[Secondary angina pectoris. Generalities]

Secondary angina pectoris (AP) resulting from an increase in myocardial oxygen demands not satisfied by increased coronary flow because of severe and usually multiple atherosclerotic lesions, contrasts with primary AP due to decreased coronary flow usually due to coronary spasm. Secondary AP corresponds clinically to Heberden's common AP induced by conditions which increase the metabolic demands of the myocardium: tachycardia, increased parietal tension and myocardial contractility, prolongation of the ejection period. In practice, secondary AP is preceded by an elevation in the rate-pressure product. Factors which give rise to tachycardia, increased after and preload, increased inotropism and ventricular ejection may cause secondary AP at a critical level of fixed reduction of the coronary vascular bed. Mixed AP is due to the association of fixed anatomical lesions and coronary spasm in variable proportions. The physiopathological principles should be born in mind when taking therapeutic decisions.