[Ca2+]i in Human Heart Failure: A Review and Discussion of Current Areas of Controversy.

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[Ca2+]i in Human Heart Failure: A Review and Discussion of Current Areas of Controversy.

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dc.contributor.author Helm, P. A.
dc.contributor.author Hajjar, R. J.
dc.contributor.author Saha, C.
dc.contributor.author Liao, Ronglih
dc.contributor.author Gwathmey, Judith Karen
dc.date.accessioned 2011-04-26T03:53:36Z
dc.date.issued 1994
dc.identifier.citation Liao, R., P. A. Helm, R. J. Hajjar, C. Saha, and J. K. Gwathmey. 1994. [Ca2+]i in human heart failure: a review and discussion of current areas of controversy. The Yale Journal of Biology and Medicine 67(5-6): 247-264. en_US
dc.identifier.issn 0044-0086 en_US
dc.identifier.uri http://nrs.harvard.edu/urn-3:HUL.InstRepos:4875902
dc.description.abstract Multiple abnormalities have been reported in the setting of human heart failure. It is unclear whether detected changes reflect adaptive alterations in myocardium subjected to increased and sustained hemodynamic overload or are pathogenic to the disease process. As a result of the observation that the primary defect in heart failure is decreased pump function, investigators have concentrated their efforts on determining systolic [Ca2+]i as a logical corollary and a causative mechanism for contractile dysfunction. A simple cause and effect relationship has therefore been proposed with regard to contractile dysfunction and [Ca2+]i. Yet some investigators have found no difference in peak systolic [Ca2+]i between failing and non-failing human myocardium, whereas others have found peak [Ca2+]i to be significantly reduced in failing hearts. Resting calcium concentrations have been reported either to be elevated in failing human myocardium or not different from non-failing human myocardium. Investigators should now appreciate that the force-calcium relationship is not a simple relationship. One must take into account the prolonged time course and slowed mobilization of [Ca2+]i as opposed to simply peak [Ca2+]i. When put in perspective of mechanisms and determinants of the Ca(2+)-force relationship, we begin to realize that failing human myocardium has the "potential" to generate normal levels of force. Only when stressed by [Ca2+]i overload and/or frequency perturbation does myocardium from patients with end-stage heart disease demonstrate contractile failure. Although [Ca2+]i availability and mobilization are likely to play a role in the systolic as well as diastolic dysfunction reported in human heart failure, it is likely that other mechanisms are involved as well (e.g., myocardial energetics). Myocardial energetics is directly related to [Ca2+]i and mobilization in failing human myocardium, because metabolites, e.g., ADP, inhibit pumps, such as sarcoplasmic reticulum Ca2+ ATPase activity. We therefore conclude that there is a role for intracellular calcium mobilization and myocardial energetics for systolic and diastolic dysfunction seen in human heart failure. en_US
dc.language.iso en_US en_US
dc.publisher Yale Journal of Biology and Medicine en_US
dc.relation.hasversion http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2588906/pdf/ en_US
dash.license LAA
dc.title [Ca2+]i in Human Heart Failure: A Review and Discussion of Current Areas of Controversy. en_US
dc.type Journal Article en_US
dc.description.version Version of Record en_US
dc.relation.journal The Yale Journal of Biology and Medicine en_US
dash.depositing.author Liao, Ronglih
dc.date.available 2011-04-26T03:53:36Z
dash.affiliation.other HMS^Medicine-Brigham and Women's Hospital en_US
dash.affiliation.other HMS^Medicine- Beth Israel-Deaconess en_US

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