Hypercholesterolemia exacerbates ventricular remodeling in the rat model of myocardial infarction
Michał Maczewski1, Joanna Maczewska
1Department of Clinical Physiology, Medical Center of Postgraduate Education, Warsaw, Poland.
Insights
High cholesterol intake worsens left ventricular (LV) remodeling and heart failure after myocardial infarction in rats. This effect is independent of infarct size, highlighting cholesterol
Area of Science:
- Cardiovascular Biology
- Heart Failure Research
- Metabolic Syndrome Studies
Background:
- Hypercholesterolemia exacerbates left ventricular (LV) remodeling post-myocardial infarction (MI).
- The independent contribution of hypercholesterolemia to LV remodeling, separate from infarct size, remains unclear.
- Understanding this relationship is crucial for managing heart failure in hypercholesterolemic patients.
Purpose of the Study:
- To investigate if high cholesterol feeding worsens LV remodeling and heart failure in a rat model of MI.
- To determine if this exacerbation is independent of cholesterol's effect on infarct size.
- To elucidate the specific impact of hypercholesterolemia on post-MI cardiac function.
Main Methods:
- Myocardial infarction (MI) induced by permanent ligation of the left coronary artery in rats.
- Rats were fed either a normal or high-cholesterol diet and observed for 8 weeks.
- Echocardiography and pressure-volume loop analysis were used to assess LV remodeling and function.
Main Results:
- Hypercholesterolemic rats, matched for infarct size, showed significantly greater LV dilation.
- LV systolic/diastolic diameters were larger in hypercholesterolemic rats (8.1/10.2 mm) vs. controls (6.7/8.9 mm).
- Higher diastolic LV volumes and LV end-diastolic pressure were observed in hypercholesterolemic rats.
Conclusions:
- High-cholesterol diet significantly exacerbates LV remodeling and heart failure post-MI in rats.
- This detrimental effect is independent of the impact of hypercholesterolemia on initial infarct size.
- Findings suggest hypercholesterolemia directly promotes adverse cardiac remodeling irrespective of MI severity.
Background:
Detrimental left ventricular (LV) remodeling is exacerbated in hypercholesterolemic patients with myocardial infarction; however, this could result from either larger infarcts or more extensive remodeling itself in this population. Therefore, we sought to investigate whether high cholesterol feeding exacerbates LV remodeling and heart failure in rats with myocardial infarction independently from its influence on infarct size.
Methods And Results:
Myocardial infarction was induced by permanent ligation of left coronary artery in rats fed normal and high-cholesterol diet and the animals were followed for 8 weeks. Hypercholesterolemic rats were matched with normocholesterolemic animals for infarct size 24 hours after infarction and exhibited more pronounced LV dilation at 8 weeks after infarction (LV systolic/diastolic diameter 8.1 +/- 0.2/10.2 +/- 0.3 versus 6.7 +/- 0.2/8.9 +/- 0.2, respectively, measured by echocardiography, P < .05 each). Pressure-volume curves obtained in isolated Langendorff-perfused hearts revealed higher diastolic LV volumes (1677 +/- 102 versus 1385 +/- 46 muL/kg body weight, P < .05) and hemodynamic examination demonstrated higher LV end-diastolic pressure (21.8 +/- 0.7 versus 18.7 +/- 1.0 mm Hg, P < .05) in hypercholesterolemic rats compared with normocholesterolemic animals.
Conclusion:
In a rat model of myocardial infarction, LV remodeling and heart failure are more pronounced in rats fed high-cholesterol diet in comparison to animals fed normal chow. This effect is independent from effect of hypercholesterolemia on infarct size.
