Key result
Idiopathic dilated cardiomyopathy was associated with a markedly increased caffeine threshold for sarcoplasmic reticulum Ca2+ release compared to normal myocardium (1.94 vs 0.29 mmol/l).
Why the study?
Does idiopathic dilated cardiomyopathy alter the Ca2+ sensitivity of the contractile apparatus or Ca2+ release activity of the sarcoplasmic reticulum compared to normal myocardium?
Population
Chemically skinned myocardial fibers from 13 excised hearts from patients with idiopathic dilated…
Comparison
In vitro testing with solutions of decreasing… vs Normal myocardium
Design
Preclinical
Authors
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Skinned-fiber findings in DCM warrant no clinical action; leaves open SR Ca2+ release defects as drivers of human contractile dysfunction.
Observational (n=17)
Does idiopathic dilated cardiomyopathy alter the Ca2+ sensitivity of the contractile apparatus or Ca2+ release activity of the sarcoplasmic reticulum compared to normal myocardium?
Absolute Event Rate: 1.94% vs 0.29%
In idiopathic dilated cardiomyopathy, the gating mechanism of the sarcoplasmic reticulum Ca2+ release channel is abnormal, while contractile and regulatory proteins remain unaltered.
D’Agnolo et al. (1992) conducted an observational in Idiopathic dilated cardiomyopathy (n=17). Idiopathic dilated cardiomyopathy vs. Nonfailing human hearts was evaluated on Caffeine threshold for Ca2+ release. Idiopathic dilated cardiomyopathy was associated with a markedly increased caffeine threshold for sarcoplasmic reticulum Ca2+ release compared to normal myocardium (1.94 vs 0.29 mmol/l).
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