Aims: To define which echocardiographic parameters are related to the degree of functional mitral regurgitation (FMR) and to establish their relationship with clinical status, plasma B-type natriuretic peptide (BNP) levels, and prognosis in patients with non-ischaemic dilated cardiomyopathy (NICMP). Methods and results: Ninety patients (mean age: 50 ± 14, 31% females) with NICMP and FMR were prospectively analysed by echocardiography. Global and local left ventricular remodelling parameters such as ejection fraction and sphericity index, inter-papillary muscle distance, coaptation to septal distance, and mitral annular area, as well as mitral valve deformation indices such as tenting area (TA) and tenting distance, were measured as indicators of FMR. Patients were defined as having severe FMR [effective regurgitant orifice area (EROA) ≥ 0.2 cm2, n = 41] or non-severe FMR (EROA < 0.2 cm2, n = 49) and followed for 15 ± 3 months. Multivariate regression analysis revealed that TA had the greatest ability to predict severe FMR at a cut-off level of 3.4 cm2 with 82% sensitivity and 77% specificity. Patients with higher TA values (>3.4 cm2) had statistically higher BNP levels, worse functional status, more hospitalizations, and higher death rates. The plasma BNP level (P: 0.012) and TA (P: 0.056) were predictors of all-cause mortality. New York Heart Association class (P < 0.001) and TA (P: 0.005) were predictors of combined death or hospitalization on multivariate Cox's regression analysis. Conclusion: Tenting area accurately reflects the degree of FMR at a cut-off value of 3.4 cm2 and has a strong correlation with functional status, plasma BNP, mortality, and hospitalization rates. Tenting area is also an independent predictor of mortality and hospitalizations in patients with NICMP and FMR.

The effects of spironolactone or metoprolol added to a conventional treatment protocol on QT dispersion, which is accepted as a sudden cardiac death predictor, were evaluated in heart failure patients.? A total of 105 New York Heart Association class III patients were included in this study. The conventional treatment protocol was standardized by giving ramipril, furosemide, and digoxin to all patients for 3 weeks at the same doses. At the end of this period, the patients were divided into three groups. Conventional treatment was continued in group 1, 25 mg spironolactone was added in group 2, and 12.5 mg metoprolol was added in group 3. Patients were followed for 12 weeks and clinical and laboratory tests were conducted at 3 week intervals. No significant change in corrected QT dispersion was observed in group 1 at the end of 12 weeks (corrected QT dispersion: 80 +/- 2 msc to 79 +/- 2 msc, P: 0.22). However, corrected QT dispersion in group 2 was reduced by 32.5% (83 +/- 2 msc to 56 +/- 1 msc; P: 0.01). A 32.9% reduction in corrected QT dispersion (79 +/- 2 msc to 53 +/- 2 msc; P: 0.01) was observed in group 3. In conclusion, the addition of spironolactone or metoprolol to a conventional treatment in heart failure patients resulted in improved clinical conditions and the significant decrease in sudden death predictors corrected QT dispersion. The effects of spironolactone and metoprolol on corrected QT dispersion were similar.

Recent studies demonstrate that the serum inflammatory markers increase in patients with atherosclerosis. We aimed to assess whether a difference exists between patients with acute coronary syndrome and patients with stable angina pectoris in respect to serum neopterin, procalcitonin (PCT) and C-reactive protein (CRP) levels. A total of 52 patients (42 male, 10 female) who had atherosclerosis confirmed by angiography and were being followed up for an acute coronary syndrome were recruited and for control group, 45 patients with stable angina pectoris (SA) (35 male and 10 female) who underwent coronary angiography, were examined. Serum concentrations of neopterin, CRP and PCT in the study group (acute coronary syndrome) were compared to control group (stable angina pectoris). The mean neopterin level of the study group was 22.47 +/- 2.93 nmol/l, the mean CRP level was 30.40 +/- 8.05 mg/l and the mean PCT level was 0.40 +/- 0.04 ng/ml. In control group these levels were 12.26 +/- 0.61 nmol/l (p < 0.05), 5.26 +/- 0.64 mg/l (p < 0.001) and 0.19 +/- 0.02 ng/ml (p < 0.001), respectively. In the presented study our results showed that these markers can be useful for the assessment of inflammation related to atherosclerosis.