Mitral peak early diastolic filling velocity to deceleration time ratio as a predictor of prognosis in patients with chronic heart failure and preserved or reduced ejection fraction.

OBJECTIVE: Doppler derived mitral peak early diastolic filling velocity to deceleration time ratio (E/DT) has been proposed as parameter for predicting prognosis in general population. This study prospectively investigates the incremental prognostic value of E/DT over clinical, conventional echocardiographic and mitral-Doppler variables in patients hospitalized for decompensated heart failure (HF). METHODS: We analyzed 95 HF patients (mean age 64.8 ± 12.2 years) hospitalized at our institution from January 2010 to March 2012. The primary end-point was cardiac death or hospitalization, whichever occurred first. Cox regression analysis was performed to identify significant predictors of outcomes. RESULTS: During follow-up (median 37.7 months) 13 patients died and 44 were hospitalized for a cardiac event. At univariable analysis, New York Heart Association (NYHA) functional class, furosemide dosage, lateral tricuspidal annular plane systolic excursion, deceleration time and E/DT were predictive of outcome. At multivariable analysis, E/DT was the only predictor of prognosis (hazard ratio = 1.02, P = 0.018), giving incremental prognostic information to clinical and other echocardio-graphic measures (global chi-square from 15.4 to 25.2; P = 0.032). CONCLUSIONS: E/DT gives independent and incremental prognostic information in HF patients.

Arterial wave reflections and ventricular-vascular interaction in patients with left ventricular systolic dysfunction.

Central aortic pressure waveform (AoPW) is the summation of a forward-traveling wave generated by the left ventricle and a backward-traveling wave caused by the reflection of the forward wave. The aim of this study was to evaluate the effect of ventricular-vascular coupling on the morphology of AoPW in chronic heart failure patients with different degrees of left ventricular systolic dysfunction (LVSD) using pulse wave analysis (PWA). PWA of AoPW and left ventricular (LV) function were evaluated by applanation tonometry in 26 control subjects, in 12 patients with left ventricular ejection fraction (LVEF) ≤ 30%, and in 14 patients with LVEF > 30%. Augmentation pressure, augmentation index, wasted energy, and ejection duration were lower in patients with LVEF ≤ 30% than in those with LVEF > 30% and in control subjects. Furthermore, augmentation index showed an inverse correlation with Doppler mitral E-wave amplitude (r = -0.40; P = 0.04) and E/A ratio (r = -0.42; P = 0.03) and a direct correlation with deceleration time of mitral E-waves (r = 0.39; P = 0.04). In patients with severe LVSD (LVEF ≤ 30%), aortic wave reflections negatively interfere with LV function and induce a shortening of ejection duration. In contrast, AoPW is similar in patients with moderate LVSD (LVEF > 30%) and in control subjects.

Progression of coronary artery calcification and cardiac events in patients with chronic renal disease not receiving dialysis.

We tested for the presence of coronary calcifications in patients with chronic renal disease not on dialysis and studied its progression in 181 consecutive non-dialyzed patients who were followed for a median of 745 days. Coronary calcifications (calcium score) were tallied in Agatston units by computed tomography, and the patients were stratified into two groups by their baseline calcium score (100 U or less and over 100 U). Survival was measured by baseline calcium score and its progression. Cardiac death and myocardial infarction occurred in 29 patients and were significantly more frequent in those patients with calcium scores over 100 U (hazard ratio of 4.11). With a calcium score of 100 U or less, the hazard ratio for cardiac events was 0.41 and 3.26 in patients with absent and accelerated progression, respectively. Thus, in non-dialyzed patients, the extent of coronary calcifications was associated to cardiac events, and progression was an independent predictive factor of cardiac events mainly in less calcified patients. Hence, assessment of coronary calcifications and progression might be useful for earlier management of risk factors and guiding decisions for prevention of cardiac events in this patient population.

Prognostic value of reduced kidney function and anemia in patients with chronic heart failure.

OBJECTIVES: The present study aimed to evaluate the prognostic value of B-type natriuretic peptide (N-proBNP), renal dysfunction and anemia in chronic heart failure (CHF) patients. METHODS: We analyzed data from a prospective cohort of 153 patients (mean age 64 years) with CHF referred to our hospital center. Clinical, echocardiographic and laboratory data were drawn during hospital recovery in all patients. Kidney dysfunction was defined as a glomerular filtration rate (GFR) < 60 ml/min and anemia as a hematocrit < 35%. After discharge, patients attended the outpatient clinic of our institution. RESULTS: Kidney dysfunction was diagnosed in 37% of cases, whereas anemia was present in 25% of patients. During follow-up (median time 456 days), 32 patients died. Multivariate Cox proportional hazard model revealed that N-proBNP [hazard ratio (HR) = 1.002; P < 0.001] and GFR (HR = 0.972; P < 0.005) were significant predictors for mortality after adjustment for confounding variables. Kaplan-Maier analysis demonstrated a progressive decrease in survival from lowest to highest tertiles of N-proBNP values (log rank = 28.7; P < 0.001) and from higher to lower GFR values (log rank = 5.63; P < 0.01). Moreover, parametric survival analysis by the Weibull model demonstrated that the estimated probability of survival adjusted for N-proBNP values was higher in patients with GFR > or = 60 ml/min than in those with GFR < 60 ml/min (P < 0.001). CONCLUSION: Increased N-proBNP and decreased kidney function, but not anemia, are independent risk factors for mortality in patients with CHF.

Novel deletion at the M and P promoters of the human dystrophin gene associated with a Duchenne muscular dystrophy.

Despite numerous reports about dystrophin alterations in Duchenne and Becker muscular dystrophies and dilated cardiomyopathy, the function of dystrophin gene promoters has not yet been completely elucidated. We report the first case of a DNA segment deletion encompassing promoters M and P of the human dystrophin gene, which caused a very severe muscle phenotype without cardiomyopathy, in a 13-year-old boy. These data indicate that the simultaneous lack of promoters P and M results in dramatic consequences in skeletal muscle but not in the heart.