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Congestive Heart failure, including systolic and diastolic heart failure, is a major public health hazard and its prevalence continues to rise. While the mortality of systolic heart failure has significantly reduced over the past decade thanks to the advances in pharmacological therapy, there has not been a single therapy that has shown to be survival benefit on diastolic heart failure. A significant gap in knowledge on diastolic heart failure has to be bridged before we may design a therapeutic strategy to target this disease. Recent elegant studies have revealed evidence of systemic and myocardial inflammation in endomyocardial tissues. A new paradigm of the pathophysiology of diastolic heart failure has been proposed - systemic proinflammatory state, coronary endothelial inflammation, impairment in endothelial-cardiomyocyte nitric oxide signaling, inflammatory cell infiltration and proinflammatory cytokines, collectively lead to diastolic dysfunction. Therefore, our central hypothesis is endothelial dysfunction contributes to diastolic function and clinical exacerbation of heart failure.
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