Abstract

The proposition that cardiomyocyte “stretch” is a key determinant of brain natriuretic peptide (BNP) release has been a widely accepted concept that has contributed to the broad use of plasma BNP measurement in the diagnosis and evaluation of heart failure. In our study,1 we showed that the R 2 value for the association between the transcardiac BNP gradient and left ventricular end-systolic wall stress was ≈0.5, indicating that 50% of the variability of cardiac BNP release was …

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