Abstract
Purpose of ReviewThe balance between inflammation and its resolution plays an important and increasingly appreciated role in heart failure (HF) pathogenesis. In humans, different chronic inflammatory conditions and immune-inflammatory responses to infection can lead to diverse HF manifestations. Reviewing the phenotypic and mechanistic diversity of these HF presentations offers useful clinical and scientific insights.Recent FindingsHF risk is increased in patients with chronic inflammatory and autoimmune disorders and relates to disease severity. Inflammatory condition–specific HF manifestations exist and underlying pathophysiologic causes may differ across conditions.SummaryAlthough inflammatory disease–specific presentations of HF differ, chronic excess in inflammation and auto-inflammation relative to resolution of this inflammation is a common underlying contributor to HF. Further studies are needed to phenotypically refine inflammatory condition–specific HF pathophysiologies and prognoses, as well as potential targets for intervention.
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