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Editorial
This editorial discusses the pathophysiological mechanisms by which right ventricular adaptation to pulmonary arterial hypertension eventually leads to dilation and tricuspid regurgitation.
Right ventricular (RV) function is the linchpin in the natural history of pulmonary arterial hypertension (PAH) [1]. Patients with PAH feel well, function better and live longer if RV function is preserved [1]. The RV initially adapts to the increased afterload in the pulmonary circulation by hypertrophy and increased contractility, which maintains stroke volume. This is called the homeometric adaptation or the Anrep effect [1]. Eventually when the homeometric adaption is not enough to maintain cardiac output, the RV dilates, which maintains stroke volume by increasing the RV end-diastolic volume based on the Starling principle, which is referred to as the heterometric adaption [1]. Progressive RV dilation can lead to dilatation of the tricuspid valve annulus, malcoaptation of the tricuspid valve leaflets, and ultimately tricuspid regurgitation [2]. Tricuspid regurgitation in PAH: food for thought <https://bit.ly/3ylWgmm> The author would like to acknowledge E.K. Weir from the University of Minnesota for scientific review of this editorial.
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Thenappan Thenappan (2024) studied this question.
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