Myocardial hypertrophy and its role in XXXX with preserved ejection fraction.

@entity1 @entity712 @entity296 @entity101 @entity6 @entity455 @entity1184 @entity740 @entity4346 @entity141 @entity67
@entity4346 ( @entity4346 ) is the most common @entity296 associated with @entity712 with preserved ejection fraction (HFpEF). @entity4346 is driven by neurohumoral activation, increased mechanical load, and cytokines associated with arterial @entity101 , @entity740 , @entity6 , and other comorbidities. Here we discuss the experimental and clinical evidence that links @entity4346 to @entity67 and qualifies @entity4346 as one diagnostic marker for HFpEF. Mechanisms leading to @entity67 in @entity4346 are incompletely understood, but may include extracellular matrix changes, @entity455 , as well as altered cardiomyocyte mechano-elastical properties. Beating cardiomyocytes from HFpEF @entity1 have not yet been studied, but we and others have shown increased @entity141 turnover and impaired relaxation in cardiomyocytes from @entity1184 hearts. @entity296 can lead to heterogeneity in regional myocardial contractile function, which contributes to @entity67 in HFpEF. In the clinical setting of @entity1 with compound comorbidities, @entity67 may occur independently of @entity4346 . This may be one explanation why current approaches to reduce @entity4346 have not been effective to improve symptoms and prognosis in HFpEF. Exercise training, on the other hand, in clinical trials improved exercise tolerance and diastolic function, but did not reduce @entity4346 . Thus current clinical evidence does not support regression of @entity4346 as a surrogate marker for (short-term) improvement of HFpEF.
