Metabolic syndrome (MS) identifies cardiovascular risk; however, there is little information regarding the evolution of patients with MS after stent implantation. The aim of this single-center study is to evaluate the possible association between MS and clinical restenosis, after adjustment for highsensitivity C-reactive protein (hs-CRP) and angiographic predictors of restenosis. In a longitudinal study, 159 patients (89 with and 70 without MS) were studied. Criteria for MS were: elevated blood pressure (systolic >or=130 mmHg, diastolic >or=85 mmHg or drug treatment for hypertension; elevated fasting glucose (>100 mg/dl) or drug treatment for elevated glucose; reduced HDL-cholesterol (<40 mg/dl in men and <50 mg/dl in women) or drug treatment for reduced HDL-cholesterol; elevated triglycerides (>or=150 mg/dl) or drug treatment for elevated triglycerides; and obesity (body mass index >28.8 kg/m2). The primary end point was the rate of major adverse clinical events (MACE): cardiovascular death, myocardial infarction, or target lesion revascularization (TLR) during the 12-month follow-up period. The secondary end point was the rate of TLR. MS was neither identified as predictor of MACE [hazard ratio (HR): 0.844; 95% CI: 0.41-1.74; p=0.648], nor TLR (HR: 1.05; 95% CI: 0.44-2.50; p=0.91), even when controlled for hs-CRP levels and angiographic predictors of restenosis. Also, no significant interaction between MS and hs-CRP was found (p=0.135 and p=0.194, for MACE and TLR, respectively). This study shows that patients with MS do not have an additional risk of MACE, even when controlled for angiographic predictors of restenosis and hs-CRP.

No abstract

AtualizaçãoO endotélio, mais que simples barreira natural que separa os constituintes da parede dos elementos do sangue, é órgão secretor que libera diversas substâncias, muitas delas com efeitos antagonistas, como fatores que promovem o crescimento de células do músculo liso vascular e outras, que o inibem, substâncias pró e antiagregantes plaquetárias, vasodilatadoras e vasoconstritoras, pró e antifibrinolíticas [1][2][3] . A homeostase da parede vascular resulta do equilíbrio desta atividade secretora.São apresentadas a seguir as evidências da literatura sobre as propriedades do fator relaxante derivado do endotélio (FRDE) e sua similitude com o óxido nítrico (NO), os efeitos do FRDE, do precursor e doadores de NO sobre as plaquetas, polimorfonucleares, monócitos e células de músculo liso vascular; a interação do NO com espécies reativas de oxigênio e lipoproteínas, além de outras propriedades farmacológicas destas substâncias, propriedades estas que indicam que o FRDE cumpre um papel importante na homeostase da parede vascular. Disfunção endotelialO termo disfunção endotelial é empregado para definir as situações em que o endotélio perdeu sua propriedade vasoprotetora, representando a etapa inicial de vários processos de lesão vascular, como a injúria mecânica, hipercolesterolemia, aterosclerose, hipertensão arterial sistêmica, entre outros [4][5][6] . Do ponto de vista farmacológico, a disfunção endotelial consiste numa resposta parodoxal à administração de acetilcolina ou a de outro vasodilatador dependente do endotélio, causando vasoconstrição e queda do fluxo sangüíneo no vaso estudado 7,8 . São vários os mecanismos propostos para explicar esta reatividade vascular anormal, entre eles, menor síntese e liberação do FRDE-NO pelo endotélio 9,10 ou inativação do mesmo mediada, principalmente, pelo radical superóxido ou por produtos da lipoperoxidação [11][12][13][14] . A resposta vascular coronária alterada está relacionada com a presença de fatores de risco para doença coronária, como hipercolesterolemia, hipertensão, idade, aterosclerose instituída, diabetes mellitus [15][16][17][18][19][20] , podendo ocorrer também após angioplastia no segmento distal ao procedimento 21 . A disfunção endotelial está também envolvida na patogênese da síndrome X . A importân-cia da síntese do FRDE-NO a partir da L-arginina, a chamada via L-arginina-NO, baseia-se no fato de que são vários os tecidos que têm a propriedade de síntese do FRDE-NO, entre eles o endotélio, e que esta molécula cumpre importantes funções no organismo 45 . Esta síntese, a partir da L-arginina, é devida à ação da enzima constitutiva NO sintase endotelial (NOSe), que é estimulada por vários agentes 46-48 (quadro I).Quadro I -Ativadores da NO sintase [46][47][48]

The 894G>T polymorphism of the endothelial constitutive nitric oxide synthase gene consists of the substitution of a guanine base by a thymine at the 894th nucleotide of the gene. An association of this polymorphism with acute coronary syndromes has been described, only when in combination with other polymorphisms of this gene. The aim of the present study was to search for an association between this polymorphism and unstable angina in a southern Brazilian population. In a case-control study, 156 patients (group 1 (N = 83): unstable angina, group 2 (N = 73): stable angina) were genotyped by PCR and digestion of the product. Univariate analysis demonstrated that the minimal luminal diameter and the degree of stenosis of the culprit lesion differed between groups (P = 0.006 and 0.005, respectively). In addition, the frequencies of the T allele and of the T allele carriers (combined TT and TG genotypes) were significantly higher in the group with unstable angina (41.6 vs 28.8%; P = 0.025, Pearson chisquare test, and 73.5 vs 45.2%; P = 0.001, Pearson chi-square test, respectively). Multivariate logistic regression showed that the frequency of the T allele carriers was the only variable with a predictive value for unstable angina, when controlled for the other variables (6.1 (95% CI = 2.55-14.43); P < 0.001). Thus, in a homogenous group of patients, the endothelial constitutive nitric oxide synthase 894G>T polymorphism was associated with unstable angina. We suggest that this polymorphism may be a genetic risk factor for unstable angina.

Despite the extensive research on the pharmacology of L-arginine, there are only few data on its antithrombotic properties. We studied the effect of oral L-arginine administration in a model of arterial thrombosis in rabbits divided into three groups: group 1, group without intervention; group 2, control group, treated with normal diet and submitted to the thrombosis-triggering protocol; group 3, treated for 2 weeks with L-arginine (2.25%) prior the protocol. L-Arginine did not alter platelet aggregation nor coagulation parameters but reduced vascular activities of both ADPase (49.1 +/- 8.5 versus 28.9 +/- 8.3 versus 18.8 +/- 10.3 nmoles inorganic phosphate/min per mg protein; mean +/- SD; group 1 versus group 2 versus group 3, respectively; ANOVA F = 19.21; P < 0.0001) and ATPase (97.8 +/- 15.8 versus 52.1 +/- 11.6 versus 31.9 +/- 16.3 nmoles inorganic phosphate/min per mg protein; mean +/- SD; group 1 versus group 2 versus group 3, respectively; ANOVA, F = 34.65; P < 0.0001). L-Arginine did not reduce the thrombi area (17.1 mm, 9.02 and 48.07, versus 27.04 mm, 25.4 and 70.39, median, percentile 25 and 75 respectively, P = 0.079; group 2 versus group 3, respectively). In conclusion, oral L-arginine administration did not inhibit thrombosis, and, conversely, it significantly reduced the arterial wall ADPase and ATPase activities. This effect may limit its antithrombotic properties.