Nevzat Uslu

Influence of weight loss on myocardial performance index

Obese patients may have a phase of asymptomatic left ventricular dysfunction. A combined myocardial performance index (MPI) has been demonstrated to be a useful index to estimate left ventricular function and to predict the prognosis of patients with heart failure. The objective of the study was to determine the influence of weight loss on MPI. A total of 18 obese patients (3 men, 15 women, mean age 49.6 ± 5.5 years, body mass index [BMI] >30 kg/m2) were investigated in the study. All patients were treated with a multidisciplinary approach consisting of a hypocaloric diet and orlistat therapy (120 mg three times daily), and all of them underwent two-dimensional and Doppler echocardiographic examination two times before starting the study and after a period of weight loss. Using echo-Doppler methods, ejection fraction, peak velocities of early (E) and late (A) diastolic filling, the E/A ratio, deceleration time (DT), isovolumic contraction time (IVCT), isovolumic relaxation time, ejection time, and MPI were measured. The MPI was obtained by subtraction ejection time from the interval between cessation and onset of the mitral flow. All patients lost at least 10% of their initial body weight, with a mean decrease of 10.8 ± 3.7 kg. This was associated with significant reductions in BMI with a mean decrease 4.5 ± 1.4 kg/m2. Compared with baseline, after weight loss the E/A ratio of 1.01 ± 0.22 before treatment increased to 1.17 ± 0.26 (P = 0.012), left ventricular mass index decreased from 88 ± 23 to 82 ± 19 g/m2 (P = 0.028), IVCT from 71 ± 20 to 53 ± 30 ms (P = 0.004), DT from 233.65 ± 38.14 to 196.72 ± 47.73 s (P = 0.004), and MPI from 0.63 ± 0.13 to 0.50 ± 0.13 (P = 0.0001). Weight loss ameliorates MPI and seems to be a clinically relevant measurement of left ventricular global function, and may prove to be a valuable tool in assessing the risk of developing heart failure.

High SYNTAX score predicts worse in-hospital clinical outcomes in patients undergoing primary angioplasty for acute myocardial infarction.

ObjectiveA high SYNTAX score (SXscore) is a predictor of adverse outcomes for stable and unstable coronary syndromes. We aimed to examine whether a high SXscore will determine in-hospital clinical outcomes in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention. MethodsA total of 646 (mean age 56.1±12.5; 516 males, 130 females) patients with STEMI undergoing a primary percutaneous coronary intervention were evaluated prospectively. The study population was divided into tertiles based on the SXscore values. A high SXscore (n=196) was defined as a value in the third tertile (>21.75), and a low SXscore (n=450) was defined as a value in the lower two tertiles (⩽21.75). Patients were followed up for in-hospital clinical outcomes. ResultsIn-hospital cardiovascular mortality occurred more in the high SXscore group than in the low SXscore group (10.7 and 2.4%, respectively, P<0.001). In a receiver-operating characteristic curve analysis, an SXscore value of 21.75 was identified as an effective cut point in STEMI for in-hospital cardiovascular mortality (area under curve=0.75, 95% confidence interval: 0.66–0.83, P<0.001). An SXscore value of more than 21.75 yielded a sensitivity of 66% and a specificity of 71.5%. A significant association was noted between a high SXscore level and the adjusted risk of in-hospital cardiovascular mortality (odds ratio: 3.92, 95% confidence interval: 1.1–13.9, P=0.03). ConclusionOur findings showed that patients with a high SXscore undergoing primary angioplasty for STEMI have a poor in-hospital survival, and that a high SXscore represents an independent risk factor for in-hospital cardiovascular mortality.

Accessory Mitral Valve Tissue: Report of Two Asymptomatic Cases

Accessory mitral valve tissue is a rare anomaly of embryologic development of the endocardial cushion and may cause substantial and progressive obstruction of the left ventricular outflow tract. Subaortic obstruction resulting from accessory mitral tissue is most likely due to systolic ballooning of the tissue into the outflow tract. The obstruction can occur in the early period of life as a result of mass effect or it can develop gradually due to the continued deposition of fibrous tissues within the left ventricular outflow tract. In patients with accessory mitral valve tissue, surgery is mandatory if there is a significant obstruction in the left ventricular outflow tract. We report two cases with accessory mitral valve tissue causing mild subaortic stenoses which did not require surgery.

Acute severe occlusion of the left main coronary artery following transcatheter aortic valve implantation.

exudate. Leucocyte count was 9.080/mm3, neutrophil count was 6.470/ mm3, pH 7.51 and adenosine deaminase level was 10 U/L (<40 U/L). The albumin and lactate dehydrogenase levels of pleural fluid were 3.3 g/dL (3.5-5 g/dL), and 365 U/L (240-480 U/L), respectively. Left sided pleural fluid with mild pericardial fluid was detected on computerized tomography. The pleural fluid was thought to be due to parapneumonic effusion, antibiotherapy and methylprednisolone were started. He was referred to our clinic in August 2010. He was investigated for possible diseases that lead to pleural effusion. His erythrocyte sedimentation rate (ESR) was 94 mm/h (0-20) and C-reactive protein (CRP) level was 24 mg/dL (0-0.5). Genetic analysis for Familial Mediterranean Fever mutation was negative. Antinuclear antibodies were negative. He did not have any sign of infection or systemic disease, alhough, he was still suffering from pleural and pericardial effusion. He used colchicine for 3 months but it did not make any difference. Amiodarone was discontinued because of its possible adverse effect. One month later there was no sign of pleural effusion on the chest X-ray, ESR and CRP levels were within normal ranges. Amiodarone is a widely used anti-arrhythmic drug. Several types of pulmonary diseases such as chronic interstitial pneumonitis, organizing pneumonia, acute respiratory distress syndrome (ARDS), pulmonary fibrosis may occur in patients receiving amiodarone therapy (1). The incidence of pulmonary toxicity associated with amiodarone ranges from 1% to 10% (2). A high cumulative dose, duration of therapy, age, preexisting lung disease and surgery are defined as potential risk factors for developing pulmonary toxicity among patients treated with amiodaroneinduced (1). It is speculated that amiodaroneinduced pulmonary toxicity can be due to direct toxic injury to lung cells or indirect immunologic reaction (1). It has been reported that amiodarone-induced pleural effusion may be accompanied by the lung parenchymal involvement (3). However, one-third of the patients may have only pleural fluid accumulation (3). Corticosteroids have beneficial effects in treatment of amiodarone-induced pulmonary toxicity (1). In our case, pleuro-pericardial effusion was the only manifestation of pulmonary toxicity without a preexisting lung parenchymal involvement. Therefore, in clinical practice, serositis findings in a patient receiving amiodarone can be ascribed to amiodarone after excluding other possible causes.

HIGH SYNTAX SCORE PREDICTS WORSE IN-HOSPITAL CLINICAL OUTCOMES IN PATIENTS UNDERGOING PRIMARY ANGIOPLASTY FOR ACUTE MYOCARDIAL INFARCTION

High Syntax Score (SXscore) is predictor of adverse outcomes for stable and unstable coronary syndromes. We aimed to investigate whether high Sxscore would estimate in-hospital clinical outcomes in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary

Successful treatment of a patient with pulmonary embolism and biatrial thrombus.

A 57-year-old male patient was presented to our emergency department with the complaint of dyspnea of 10 days duration. He was normotensive with a heart rate of 82 bpm and normal respiratory rate. Transthoracic echocardiography (TTE) showed right ventricular dilatation with mild tricuspid regurgitation. Pulmonary artery systolic pressure was 50 mmHg. There were mobile masses in both atria (Fig. 1 and Video 1. See corresponding video/movie images at www.anakarder.com). Transesophageal echocardiography (TEE) revealed worm-like, elongated, highly mobile thrombi in right atrium which was extending to the left atrium by crossing the patent foramen ovale (PFO). The free edges of the thrombus were prolapsing towards both the tricuspid and mitral valves to the right and left ventricles, respectively (Fig. 2-4 and Video 2-3. See corresponding video/movie images at www.anakarder.com). Thoracoabdominal computed tomography was performed for evaluation of pulmonary vasculature and if any underlying pathology such as renal cell carcinoma. It showed multiple filling defects of both branches of pulmonary artery. Ultrasound of lower extremity showed absence of thrombus. We had consulted with the cardiovascular surgeons and also discussed the possible complications of treatment modalities with the patient. The patient refused to have an operation so we decided to apply intravenous thrombolytic therapy and it was successfully administered. No thrombi or other cardiac masses were detected on TTE and TEE performed 2 days after thrombolytic treatment and patient had an unevent-