Biomarcadores melhoram a predição de morte cardiovascular em homens idosos

Zethelius B. et AL. Use of Multiple Biomarkers to Improve the Prediction of Death from Cardiovascular Causes. NEJM. May 15, 2008;358(20):2107-2116.

A incorporação de 4 biomarcadores (troponina, peptídeo natriurético cerebral, cistatina C e proteína C reativa) aos fatores usuais de avaliação de risco cardiovascular significativamente aumenta a previsibilidade de morte por causas cardiovasculares

Incorporating four biomarkers along with the usual factors in assessing cardiovascular risk significantly increases the predictability of death from cardiovascular causes, the New England Journal of Medicine reports.

Researchers used customary risk factors, plus four biomarkers, to evaluate a cohort of some 1100 men with a mean age of 71 years. The biomarkers chosen reflect damage to or malfunction of various systems — namely, myocardium (troponin), left ventricle (brain natriuretic peptide), kidney (cystatin C), and inflammation (C-reactive protein).

After 10 years' follow-up, the inclusion of biomarkers significantly increased the predictability of death from cardiovascular disease, both in the entire cohort and in those without cardiovascular disease at baseline. Those with elevations in any two biomarkers had a 3-fold increase in risk, and elevations in all four presaged a 16-fold increase.

Editorialists say the results need validation in younger cohorts that include both men and women who don't have cardiovascular disease.

Placa carotídea: um precursor subclínico de eventos vasculares

Espessura máxima da placa carotídea é um simples e não invasivo marcador de aterosclerose subclínica associada com risco aumentado de eventos vasculares.

Rundek T, ArifMcCord H et al. Carotid plaque, a subclinical precursor of vascular events

The Northern Manhattan Study. NEUROLOGY 2008;70:1200-1207.

Carotid atherosclerosis is a known biomarker associated with future vascular disease. The risk associated with small, nonstenotic carotid plaques is less clear. The objective of this study was to examine the association between maximum carotid plaque thickness and risk of vascular events in an urban multiethnic cohort.

As part of the population-based Northern Manhattan Study, carotid plaque was analyzed among 2,189 subjects. Maximum carotid plaque thickness was evaluated at the cutoff level of 1.9 mm, a prespecified value of the 75th percentile of the plaque thickness distribution. The primary outcome measure was combined vascular events (ischemic stroke, myocardial infarction, or vascular death).

Carotid plaque was present in 1,263 (58%) subjects. After a mean follow-up of 6.9 years, vascular events occurred among 319 subjects; 121 had fatal or nonfatal ischemic stroke, 118 had fatal or nonfatal myocardial infarction, and 166 died of vascular causes. Subjects with maximum carotid plaque thickness greater than 1.9 mm had a 2.8-fold increased risk of combined vascular events in comparison to the subjects without carotid plaque (hazard ratio, 2.80; 95% CI, 2.04–3.84). In fully adjusted models, this association was significant only among Hispanics. Approximately 44% of the low-risk individuals by Framingham risk score had a 10-year vascular risk of 18.3% if having carotid plaque.

Conclusions: Maximum carotid plaque thickness is a simple and noninvasive marker of subclinical atherosclerosis associated with increased risk of vascular outcomes in a multiethnic cohort. Maximum carotid plaque thickness may be a simple and nonexpensive tool to assist with vascular risk stratification in preventive strategies and a surrogate endpoint in clinical trials.