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Can the hemodynamic model in heart failure be restored based on analysis of ventricular-arterial coupling?

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Abstract

The hemodynamic model was inappropriate to explain the disappointing effect of vasodilation and the beneficial effect of beta-blockade in chronic heart failure. A more nuanced hemodynamic analysis, taking both steady and pulsatile hemodynamics into consideration, improves insight into these apparently enigmatic effects. Of particular interest is the velocity of early systolic flow as a determinant of left ventricular afterload. Several drugs, in particular beta-blockers, directly or indirectly, influence the velocity of early systolic flow. Thus, the hemodynamic model in heart failure may deserve reconsideration.

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Correspondence to Johannes Soma.

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All human and (animal studies) that were performed, and which forms the basis for the arguments in this manuscript were approved by the appropriate ethics committee and have therefore been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments. All study participants gave their informed consent prior to their inclusion in those studies. However, the actual manuscript does not contain clinical studies or patient data.

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Soma, J. Can the hemodynamic model in heart failure be restored based on analysis of ventricular-arterial coupling?. Heart Fail Rev 29, 463–464 (2024). https://doi.org/10.1007/s10741-023-10374-7

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