ABSTRACT
While most prior studies examined late stages of heart failure, we determined initial changes of beta-adrenergic receptors (beta-AR) during left ventricular chronic volume and pressure overload. We investigated right auricular (RA) and left ventricular (LV) beta-AR density (Bmax, fmoles/mg protein) and beta 1-AR percentage in two groups of patients undergoing valve replacement without LV systolic dysfunction (LV ejection fraction > or = 60%), with normal plasma catecholamine levels and echocardiography LV hypertrophy. These results were compared with the values of a control group, composed by 8 patients with mitral stenosis and 5 cardiac transplant donors, and the values of 5 patients undergoing heart transplantation because of end-stage idiopathic dilated cardiomyopathy. These results show that, before alteration of LV systolic function occurs, left ventricular chronic overload induces a selective down-regulation of LV beta 1-AR compensated by an increase in beta 2-AR. These variations may be due to LV hypertrophy induced by volume or pressure overload.
Subject(s)
Hypertrophy, Left Ventricular/physiopathology , Myocardium/chemistry , Receptors, Adrenergic, beta/analysis , Catecholamines/blood , Down-Regulation , Female , Heart Valve Diseases/complications , Humans , Hypertrophy, Left Ventricular/etiology , Male , Middle Aged , Receptors, Adrenergic, beta/physiologyABSTRACT
The anti-ischemic and cardioprotective effects of various angina drugs have been evaluated during angioplasty. This special situation of transitory regional ischemia was used to test verapami given by intra-coronary injection in 15 patients undergoing balloon dilatation of the left anterior descending artery, suffering from stable angina and with normal left ventricular kinetics. Each patient serving as his own control, parameters indicating oxygen consumption and clinical and electrocardiographic (ST segment changes) markers were measured during two successive inflations. Continuous monitoring of comparative variations between a first inflation without treatment and a second inflation after intra-coronary administration of 1 mg of verapamil revealed, following 60 seconds of ischemia, the absence of any change in heart rate, a moderate fall in mean blood pressure (101.7 as against 96.8 mmHg, p = 0.033) and a notable 60% reduction in the amplitude of maximal ST depression (5.07 +/- 3.08 mm as against 2.07 +/- 1.44 mm, p = 0.0002). These results confirm the anti-ischemic properties of verapamil, the action of which is based upon an indirect peripheral vasodilator model but also on a probable direct cardioprotective effect on anoxic myocardial regions.