminal changes (n = 27) induced by sublingual nitroglycerin were compared with those induced by verapamil. Nitroglycerin induced a significantly greater increase in coronary caliber in both normal and diseased segments; estimated stenosis flow resistance decreased 28% with nitroglycerin compared with 14% with verapamil (p less than 0.01). Thus, verapamil moderately dilates the systemic and coronary small vessel resistance bed without apparently increasing myocardial metabolic demand. Furthermore, verapamil mildly dilates large coronary conductance vessels in both "normal" and diseased segments, although significantly less than does nitroglycerin.