Effect of myocyte necrosis on strength, strain, and stiffness of isolated myocardial strips.
Cardiac rupture accounts for 8% to 10% of patient deaths after acute myocardial infarction, suggesting that myocyte necrosis weakens the ventricular wall in the initial days after occlusion. To test this theory, permanent occlusion of the left anterior descending coronary artery was performed in dogs. Twenty-four hours after occlusion, the tensile strength, strain at rupture, and stiffness of necrotic epicardium, midmyocardium, endocardium, subepicardium, and the visceral pericardium (VP) were quantified and compared with those of noninfarcted cardiac tissue. The relationship between tensile strength, stiffness, and collagen content was also examined. These material properties did not differ between necrotic and normal myocardium in any of the layers, indicating that myocyte necrosis, per se, does not weaken the myocardium. In both necrotic and normal tissue, marked transmural heterogeneity was observed; tensile strength of the endo- and epicardium (21.3 +/- 3.3 and 21.3 +/- 3.2 gm/mm2) was significantly greater (p less than 0.01) than that of the midmyocardium (4.0 +/- 0.3 gm/mm2) and subepicardium (5.0 +/- 0.5 gm/mm2), whereas the VP was substantially stronger (greater than 100 gm/mm2) than any myocardial layer. Similar results were obtained for stiffness. In contrast, strain at rupture did not vary significantly among myocardial layers and ranged from 0.40 +/- 0.03 (VP) to 0.53 +/- 0.03 (endocardium). Both tensile strength and stiffness of the myocardial layers were found to correlate directly with their collagen content: the higher the hydroxyproline concentration, the greater the tensile strength (r = 0.83). These results support the concept that the collagen fibroskeleton is an important determinant of the material properties of the myocardium. As myocyte necrosis, per se, did not affect tensile strength, we tentatively conclude that cardiac rupture may be a consequence of a defect or weakness in the collagenous framework of the heart.
Przyklenk
K
K
Department of Medicine, Harvard University, Boston, Mass.
Connelly
C M
CM
McLaughlin
R J
RJ
Kloner
R A
RA
Apstein
C S
CS
D000818:Animals; D001696:Biomechanical Phenomena; D003094:Collagen / Q000032:analysis; D004285:Dogs; D004699:Endocardium / Q000473:pathology; D005260:Female; D006341:Heart Rupture / Q000503:physiopathology; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology*; D009206:Myocardium / Q000032:analysis / Q000473:pathology*; D009336:Necrosis; D010496:Pericardium / Q000473:pathology; D013718:Tensile Strength
D003094:Collagen