Markers of inflammation and cardiovascular disease: clinical applications of C-reactive protein determination.

C-reactive protein (CRP) is produced by the macrophages in the liver and adipocytes and is integrated in the acute-phase response pathway. Being a nonspecific marker of inflammation, it increases in response to inflammation. The results of recent studies that have analyzed the role of CRP have not yet influenced current clinical practice. When used in combination with other established biomarkers for the prediction of the first major cardiovascular event or death, CRP does not improve the risk stratification obtained with the current guidelines. The reduction of CRP levels itself or as a statin-related pleiotropic effect has been assessed in different scenarios, including the acute phase of myocardial infarction; secondary prevention of cardiovascular diseases; special patient populations, such as diabetic patients; and finally in a primary prevention study (JUPITER [Justification for the Use of statins in primary Prevention: an Intervention Trial Evaluating Rosuvastatin]). Risk stratification in all the examined scenarios was related to serum LDL-C levels; in other words, the degree of cardiovascular risk was always lipid dependent.

[Advances in hypertension and diabetes in 2007]. / Temas de actualidad en hipertensión arterial y diabetes.

This article contains a review of some of the main developments reported in 2007 on the topics of hypertension and diabetes. The most important was the publication of the European Society of Cardiology's clinical practice guidelines on the two conditions, both of which have been adopted by the Spanish Society of Cardiology. Elsewhere, we have recently been witnessing crucial debates on the use of rosiglitazone for the treatment of diabetes and on the drug's effect on cardiovascular outcomes. The evidence available up to the present time is assessed. Finally, we will review the results of the most recent large clinical trial on the prevention of vascular complications in diabetics, which employed an antihypertensive approach.

Mitochondrial changes induced by trimetazidine in the myocardium.

BACKGROUND: The aim was to assess the effect of trimetazidine (TMZ) on mitochondrial alterations induced in a canine model of brief, repeated episodes of ischemia. MATERIAL/METHODS: Twelve crossbred dogs were analyzed, after double-blind randomization, to a 7-day treatment with either TMZ or placebo. Twenty brief, complete occlusions of the left anterior descending coronary artery were performed. Mitochondrial analysis entailed a qualitative (percentage of mitochondrial damage, merging, pairing, vacuoles, and lipofucsin granules) and a quantitative size analysis (major and minor axes, perimeter, and area) of the mitochondria in the ischemic and control zones. RESULTS: Comparative study of the control zones revealed an increase in lipofucsin granules in the TMZ series and a greater percentage of damaged mitochondria and vacuoles. The control-zone mitochondria treated with TMZ presented a significant increase in the perimeter and major axis and a decrease in the minor axis (p<0.005). No significant differences were found between the series in the qualitative analysis of mitochondrial damage in the ischemic zone. The mitochondria in the TMZ series presented a greater major axis and perimeter than those in the placebo series (p<0.05), which presented a smaller minor axis. CONCLUSIONS: TMZ made the mitochondria adopt an elongated, "rod-like" morphology in both the control and ischemic zones. This is interpreted as an increase in the membrane surface. In the non-ischemic zone, TMZ produced an increase in mitochondrial turnover. There were no differences in the myocardium subjected to ischemia in both series in terms of observable mitochondrial damage.