Objectives: Low plasma levels of testosterone in men are associated with increased risk for atherosclerosis. In this study, we assessed plasma testosterone levels in patients with metabolic syndrome (MS) and its relationship with MS parameters. Study design: The study consisted of 36 men (mean age 50.2±7.2 years) with a diagnosis of MS according to the NCEP (National Cholesterol Education Program) criteria. An age-matched control group comprising 39 healthy volunteers (mean age 48.3±8.1 years) was also included. Plasma testosterone levels were determined by electrochemiluminescence immunoassay on the Roche Elecsys 2010 analyzer. Fasting blood samples were analyzed for glucose and insulin levels, and lipid profiles (total cholesterol, triglyceride, LDL, and HDL). In addition, HOMA (Homeostasis Model Assessment) index was calculated. Results: The mean plasma testosterone level was significantly lower in the patient group (3.6±0.8 vs 4.8±1.9 ng/ml, p=0.001). There was a significant correlation between the levels of testosterone and HDL cholesterol (r=0.25, p<0.05). Testosterone levels were inversely correlated with the following: body mass index (r= -0.41, p<0.001), waist circumference (r= -0.40, p<0.001), HOMA index (r= -0.31, p=0.008), insulin (r= -0.28, p<0.05), glucose (r= -0.29, p<0.05), triglyceride (r= -0.28, p<0.05), and very low density lipoprotein (r= -0.28, p<0.05). Multivariate analysis identified only body mass index as an independent correlate of testosterone (b= -0.36, p=0.038). Conclusion: Our results show that plasma testosterone levels are significantly decreased in MS. This may be of clinical importance for the assessment of cardiovascular risks in male patients with MS.

Objectives: This study was planned to assess the relationship between serum myeloperoxidase (MPO) levels and major cardiovascular events in patients with acute coronary syndrome. Study design: Serum MPO levels were measured by ELISA on admission of 243 consecutive patients with acute coronary syndrome (153 acute myocardial infarction, 90 unstable angina). Major cardiac events that occurred during hospitalization and 30-day follow-up period included recurrent angina, reinfarction, ventricular (ventricular tachycardia, ventricular fibrillation) and supraventricular (atrial fibrillation, supraventricular tachycardia) arrhythmias, complete atrioventricular block, clinical heart failure, and death. Correlations were sought between high (n=70, >350 µg/l) and low (n=173, ?350 µg/l) MPO levels and major events. Relative risks were estimated using the Cox proportional hazards regression model. Results: The incidence of hypercholesterolemia was significantly higher in patients with high levels of MPO (p=0.008). A significant association was found between high levels of MPO and increased mortality risk during both hospitalization (hazard ratio-HR, 3.91; 95% CI 1.12-13.6; p=0.03) and 30-day follow-up period (HR 5.08, 95% CI 1.64-15.7; p=0.005). No significant differences were observed between patients with high and low MPO levels with respect to the development of arrhythmia, reinfarction, recurrent angina, and clinical heart failure (p>0.05). Conclusion: The results of this study demonstrate that elevated MPO levels predict death during hospital stay and 30-day follow-up period in patients with acute coronary syndrome.

Objectives: The diagnosis of rheumatic carditis with auscultation can be difficult especially in subclinical cases. We investigated the effectiveness of auscultation in detecting valvular regurgitation in rheumatic fever (RF). Study design: The study included 112 patients (51 males, 61 females; mean age 11.0±2.4 years; range 6 to 16 years) with RF (n=75) and rheumatic heart disease (n=37). The presence of murmurs of mitral (MR) and aortic (AR) regurgitation on precordial auscultation were noted. Two-dimensional and color Doppler echocardiographic examinations were performed in all the patients to determine pericardial effusions, prolapse and thickening of the mitral valve, and pathologic valvular regurgitations. The sensitivity, specificity, and predictive values of auscultation were calculated for MR and AR. Results: Seventy-seven patients had cardiac involvement (68.8%; 47 mild, 13 moderate, 17 severe), which was demonstrated by auscultation in 60 patients (77.9%). There were 17 patients with silent carditis. Auscultation enabled detection of MR and AR in 60 (60/72; 83.3%) and 21 (21/37; 56.8%) patients, respectively. Echocardiography revealed silent MR in 12 patients and silent AR in 16 patients. The degree of valvular insufficiency was significantly lower in silent cases than those with evident MR (p=0.003) and AR (p=0.005). Of 12 patients with silent MR, only one patient had mitral valve prolapse and another had thickening of the mitral valve. The sensitivity, specificity, positive and negative predictive values of auscultation were found as 83.3%, 85.0%, 90.9% and 73.9% for MR, and 56.8%, 98.7%, 95.5% and 82.2% for AR, respectively. Conclusion: Auscultation was found to be more sensitive for MR and more specific for AR. Given considerably low negative predictive value of auscultation for MR and AR, the role of echocardiographic examination to detect cardiac involvement is indispensable in patients with RF.

Objectives: It has been shown that mutations in the endothelial nitric oxide synthase (eNOS) gene are associated with an increased risk for coronary artery disease (CAD), myocardial infarction, and hypertension. We investigated the association of eNOS gene polymorphism (T-786 C) with coronary artery disease in a Turkish population. Study design: The study included 211 patients (144 males, 67 females, mean age 59 years; range 27 to 85 years) who underwent coronary angiography. While 159 patients (75.4%) had angiographically shown CAD (?50% stenosis at least in one vessel), 52 subjects (24.6%) were free of the disease. Those with CAD were classified according to the number of vessels affected. Polymerase chain reaction was used for genotyping. Risk factors for CAD were analyzed by a multivariate logistic regression analysis. Results: Genotypical and allelic distribution significantly differed between the two groups (p<0.05). The CC genotype was more prevalent in patients with three-vessel disease (p<0.001). Compared with TT homozygotes, the number of patients carrying at least one C allele (TC+CC, C dominant model) was significantly higher among CAD patients (p<0.01) and in those with three-vessel disease (p<0.001). With respect to allelic distribution (T vs C, additive model), the frequency of the C (cytosine) allele was higher in CAD (p<0.05). Multivariate logistic regression showed that C-dominant individuals had a 2.9-fold likelihood for CAD (odds ratio 2.902, 95% confidence interval 1.272-6.622; p<0.05). Conclusion: Our data suggest that the T-786 C polymorphism of the eNOS gene may be involved as a risk factor in the prevalence of CAD in Turkish patients.

A 23-year-old male patient was referred to our hospital following detection of a cardiac murmur at a center where he had sought treatment for his complaint of dyspnea due to blunt chest trauma of a-month history. Transthoracic and transesophageal echocardiography showed papillary muscle rupture and severe mitral regurgitation. At surgery, it was noted that papillary muscle rupture was accompanied by complete rupture of the chordae tendineae of the anterior leaflet, making reconstruction unfeasible. The valve was excised and a prosthetic valve was implanted.

A 50-year-old male patient who presented with chest pain was hospitalized with a diagnosis of non-Q-wave myocardial infarction. Treatment with aspirin, clopidogrel, nitrates, beta-blocker, and heparin did not relive pain. Coronary angiography showed slow flow in the left anterior descending coronary artery and massive thrombotic occlusion in the septal artery. Tirofiban administration resulted in relief of chest pain. Control coronary angiography performed at 72 hours showed complete disappearance of the intracoronary thrombus, but slow flow in the left anterior descending coronary artery persisted. The patient was asymptomatic during a follow-up of three months.

Although aspirin is the most commonly used antithrombotic drug in the treatment of cardiovascular diseases, the appearance of vascular thromboembolic events in some patients receiving aspirin has brought into question its safety and development of aspirin resistance. This article reviews the most current information concerning the cause of aspirin resistance and clinical results and discusses therapeutic implications.

Toxic effects associated with the production of significant amounts free oxygen radicals at the cellular level are eliminated by the antioxidant defense system within the body. Oxidative stress which arises from insufficiency or failure of this defense system plays an important role in aging and pathogenesis of many diseases. This article revisits the role of oxidative stress in the formation and progression of many heart diseases such as endothelial dysfunction, atherosclerosis, hypertension, heart failure, and reperfusion injury.