Endotheliale Funktionsstörung bei Patienten mit akutem Koronarsyndrom

Abstract

Increased vasoconstriction, activation of platelet vessel wall interaction and invasion of monocytes into the subintima as well as vascular smooth muscle cell proliferation play a fundamental role in the pathogenesis of coronary artery disease. Acute coronary syndromes such as myocardial infarction and unstable angina pectoris are characterized by plaque rupture or erosion, activation of platelets and the coagulation system and vasoconstriction. Endothelial dysfunction may be one of the underlying mechanisms linking coronary artery disease and acute coronary syndromes. Both of these are often temporarily limited. Therefore, "non-invasive examination" of endothelial function by venous occlusion plethysmography or high resolution ultrasound might be useful for monitoring high-risk patients.

Expression of vascular endothelial growth factor and its receptors is increased, but microvascular relaxation is impaired in patients after acute myocardial ischemia

“…First, although it is already well known from studies in rats that the expression of VEGF and its receptors is increased in myocardium early after the onset on acute ischemia, 18,19 extrapolating a heightened physiologic effect may not be justified because VEGF, FGF2, and several other angiogenic substances may operate through the stimulated release of nitric oxide by activation of tyrosine kinase receptors. [20][21][22] Because endothelial dysfunction is known to occur during acute myocardial ischemia, [23][24][25] it is plausible that the physi-ologic actions of endogenous growth factors may be impaired. This was suggested by the findings of this study.…”

Reconstituted HDL in Acute Coronary Syndromes

“…Since endothelial function is severely impaired in patients with ACS [12] and has been identified as an independent denominator of future cardiovascular events [13], the goal of the present study was to investigate the acute effects of human rHDL on vascular function, markers of vascular inflammation, and oxidative stress in patients with ACS on optimal background therapy, including statins and antithrombotics.…”