The pathophysiology of angina pectoris and the effect of lidoflazine.

Abstract

Angina pectoris results from a deficiency in myocardial oxygen supply. The rate-pressure product is an important predictor of myocardial oxygen requirements in patients with ischemic heart disease and in normal persons. The rate-pressure product at the onset of angina pectoris is reproducible under a variety of circumstances with a suitable protocol. In some patients, coronary artery spasm may reduce myocardial blood flow and contribute to the development of angina pectoris. Lidoflazine is a synthetic drug that appears to be a calcium-entry blocker and results in symptomatic improvement in patients with angina pectoris. Lidoflazine reduces the exercising rate-pressure product by its effect on heart rate and by decreasing systemic vascular resistance. It decreases coronary vascular resistance and antagonizes processes leading to an increase in coronary vasomotor tone.

• Authors: F L Gobel, L A Nordstrom, R R Nelson, Y Wang
• Journal: Circulation (Circulation) Vol. 65 Issue 1 Pt 2 Pg. I27-32 (Jan 1982) ISSN: 0009-7322 [Print] United States
• PMID: 7030519 (Publication Type: Journal Article, Review)

Chemical References

• Piperazines
• Lidoflazine

Topics

• Angina Pectoris (physiopathology)
• Blood Pressure (drug effects)
• Coronary Disease (physiopathology)
• Coronary Vessels (physiopathology)
• Heart Rate (drug effects)
• Humans
• Lidoflazine (therapeutic use)
• Myocardial Contraction (drug effects)
• Myocardium (metabolism)
• Oxygen Consumption
• Physical Exertion
• Piperazines (therapeutic use)