Contractility in the borderzone (BZ) after antero-apical myocardial infarction (MI) is depressed. We tested the hypothesis that BZ contractility is also decreased after postero-lateral MI.
Five sheep underwent postero-lateral MI. Magnetic resonance imaging (MRI) was performed 2 weeks before and 16 weeks after MI, and left ventricular (LV) volume and regional strain were measured. Finite element (FE) models were constructed and the systolic material parameter, Tmax, was calculated in the BZ and remote myocardium by minimizing the difference between experimentally measured and calculated LV strain and volume. Sheep were sacrificed 17 weeks after MI and myocardial muscle fibers were taken from the BZ and remote myocardium. Fibers were chemically demembranated, and isometric developed force, Fmax, was measured at supra-maximal [Ca2+]. Routine light microscopy was also performed.
There was no difference in Tmax between pre-MI and remote myocardium 16 weeks after MI. However, there was a large decrease (63.3%, p=0.005) in Tmax in the BZ when compared with the remote myocardium 16 weeks after MI. In addition, there was a significant reduction of BZ Fmax for all samples (18.9%, p=0.023). Myocyte cross-sectional area increased by 61% (p=0.021) in the BZ, but there was no increase in fibrosis.
Contractility in the borderzone is significantly depressed relative to the remote myocardium after postero-lateral MI. The reduction in contractility is due at least in part to a decrease in contractile protein function.
Keywords: myocardial infarction, remodeling, borderzone, ventricular function, cardiac mechanics, contractility, magnetic resonance imaging, finite element