Background: Red cell distribution width (RDW) in acute heart failure (AHF) is accepted as a prognostic indicator with unclear pathophysiological ties. The aim of this study was to evaluate the prognostic value of RDW in AHF patients in relation to clinical and echocardiographic data. Methods: 170 patients with AHF were retrospectively studied. All patients had laboratory testing and an echocardiogram performed within 24 h of admission to the Cardiology Department. Results: During the mean 193 ± 111 days of follow-up, 33 patients died. More advanced age, high RDW and low peak early diastolic velocity of the lateral mitral annulus (MVe') were independent predictors of all-cause mortality with hazard ratios of: 1.05 (95% CI 1.02-1.09), p < 0.005, 1.40 (95% CI 1.22-1.60), p < 0.001, and 0.77 (95% CI 0.63-0.93), p < 0.007, respectively. In a stepwise multiple linear regression model, RDW was correlated with hemoglobin concentration (standardized b =-0.233, p < 0.001), mean corpuscular volum (standardized b =-0.230, p < 0.001), mean corpuscular hemoglobin concentration (standardized b =-0.207, p < 0.007), the natural logarithm of C-reactive protein (CRP) (standardized b = 0.184, p < 0.004) and tricuspid regurgitation peak gradient (TRPG) values (standardized b = 0.179, p < 0.006), whereas MVe' was correlated with atrial fibrillation (standardized b = 0.269, p < 0.001). Conclusions: The present data demonstrates a novel relation between higher levels of RDW and elevated TRPG and high sensitivity CRP values in patients with AHF. These findings suggest that RDW, the most important mortality predictor, is independently associated with elevated pulmonary pressure and systemic inflammation in patients with AHF. Moreover, in AHF patients, more advanced age and decreased MVe' are also independently associated with total mortality risk.
Current data indicate that heart failure (HF) is associated with inflammation and microvascular dysfunction and remodeling. These mechanisms could be involved in HF development and progression, especially in HF with preserved ejection fraction (HFpEF). We aimed to compare structural changes in retinal arterioles and carotid arteries between HF patients and patients without heart failure. This preliminary, retrospective, case-control study included 28 participants (14 patients with HFpEF and 14 age- and sex-matched healthy controls). Carotid intima-media thickness to lumen ratio (cIMTLR) was assessed using B-mode ultrasonography. Retinal arterioles wall- to-lumen ratio (rWLR) was assessed by adaptive optics camera rtx1. The HF patients had higher IMTLR (Dmedian [HFpEF–control group] 0.07, p = 0.01) and eWLR (Dmedian 0.03, p = 0.001) in comparison to patients without HF. In the whole study group, rWLR correlated significantly with IMTLR (r = 0.739, p = 0.001). Prevalence of arterial hypertension was similar in both groups, however, patients with HF had a significantly lower office, central and 24-hour ambulatory blood pressure (systolic Dmedian −21 to −18 mmHg; diastolic Dmedian −23 to −10 mmHg). Our data suggests gradual and simultaneous progression of vascular remodeling in both retinal arterioles and carotid arteries in HFpEF patients. This process could be a marker of HF development. Significantly lower blood pressure values in HF group may indicate that vascular remodeling could be independent of BP control. Nevertheless, further and larger prospective studies allowing to reduce the impact of confounding and address temporality are warranted.
The limitations of diuretics in the treatment of acute decompensated heart failure (ADCHF) are progressive worsening of renal function and resistance to up-titrated doses. The occurrence of resistance to loop diuretics in patients with ADCHF is associated with worsening prognosis and increased mortality. In this study, we report two patients with ADCHF and resistance to loop diuretics suspected for venous thromboembolism, suggesting that heparin administered to ADCHF patients treated for venous thromboembolism with cardiorenal syndrome decreases right-ventricular overload and improves renal function. To our knowledge, these are the first reported cases describing restored responsiveness to loop diuretics in ADCHF patients after additional heparin administration.
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