(Circulation. 1995;91:1143-1153.)
© 1995 American Heart Association, Inc.
Articles |
From the Division of Cardiology, Department of Medicine, University of California, San Diego, La Jolla.
Correspondence to John Ross, Jr, MD, Department of Medicine, 0613B, University of California, San Diego, 9500 Gilman Dr, La Jolla, CA 92093-0613.
Background The effects of reperfusion after coronary
occlusion on transmural remodeling of the ischemic region early and
late after nontransmural infarction must importantly affect the
recovery of regional function. Accordingly, analysis of local
volume and three-dimensional strain was performed using a finite
element method to determine regional remodeling. Systolic and
remodeling strains were measured using radiographic imaging of three
columns (
1 cm apart) of four to six gold beads implanted across the
left ventricular posterior wall in 6 dogs.
Methods and Results After a control study, infarction was produced by 2 to 4 hours of proximal left circumflex coronary artery occlusion followed by reperfusion. Follow-up studies were performed at 2 days, 3 weeks, and 12 weeks with the dogs under anesthesia and in closed-chest conditions. Biplane cineradiography was performed to obtain the three-dimensional coordinates of the beads. At 2 days, end-systolic strains were akinetic with loss of normal transmural gradients of shortening and thickening. Remodeling strains (RS) were determined by use of a nonhomogeneous finite element method by referring the end-diastolic configuration during follow-up studies to its control state at matched end-diastolic pressures and heart rates. Tissue volume at 2 days increased substantially, more at the endocardium (30±7%) than at the epicardium (5±12%, P<.01); the increase was associated with an average RS in the wall-thickening direction of 0.18±0.15 (P<.01) with all other RS near zero. At 12 weeks systolic function partially recovered, with normal wall thickening in the epicardium (radial strain, 0.081±0.056 [control] versus 0.113±0.088 [12 weeks]) but with dysfunction in the endocardium (0.245±0.108 [control] versus 0.111±0.074 [P<.01] [12 weeks]). This inability of the inner wall to recover function may be related to increased transmural torsional shear and negative longitudinal-radial transverse shear in the inner wall. Volume loss occurred at 12 weeks in the endocardium (-36±16%) corresponding to transmural gradients in longitudinal RS and both transverse shear RS. Negative longitudinal RS was greater at the endocardium (-0.20±0.10) than at the epicardium (-0.06±0.05, P<.01).
Conclusions These results indicate the presence of marked subendocardial edema 2 days after reperfusion following 2 to 4 hours of coronary occlusion. At 3 months after reperfusion, however, there was volume loss in the inner wall due to shrinkage along the myofiber direction with reduced transmural function and loss of longitudinal shortening, while both tissue volume and function recovered completely in the outer wall.
Key Words: myocardial contraction myocardial infarction edema radiography
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