Francesca Donati

Right ventricular dysfunction is associated with chronic kidney disease and predicts survival in patients with chronic systolic heart failure.

Chronic kidney disease (CKD) and right ventricular (RV) dysfunction are important predictors of prognosis in heart failure (HF). We investigated the relationship between RV dysfunction and CKD in outpatients with chronic systolic HF, an association which remains poorly defined.

Patterns of left ventricular remodeling in chronic heart failure: prevalence and prognostic implications.

BACKGROUND AND AIM Many descriptors of left ventricular (LV) remodeling have important prognostic implications in patients with chronic systolic heart failure (HF). We sought to assess the prognostic value of the combination of increased LV mass with a disproportion between wall thickness and internal diameter. METHODS AND PATIENTS Patients (n = 536) with chronic HF, ejection fraction <50% and LV end-diastolic volume index >91 mL/m(2), classified according to LV mass index and relative wall thickness (RWT), were followed up for 33 ± 21 months. Ventricular mass was determined using a standard M-mode echocardiographic method. Relative wall thickness was defined as the ratio of (sum of interventricular septum thickness in diastole + posterior wall thickness in diastole)/LV end-diastolic diameter. RESULTS Prevalence of the pattern of increased LV mass index, defined as LV mass index >148 g/m(2) in men and >122 g/m(2) in women, and decreased RWT (<0.34) was 29%. Multivariable predictors of all-cause mortality were age >70 years (P < .0001), New York Heart Association class >2 (P < .0001), increased LV mass index, and decreased RWT (P = .003), E wave deceleration time ≤140 ms (P = .005), and male gender (P = .025). Patients with increased LV mass index and decreased RWT had a worse survival (33%) than patients with less LV mass index and normal to reduced RWT (log-rank 23.92; P < .0001). Comparisons of Cox models showed that the combination of increased mass index and decreased RWT added prognostic value to a model that included ejection fraction and end-systolic volume index. CONCLUSION In patients with systolic HF, an independent and incremental risk of adverse outcome was associated with increased mass index and decreased RWT.

Association of furosemide dose with clinical status, left ventricular dysfunction, natriuretic peptides, and outcome in clinically stable patients with chronic systolic heart failure.

In chronic heart failure (HF), high daily doses of furosemide have been associated with increased mortality. The authors sought to evaluate the relationships between orally administered furosemide doses, clinical status, left ventricular (LV) dysfunction, N-terminal proBNP (NT-proBNP), and outcome in 400 outpatients with chronic HF and LV ejection fraction (EF) ≤ 45%. Clinical status, NT-proBNP levels, and estimated glomerular filtration rate (eGFR) were evaluated. Median follow-up duration was 32 months. The median values of daily-dose furosemide and of furosemide dose normalized to body surface area were 25 mg (12.5-62.5 mg) and 15 mg/m(2) (13-34 mg/m(2)), respectively. A total of 32% of patients had decompensated HF according to Framingham score and criteria for congestion. In clinically stable patients, a multivariable Cox model, which included clinical and echocardiographic parameters plus NT-proBNP, hemoglobin, and eGFR, showed that normalized furosemide dose (P=.017), anemia (P=.060), age (P=.080), and New York Heart Association class (P=.080) were predictors of all cause-mortality. In patients with decompensated HF, LV end-systolic volume index (P=.018), NT-proBNP (P=.060), and reduced eGFR (P=.070) were independently related to the outcome. Normalized furosemide dose was a major determinant of prognosis in patients with chronic HF but without ongoing signs and symptoms, and this suggests a possible negative interaction of this drug in clinically stable patients.

Therapy Against Ischemic Injury

The advent of reperfusion therapy constituted a historical change for the management of myocardial infarction (MI) patients. However, shortly after, experimental models recognized an intrinsic damage, related to reperfusion itself, which was termed as ischemiareperfusion injury (IRI). Clinical studies attribute IRI a significant burden of morbidity and mortality observed in patients undergoing successful epicardial reperfusion. Several mechanisms have been identified and, as many strategies, have been investigated to address the phenomenon. In this review we will discuss the current evidence for IRI, pharmacological and non-pharmacological preventive strategies adopted both in experimental models and in clinical practice. Finally, we will try to provide a critical appraisal to the lack of consistent benefit observed in translational medicine.