Prognostic significance of right ventricular dysfunction in patients presenting with acute left-sided heart failure.

BACKGROUND: The prognostic value of right ventricular (RV) function in chronic heart failure (HF) has lately been well established. However, research on its role in acute heart failure (AHF) is sparse. RESULTS: This study comprised 195 patients, aged between 18 and 80 years, with acute left-sided heart failure (HF) and a left ventricular ejection fraction (LVEF) < 50%. Patients with LVEF ≥ 50%, mechanical ventilatory or circulatory support, poor echocardiographic windows, prosthetic valves, congenital heart diseases, infective endocarditis, and/or life expectancy < 1 year due to non-cardiac causes were excluded. The study participants' mean age was 57.7 ± 10.9 years, and 74.9% were males. Coronary artery disease was present in 80.5% of patients. The mean LVEF was 31% ± 8.7. RV dysfunction (RVD), defined as tricuspid annular plane systolic excursion (TAPSE) < 17 mm, RV S' < 9.5 cm/s and/or RV fractional area change (FAC) < 35%, was identified in 48.7% of patients. The RV was dilated in 67.7% of the patients. RVD was significantly associated with a longer HF duration, atrial fibrillation, and idiopathic dilated cardiomyopathy. The primary outcome, a 6-month composite of cardiovascular death or hospitalization for worsening HF (HHF), occurred in 42% of the participants. Cardiovascular mortality and HHF occurred in 30.5% and 23.9% of the patients, respectively. The primary endpoint and longer CCU stays were significantly more common in patients with RVD than in those with normal RV function. RV dilatation was significantly associated with the primary outcome, whether alone or in combination with RVD. Multivariate regression analysis showed that only RV global longitudinal strain (GLS) independently predicted poor outcomes. CONCLUSIONS: RVD and RV dilatation strongly predict CV death and HHF in patients with AHF and LVEF < 50%. Multivariate analysis showed that RV GLS was the only predictor of a composite of CV death and HHF.

Folic acid protects against experimental prenatal nicotine-induced cardiac injury by decreasing inflammatory changes, serum TNF and COX-2 expression.

Nicotine administration has been shown to increase the risk for cardiovascular diseases and death. The present study was designed to investigate the impact of nicotine administration on serum level tumor necrosis factor and cycloxygenase -2 (COX-2) expression mediated cardiac injury in rat off springs, and the possible protective effect of folic acid. Eighteen pregnant female rats were randomly divided into three groups, six animals each. Control group received the vehicle, nicotine group received a dose of nicotine 0.1 mg/kg body weight, daily with subcutaneous injection from day 3 of gestation until weaning on postnatal day 21. Nicotine treated group received daily oral supplementation with folic acid 200 mg/kg body weight by intragastric tube prior to injection of nicotine. In serum of the pups, levels of tumor necrosis factor (TNF), nitric oxide (NO), total antioxidant capacity (TAC) and malondialdehyde (MDA) were measured. Histopathological studies of cardiac tissues using hematoxylin-eosin (H&E) were carried out. The expression of COX-2 was evaluated using immunohistochemistry. Serum TNF and MDA were significantly increased, while serum NO and TAC were significantly decreased in nicotine group. Moreover, nicotine-exposed rats showed complete lysis of cardiac myocytes, marked cytoplasmic vacuolation of myocytes, muscle fibers show loss of striation and increased COX-2 expression. Concomitant folic acid administration resulted in a significant alleviation of biochemical and structural alteration-induced by nicotine. In conclusion, folic acid has a protective role against nicotine induced cardiac injury by reduction of COX-2 expression, decreasing TNF production and lipid peroxidation mediated cell injury.