Effect of lidoflazine on systemic arteries and veins

Abstract

Lidoflazine, 4 4,4-bis(4 fluorophenyl)butyl-N-(2,6dimethylphenyl)-1-piperazineacetamide, helps improve work tolerance in patients with ischemic heart disease. Chronic treatment with the drug in patients with angina pectoris increase stroke volume, decreases systemic vascular resistance, and reduces mean arterial pressure at rest. Similar results were described in intact animals on acute administration of the compound. In both normal volunteers and patients with ischemic heart disease, chronic administration of lidoflazine augments stroke volume and cardiac output, and decreases mean arterial pressure and systemic vascular resistance during exercise. These hemodynamic findings indicate that the myocardium is shifted from pressure work to volume work, and that its total load (preload and afterload) is reduced by lidoflazine. The major dynamic determinants of preload and afterload of the heart are the degree of constriction of the venous and arterial segments of the circulation, respectively. This study was designed to determine the direct effects of lidoflazine on arterial and venous smooth muscle.