Inflammatory alterations in the myocardial microcirculation.
Inflammatory mechanisms are involved in the pathophysiology of cardiovascular disease and the present review focus us on the association between inflammation and microvascular endothelial dysfunction in the heart, i.e. reduced endothelium dependent vasodilation of coronary resistance vessels. This abnormality is caused by reduced bioactivity of nitric oxide (NO), and it is found in a variety of conditions, including ischemic heart disease, cardiac allograft vasculopathy, diabetes, hypercholesterolemia, and smoking. At the level of the myocardial microcirculation, reperfusion injury manifests itself as endothelial dysfunction, no-reflow, and increased permeability, which are all probably the result of reperfusion-induced augmentation of the inflammatory response. In other animal models of cardiovascular disease, inflammatory alterations have been described that can contribute to microvascular endothelial dysfunction and reactive oxygen species, neutrophils, tumour necrosis factor-alpha, and inducible NO synthase are among the mediators that have been incriminated. Circulating levels of inflammatory mediators may serve as molecular markers of cardiovascular disease, and antiinflammatory interventions hold some promise for future cardiovascular therapy.
Hansen
P R
PR
Department of Cardiology P, Gentofte University Hospital, Hellerup, Denmark.
D004730:Endothelium, Vascular / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D008833:Microcirculation / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology*