Myocardial cell death and apoptosis in hibernating myocardium

Chunguang Chen, Lijie Ma, Douglas R. Linfert, Tianjie Lai, John T. Fallon, Linda D. Gillam, David D. Waters, Gregory J. Tsongalis

Research output: Contribution to journalArticle

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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 ≤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.

Original languageEnglish (US)
Pages (from-to)1407-1412
Number of pages6
JournalJournal of the American College of Cardiology
Volume30
Issue number5
DOIs
StatePublished - Nov 1 1997

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Myocardium
Cell Death
Apoptosis
Muscle Cells
Swine
Coronary Stenosis
Infarction
Fibrosis
Myocardial Infarction
Agar Gel Electrophoresis
Regional Blood Flow
Echocardiography
DNA

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Chen, Chunguang ; Ma, Lijie ; Linfert, Douglas R. ; Lai, Tianjie ; Fallon, John T. ; Gillam, Linda D. ; Waters, David D. ; Tsongalis, Gregory J. / Myocardial cell death and apoptosis in hibernating myocardium. In: Journal of the American College of Cardiology. 1997 ; Vol. 30, No. 5. pp. 1407-1412.
@article{1547a719e2994668b56680fa85bd4b67,
title = "Myocardial cell death and apoptosis in hibernating myocardium",
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 ≤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.",
author = "Chunguang Chen and Lijie Ma and Linfert, {Douglas R.} and Tianjie Lai and Fallon, {John T.} and Gillam, {Linda D.} and Waters, {David D.} and Tsongalis, {Gregory J.}",
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Chen, C, Ma, L, Linfert, DR, Lai, T, Fallon, JT, Gillam, LD, Waters, DD & Tsongalis, GJ 1997, 'Myocardial cell death and apoptosis in hibernating myocardium', Journal of the American College of Cardiology, vol. 30, no. 5, pp. 1407-1412. https://doi.org/10.1016/S0735-1097(97)00309-4

Myocardial cell death and apoptosis in hibernating myocardium. / Chen, Chunguang; Ma, Lijie; Linfert, Douglas R.; Lai, Tianjie; Fallon, John T.; Gillam, Linda D.; Waters, David D.; Tsongalis, Gregory J.

In: Journal of the American College of Cardiology, Vol. 30, No. 5, 01.11.1997, p. 1407-1412.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Myocardial cell death and apoptosis in hibernating myocardium

AU - Chen, Chunguang

AU - Ma, Lijie

AU - Linfert, Douglas R.

AU - Lai, Tianjie

AU - Fallon, John T.

AU - Gillam, Linda D.

AU - Waters, David D.

AU - Tsongalis, Gregory J.

PY - 1997/11/1

Y1 - 1997/11/1

N2 - 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 ≤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.

AB - 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 ≤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.

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