Why the study?
Do elevated circulating adipokine levels predict major adverse cardiac events in patients with chronic heart failure?
Do elevated circulating adipokine levels predict major adverse cardiac events in patients with chronic heart failure?
Elevated circulating adiponectin levels, corrected for BMI, independently predict major adverse cardiac events in patients with chronic heart failure, particularly those with elevated NT-proBNP.
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May refine MACE prognostication in chronic HF; hypothesis-generating and requires prospective validation before practice change.
BACKGROUND: The aim of this study was to ascertain whether expressions of adipokines in the myocardium or their circulating levels can provide prognostic information concerning patients with chronic heart failure (HF). METHODS AND RESULTS: Circulating levels of 3 adipokines (leptin, adiponectin, and resistin), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and high-sensitivity C-reactive protein were measured in 96 patients with chronic HF. Major adverse cardiac events (MACE) involving death, heart transplantation, and hospitalization with deteriorating HF during a median follow-up period of 288 days were recorded. From that group, immunohistochemistry and Western blotting studies of the myocardial tissues were conducted on 7 patients with end-stage HF undergoing heart transplantation. The levels of the 3 adipokines significantly correlated with that of NT-proBNP; however, only adiponectin concentration increased with the severity of HF, after correction for body mass index. Cox proportional hazards analyses revealed that high levels of corrected adiponectin were predictive of the development of MACE (hazard ratio, 2.947, P=0.037). Moreover, adiponectin was significantly expressed in the myocardium, and its tissue expression positively correlated with the severity of HF. CONCLUSIONS: This study showed that adiponectin is associated with clinical outcomes and severity of HF. Further research into the precise mechanisms of these adipokine derangements in HF is important to help clarify the exact role of adipokines in the pathophysiology of HF.
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Yin et al. (2012) studied this question.
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