Key result
Cardiac support device reduces end-diastolic volume ~39% and improves LVEF after myocardial infarction.
Why the study?
Limiting progressive left ventricular dilatation after myocardial infarction by passive constraint may improve cardiac function and myocardial energetics but requires investigation.
Does a woven polyester jacket cardiac support device improve left ventricular function and mechanics in an ovine model of heart failure secondary to acute myocardial infarction?
Does a woven polyester jacket cardiac support device improve left ventricular function and mechanics in an ovine model of heart failure secondary to acute myocardial infarction?
Absolute Event Rate: 67.6% vs 110.3%
p-value: p=.006
Passive constraint with a cardiac support device prevents further remodeling and improves cardiac function and energetics in an ovine model of post-infarction heart failure.
May reduce post-MI wall stress in experimental models; leaves open whether passive constraint improves clinical outcomes.
OBJECTIVE: This study investigated the effects on global cardiac function and myocardial energetics of limiting progressive dilatation after infarction by means of a woven polyester jacket cardiac support device. We hypothesized that placement of the cardiac support device results in a decrease in myocardial wall stress and improvement in cardiac function and myocardial energetics. METHODS: To investigate the effect of passive constraint on left ventricular function and mechanics, a total of 10 sheep were studied with pressure-volume analysis and magnetic resonance imaging. A baseline study was followed by the creation of an anterior infarct. After 1 week, the animals underwent a second study. The cardiac support device was then placed over the epicardium in 5 sheep; the remaining animals served as controls. A terminal study was performed at 2 months after the infarct. RESULTS: The cardiac support device group at the terminal study exhibited a decrease in end-diastolic volume (control 110.3 +/- 19.8 mL vs cardiac support device 67.6 +/- 4.7 mL, P =.006) and an improved ejection fraction (control 15.5% +/- 5.7% vs cardiac support device 29.46% +/- 4.42%, P =.008) relative to the control group. Myocardial energetics were also enhanced in the cardiac support device group, as evidenced by the significant improvements in potential energy (control 2015 +/- 503 mL. mm Hg/beat vs cardiac support device 885 +/- 220 mL. mm Hg/beat, P =.006), efficiency (control 39.4% +/- 13.6% vs cardiac support device 59.8% +/- 8.5%, P =.044), and oxygen consumption (control 0.072 +/- 0.013 mL O(2)/beat vs cardiac support device 0.052 +/- 0.007 mL O(2)/beat, P =.034). CONCLUSION: Passive constraint with the cardiac support device after infarct prevents further remodeling and may stimulate reverse remodeling in heart failure secondary to acute myocardial infarction. These results suggest that in human beings placement of the cardiac support device after a large anterior myocardial infarction may be effective in halting the remodeling process that often leads to end-stage heart failure. If proved effective, placement of a cardiac support device after large heart attacks has the potential to decrease the incidence of heart failure that results after large myocardial infarctions.
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Pilla et al. (2003) studied heart failure secondary to acute myocardial infarction (n=10). woven polyester jacket cardiac support device vs. no device (control) was evaluated on end-diastolic volume (p=.006). Placement of a cardiac support device in an ovine infarct model significantly decreased end-diastolic volume (67.6 vs 110.3 mL, P=0.006) and improved ejection fraction (29.5% vs 15.5%, P=0.008).
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