Key result
PAH linked to ~30% smaller LV cardiomyocytes and reduced force-generating capacity versus healthy donors.
Why the study?
The pathophysiology of left ventricular dysfunction in pulmonary arterial hypertension is incompletely understood, and the contribution of cardiomyocyte atrophy and contractility remains unclear.
Population
9 PAH patients and 10 donors
Comparison
PAH patients vs donors
Design
Case-control study
Authors
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LV cardiomyocyte atrophy and weakness may contribute to PAH-related LV impairment; hypothesis-generating for targeted therapies, needs prospective validation.
Observational (n=19)
Left ventricular cardiomyocyte atrophy and reduced contractile function at the cellular level contribute to the reduced in vivo LV contractility observed in patients with pulmonary arterial hypertension.
Manders et al. (2014) conducted an observational in Pulmonary Arterial Hypertension (n=19). Pulmonary arterial hypertension vs. Donors was evaluated on Cross-sectional area and force-generating capacity of isolated single cardiomyocytes. Pulmonary arterial hypertension was associated with a ~30% reduction in LV cardiomyocyte cross-sectional area and a ~25% reduction in maximal force-generating capacity compared to donors.
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