“…Other authors have demonstrated several pathomechanisms probably involved in poststenotic vasoconstriction after PTCA such as endothelium-dependent (Fischell et al 1989) or myogenic (Fischell et al 1990) response to sudden increases in pressure following PTCA, increased vasoreactivity to stimuli such as serotonin released from platelets adhering and aggregating at the PTCA-site (Zeiher et al 1991, Golino et al 1994, loss of flowmediated vasodilation (Cox et al 1989), alteration of coronary autoregulatory tone (Fischell et al 1990) and sympathetic reflex diffusely distributed to the coronary tree (Gregorini et al 1994). In contrast to poststenotic coronary diameter, poststenotic coronary Doppler flow velocity showed a highly significant increase after PTCA, as observed by us (Dill et al 1994, Altstidl et al 1995a, 1997b and other groups (Segal et al 1992, Ofili et al 1993a, Segal 1993, Serruyys et al 1993, Anderson et al 1993 before. Since poststenotic coronary artery vasoconstriction routinely occurs during PTCA (Fischell et al 1988, Altstidl et al 1997a, increase of poststenotic flow velocity may be due to both reduction in diameter stenosis and decrease in coronary diameter according to the continuity equation.…”