Uğur Abbas Bal

Epicardial adipose tissue thickness by echocardiography is a marker for the presence and severity of coronary artery disease

BACKGROUND AND AIM Epicardial adipose tissue (EAT), which is thought to be a component of visceral adiposity, is associated with the metabolic syndrome. We aimed to test the hypothesis that echocardiographic EAT thickness can be a marker for the presence and severity of coronary artery disease (CAD). METHOD AND RESULTS In all, 150 patients (100 patients with CAD and 50 patients with normal coronary arteries by diagnostic coronary angiography; 65 women, 85 men; mean age 55.7+/-7.4 years) were enrolled. EAT thickness was measured using 2-D echocardiographic parasternal long- and short-axis views. EAT thickness measurements were compared with angiographic findings. EAT thickness was significantly higher in patients with CAD in comparison to those with normal coronary arteries (6.9+/-1.5 mm vs. 4.4+/-0.8 mm; P<0.001). Furthermore, EAT thickness increased with the severity of CAD (multivessel disease 7.4+/-1.2 mm vs. single vessel disease 5.7+/-1.7 mm; P<0.001). Gensinis score significantly correlated with EAT thickness (r=0.600, P<0.001). EAT thickness of > or = 5.2 mm had 85% sensitivity and 81% specificity (ROC area 0.914, P<0.001, 95% CI [0.86-0.96]) for predicting CAD. CONCLUSION EAT thickness, which is easily and non-invasively evaluated by transthoracic echocardiography, can be an adjunctive marker to classical risk factors for the prediction of CAD.

Prevention of contrast-induced impairment of renal function by short-term or long-term statin therapy in patients undergoing elective coronary angiography

A decline in kidney function after contrast exposure is associated with a high risk of morbidity and mortality during hospitalization and over long-term periods. Several retrospective and recent prospective clinical trials have shown that statin therapy might prevent contrast-induced nephropathy in patients undergoing percutaneous coronary intervention. In this study, we aimed to assess the effects of statin therapies on renal function parameters in patients undergoing elective coronary angiography. One hundred and sixty patients undergoing elective coronary angiography were randomized equally into two groups: atorvastatin 40 mg/day group (statin started 3 days before coronary angiography) and an untreated control group. An additional 80 patients were included as a chronic statin therapy group. Serum creatinine, serum cystatin C, and glomerular filtration rate (GFR) were measured before and 48 h after coronary angiography. Cockcroft–Gault and Modification of Diet in Renal Disease (MDRD) equations were used to determine GFR. After coronary angiography, serum creatinine and GFR determined by MDRD were significantly better in patients using atorvastatin than those in controls (P = 0.002 and P = 0.004, respectively). Postprocedure serum creatinine, cystatin C, and GFR determined by MDRD were also significantly better in chronic statin therapy group than those in controls (P = 0.006, P = 0.003, and P = 0.004, respectively). There were no differences in renal function parameters between the short-term atorvastatin group and the chronic statin therapy group. Our data demonstrate that the use of short-term atorvastatin and chronic statin therapy may have a role in protecting renal function after elective coronary angiography.

Value of Stress Myocardial Perfusion Scanning in Diagnosis of Severe Coronary Artery Disease in Liver Transplantation Candidates

BACKGROUND The significant potential for perioperative and late cardiovascular complications makes careful preoperative cardiac risk assessment imperative in liver transplantation candidates. OBJECTIVE To determine the sensitivity and specificity of myocardial perfusion scanning for detection of coronary artery disease (CAD) in liver transplantation candidates. PATIENTS AND METHODS We prospectively evaluated 93 liver transplantation candidates. Patients with known CAD were excluded. All patients, regardless of symptoms and risk factors, underwent myocardial perfusion scanning and coronary angiography. RESULTS Results of myocardial perfusion scanning were abnormal in 64 patients (68.8%) and normal in 29 patients (31.2%). Of patients with abnormal scans, only 6 (9.4%) had severe CAD at coronary angiography. None of the 29 patients with normal perfusion scans and the 24 patients with fixed defects had severe CAD; however, 6 of 40 patients (15.0%) with reversible perfusion defects had severe CAD at coronary angiography (P = .005). Alcoholic liver disease, reversible perfusion defects at myocardial perfusion scanning, left ventricular systolic dysfunction, and higher low-density lipoprotein (LDL) cholesterol and triglyceride levels were significantly associated with CAD. Defining reversible perfusion defects as a sign of ischemia, and fixed defects and normal perfusion as nonischemic, myocardial perfusion scanning had 100% sensitivity but 61% specificity for severe CAD. The tests accuracy was low (38%). CONCLUSIONS The results of reversible perfusion defects on myocardial perfusion scanning were sensitive but not specific for CAD in liver transplantation candidates. The high number of false-positive results decreased the tests accuracy.

Incidence of Aspirin Resistance and Its Relationship With Cardiovascular Risk Factors and Graft Function in Renal Transplant Recipients

BACKGROUND Aspirin (ASA) is frequently used to prevent cardiovascular events and improve renal graft function after renal transplantation. Clinical studies have demonstrated that decreased responsiveness to ASA therapy is associated with an increased risk of atherothrombotic events. However, no clinical trial to date has evaluated the incidence and clinical importance of ASA resistance among renal transplant recipients. AIM To assess the incidence of ASA resistance and its association with cardiovascular risk factors (CRF) and renal graft function after renal transplantation. METHODS We prospectively included 40 patients undergoing living related donor renal transplantation using ASA (80 mg/d) in the study. ASA resistance was defined using a platelet function analyzer (PFA-100). Glomerular filtration rate (GFR) was measured by postoperative Tc-99m diethylenetriaminepentaacetic acid renal scintigraphy. We investigated the incidence of ASA resistance and its relationship to CRF and renal graft function. RESULTS ASA resistance was noted in 11 patients (27.5%). The demographic characteristics of the patients were similar in both groups (P > .05). Compared with patients in the ASA-sensitive group, patients in the ASA-resistant group showed significantly higher total cholesterol, low-density lipoprotein cholesterol, triglyceride, C-reactive protein, and fibrinogen levels and lower GFRs (44 +/- 21 mL/min vs 63 +/- 26 mL/min, P = .03). The incidence of ASA resistance was higher among patients with GFRs < 60 mL/min compared with those with a GFR >or= 60 mL/min (10% vs 1%; P = .012). CONCLUSION ASA resistance is associated with higher lipid levels and inflammatory and thrombotic cardiovascular risk factors and lower GFRs in renal transplant recipients.

Coronary anatomy, anatomic variations and anomalies: a retrospective coronary angiography study.

INTRODUCTION The incidence of coronary artery anomalies (CAAs) varies from 0.2% to 8.4%. Knowledge of such anatomical variations is important as coronary procedures are regularly performed these days. We aimed to find the coronary dominance pattern, intermediate artery (IMA) frequency and CAA incidence in our clinic, and compare them to those in the literature. METHODS The medical reports of 5,548 patients who had undergone coronary angiography (CAG) between 2005 and 2009 were retrospectively investigated. Dominance pattern and presence of IMA and CAA were recorded. CAAs were described using two different classifications: Angelini and Khatamis classification, and a new modified classification that was derived from Angelini and Khatamis classification. Some procedural details and clinical features of the patients with CAA were also investigated. RESULTS Coronary dominance pattern was: 81.6% right coronary artery, 12.2% circumflex artery and 6.2% co-dominant. IMA was present in 613 (11.0%) patients. The incidences of overall anomaly were 2.7% and 1.4%, according to the different classifications. Absent left main coronary artery, which was the most common anomaly in the present study, was found in 51 (0.9%) patients. Incidences of myocardial bridge, coronary arteriovenous fistulae and aneurysms were 1.1%, 0.2% and 0.3%, respectively. CONCLUSION CAAs are generally asymptomatic, isolated lesions. Some may lead to anginal symptoms, myocardial infarction or sudden death. We found that CAA was associated with increased radiation and contrast exposure in patients who underwent CAG. This risk could be reduced if appropriate catheters were designed and training programmes on ostial cannulation were developed.

Differential influence of vitamin D analogs on left ventricular mass index in maintenance hemodialysis patients.

Purpose Secondary hyperparathyroidism (SHPT) is a common feature in maintenance hemodialysis (MHD) patients. Inadequate treatment of SHPT has been associated with cardiovascular complications, and vitamin D therapy might influence the development of cardiovascular diseases. In the present study, we aimed to evaluate the effects of intravenous paricalcitol and calcitriol treatments on left ventricular mass index changes in MHD patients. Methods We conducted an observational study with a 12-month follow-up duration to compare the outcomes of intravenous paricalcitol and calcitriol treatments in MHD patients. Eighty patients with moderate to severe SHPT were enrolled in the study. All the patients had normalized total serum Ca concentration <10.5 mg/dL, serum calcium-phosphorus product (Ca × P) <75, and parathyroid hormone level (PTH) level ≥300 pg/mL at the begining of the follow-up period. Results The patients were divided into a paricalcitol group (n = 40) and a calcitriol group (n = 40). The demographic, clinical, and biochemical characteristics of the patients were similar at baseline. We observed significantly superior control of SHPT; lesser frequency of hypercalcemia and hyperphosphatemia, and Ca × P level elevations; and interruption of vitamin D treatment in the paricalcitol group. Moreover, we found no significant change in left ventricular mass index in the paricalcitol group, but found a significantly increased left ventricular mass index in the calcitriol group during the follow-up period (from 136.6 ± 35.2 g/m2 to 132.9 ± 40.4 g/m2 vs. from 137.2 ± 30.1 g/m2 to 149.4 ± 31.0 g/m2; p<0.044). Conclusion We observed that, compared with calcitriol therapy, paricalcitol therapy reduced the PTH concentrations more effectively without causing hypercalcemia and hyperphosphatemia and might have a substantial beneficial effect on the development of left ventricular hypertrophy.

The clinical importance of laboratory-defined aspirin resistance in patients presenting with non-ST elevation acute coronary syndromes.

In this study, we aimed to assess the factors associated with laboratory-defined aspirin resistance and the relationship of this laboratory-defined aspirin resistance with thrombolysis in myocardial infarction risk score, markers of cardiac necrosis, and inflammatory and thrombotic risk factors in patients with unstable angina or non-ST elevation myocardial infarction. Ninety-seven patients who were under aspirin therapy and hospitalized with unstable angina/non-ST elevation myocardial infarction were included in the study. Laboratory-defined aspirin sensitive and resistant groups were determined by platelet function analyzer; aspirin resistance was defined as collagen/epinephrine closure time less than 165 s. Laboratory-defined aspirin resistance was noted in 29 patients (29.9%), and non-ST elevation myocardial infarction was observed in 46 patients (47.4%). Patients in the group with laboratory-defined aspirin resistance had significantly higher thrombolysis in myocardial infarction risk scores (P < 0.001). When the details of cardiac myonecrosis markers were compared, baseline and follow-up creatine kinase-myocardial band and troponin I values were higher in laboratory-defined aspirin-resistant group. Multivariate analyses revealed that laboratory-defined aspirin resistance was an independent predictor of non-ST elevation myocardial infarction (P = 0.022). Laboratory-defined aspirin resistance is associated with non-ST elevation myocardial infarction, higher markers of cardiac necrosis and thrombolysis in myocardial infarction risk score in patients hospitalized with unstable angina/non-ST elevation myocardial infarction.

Assessment of biochemical aspirin resistance at rest and immediately after exercise testing

Some aspirin-treated patients experience thromboembolic events, a phenomenon termed ‘aspirin resistance’, which may be clinical or biochemical by definition. Physical exercise is known to enhance platelet secretion and aggregability. To evaluate the presence of biochemical aspirin resistance at rest and immediately after exercise in individuals with stable coronary artery disease or coronary artery disease risk factors. We prospectively enrolled 101 patients who had received 100 or 300 mg/day enteric-coated aspirin for at least 7 days. Biochemical aspirin resistance (defined as normal collagen-epinephrine closure time < 165 s) was studied using the standardized platelet function analyzer. Of the 101 patients, 63 were aspirin sensitive both at rest and immediately after exercise, 18 exhibited biochemical aspirin resistance both at rest and after exercise, and 20 were aspirin sensitive at rest but exhibited biochemical aspirin resistance immediately after exercise. The results of exercise testing were similar in all three groups (each P > 0.05). Our results indicate that in almost 20% of the patients, aspirin did not seem to protect against exercise-induced platelet activation, despite the presence of aspirin sensitivity at rest. We did not, however, determine the extent to which the biochemical aspirin resistance noted in our study applied to clinical events.

Effects of Carvedilol Compared to Nebivolol on Insulin Resistance and Lipid Profile in Patients With Essential Hypertension.

Background and aim: Beta-blockers have unfavorable effects on metabolic parameters in hypertensive treatment. New generation beta-blockers with vasodilatory capabilities are superior to traditional beta-blockers, but studies examining their effects on metabolic parameters are still lacking. This study aimed to compare the effects of 2 new generation beta-blockers, carvedilol and nebivolol, on insulin resistance (IR) and lipid profiles in patients with essential hypertension. Methods: This was a prospective, randomized, open-label, single-center clinical trial. A total of 80 patients were randomized into 2 groups: the carvedilol group (n = 40, 25 mg of carvedilol daily) and the nebivolol group (n = 40, 5 mg of nebivolol daily). Follow-up was performed for 4 months. Fasting plasma glucose, insulin levels, and the lipid profile (high-density lipoprotein [HDL], low-density lipoprotein [LDL], total cholesterol, triglyceride, apolipoprotein AI, and apolipoprotein B levels) were measured and IR was calculated by the homeostasis model assessment (HOMA) index. These variables were compared before and 4 months after treatment. Results: Blood pressure and heart rate were significantly and similarly reduced in the carvedilol and nebivolol groups after treatment compared to those before treatment (both P < .001). Serum glucose (P < .001), insulin (P < .01), HOMA-IR (P < .01), HDL (P < .001), LDL (P < .001), total cholesterol (P < .001), and apolipoprotein B (P < .05) levels decreased in a similar manner in the carvedilol and nebivolol groups after treatment compared to those before treatment. Serum triglyceride and apolipoprotein AI levels did not change after treatment with both drugs. Conclusion: New generation beta-blockers, carvedilol and nebivolol, efficiently and similarly decrease blood pressure. They have similar favorable effects on glucose, insulin, IR, and the lipid profile.

Treatment-associated change in apelin concentration in patients with hypertension and its relationship with left ventricular diastolic function

Objective: We examined the change in apelin concentration and its relationship with left ventricular diastolic function in patients treated for hypertension. Methods: Ninety treatment-naive patients with newly diagnosed hypertension and 33 age- and sex-matched control subjects were prospectively enrolled. Patients with hypertension were randomized to treatment either with telmisartan 80 mg or amlodipine 10 mg. Apelin concentration was measured and echocardiography was performed at baseline and after 1 month of treatment. Results: The data of 77 patients and 33 controls were analyzed. Mean age, gender, baseline blood pressure, apelin levels, and echocardiographic measurements were similar between the treatment groups (p>0.05 for all). Apelin concentration was significantly lower in patients with hypertension than in controls. There was a significant increase in apelin level after 1 month of treatment in both groups (0.32±0.17 vs. 0.38±0.17 ng/dL in telmisartan group, p=0.009, and 0.27±0.13 vs. 0.34±0.18 ng/dL in amlodipine group, p=0.013). Diastolic function improved significantly in both groups (p<0.05) but was not significantly associated with change in apelin concentration. Conclusion: Apelin concentration increased significantly after 1 month of effective treatment with telmisartan or amlodipine to a similar extent. Change in apelin concentration was not associated with improvement in diastolic function.