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Left ventricular aneurysm repair in rats: structural, functional, and molecular consequences
G Sakaguchi1, R L Young, M Komeda
1Departments of Clinical Pharmacology and Therapeutics and Cardiac Surgery, Austin and Repatriation Medical Centre, Heidelberg, Victoria 3084, Australia.
The Journal of Thoracic and Cardiovascular Surgery
|March 30, 2001
Summary
Surgical repair of left ventricular aneurysms in rats after myocardial infarction improved heart function. This procedure also normalized gene expression related to cardiac hypertrophy and contractile proteins.
Area of Science:
- Cardiovascular Research
- Molecular Cardiology
- Regenerative Medicine
Background:
- Myocardial infarction (MI) often leads to left ventricular (LV) aneurysm formation, impairing cardiac function.
- LV aneurysm is associated with adverse cardiac remodeling, including hypertrophy and altered gene expression.
Purpose of the Study:
- To investigate the impact of surgical aneurysm repair on cardiac function and gene expression in a rat model of MI.
- To assess the spatiotemporal distribution of cardiac contractile protein and natriuretic peptide messenger RNA (mRNA) after aneurysm repair.
Main Methods:
- A rat model of MI was established, and LV aneurysms were surgically plicated 4 weeks post-infarction.
- At 30 weeks, heart sections were analyzed using in situ hybridization histochemistry to quantify regional mRNA levels of key cardiac genes.
Main Results:
- Plication significantly reduced LV endocardial circumference, heart weight ratio, and LV end-diastolic pressures.
- Improved cardiac function was indicated by increased +/-dP/dt.
- Aneurysm repair led to reduced mRNA levels of pre-pro-atrial natriuretic peptide, skeletal alpha-actin, beta-myosin heavy chain, and myosin light chain-2v in specific cardiac regions.
Conclusions:
- Surgical plication of LV aneurysms post-MI effectively reduces cardiac hypertrophy and enhances cardiac function in rats.
- The procedure normalizes the expression of genes associated with cardiac hypertrophy and fetal/adult contractile protein isoforms.