Left ventricular remodeling in myocardial hibernation

Chunguang Chen, Lijie Ma, William Dyckman, Federico Santos, Tianjie Lai, Linda Gillam, David D. Waters

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Background: Left ventricular (LV) remodeling as a consequence of extensive myocardial infarction has been well established in animal and human studies. This study was designed to determine whether regional LV dysfunction with myocardial hibernation without transmural or extensive infarction could initiate the remodeling process. Methods and Results: A severe left anterior descending coronary artery stenosis was created to reduce resting flow by ≃40% (from 0.99±0.10 to 0.56±0.11 mL · min-1 · g-1) and was maintained for 7 days in 13 pigs. The reduction of regional coronary flow initially produced acute myocardial ischemia, as evidenced by reduced regional wall thickening, from 37±3% at baseline to 9±7%, regional lactate production and a decrease in regional coronary venous pH. All pigs had significant regional LV dysfunction and reduced LV ejection fraction (41±11%). The LV end-diastolic volume increased from 59±9 mL at baseline to 74±13 mL immediately after placement of the stenosis and to 78±17 mL 7 days later with hibernating myocardium. The LV mass did not change immediately (60±8 g baseline versus 59±11 g immediately after creation of the stenosis) but increased modestly yet significantly to 67±15 g after 7 days of myocardial hibernation subtending the severe LAD stenosis. The reductions of coronary flow and wall thickening were unchanged at 7 days, whereas myocardial lactate production recovered. By 4 weeks after restoration of LAD flow, regional function had recovered in all 7 pigs with follow-up. Of the 13 pigs, 6 were free from any evidence of myocardial infarction, and 4 had patchy necrosis involving less than 6% of the area at risk. Conclusions: LV remodeling, which is commonly associated with extensive myocardial infarction, can be initiated by regional dysfunctional hibernating myocardium resulting from a severe coronary stenosis. Myocardial necrosis is not a prerequisite for LV remodeling in response to regional dysfunction.

Original languageEnglish (US)
JournalCirculation
Volume96
Issue number9 SUPPL.
StatePublished - Nov 4 1997
Externally publishedYes

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Myocardial Stunning
Ventricular Remodeling
Swine
Pathologic Constriction
Coronary Stenosis
Myocardial Infarction
Left Ventricular Dysfunction
Stroke Volume
Lactic Acid
Myocardium
Necrosis
Infarction
Myocardial Ischemia

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Chen, C., Ma, L., Dyckman, W., Santos, F., Lai, T., Gillam, L., & Waters, D. D. (1997). Left ventricular remodeling in myocardial hibernation. Circulation, 96(9 SUPPL.).
Chen, Chunguang ; Ma, Lijie ; Dyckman, William ; Santos, Federico ; Lai, Tianjie ; Gillam, Linda ; Waters, David D. / Left ventricular remodeling in myocardial hibernation. In: Circulation. 1997 ; Vol. 96, No. 9 SUPPL.
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abstract = "Background: Left ventricular (LV) remodeling as a consequence of extensive myocardial infarction has been well established in animal and human studies. This study was designed to determine whether regional LV dysfunction with myocardial hibernation without transmural or extensive infarction could initiate the remodeling process. Methods and Results: A severe left anterior descending coronary artery stenosis was created to reduce resting flow by ≃40{\%} (from 0.99±0.10 to 0.56±0.11 mL · min-1 · g-1) and was maintained for 7 days in 13 pigs. The reduction of regional coronary flow initially produced acute myocardial ischemia, as evidenced by reduced regional wall thickening, from 37±3{\%} at baseline to 9±7{\%}, regional lactate production and a decrease in regional coronary venous pH. All pigs had significant regional LV dysfunction and reduced LV ejection fraction (41±11{\%}). The LV end-diastolic volume increased from 59±9 mL at baseline to 74±13 mL immediately after placement of the stenosis and to 78±17 mL 7 days later with hibernating myocardium. The LV mass did not change immediately (60±8 g baseline versus 59±11 g immediately after creation of the stenosis) but increased modestly yet significantly to 67±15 g after 7 days of myocardial hibernation subtending the severe LAD stenosis. The reductions of coronary flow and wall thickening were unchanged at 7 days, whereas myocardial lactate production recovered. By 4 weeks after restoration of LAD flow, regional function had recovered in all 7 pigs with follow-up. Of the 13 pigs, 6 were free from any evidence of myocardial infarction, and 4 had patchy necrosis involving less than 6{\%} of the area at risk. Conclusions: LV remodeling, which is commonly associated with extensive myocardial infarction, can be initiated by regional dysfunctional hibernating myocardium resulting from a severe coronary stenosis. Myocardial necrosis is not a prerequisite for LV remodeling in response to regional dysfunction.",
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Chen, C, Ma, L, Dyckman, W, Santos, F, Lai, T, Gillam, L & Waters, DD 1997, 'Left ventricular remodeling in myocardial hibernation', Circulation, vol. 96, no. 9 SUPPL..

Left ventricular remodeling in myocardial hibernation. / Chen, Chunguang; Ma, Lijie; Dyckman, William; Santos, Federico; Lai, Tianjie; Gillam, Linda; Waters, David D.

In: Circulation, Vol. 96, No. 9 SUPPL., 04.11.1997.

Research output: Contribution to journalArticle

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T1 - Left ventricular remodeling in myocardial hibernation

AU - Chen, Chunguang

AU - Ma, Lijie

AU - Dyckman, William

AU - Santos, Federico

AU - Lai, Tianjie

AU - Gillam, Linda

AU - Waters, David D.

PY - 1997/11/4

Y1 - 1997/11/4

N2 - Background: Left ventricular (LV) remodeling as a consequence of extensive myocardial infarction has been well established in animal and human studies. This study was designed to determine whether regional LV dysfunction with myocardial hibernation without transmural or extensive infarction could initiate the remodeling process. Methods and Results: A severe left anterior descending coronary artery stenosis was created to reduce resting flow by ≃40% (from 0.99±0.10 to 0.56±0.11 mL · min-1 · g-1) and was maintained for 7 days in 13 pigs. The reduction of regional coronary flow initially produced acute myocardial ischemia, as evidenced by reduced regional wall thickening, from 37±3% at baseline to 9±7%, regional lactate production and a decrease in regional coronary venous pH. All pigs had significant regional LV dysfunction and reduced LV ejection fraction (41±11%). The LV end-diastolic volume increased from 59±9 mL at baseline to 74±13 mL immediately after placement of the stenosis and to 78±17 mL 7 days later with hibernating myocardium. The LV mass did not change immediately (60±8 g baseline versus 59±11 g immediately after creation of the stenosis) but increased modestly yet significantly to 67±15 g after 7 days of myocardial hibernation subtending the severe LAD stenosis. The reductions of coronary flow and wall thickening were unchanged at 7 days, whereas myocardial lactate production recovered. By 4 weeks after restoration of LAD flow, regional function had recovered in all 7 pigs with follow-up. Of the 13 pigs, 6 were free from any evidence of myocardial infarction, and 4 had patchy necrosis involving less than 6% of the area at risk. Conclusions: LV remodeling, which is commonly associated with extensive myocardial infarction, can be initiated by regional dysfunctional hibernating myocardium resulting from a severe coronary stenosis. Myocardial necrosis is not a prerequisite for LV remodeling in response to regional dysfunction.

AB - Background: Left ventricular (LV) remodeling as a consequence of extensive myocardial infarction has been well established in animal and human studies. This study was designed to determine whether regional LV dysfunction with myocardial hibernation without transmural or extensive infarction could initiate the remodeling process. Methods and Results: A severe left anterior descending coronary artery stenosis was created to reduce resting flow by ≃40% (from 0.99±0.10 to 0.56±0.11 mL · min-1 · g-1) and was maintained for 7 days in 13 pigs. The reduction of regional coronary flow initially produced acute myocardial ischemia, as evidenced by reduced regional wall thickening, from 37±3% at baseline to 9±7%, regional lactate production and a decrease in regional coronary venous pH. All pigs had significant regional LV dysfunction and reduced LV ejection fraction (41±11%). The LV end-diastolic volume increased from 59±9 mL at baseline to 74±13 mL immediately after placement of the stenosis and to 78±17 mL 7 days later with hibernating myocardium. The LV mass did not change immediately (60±8 g baseline versus 59±11 g immediately after creation of the stenosis) but increased modestly yet significantly to 67±15 g after 7 days of myocardial hibernation subtending the severe LAD stenosis. The reductions of coronary flow and wall thickening were unchanged at 7 days, whereas myocardial lactate production recovered. By 4 weeks after restoration of LAD flow, regional function had recovered in all 7 pigs with follow-up. Of the 13 pigs, 6 were free from any evidence of myocardial infarction, and 4 had patchy necrosis involving less than 6% of the area at risk. Conclusions: LV remodeling, which is commonly associated with extensive myocardial infarction, can be initiated by regional dysfunctional hibernating myocardium resulting from a severe coronary stenosis. Myocardial necrosis is not a prerequisite for LV remodeling in response to regional dysfunction.

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Chen C, Ma L, Dyckman W, Santos F, Lai T, Gillam L et al. Left ventricular remodeling in myocardial hibernation. Circulation. 1997 Nov 4;96(9 SUPPL.).