Key result
End-stage heart failure was associated with significantly stronger ET-1-like immunoreactivity in the left atrial myocardium compared to donor hearts.
Observational (n=20)
Endothelin peptide levels are increased in the myocardium of patients with end-stage heart failure, suggesting a role in cardiac remodeling.
Association with elevated myocardial ET-1 in end-stage HF is hypothesis-generating; should not yet change practice or guide therapy.
Endothelin (ET) induces hypertrophy of cardiomyocytes and increases synthesis of collagen in vitro. Interestingly, these features are hallmarks of the cardiac remodeling taking place in heart failure. The aim of the present study was to examine cardiac ET peptide and preproET-1 mRNA synthesis in human heart failure. Cardiac tissue was obtained from 11 patients with end-stage heart failure undergoing orthothopic heart transplantation (NYHA III-IV). Cardiac tissue from nine organ donors served as controls. The specimens were examined by immunohistochemistry and mRNA slot blot analyses. Significantly stronger ET-1-like immunoreactivity (ET-1-ir) was seen in the left atrial myocardium of failing hearts compared to the left atrial myocardium of donor hearts. Within each heart, the epicardium showed the strongest ET-1-ir. Left ventricular preproET-1 mRNA expression in the entire group of patients did not differ significantly from that of donor hearts. However, hypertrophic obstructive cardiomyopathy may be associated with a twofold increase in left ventricular preproET-1 mRNA. We report an increase in cardiac ET peptide in human heart failure.
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Torstein Lyberg Theis Tønnessen (2000) conducted an observational in Heart failure (n=20). End-stage heart failure vs. Organ donors was evaluated on Cardiac ET-1-like immunoreactivity and preproET-1 mRNA expression. End-stage heart failure was associated with significantly stronger ET-1-like immunoreactivity in the left atrial myocardium compared to donor hearts.
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