Cardiac support device modifies left ventricular geometry and myocardial structure after myocardial infarction

Article

关键词: MATRIX-METALLOPROTEINASE INHIBITION;    HEART-FAILURE;    TISSUE INHIBITOR;    MATRIX-METALLOPROTEINASE-9;    DYSFUNCTION;    PROGRESSION;    ENALAPRIL;    EXPANSION;   

DOI  :  10.1161/CIRCULATIONAHA.104.499202

来源: SCIE

【 摘 要 】

Background - Whether mechanical restraint of the left ventricle ( LV) can influence remodeling after myocardial infarction ( MI) remains poorly understood. This study surgically placed a cardiac support device ( CSD) over the entire LV and examined LV and myocyte geometry and function after MI. Methods and Results - Post- MI sheep ( 35 to 45 kg; MI size, 23 +/- 2%) were randomized to placement of the CorCap CSD ( Acorn Cardiovascular, Inc) ( MI + CSD; n = 6) or remained untreated ( MI only; n = 5). Uninstrumented sheep ( n = 10) served as controls. At 3 months after MI, LV end- diastolic volume ( by MRI) was increased in the MI only group compared with controls ( 98 +/- 8 versus 43 +/- 4 mL; P < 0.05). In the MI + CSD group, LV end- diastolic volume was lower than MI only values ( 56 +/- 7 mL; P < 0.05) but remained higher than controls ( P < 0.05). Isolated LV myocyte shortening velocity was reduced by 35% from control values ( P < 0.05) in both MI groups. LV myocyte beta-adrenergic response was reduced with MI but normalized in the MI + CSD group. LV myocyte length increased in the MI group and was reduced in the MI + CSD group. Relative collagen content was increased and matrix metalloproteinase- 9 was decreased within the MI border region of the CSD group. Conclusions - A CSD beneficially modified LV and myocyte remodeling after MI through both cellular and extracellular mechanisms. These findings provide evidence that nonpharmacological strategies can interrupt adverse LV remodeling after MI.

【 授权许可】

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