Valvular aortic stenosis and coronary atherosclerosis: pathophysiology and clinical consequences

New methods of investigation (ECG, echocardiography, angiography, histology) allow a better understanding of the pathophysiology of valvular aortic stenosis (VAS) associated with coronary atherosclerosis. The progressive decrease in valvular aortic area modifies the coronary blood flow and leads to myocardial ventricular hypertrophy. These two mechanisms worsen left ventricular function. A significant atherosclerotic stenosis on a large coronary artery creates a considerable reduction of the available coronary blood flow. This reduction is permanent: present at rest, it is obviously increased during exercise. The study of the relationship between the severity of the VAS and the myocardial hypertrophy (MH) is of great interest. It seems that in VAS with coronary artery disease, different situations exist: (i) when the hypertrophy is severe (left ventricular mass greater than 180 g m-2), the angina pectoris is more attributable to the VAS than to the coronary lesions. Thus the removal of the aortic outflow obstruction is the most essential therapy; (ii) when the hypertrophy is less severe (left ventricular mass less than 180 g m-2), surgical treatment of the valvular lesion and myocardial revascularization are justified.