Highly sensitive C-reactive protein and male gender are independently related to the severity of coronary disease in patients with metabolic syndrome and an acute coronary event

Patients with metabolic syndrome are at high-risk for development of atherosclerosis and cardiovascular events. The objective of this study was to examine the major determinants of coronary disease severity, including those coronary risk factors associated with metabolic syndrome, during the early period after an acute coronary episode. We tested the hypothesis that inflammatory markers, especially highly sensitive C-reactive protein (hsCRP), are related to coronary atherosclerosis, in addition to traditional coronary risk factors. Subjects of both genders aged 30 to 75 years (N = 116) were prospectively included if they had suffered a recent acute coronary syndrome (acute myocardial infarction or unstable angina pectoris requiring hospitalization) and if they had metabolic syndrome diagnosed according to the National Cholesterol Education Program/Adult Treatment Panel III. Patients were submitted to a coronary angiography and the burden of atherosclerosis was estimated by the Gensini score. The severity of coronary disease was correlated (Spearman’s or Pearson’s coefficient) with gender (r = 0.291, P = 0.008), age (r = 0.218, P = 0.048), hsCRP (r = 0.256, P = 0.020), ApoB/ApoA ratio (r = 0.233, P = 0.041), and carotid intima-media thickness (r = 0.236, P = 0.041). After multiple linear regression, only male gender (P = 0.046) and hsCRP (P = 0.012) remained independently associated with the Gensini score. In this high-risk population, male gender and high levels of hsCRP, two variables that can be easily obtained, were associated with more extensive coronary disease, identifying patients with the highest potential of developing new coronary events.

Taquicardia atrial e funçäo renal / Atrial tachycardia and renal function

A taquicardia atrial induzida artificialmente em cäo produziu nas nossas condiçöes, alteraçäo importante da funçäo renal. Essa alteraçäo se manifestou por significativo aumento do volume urinário por minuto (1,3 ñ 0,12 no controle para 3,2 ñ 0,6ml/min no experimental) e da fraçäo de excreçäo de sódio (FENa) (de 2,3 ñ 0,3 no controle para 3,6 ñ 0,5), na presença de queda significante do fluxo sanguíneo renal (317 ñ 30,9 para 232 ñ 26,7 ml/min), sem alterar o ritmo de filtraçäo glomerular (66,1 ñ 6,7 no controle para 70,6 ñ 6,5 ml/min no experimental). Quanto à hemodinâmica sistêmica, observamos queda signficante do débito cardíaco e aumentos significantes da resistência vascular sistêmica e da pressäo de capilar pulmonar. Esses resultados demonstram que possivelmente fatores näo relacionados à hemodinâmica sistêmica, mas relacionados a alteraçöes hormonais, sejam responsáveis por estas alteraçöes