Ventricular aneurysms and akinesis
Ramiro Rivera, M.D.
Juan Luis Delcan, M.D.
Formerly, paradoxical movement of the left ventricular wall was considered the main factor causing impaired left ventricular performance. At present, experimental and clinical studies have shown that in the area of the myocardium where wall motion is absent, insufficient tension is developed to accomplish fiber shortening, with the result that fiber shortening and tension development in the remaining areas of the ventricle must increase to maintain an adequate stroke volume. When 20% to 25% of the left ventricular wall becomes akinetic, ventricular dilatation must ensue if the limits of fiber shortening of the healthy muscle are not to be exceeded.
When ventricular dilatation occurs as a consequence of the former mechanism, the physiopathology of the left ventricular function can be explained purely on a mechanical basis by La-place’s law of membranes. Thus, for a ventricle twice as large as another, four times as much tension must be developed within its wall to maintain the same pressure.
This additional requirement in wall tension is reflected in additional myocardial oxygen requirement that an impaired coronary circulation may not be able to meet. Surgical excision permits the maintenance of the intra-ventricular pressure with less wall tension and, at the same time, improves ventricular performance and relieves angina. Adequate revascularization of the remainder of the ventricle when needed must logically insure a better prognosis in terms of control of angina and recovery of cardiac function.
According to these principles, the surgical treatment of postinfarction ventricular aneurysm and akinesis should realize the maximal reduction of . . .