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Eur J Heart Fail. 2007 Sep;9(9):857-64. Epub 2007 Jun 26.

Impaired contractile reserve in severe mitral valve regurgitation with a preserved ejection fraction.

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  • 1Cardiovascular Research Center, Temple University School of Medicine, United States. mcginleyjoseph@hotmail.com

Abstract

BACKGROUND:

Impaired contractile reserve in chronic MR results from load-independent, myocyte contractile abnormalities.

AIMS:

Investigate the mechanisms of contractile dysfunction in chronic mitral valve regurgitation (MR).

METHODS:

Mild MR was produced in eight dogs followed by pacing induced left ventricular (LV) dilatation over eight months. In-vivo LV dP/dt was measured at several pacing rates. Contractile function was measured in isolated LV trabeculae and myocytes at several stimulation rates and during changes in extracellular [Ca2+]. Identical studies were performed with six control dogs.

RESULTS:

Chronic MR resulted in a preserved ejection fraction with decreased dP/dt (p<0.01). LV trabeculae demonstrated significantly lower developed force and a negative force-frequency relation with chronic MR (p<0.05). Myocytes exhibited a negative shortening-frequency relationship in both groups with a greater decline with chronic MR (p<0.001) paralleled by decreases in peak [Ca2+](i) transients. Increases in extracellular [Ca2+] abrogated the defects in force generation in trabeculae from animals with chronic MR.

CONCLUSION:

Even with a preserved EF, chronic severe MR results in a significant reduction in intrinsic contractile function and reserve. Functional impairment was load-independent reflecting a predominant defect in calcium cycling rather than impaired peak force generating capacity due to myofibrillar attenuation.

PMID:
17594913
[PubMed - indexed for MEDLINE]
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