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Updated: Mar 1, 2026
Surgical Swine Model of Chronic Cardiac Ischemia Treated by Off-Pump Coronary Artery Bypass Graft Surgery
Published on: March 27, 2018
Diastolic dysfunction persists 3 months after surgical revascularization in a large animal model of hibernating
Koray N Potel1, Annie Shao1, Nolan McLaughlin1
1Department of Surgery, University of Minnesota, Minneapolis, Minn.
Insights
Diastolic dysfunction in hibernating myocardium (HM) persists after coronary artery bypass grafting (CABG), even at three months. Persistent fibrosis and stiffness limit recovery, indicating a need for additional therapies alongside revascularization.
Area of Science:
- Cardiology
- Cardiovascular Research
- Myocardial Ischemia
Background:
- Diastolic heart failure with preserved ejection fraction (HFpEF) from coronary artery disease (CAD) causes significant morbidity and mortality.
- Chronic myocardial ischemia leads to diastolic dysfunction, but recovery after revascularization is poorly understood.
Purpose of the Study:
- To assess systolic and diastolic myocardial recovery in a swine model of hibernating myocardium (HM) after coronary artery bypass grafting (CABG).
Main Methods:
- A swine model of chronic myocardial ischemia without infarction was created using a LAD constrictor.
- Groups included controls, HM without revascularization, and HM with CABG and 1- or 3-month recovery.
- Cardiac MRI evaluated systolic and diastolic function at rest and stress; histopathology examined tissue changes.
Main Results:
- Hibernating myocardium (HM) showed depressed systolic and diastolic function, which improved post-CABG.
- Diastolic relaxation remained significantly impaired at 3 months post-CABG compared to controls.
- Histology revealed persistent interstitial fibrosis and myofibroblasts in HM and post-CABG tissues.
Conclusions:
- Diastolic dysfunction persists in hibernating myocardium (HM) under stress, even 3 months after CABG.
- Persistent fibrosis and diastolic stiffness impede full recovery.
- Adjunctive pharmacologic or regenerative therapies are needed at revascularization.
Objective:
Diastolic heart failure with preserved ejection fraction secondary to coronary artery disease is associated with a significant morbidity and mortality. Diastolic dysfunction due to chronic myocardial ischemia is an important clinical entity though recovery of diastolic relaxation with revascularization is poorly understood. A swine model of hibernating myocardium (HM) was used to assess systolic and diastolic myocardial recovery following coronary artery bypass grafting (CABG).
Methods:
Study animals included 18 juvenile pigs who underwent placement of a constrictor around the left anterior descending artery to gradually create chronic ischemia without infarction. Study groups included 5 healthy age- and weight-matched controls, 6 HM animals without revascularization, 7 HM + CABG + 1 month recovery and 5 HM + CABG + 3 months recovery. Cardiac magnetic resonance imaging was used to assess global systolic and diastolic function at rest and with dobutamine stress. Histopathology assessed tissue structural and molecular changes.
Results:
Systolic and diastolic myocardial function were significantly depressed in HM. Both improved with CABG; however, diastolic relaxation remained significantly impaired even at 3 months post-CABG compared with controls. Histological analysis showed interstitial fibrosis in HM tissue with residual fibrosis seen post-CABG. Alpha-smooth muscle actin stain identified myofibroblasts in both HM and post-CABG animals.
Conclusions:
In a large animal model of HM, diastolic dysfunction persists under stress despite CABG and is present even after 3 months of recovery. Persistent fibrosis and diastolic stiffness prevent full recovery. These findings highlight a therapeutic need for pharmacologic or regenerative adjunctive therapies at the time of revascularization.
