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Published on: April 17, 2021
Heat shock treatment prior to myocardial infarction results in reduced ventricular remodeling
Olivier Heimrath1, Adam Oxner, Tanya Myers
1Department of Surgery, Dalhousie University, Halifax, Nova Scotia, Canada.
Insights
Heat shock (HS) treatment before myocardial infarction (MI) improved heart function and reduced left ventricular (LV) remodeling weeks later. This cardiac protection occurred without altering initial infarct size.
Area of Science:
- Cardiology
- Cardiovascular Research
- Cellular Biology
Background:
- Heat shock (HS) is explored for potential myocardial protection post-ischemia.
- Limited data exists on HS effects on left ventricular (LV) remodeling weeks after myocardial infarction (MI).
Purpose of the Study:
- To investigate the impact of pre-conditioning heat shock treatment on LV remodeling following experimental myocardial infarction.
Main Methods:
- Myocardial infarction (MI) induced by coronary ligation in Lewis rats.
- Two groups: Heat Shock + MI (HS+MI) and MI alone.
- HS treatment: 42°C for 15 min, 24 hr before MI.
- LV remodeling assessed via echocardiography and histology at various time points.
Main Results:
- No significant difference in infarct size between HS+MI and MI groups.
- HS+MI group showed preserved LV ejection fraction and fractional shortening at 7 and 28 days post-MI.
- HSP27 expression remained elevated at infarct borders in both groups at 28 days.
Conclusions:
- Pre-conditioning heat shock treatment significantly reduces LV remodeling after MI.
- This protective effect is independent of changes in infarct size.
- HS treatment offers a potential therapeutic strategy for post-MI cardiac remodeling.
Background:
Heat shock (HS) treatment has been suggested to confer myocardial protection following ischemia. However, the effects of HS on left ventricular (LV) remodeling weeks after infarction have yet to be described.
Methods:
Myocardial infarction (MI) was created by coronary ligation in Lewis rats. Two experimental groups of animals were created: HS+MI group (n = 13) and MI group (n = 13). HS treatment consisted of an elevation in core temperature to 42 degrees C for 15 min, 24 hr prior to MI. LV remodeling was assessed by transthoracic echocardiography (day 0, 1, 7, and 28) and by morphometric histology (day 28).
Results:
There was no significant difference in infarct size (TTC stain 24 hr) between HS+MI and MI groups. Using transthoracic echo there was a significant preservation of LV ejection fraction and fractional shortening in the HS+MI group as compared to MI group (7 and 28 days). Similar trends were seen by histology at 28 days but failed to reach significance. HSP27 expression by myocardial cells was shown to remain up-regulated (at 28 days) in both groups at the edges of the infarct area as compared to control myocardium.
Conclusions:
Our findings suggest that HS treatment prior to MI can result in a significant decrease in LV remodeling independent of a reduction in infarct size.
