Plasma C-Reactive Protein and Lipoprotein Levels, and Progression of Coronary Artery Disease after Myocardial Infarction Treated with Thrombolysis

Abstract

Background: There is a paucity of studies using quantitative coronary angiography (QCA) to determine progression of coronary artery disease (CAD) after an acute coronary event. Furthermore, despite a great interest in effects of inflammation and ‘early’ lipid lowering therapy, no data have been published on the role of plasma C-reactive protein (CRP) and lipoprotein levels in CAD progression after myocardial infarction. Methods: Seventy-two patients with myocardial infarction treated with thrombolysis, but not with statins, were investigated with QCA during admission and after 6 months. Plasma CRP concentrations were measured by a high sensitive method 2 days after the acute event, and plasma high-sensitive CRP and lipoprotein levels were determined 3 months after myocardial infarction. Results: Overall, there was no significant progression of CAD, but when stenoses were grouped into those reducing the lumen diameter greater or less than 50%, progression was seen in stenoses originally <50%, whereas regression was seen in stenoses >50%. No consistent associations were seen between plasma CRP, lipoprotein lipid or lipoprotein(a) levels and CAD. Conclusions: Progression of stenoses <50% might be of clinical importance since these stenoses are more prone to rupture. Furthermore, the lack of associations between change in minimum lumen diameter and plasma CRP and lipoprotein concentrations suggests that positive effects on CAD progression of early treatment with anti-inflammatory or lipid-lowering drug therapy may not be expected in this subset of patients.

Endothelial function and cardiovascular diseases in HIV infected patient

“…High levels of this adhesion molecules represent early markers of the development of atherosclerosis [66,67]. Of interest, beside soluble adhesion molecules, other factors such as fibrinolytic factors, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) have also been considered to be markers of endothelial dysfunction [68][69][70].…”