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In addition to the diagnostic performance, coronary computed tomography angiography (CTA) can give important data regarding the prognosis of coronary artery disease (CAD). In this study we aimed to evaluate the prognostic role of coronary CTA in patients with suspected CAD and mild-moderate coronary stenosis.A total of 1115 patients (602 male, 54%; age 58.4 ± 11.4) without previous CAD were enrolled. Patients underwent coronary CTA imaging using dual-source 64-slice CT scanner. For categorization of the coronary atherosclerotic plaques (CAP), the coronary system was divided into 16 separate segments. For each segment, CAPs were categorized as: calcified, noncalcified and mixed.During follow-up of 29.7 ± 13.2 months, cardiovascular events defined as ST segment elevation myocardial infarction (4 patients), non-ST segment elevation myocardial infarction (5 patients) and unstable angina pectoris (20 patients) requiring revascularization or hospital admission were recorded. Cox hazard regression analysis revealed an association between the severity of luminal stenosis (HR: 4.73, 95% CI: 1.36-16.47, p0.05) and extent (HR: 1.10, 95% CI: 1.00-1.22, p=0.051) and the adverse coronary events in the follow-up. Multivariate Cox hazard regression analysis revealed that nonobstructive (≤ 50%) lesions were the only factor causing increased probability of coronary events in the follow-up (HR: 4.77, 95% CI: 1.36-16.74, p0.05).The presence and severity of luminal stenosis shown by coronary CTA were associated with prognosis of coronary events in the follow-up. These results may improve the risk stratification in patients evaluated by coronary CTA and provide strategies for the individualized prevention programs.

There is controversy regarding the role of family history (FH) of premature coronary artery disease (CAD) as an independent risk factor for CAD. Herein, we aimed to assess the role of FH of premature CAD in prediction of coronary atherosclerosis shown by multidetector computed tomography (MDCT) coronary angiography.We analyzed consecutive subset of 349 patients in whom MDCT coronary angiography was performed for suspected CAD. All patients underwent coronary MDCT imaging using dual-source MDCT scanner. Coronary arteries were evaluated on 16-segment basis, critical CAP was described as luminal narrowing50%, whereas plaque morphology was assessed on per segment basis.Study population consisted of 202 (57.9%) male and 147 (42.1%) female patients with mean age of 57.8 ± 10.8 years. The presence of CAP was higher in patients with FH of premature CAD in LAD and Cx compared to patients without FH of premature CAD (70.8% vs 58.0%, p=0.013 for LAD; 42.3% vs 30.4%, p=0.021 for Cx; 34.5% vs 29.8%, p=0.348 for RCA).In multinominal logistic regression analysis age, male gender, dyslipidemia and FH of premature CAD seemed significant predictors of primarily noncalcified CAP(OR:1.17, 95% CI:1.07-1.15, p0.001; OR:0.19, 95% CI:0.09-0.38, p0.001; OR:2.26, 95% CI:1.21-4.24, p=0.01; OR:3.32, 95% CI:1.74-6.34, p0.001 respectively) after adjustment for other risk factors.Our study results indicate that FH of premature CAD is associated with severity, extent and noncalcified CAP shown by MDCT. Further investigation is needed to clarify the exact diagnostic and prognostic role of MDCT coronary angiography in subjects with positive FH and suspected CAD.

Human epicardial adipose tissue (EAT) is a type of visceral adipose tissue functioning as a metabolically active endocrine organ by secreting several hormones and adipocytokines. In this study, we aimed to assess the relationship between EAT measured by dual source multidetector computed tomography (MDCT) and the presence and components of metabolic syndrome (MS).A total of 83 patients (43.4% male, mean age 56.1 ± 11.9) who underwent MDCT for suspected coronary artery disease were enrolled in this study. Thickness of the EAT was measured on contrast enhanced multiplanar reformat images with parasternal short axis view at basal, mid-ventricular and apical levels and horizontal long axis view.The mean EAT thickness was significantly increased in patients with MS compared to those without MS (8.49 ± 1.43 mm vs 7.39 ± 2.10 mm, p0.001). Additionally there was a graded relationship between increasing number of MS components and mean total EAT and pericoronary fat thickness (p0.05). Simple regression analysis revealed that the presence of MS, age and body mass index (BMI) were correlated with mean EAT thickness (r=0.398, r=0.376 and r=0.371 respectively, p0.001). Multiple regression analysis revealed that the presence of MS, age and BMI were the strongest independent variables related to EAT.In this study we demonstrated that EAT and pericoronary fat thickness were associated with the presence of MS. Those findings may implicate that, EAT and pericoronary fat may be a novel and useful indicator for MS.

Methods: A 63-year-old-woman was admitted to the emergency department with complaints of palpitation, breathlessness and dizziness. At the admission she was conscious and her systolic blood pressure was 80mmhg. At the ECG there was sustained ventricular tachycardia (Figure 1). In the ED, because of hemodynamic impairment, defibrillation with 30 j was performed and sinus rhythm was restored. After 600mg loading dose of amiodorone, intravenous maintenance therapy was continued. At the same hour two non-sustained ventricular tachycardia attacks happened. Her biochemical parameters demonstrated a potasium concentration of 2.8mmol/L, creatinine 0.8mg/dl (0.72–1.25) and sodium 137mmol/L (136–145). Transthoracic echocardiography was performed and ejection fraction was found 60% and other measurements were normal. 60mEq/L potassium replacement was given to the patient and the control potassium was 3.7mmol/L. The patient had been using amlodipine 10mg, indapamide 1.5mg and acetylsalicylic acid 100mg per day for ten years because of hypertension. The patient was complaining from intermittent chest pain so coronary angiography was performed and normal coronary arterial anatomy was observed. It was thought that VT had occurred because of hypokalemia induced by indapamide so indapamide treatment was stopped. The K was 4.5mmol/L after one week follow up. The patient was followed-up in the coronary care unit and was discharged on the eighth day of admission without any VT attacks. Conclusions: Clinicians should keep in mind that the antihypertensive drug indapamine can cause life threatening ventricular tachycardias because of its hypokalemia side effect. Therefore we emphasize that serum potassium and ECG must be carefully monitored during indapamide therapy.

LA thrombus prior to DC cardioversion were identified from our department. A CHA2DS2-VASc score was calculated for each patient. 3D TEE examination were performed for the presence of LA thrombus and LAA volume evaluation. Results: The mean CHA2DS2-VASc score was 3.7±1.5. among 64 patients with nonvalvular atrial fibrillation only 32% had been taken oral anticoagulants. From all patients 81.8% of patients with stroke were under 65 years old. Hypertension was present in 81%, diabetes mellitus in 32%, CAD in 20%, Stroke in 25%, PAH in 12%, and congestive heart failure was present in 21% of patients with AF. The mean LAA volume (3mm) was 9.3±2.6. A significant association was present between CHA2DS2-VASc score and LAA volume (p < 0.001). There were 5 patients with low CHA2DS2VASc score (0–1), 37 patients with intermediate score (2–4), and 22 patients with high (5–9) score. The volume of LAA in low, intermediate and high CHA2DS2-VASc score groups was 8.8±1.1, 8.7±2.3, 10.8±2.6, respectively. Conclusion: High CHA2DS2-VASc score is significantly associated with LAA volume in patients with non valvular AF.

Objective: Alport syndrome (AS) is a rare inherited disorder characterized by involvement of the kidneys because of the defect in the genes encoding a connective tissue protein, one of several subunits of collagen (particularly type IV) ultimately leading to renal failure at an early age. Cardiac involvement have been reported rarely which most commonly includes conduction system abnormalities. Valvular abnormalities in AS have not been reported previously. In our case, concomitant occurrence of previously unreported AS with MVP may be due to mutation at the level of collagen synthesis. Also single coronary ostium may contribute to this association coincidentally. Methods: A 23-year-old female with chronic renal failure because of Alport syndrome (AS) consulted for cardiac evaluation before renal transplantation. She described dyspnea with minimal effort and atypical chest pain. Past medical history includes AS, hypertension and chronic renal failure for 4 years. She was taking carvedilol and amlodipine for hypertension.