The presence and the duration of obesity were associated with impairment of subclinical biventricular systolic and diastolic function. These findings have the potential to increase awareness of subclinical cardiac manifestations in patients with isolated obesity and influence their early management.

Previous studies revealed that there were various mutations on endothelial nitric oxide synthase (eNOS) gene and these mutations might be a risk factor for coronary artery disease (CAD), myocardial infarction (MI), and hypertension (HT). In this study, we aimed to investigate the relationship between eNOS gene polymorphism (T-786 C) and coronary artery disease in the Turkish population. Two hundred and eleven unrelated individuals (152 male, 59 female, mean age 59 years, range 27-85) whose angiographic examinations were performed in our hospital were enrolled into the study; 159 of these had angiographically determined coronary artery lesions (>or=50% stenosis at least in one vessel). Fifty-two individuals were free of coronary artery disease on their coronary angiography. The Gensini scoring system was used to determine the severity of the CAD. The polymerase chain reaction (PCR) method was used for genotyping the individuals. To determine the independent risk factors for coronary artery disease, multivariate logistic regression analysis was used. The variant distribution of the T-786 C polymorphism was as follows. For all individuals: TT 94 (44.5%), TC 88 (41.7%), CC 29 (13.8%); in CAD patients: TT 63 (39.6%), TC 73 (45.9%), CC 23 (14.5%); and in normal individuals: TT 31 (59.6%), TC 15 (28.8%), CC 6 (11.5%). There was a statistically significant difference in the variant distribution between CAD and normal individuals (P<0.05). On the other hand, when we compared the frequency of the at-least-one-C-allele carriers (CC+TC, dominant model) and TT homozygous, those with at least one C allele were more prevalent in CAD patients. The results were as follows. In coronary artery disease patients: CC+TC 96 (60.4%), TT 63 (39.6%); in normals: TC+CC 21 (40.4%), TT 31 (59.6%) (P<0.01). When we compared the allele distribution (T vs C, additive model) between CAD patients and normal controls, the results were as follows: T 0.625 vs 0.740, C 0.375 vs 0.260; there was also a statistically significant association between CAD and C allele (P<0.05). When we compared the means of the Gensini scores between each genotype of the T-786 C mutation, there was a statistically significant difference. The results were TT (48.6+/-37.3, median 43.0), TC (55.4+/-41.2, median 41.0), CC (77+/-43.6, median 80.0) (P<0.05). Multivariate logistic regression analysis revealed that C-dominant (CC+TC) individuals had 2.9-fold more likelihood to suffer from CAD (odds ratio: 2.902; confidence interval: 1.272-6.622) (P<0.05). We conclude that the T-786 C polymorphism of eNOS gene might be a risk factor for coronary artery disease in the Turkish population.

After successful percutaneous coronary interventions (PCI), elevations of cardiac enzymes are not rare, but it is still not clear whether those elevations are associated with adverse late outcome. The purpose of the study was to investigate the relation between cardiac troponin I (cTn-I) increase after successful percutaneous intervention and late outcome. The study consisted of 100 consecutive patients (mean age 56 +/-9.8, 84% male) who had successful elective coronary balloon angioplasty with or without stent implantation. Patients with stable angina (n=54) and unstable angina (n=46) were included in the study. Blood samples for measurement of cTn-I were taken before and immediately after the procedure, and every 6 hours for the first 24 hours. Patients with preprocedural cTn-I elevation were excluded from the study. Postprocedural cTn-I elevation was detected in 34 patients (34%, troponin (+) group) and cTn-I levels were normal in 66 patients (66%, troponin (-) group). Logistic regression analysis showed that intervention in patients with unstable angina, stent implantation following balloon dilation, and maximal inflation pressure were the predictors of cTn-I elevation (p=0.035, p=0.038, and p=0.014, respectively). During the prospective follow-up period for 21 +/-7.5 months, the incidence of major cardiac events including recurrent angina, acute myocardial infarction, death, and revascularization were not different in patients with and without cTn-I elevation. Overall, major cardiac events occurred in 9 patients (26%) in the troponin (+) group and in 13 patients (20%) in the troponin (-) group. Kaplan-Meier survival analysis showed that cTn-I elevation was not an important correlate of overall cardiac events (log-rank: 1.66, p=0.19). The authors conclude that postprocedural cTn-I elevation is related to unstable angina, stent implantation following predilation, and inflation pressure, and there is no association with minor myocardial injury occurring after successful percutaneous coronary intervention and late adverse cardiac events.

SUMMARYLeft atrial (LA) function is associated with left ventricular (LV) diastolic filling and cardiac output response to exercise. But the relation between LA function and exercise performance has not been adequately evaluated.The aim of this study was to investigate the relation between LA function and exercise capacity in dilated cardiomyopathy (DCM) with cardiopulmonary exercise testing.Forty-four patients with a left ventricular end-diastolic dimension (LVDd) ≥ 60 mm and an ejection fraction (EF) ≤ 40%, and in normal sinus rhythm were included in this study. Patients were divided into group 1 and group 2 according to their exercise peak oxygen uptake (VO 2 ) (group 1: peak VO 2 >14 mL/kg/min, group 2: peak VO 2 ≤ 14 mL/ kg/min). LA function indices were defined as follows: LA end-systolic diameter (LASd), end-diastolic diameter (LADd), LA systolic volume (LASV), LA diastolic volume (LADV), LA ejection volume (LAEV), and LA ejection fraction (LAEF).LASd, LADd, LASV, and LADV were significantly increased in group 2 (P < 0.001, P < 0.001, P < 0.05, P < 0.005). Group 1 had significantly higher LAEF (P < 0.001 ) and LVEF (P < 0.05). Group 2 had significantly shorter exercise duration, and decreased anaerobic threshold levels and minute ventilation volumes (P < 0.001, P < 0.001, P < 0.005 ). There was a positive correlation between peak VO 2 and LVEF (r = 0.46, P = 0.002), and LAEF (r = 0.61, P < 0.001), peak A wave velocity (r = 0.39, P = 0.009), E wave deceleration time (r = 0.56, P < 0.001), and isovolumic relaxation time (IVRT) (r = 0.35, P = 0.04). There was a negative correlation between peak VO 2 and LASd (r = -0.53, P < 0.001) LADd (r = -0.59, P < 0.001), LASVI (r = -0.34, P = 0.027), LADVI (r = -0.37, P = 0.001), and the E/A ratio (r = -0.41, P = 0.006), Decreased LAEF and increased LA sizes were associated with decreased peak VO 2 . The results clearly demonstrate that LA functions at rest are related to exercise performance in patients with heart failure. (Int Heart J 2005; 46: 123-131)

Elevated NLR and increased LVESD were independent prognostic factors in predicting persistent LV dysfunction in patients with PPCM. The NLR might assist in identifying high risk patients with PPCM.

SUMMARYCoronary artery ectasia (CAE) is characterised by irregular, diffuse, saccular, or fusiform dilatation of the coronary arteries. Although the underlying mechanisms are not fully understood, CAE is considered to be an original form of vascular remodelling in response to atherosclerosis. However, it is not clear why some patients develop CAE while most do not. Experimental data suggest that activation of the renin angiotensin system may lead to an increased inflammatory response in the vessel wall or to an activation of matrix metalloproteinases. In addition, an insertion/deletion (ID) polymorphism of angiotensin converting enzyme (ACE) has been associated with coronary vascular tone and the development of aneurysms. Accordingly, we hypothesised that the gene polymorphism of ACE may be a potential factor influencing the genesis of CAE. We retrospectively evaluated 112 patients who underwent coronary angiography. ACE ID genotype was determined in two groups of patients. Group 1 consisted of 56 patients who were found to have CAE. Group 2 consisted of 56 patients with significant coronary artery disease (CAD) (> 50% stenosis in any of the major epicardial coronary arteries or their branches) but without any evidence of coronary ectasia. Polymerase Chain Reaction (PCR) was used to detect ACE genotype. The ratio of DD genotype was found to be greater in group 1 than group in 2 (39% versus 18%, respectively, P < 0.05). When assessed according to the presence of the I allele, it was greater was greater in group 2 than in group 1 (82.1% versus 60.7%, respectively, P < 0.05). The results indicate that an ACE DD genotype may be a risk factor for CAE. (Int Heart J 2005; 46: 89-96) Key words: Coronary artery ectasia, ACE genotype, Coronary artery disease IN addition to major and predisposition risk factors, the roles of the nontraditional risk factors are the current subjects of study in cardiology. One of these risk factors being studied is ACE ID genotype.

This report sought to compare live/real-time three-dimensional transesophageal echocardiography (3D-TEE) with two-dimensional transesophageal echocardiography (2D-TEE) and to determine whether there are advantages to using 3D-TEE on patients with pulmonary stenosis (PS). Sixteen consecutive adult patients (50 % male and 50 % female; mean age 33 ± 13.4 years) with PS and indications of TEE were prospectively enrolled in this study. Following this, initial 2D-TEE and 3D-TEE examinations were performed, and 3D-TEE images were analyzed using an off-line Q-lab software system. Finally, the 2D-TEE and 3D-TEE findings were compared. In the present study, 3D-TEE allowed us to obtain the en face views of pulmonary valves (PVs) in all but one patient. While this patient was without a PV due to a previous tetralogy of Fallot operation, we could detect the type of PV in the other 15 (93.7 %) patients by using 3D-TEE. Due to poor image quality, the most stenotic area was not measurable in only one (6.2 %) of the patients. In eight (50 %) of the patients, severity and localization of stenosis were more precisely determined with 3DTEE than with 2D-TEE. The PVs' maximal annulus dimensions were found to be significantly larger when they were measured using 3D modalities. This study provides evidence of the incremental value of using 3D-TEE rather than 2D-TEE during assessments of PS, specifically in cases where special conditions (pregnancy, pulmonary regurgitation, and concomitant atrial septal defects) cause recordings of the transvalvular peak gradient to be inaccurate. Therefore, 3D-TEE should be used as a complementary imaging tool to 2D-TEE during routine echocardiographic examinations.

Background: In our study, we assessed the effect of glycoprotein (GP) IIb/IIIa receptor inhibition on microvascular flow after acute coronary occlusion using the early sum of ST segment resolution in electrocardiography. Platelets may play a major role in the dissociation of epicardial artery recanalization and tissue level reperfusion, referred to as the ‘no-reflow phenomenon’. Therefore, GP IIb/IIIa receptor inhibition might improve myocardial reperfusion, distinct from its effects on epicardial patency. Methods and Results: One hundred and fifteen patients (mean age 57.7 ± 12.2 years, 96 males, 19 females) with ≤12-hour acute ST segment elevation myocardial infarction who underwent successful primary percutaneous coronary intervention were retrospectively enrolled into the study. Patients were grouped according to whether they received tirofiban therapy or not. Clinical and electrocardiographic parameters were evaluated. The first sum of ST segment elevation amounts in millimeters was obtained immediately before angioplasty and the second 60 min after restoration of thrombolysis in myocardial infarction III flow. The difference between the two measurements was accepted as resolution of the sum of ST segment elevation and expressed as ΣSTR. There were no significant differences between the groups regarding age, gender, cardiovascular risk factors, and laboratory parameters, duration from angina onset to the emergency unit, and from door to angioplasty. ΣSTR was higher in patients who received tirofiban than in those who did not (7.2 ± 2.8 and 4.2 ± 2.6 mm, respectively; p < 0.001). There was a significant and positive correlation between GP IIb/IIIa inhibition and ΣSTR (r = 0.336, p < 0.001), as well as between ejection fraction and ΣSTR (r = 0.310, p < 0.001). GP IIb/IIIa inhibition was the only independent determinant of ΣSTR in a multivariate linear regression model which contains 10 variables (p < 0.001). The incidence of in-hospital post-myocardial infarction refractory angina, reinfarction, and heart failure was significantly lower in the tirofiban group (p < 0.05, p < 0.05, and p < 0.05, respectively). Additionally, after 30 days, reinfarction and heart failure were lower in the tirofiban group (p < 0.05 and p < 0.05, respectively). Conclusions: It is well known that ΣSTR determines microvascular perfusion. This study shows that GP IIb/IIIa inhibition with tirofiban is of value in preserving microvascular perfusion after restoring coronary thrombolysis in myocardial infarction III flow.