Changes in passive mechanical stiffness of myocardial tissue with aneurysm formation.

BACKGROUND Myocardium undergoes complex cellular and histochemical alterations after acute myocardial infarction. These structural changes directly affect the mechanical stiffness of infarcted and remote myocardia. 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 the first serial measurements of biaxial mechanical properties of sheep myocardium after anteroapical infarction.

METHODS AND RESULTS Anteroapical infarctions of 23.7 +/- 2.5% of the left ventricular mass were produced by coronary arterial ligation in sheep. Biaxial force-extension measurements were made on freshly excised squares (6.45 cm2) of remote, noninfarcted, and infarcted myocardia before and 4 hours, 1 week, 2 weeks, and 6 weeks after ligation. Adjacent myocardial samples were assayed for hydroxyproline content. Force-extension data and a derived constitutive equation were used to describe stresses and strains and material properties of each sample. In sheep, anteroapical infarctions evolve into thin left ventricular aneurysms that consist of predominantly fibrous tissue with disrupted groups of muscle cells encased in scar. In the infarct, Cauchy stresses at 15% extensions (control stresses: circumferential, sigma C, 19.4 +/- 3.3 g/cm2; longitudinal, sigma L, 54.8 +/- 34.8 g/cm2) increase within 4 hours, peak at 1 to 2 weeks (sigma C, 338.5 +/- 143.6 g/cm2; sigma L, 310.7 +/- 45.9 g/cm2), and then decrease 6 weeks after infarction (sigma C, 115 +/- 47.2 g/cm2; sigma L, 53.2 +/-28.9 g/cm2). Stresses in the remote myocardium follow a similar time course but to a lesser extent than the infarcted region. Hydroxyproline content, a measure of collagen content, does not correlate with infarct stiffness but progressively increases to 69.7 +/- 7.6 micrograms/mg after 6 weeks. Stress-extension curves demonstrate directional anisotropy of both infarcted and remote myocardia.

CONCLUSIONS The findings indicate that infarcted myocardium becomes more stiff during the first 1 to 2 weeks after anteroapical infarction and then more compliant. The infarct also exhibits directional anisotropy. These observations underscore the importance of ventricular material properties 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 anteroapical infarction.