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Inflammation plays a central role in the pathogenesis and progression of heart failure (HF).Over the past 3 decades, observational and mechanistic studies have implicated inflammation as both a cause and consequence of HF.(1, 2) Yet, until recently, approaches targeting inflammation in HF failed to yield clinical benefit.Recently, direct and indirect approaches to modulating inflammation in HF have been somewhat more promising.
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Matthew J. Feinstein (2024) studied this question.
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