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Effect of long-term captopril therapy on left ventricular remodeling and function during healing of canine myocardial
B I Jugdutt1, B L Schwarz-Michorowski, M I Khan
1Cardiology Division, University of Alberta, Edmonton, Canada.
Insights
Captopril treatment attenuated left ventricular remodeling and improved function after myocardial infarction in dogs. This ACE inhibitor reduced adverse cardiac changes, enhancing recovery and ejection fraction.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Regenerative Medicine
Background:
- Acute anterior myocardial infarction can lead to detrimental left ventricular remodeling.
- Left ventricular remodeling involves changes in size, shape, and function post-infarction.
- Attenuating remodeling is crucial for improving outcomes after myocardial infarction.
Purpose of the Study:
- To investigate if long-term reduction of preload and afterload by captopril can attenuate left ventricular remodeling and improve function after myocardial infarction.
- To assess the effects of captopril on scar topography, collagen content, and cardiac function in a canine model.
Main Methods:
- 30 dogs with induced anterior myocardial infarction were randomized to placebo or captopril (50 mg twice daily) for 6 weeks.
- Serial hemodynamic measurements, echocardiography, and scar analysis (planimetry, arteriography, hydroxyproline) were performed.
- Left ventricular remodeling was assessed by measuring infarct scar thinning, expansion, and aneurysm formation.
Main Results:
- Captopril significantly reduced mean arterial pressure and mean left atrial pressure compared to placebo.
- While scar mass and collagen were similar, captopril treatment resulted in less scar thinning and expansion.
- Echocardiography revealed less left ventricular aneurysm formation and improved global ejection fraction with captopril.
Conclusions:
- Long-term captopril therapy effectively attenuates adverse left ventricular remodeling after myocardial infarction in dogs.
- Captopril improves cardiac function by reducing infarct expansion, thinning, and aneurysm formation.
- These findings suggest captopril's potential therapeutic benefit in post-myocardial infarction recovery.
Abstract:
To determine whether the long-term reduction of preload and afterload by captopril during healing after acute anterior myocardial infarction might attenuate left ventricular remodeling and improve function, 30 chronically instrumented dogs with infarction produced by left anterior descending coronary artery ligation were randomized 2 days later to oral therapy with placebo (n = 15) or captopril, 50 mg twice daily (n = 15), for 6 weeks. Serial hemodynamic as well as topographic and functional variables (two-dimensional echocardiography) were measured over 6 weeks. Scar topography (planimetry), occluded bed size (coronary arteriography) and collagen (hydroxyproline) content were measured at 6 weeks. Between 2 days and 6 weeks, captopril decreased (p less than 0.001) mean arterial pressure and mean left atrial pressure more than did placebo, but it did not influence heart rate. Infarct scar mass, transmurality and collagen content at 6 weeks were similar in the two groups but scars showed less (p less than 0.001) thinning and expansion with captopril than with placebo. Echocardiograms showed similar infarct expansion and thinning in the two groups at 2 days but less aneurysm with captopril at 6 weeks. Between 2 days and 6 weeks, expansion index (infarct-/noninfarct-containing segment length) decreased (p less than 0.001) with captopril but increased (p less than 0.001) with placebo. Also, thinning ratio (infarct/normal wall thickness) decreased (p less than 0.001) with placebo but did not change (p = NS) with captopril. By 6 weeks, left ventricular asynergy and volumes showed a greater decrease (p less than 0.01) and global ejection fraction a greater increase (p less than 0.05) with captopril.(ABSTRACT TRUNCATED AT 250 WORDS)