Objective: Coronary artery disease (CAD) risk increases with the elevation of low-density lipoprotein cholesterol (LDL-C), triglyceride (TG) and low level high-density lipoprotein cholesterol (HDL-C) levels. However, the magnitude at which CAD risk increases with every lipid parameter is controversial. We developed a new index called CHOLINDEX, in order to evaluate CAD risk, and investigated its reliability. Methods: Three hundred and seven patients (190 males and 117 females, aged between 26-80 years, mean 53.6±10.2 years) who underwent diagnostic coronary angiography were included in the study. Risk factors and lipid profiles of all patients were noted. CHOLINDEX was calculated by using a formula as follows: CHOLINDEX=LDL-C-HDL-C (TG < 400 mg/dL), LDL-C-HDL-C + 1/5 of TG (TG ≥ 400mg/dL). Results: Of the 307 patients, 180 had CAD. We found that age, male gender, hypertension, diabetes mellitus, smoking and CHOLINDEX were independent predictors of CAD. The logistic regression analysis showed that the CHOLINDEX had a much more significant relation with CAD (odds ratio=1.011, 95% CI=1.003-1.019) compared with other lipid parameters. Conclusion: CHOLINDEX is a simple index which can be used reliably in prediction of CAD like other lipid parameters in daily clinical practice. (Anadolu Kardiyol Derg 2013; 13: 315-9)

Genetic factors are important in the pathogenesis of coronary artery disease (CAD). Angiotensin converting enzyme (ACE) gene insertion(I)/deletion(D) polymorphism is one of the genetic factor found to be related with CAD. We investigated the association between I/D polymorphism of the ACE gene and the presence of CAD. Three hundred and seven patients (187 males and 120 females, aged between 35-80, mean 54.3 +/-9.8 years) who underwent diagnostic coronary angiography were included in the study. ACE I/D polymorphism was detected by polymerase chain reaction. Of the 307, 176 had CAD. The most frequently observed genotype in all subjects was ID (47.9 %). However, in patients with CAD the frequency of II genotype was lower whereas DD genotype was higher compared to the controls (p < 0.05). The number of D allele carrying subjects were also higher (p < 0.05) in CAD patients. The logistic regression analysis indicated that the ACE D allele is an independent risk factor (odds ratio = 1.48, 95 % CI = 1.01-2.18, p < 0.05). In conclusion, the I/D polymorphism of ACE gene (carrying D allele) is an independent risk factor for CAD in the studied Turkish population.

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SUMMARYThe frequency of Brugada sign was found to differ among ethnic groups. Yet, there is no data regarding the prevalence of Brugada syndrome and sign in our country. The aim of this study was to determine the frequency of a Brugada-type electrocardiogram (ECG) pattern in southern Turkey.A total of 1238 subjects (males, 671, females, 567) were included in the study. The previously archived ECGs of 807 subjects without any evidence of structural heart disease were chosen randomly and evaluated. In addition, prospective analysis of the ECGs of 431 subjects (males, 293, females, 138) randomly chosen from healthy university students were also included. The mean age was 38.9 ± 17.6 years. Six subjects (0.48%) had a Brugada-type ECG pattern. One (0.08%) of them had the coved-type and 5 (0.40%) had the saddleback-type. All subjects were asymptomatic.A Brugada-type ECG pattern was obtained in 1 (0.17%) female and in 5 (0.74%) males (OR: 4.2 CI: 0.5-36.4, P = 0.2). The Brugada-type ECG pattern frequency was 0.12% in subjects ≥ 25 years old and 1.16% in subjects between 17-24 years old (OR: 9.4 CI: 1.1-81.2, P = 0.02). Young males between 17-24 years had the highest (1.70%) frequency.The results indicate that the frequency of the Brugada-type ECG pattern was 0.48% in the general population, being more prevalent in young males in our region. These results are similar to the findings of studies performed in other countries. (Int Heart J 2006; 47: 541-547)

Background. Arterial stiffness parameters in patients who experienced MACE after acute MI have not been studied sufficiently. We investigated arterial stiffness parameters in patients with ST segment elevation (STEMI) and non-ST segment elevation myocardial infarction (NSTEMI). Methods. Ninety-four patients with acute MI (45 STEMI and 49 NSTEMI) were included in the study. Arterial stiffness was assessed noninvasively by using TensioMed Arteriograph. Results. Arterial stiffness parameters were found to be higher in NSTEMI group but did not achieve statistical significance apart from pulse pressure (P = 0.007). There was no significant difference at MACE rates between two groups. Pulse pressure and heart rate were also significantly higher in MACE observed group. Aortic pulse wave velocity (PWV), aortic augmentation index (AI), systolic area index (SAI), heart rate, and pulse pressure were higher; ejection fraction, the return time (RT), diastolic reflex area (DRA), and diastolic area index (DAI) were significantly lower in patients with major cardiovascular events. However, PWV, heart rate, and ejection fraction were independent indicators at development of MACE. Conclusions. Parameters of arterial stiffness and MACE rates were similar in patients with STEMI and NSTEMI in one year followup. The independent prognostic indicator aortic PWV may be an easy and reliable method for determining the risk of future events in patients hospitalized with acute MI.

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SUMMARYMost cross-sectional and case-control studies indicate that an increased plasma total homocysteine (tHcy) level is an independent risk factor for coronary artery disease (CAD). However, this is still a controversial issue. Recently, it was reported that the level of tHcy is related to the extent and severity of CAD. This study was designed to investigate the relationship between plasma tHcy levels and the presence, extent, and severity of CAD.Three hundred and forty-one patients who underwent coronary angiography were included in the study. Of these patients, 195 had CAD and 146 had normal coronary arteries (control group). The mean tHcy level was found to be higher in patients with significant CAD (16.4 ± 7.4µmol/L vs 13.2 ± 3.6 µmol/L, P < 0.001). This group also had a higher rate of hyperhomocysteinemia (HHcy) (22.6% vs 5.5%, P < 0.001). There were positive relationships between tHcy levels and male gender (P = 0.03, r = 0.16), smoking (P < 0.001, r = 0.19), hyperlipidemia (P = 0.006, r = 0.15), and hypertension (P < 0.001, r = 0.20). Using regression analysis HHcy was determined to be an independent risk factor for CAD (OR = 3.69, CI 95% 1.51-9.06, P = 0.004). However, HHcy was not an independent risk factor in patients with low cardiovascular risk profiles. There was no relationship between the level of tHcy and the severity, extent, and vessel scores of CAD. On the other hand, age and diabetes mellitus were related with all scores of CAD.In conclusion, although hyperhomocysteinemia is an independent risk factor for CAD in our region, it appears to be unrelated to the extent and severity of the disease. (Jpn Heart J 2003; 44: 357-368)