Literature DB >> 9350947

Myocardial cell death and apoptosis in hibernating myocardium.

C Chen1, L Ma, D R Linfert, T Lai, J T Fallon, L D Gillam, D D Waters, G J Tsongalis.   

Abstract

OBJECTIVES: This study was designed to study apoptosis in hypoperfused hibernating myocardium subtending severe coronary stenosis.
BACKGROUND: Apoptosis contributes to myocyte death in acute myocardial infarction.
METHODS: A left anterior descending coronary artery stenosis was created in 13 pigs and maintained for 24 h (n = 4), 7 days (n = 5) and 4 weeks (n = 4) to reduce coronary blood flow by a mean of 34% with severe regional myocardial systolic dysfunction, as documented by echocardiography. Apoptosis was detected with an in situ end-labeling method and confirmed by "deoxyribonucleic acid laddering" on agarose-gel electrophoresis. The severity of apoptosis was expressed as the percentage of apoptotic myocyte nuclei and nonapoptotic myocardial nuclei.
RESULTS: Myocardial blood flow of the anterior left ventricular wall was reduced from 1.00 +/- 0.18 to 0.66 +/- 0.21 ml/min per g (p < 0.01), with a severe reduction of anterior regional wall thickening from a mean (+/-SD) of 39 +/- 4% to 9 +/- 8% (p < 0.01). There was no myocardial infarction in five pigs and minimal patchy infarction of < or = 6% of the area at risk in eight pigs. Apoptotic myocytes were observed in the hibernating myocardial region in all pigs (4.8 +/- 2.3%). Myocyte apoptosis was patchy in distribution and was found predominantly in the subendocardial myocardium (9.8 +/- 4.6%) and rarely in the subepicardial myocardium (0.32 +/- 0.45%). Apoptosis was found not only around focal fibrosis areas, but also in areas without fibrosis or patchy infarction. Apoptosis was found not only in 24-h hypoperfused myocardium, but also in 4-week hypoperfused myocardium. The severity of myocyte apoptosis correlated significantly with regional coronary blood flow reduction (r = 0.75, p < 0.01). No apoptosis was found in the normal control region.
CONCLUSIONS: This study demonstrates that there is ongoing myocyte death through myocyte apoptosis in hypoperfused hibernating myocardium.

Entities:  

Mesh:

Year:  1997        PMID: 9350947     DOI: 10.1016/s0735-1097(97)00309-4

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


  15 in total

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Review 2.  Hibernating myocardium.

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9.  Hypoxia and acidosis activate cardiac myocyte death through the Bcl-2 family protein BNIP3.

Authors:  Lori A Kubasiak; Olga M Hernandez; Nanette H Bishopric; Keith A Webster
Journal:  Proc Natl Acad Sci U S A       Date:  2002-09-11       Impact factor: 11.205

10.  Multimodality imaging of chronic ischemia.

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