Hämodynamik von Koronarstenosen

Under physiological conditions the resistance component of large epicardial coronary branches is very small in relation to total coronary resistance and can be neglected. The pressure losses across minor stenoses can be compensated by a decrease of resistance in the more peripheral coronary bed (autoregulation). This compensatory mechanism is limited to luminal obstructions less than 85%. Above this limit, when collateral vessels are not available, perfusion of the periphery becomes a function of the flow across the stenosis. As a consequence coronary reserve becomes abolished with an increasing obstruction. Coronary reserve describes an increase of coronary flow up to a factor of five, which, under normal conditions, is induced by dilation of resistors (arterioles) in the coronary bed. After exhaustion of coronary reserve the hemodynamic impact of a vascular narrowing can be expressed as the pressure loss across a coronary lesion (delta p). delta p is composed of viscous losses (AV) that are in linear relation to flow and inertial components that are related to the square of flow (B). Accordingly pressure loss across a stenosis can be expressed in a general form as delta p = AV X Q + B X Q2. In vitro data show that an approximation of delta p can be calculated on the basis of stenosis geometry including normal and minimal diameter, length, angle of entrance and exit, velocity of flow, viscosity and density of blood. Pressure losses across a stenosis can be divided in three components: the entrance, the narrow part, and the exit. Turbulence arises at the exit. This fact leads to a variable interaction of consecutive vascular lesions.(ABSTRACT TRUNCATED AT 250 WORDS