Differential progression of complex and smooth stenoses within the same coronary tree in men with stable coronary artery disease

Objectives.We sought to compare the evolution of complex and smooth stenoses within the same coronary tree in patients with stable coronary artery disease.Background.Progression of coronary stenosis has prognostic significance and may be influenced by local and systemic factors. Stenosis morphology is a determinant of disease progression, but no previous study has systematically assessed progression of complex and smooth stenoses within the same patient.Methods.We studied 50 men with stable angina who 1) had one complex coronary stenosis and one smooth stenosis in different noninfarct-related coronary vessels at initial coronary angiography, and 2) had a second angiogram after a median interval of 9 months (range 3 to 24). Patients with lesions ≥10 mm long, at a major branching point or with >85% diameter reduction were not included. Coronary lesions were measured quantitatively from comparable end-diastolic frames. Stenosis morphology was determined qualitatively by two independent observers.Results.All patients remained in stable condition during follow-up. Progression, defined as an increase in diameter stenosis by ≥15% was seen in only eight complex stenoses (16%) but in no smooth lesions (p < 0.01). The severity of complex stenoses changed more than that of corresponding smooth stenoses (mean ± 1 SD 5.8 ± 13% vs. −0.06 ± 6%, p < 0.01). On average, the annual rate of growth was 11.4 ± 28% and 1.5 ± 14% for complex and smooth lesions, respectively (p < 0.01).Conclusions.Few coronary stenoses progress rapidly in stable angina. Complex and smooth coronary stenoses progress at different rates within the same coronary tree. Complex stenosis morphology itself is an important determinant of progression of stenosis in patients with apparently clinically stable coronary artery disease

Innate and Adaptive Inflammation as a Therapeutic Target in Vascular Disease The Emerging Role of Statins

Atherosclerosis, the main pathophysiological condition leading to cardiovascular disease (CVD), is now considered to be a chronic inflammatory condition. Statins are the most widely used and promising agents in treating CVD and are renowned for their pleiotropic lipid-lowering independent effects. Statins exert their anti-inflammatory effects on the vascular wall through a variety of molecular pathways of the innate and adaptive immune systems, their impact on the circulating levels of pro-inflammatory cytokines, and their effect on adhesion molecules. By inhibiting the mevalonate pathway and isoprenoid formation, statins account for the increase of nitric oxide bioavailability and the improvement of vascular and myocardial redox state by multiple different mechanisms (directly or indirectly through low-density lipoprotein [LDL] lowering). A large number of randomized control trials have shown that statins help in the primary and secondary prevention of cardiovascular events, not only via their lipid-lowering effect, but also due to their anti-inflammatory potential as well. In this paper, we examine the molecular pathways in which statins are implicated and exert their anti-inflammatory effects, and we focus specifically on their impact on innate and adaptive immunity systems. Finally, we review the most important clinical data for the role of statins in primary and secondary prevention of cardiovascular events