Cell motion amplitude decreased 43% in ischemic and 68% in idiopathic dilated cardiomyopathy vs normal donors, with SR Ca2+ uptake dysfunction in ICM and release dysfunction in DCM.
Observational
We examined 1) contractile properties and the intracellular Ca(2+) concentration (Ca(2+)(i)) transient in cardiac myocytes and 2) sarcoplasmic reticulum (SR) Ca(2+) uptake and release function in myocardium from patients with end-stage heart failure caused by ischemic (ICM) vs. idiopathic dilated cardiomyopathy (DCM). The amplitude of cell motion was decreased 43 +/- 6% in ICM and 68 +/- 7% in DCM compared with that in normal organ donors (DN). Time to peak of shortening was increased 43 +/- 15% in DCM, but not in ICM. Prolongation of the relaxation time was more predominant in ICM. In DCM the systolic Ca(2+)(i) was decreased 27 +/- 9% and diastolic Ca(2+)(i) was increased 36 +/- 11%. In ICM the diastolic Ca(2+)(i) was increased 59 +/- 12% but the systolic Ca(2+)(i) was unchanged. A significant decrease of the ATP-dependent SR Ca(2+) uptake rate associated with the reduction of the SR Ca(2+)-ATPase protein level was found in ICM. In contrast, the significant decrease in SR Ca(2+) release rate was distinct in DCM. The large amount of Ca(2+) retained in the SR associated with a significant decrease in the maximum reaction velocity and increase in the Michaelis-Menten constant in the caffeine concentration-response curve suggests a fundamental abnormality in the SR Ca(2+) release channel gating property in DCM. We conclude that potentially important differences exist in the intracellular Ca(2+) homeostasis and excitation-contraction coupling in ICM vs. DCM. The SR Ca(2+) release dysfunction may play an important pathogenetic role in the abnormal Ca(2+) homeostasis in DCM, and the SR Ca(2+) uptake dysfunction may be responsible for the contractile dysfunction in ICM.
Sen et al. (Tue,) conducted a observational in End-stage heart failure. Ischemic cardiomyopathy vs. Idiopathic dilated cardiomyopathy and normal organ donors was evaluated on Contractile properties, intracellular Ca(2+) concentration transient, and SR Ca(2+) uptake and release function. Cell motion amplitude decreased 43% in ischemic and 68% in idiopathic dilated cardiomyopathy vs normal donors, with SR Ca2+ uptake dysfunction in ICM and release dysfunction in DCM.