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A novel paradigm in HFpEF associates comorbid conditions to an inflammatory state that increases LV stiffness and promotes HF. 71 The cellular and molecular mechanisms that lead from systemic inflammation to myocardial fibrosis (reduced nitric oxide bioactivity, cyclic guanosine monophosphate content, and protein kinase G) also promote arterial stiffening, with the endothelium being an essential component of vascular homeostasis.
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