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Updated: Dec 10, 2025
Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Hemorrhage promotes chronic adverse remodeling in acute myocardial infarction: a T1 , T2 and BOLD study
Stephania Assimopoulos1, Nancy Shie2, Venkat Ramanan2
1Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada.
Insights
Myocardial hemorrhage worsens heart attack outcomes by increasing damage, inflammation, and adverse remodeling. Understanding these effects may lead to new treatments for heart failure.
Area of Science:
- Cardiovascular Research
- Pathophysiology
- Medical Imaging
Background:
- Hemorrhage is an emerging predictor of poor outcomes after acute myocardial infarction.
- The underlying mechanisms linking hemorrhage to adverse cardiac events remain unclear.
Purpose of the Study:
- To investigate the chronic effects of myocardial hemorrhage on cardiac remodeling, inflammation, and vasodilator function.
- To elucidate the downstream consequences of hemorrhage beyond the initial ischemic insult using an experimental porcine model.
Main Methods:
- Myocardial hemorrhage was induced via intracoronary collagenase injection in a porcine model.
- Animals underwent coronary occlusion/reperfusion with or without hemorrhage, followed by MRI up to 4 weeks.
- Cardiac function, edema, hemorrhage, vasodilator function, infarct size, and microvascular obstruction were assessed.
Main Results:
- Hemorrhage significantly increased infarct size, microvascular obstruction, and adverse cardiac remodeling compared to ischemia alone.
- Hemorrhage led to compromised cardiac function, enlarged ventricular volume, and remote myocardial alterations.
- Edema and matrix expansion were greatest in the infarct zone of the hemorrhage groups.
Conclusions:
- Myocardial hemorrhage at reperfusion exacerbates myocardial damage and promotes chronic adverse remodeling.
- Hemorrhage induces inflammation and remote myocardial changes, contributing to heart failure progression.
- Understanding hemorrhage's impact is crucial for developing targeted therapies for high-risk cardiac patients.
Abstract:
Hemorrhage is recognized as a new independent predictor of adverse outcomes following acute myocardial infarction. However, the mechanisms of its effects are less understood. The aim of our study was to probe the downstream impact of hemorrhage towards chronic remodeling, including inflammation, vasodilator function and matrix alterations in an experimental model of hemorrhage. Myocardial hemorrhage was induced in the porcine heart by intracoronary injection of collagenase. Animals (N = 18) were subjected to coronary occlusion followed by reperfusion in three groups (six/group): 8 min ischemia with hemorrhage (+HEM), 45 min infarction with no hemorrhage (I - HEM) and 45 min infarction with hemorrhage (I + HEM). MRI was performed up to 4 weeks after intervention. Cardiac function, edema (T2 , T1 ), hemorrhage (T2 *), vasodilator function (T2 BOLD), infarction and microvascular obstruction (MVO) and partition coefficient (pre- and post-contrast T1 ) were computed. Hemorrhage was induced only in the +HEM and I + HEM groups on Day 1 (low T2 * values). Infarct size was the greatest in the I + HEM group, while the +HEM group showed no observable infarct. MVO was seen only in the I + HEM group, with a 40% occurrence rate. Function was compromised and ventricular volume was enlarged only in the hemorrhage groups and not in the ischemia-alone group. In the infarct zone, edema and matrix expansion were the greatest in the I + HEM group. In the remote myocardium, T2 elevation and matrix expansion associated with a transient vasodilator dysfunction were observed in the hemorrhage groups but not in the ischemia-alone group. Our study demonstrates that the introduction of myocardial hemorrhage at reperfusion results in greater myocardial damage, upregulated inflammation, chronic adverse remodeling and remote myocardial alterations beyond the effects of the initial ischemic insult. A systematic understanding of the consequences of hemorrhage will potentially aid in the identification of novel therapeutics for high-risk patients progressing towards heart failure.
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