The transthoracic echocardiographic determination of the color M-mode propagation velocity of the descending aorta is a simple practical method and correlates well with the presence of carotid and coronary atherosclerosis and brachial endothelial function.

P-wave duration and PWD increase progressively in accordance with the progression of mitral stenosis.

Downregulation of glucose and fatty acid oxidation occurs in heart failure (HF). Trimetazidine reduces fatty acid oxidation and increases glucose oxidation. In this single-blind study, trimetazidine, 20 mg three times per day (n = 51) or placebo (n = 36) was added to treatment of 87 HF patients receiving optimal HF therapy. Etiology of heart failure was coronary artery disease in 35 patients (68.6%) in the trimetazidine group and 22 (62.9%) in the placebo group. Fourteen (27.5%) patients in the trimetazidine group and 11 (31.4%) patients in the placebo group had diabetes. Peak systolic velocity (Vs), and the peak early diastolic (Vd) and late diastolic (Va) velocities of various segments left and right ventricles (RV) were obtained with tissue Doppler imaging (TDI) and averaged. Patients were re-evaluated three months later. Significant increases in mean left ventricular ejection fraction (LVEF) (33.3% +/- 5.6% to 42.4% +/- 6.3%, P < 0.001 and 30.6% +/- 8.2% to 33.2% +/- 6.6%, P = 0.021) and LV and RV myocardial velocities and mitral and tricuspid annular TDI velocities were observed in both groups. However, compared to placebo, increments in LVEF (9.1% +/- 4.2% vs. 2.5% +/- 1.4%, P < 0.001) and myocardial velocities were significantly higher with trimetazidine (P < 0.001 for LV Vs, Vd, Va; P = 0.035 for RV Vd; and P < 0.001 for RV Va and Vs). Increase in LVEF with trimetazidine was significantly correlated with presence of diabetes (r = 0.524, P < 0.001). With trimetazidine LVEF increased significantly more in diabetic patients compared to nondiabetics (P < 0.001). Also, patients having both diabetes and ischemic HF tended to have greater improvement in LVEF compared to ischemic HF patients without diabetes (P = 0.063). Addition of trimetazidine to current treatment of HF, especially for those who are diabetic, may improve LV and RV functions.

Abstract:Background: Microvascular and endothelial dysfunction have been implicated for coronary slow flow (CSF). Nebivolol, besides its beta-receptor blocking activity, causes an endotheliumdependent vasodilatation through increased nitric oxide release. Methods: This study included 27 patients with CSF and 27 subjects with normal coronary arteries. Segmental functions of the left ventricle (LV) were assessed using myocardial tissue Doppler velocities before and 3 months after treatment with nebivolol 5 mg/day. Results: Compared with the control group, mitral deceleration time (DT) was significantly longer, and E/A ratio, systolic velocity of lateral mitral annulus (S m ) and regional myocardial peak systolic and early diastolic velocities (V s , V d ) were significantly lower in patients with CSF. The reason for coronary angiography was typical angina in 21 (77.8%) and positive treadmill test in six (22.2%) CSF patients. There were significant correlations between presence of CSF in left anterior descending artery (LAD) with S m (r ¼ À0.404, p ¼ 0.002) and V s in anterior (r ¼ À0.531, p < 0.001) and lateral (r ¼ À0.495, p < 0.001) segments and between presence of CSF in RCA and V s in posterior segments (r ¼ À0.501, p < 0.001). Treatment with nebivolol significantly decreased blood pressures (128.5±12.5/82.5±8.8 to 119.8±12.6/76.4±7.4 mmHg, p < 0.001), DT (252.3±53.6 to 222.0±41.0 ms, p < 0.001) and IVRT (115.7±19.9 to 103.3±17.0 ms, p < 0.001), and increased exercise capacity (8.7±1.3 to 10.4±0.9 METs, p < 0.001), E/A ratio (0.87±0.26 to 1.08±0.23, p < 0.001) and myocardial velocities (p < 0.001). All the patients were free of angina after treatment. Patients with CSF had impaired diastolic and regional LV functions. Conclusions: Nebivolol may therefore be useful in improving angina, exercise capacity and LV functions in patients with CSF.

Brucella endocarditis, a rare complication of brucellosis, is the main cause of death attributable to this disease. There are difficulties in the diagnosis and uncertainty regarding many aspects of the treatment of Brucella endocarditis. We retrospectively examined the clinical characteristics and outcome of patients diagnosed with Brucella endocarditis. Of the six patients diagnosed as having Brucella endocarditis, four had valvular disease, one had aortic and mitral mechanic valve prosthesis (AVR+MVR) and one had secundum type atrial septal defect. Transesophageal echocardiography showed vegetations in four patients. Blood culture grew Brucella mellitensis only in two patients. Standard agglutination tests were elevated in all patients (range 1/320-1/10240). Four patients were managed with combined antibiotherapy and surgery. One refused further treatment and one refused an operation and follow-up was lost for that patient. Two patients died during follow-up; one having had a previous AVR+MVR operation refused further treatment and the other suffering renal failure. Due to the fulminant course of the disease, treatment should be initiated when there is a clinical suspicion, even if the culture results are unknown or negative. Agglutination titres aid in the diagnosis. A combination of antibiotherapy and surgery seems to be preferable treatment modality.