CHANGES IN PASSIVE MECHANICAL STIFFNESS OF MYOCARDIAL TISSUE WITH ANEURYSM FORMATION

Background Myocardium undergoes complex cellular and histochemical alt erations after acute myocardial infarction. These structural changes d irectly affect the mechanical stiffness of infarcted and remote myocar dia. Previous investigations of infarct stiffness have been limited to uniaxial testing, which does not provide a unique description of the tissue's three-dimensional material properties. This study describes t he first serial measurements of biaxial mechanical properties of sheep myocardium after anterioapical infarction. Methods and Results Anteri oapical infarctions of 23.7+/-2.5% of the left ventricular mass were p roduced by coronary arterial ligation in sheep. Biaxial force-extensio n measurements were made on freshly excised squares (6.45 cm(2)) of re mote, noninfarcted, and infarcted myocardia before and 4 hours, 1 week , 2 weeks, and 6 weeks after ligation. Adjacent myocardial samples wer e assayed for hydroxyprorine content. Force-extension data and a deriv ed constitutive equation were used to describe stresses and strains an d material properties of each sample. In sheep, anterioapical infarcti ons evolve into thin left ventricular aneurysms that consist of predom inantly fibrous tissue with disrupted groups of muscle cells encased i n scar. In the infarct, Cauchy stresses at 15% extensions (control str esses: circumferential, sigma(c), 19.4+/-3.3 g/cm(2); longitudinal, si gma(L), 54.8+/-34.8 g/cm(2)) increase within 4 hours, peak at 1 to 2 w eeks (sigma(c), 338.5+/-143.6 g/cm(2); sigma(L), 310.7+/-45.9 g/cm(2)) , and then decrease 6 weeks after infarction (sigma(c), 115+/-47.2 g/c m(2); sigma(L), 53.2+/-28.9 g/cm(2)). Stresses in the remote myocardiu m follow a similar time course but to a lesser extent than the infarct ed region. Hydroxyproline content, a measure of collagen content, does not correlate with infarct stiffness but progressively increases to 6 9.7+/-7.6 mu g/mg after 6 weeks. Stress-extension curves demonstrate d irectional anisotropy of both infarcted and remote myocardia. Conclusi ons The findings indicate that infarcted myocardium becomes more stiff during the first 1 to 2 weeks after anterioapical infarction and then more compliant. The infarct also exhibits directional anisotropy. The se observations underscore the importance of ventricular material prop erties during the remodeling process after acute myocardial infarction and may partially explain the progressive left ventricular dilatation and functional deterioration that occur in some patients after anteri oapical infarction.