Why the study?
Does a flexible ventricular restraint device prevent left ventricular remodeling in an ovine model of acute myocardial infarction?
Does a flexible ventricular restraint device prevent left ventricular remodeling in an ovine model of acute myocardial infarction?
A flexible nitinol mesh ventricular restraint device successfully attenuated left ventricular dilatation and hypertrophy at 6 weeks in an ovine model of acute myocardial infarction.
Hypothesis-generating for post-MI restraint devices; leaves open translation to human therapy.
OBJECTIVES. This study examines the effects of a flexible ventricular restraint device on LV dilatation and hypertrophy after transmural infarction in an ovine model. BACKGROUND. Left ventricular (LV) remodeling and dilatation occurs after extensive myocardial infarction. METHODS. A flexible ventricular restraint made from a nitinol mesh was evaluated in adult female sheep (n=14). Cardiac MRI scans and hemodynamic measurements were completed before and six weeks after anterior myocardial infarction. Treatment animals (n=7) received passive ventricular restraint concurrently with LV infarction. The others (n=7) served as controls. RESULTS. Increases in LV end-diastolic volume index were significantly less in the restraint group than in controls (0.20 ± 0.41vs. 0.83 ± 0.50 mL/kg, p < .03). Likewise, end-systolic volumes increased less in treatment animals (0.43 ± 0.28 vs. 0.90 ± 0.38 mL/kg, p < .03). Control hearts showed an increase in LV mass after infraction, whereas the restrained hearts had a decrease in LV mass (0.14 ± 0.19 vs. –0.25 ± 0.36 g/kg, p < 0.03). Hemodynamic studies showed similar changes after infarction for the control and the device group. Gross and microscopic examination showed no device-induced epicardial injury. CONCLUSIONS. A flexible ventricular restraint device attenuated remodeling following acute myocardial infarction in sheep.
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Magovern et al. (2005) studied this question.
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