Author + information
- Received April 21, 1987
- Revision received July 23, 1987
- Accepted August 7, 1987
- Published online January 1, 1988.
- David A Kass, MD∗,2,
- W.Lowell Maughan, MD3,
- Allen Ciuffo, MD,
- Willard Graves, PhD,
- Bernadine Healy, MD, FACC1 and
- Myron L Weisfeldt, MD, FACC
- ↵∗Address for reprints: David A. Kass, MD, Division of Cardiology, Carnegie 565A, Johns Hopkins Medical Institutions, 600 North Wolfe Street, Baltimore, Maryland 21205.
The relation between acute disproportionate infarct dilation and late postinfarct left ventricular remodeling was examined by implanting multiple radiopaque epicardial markers in the left ventricle of eight dogs and determining regional surface deformation after acute and chronic transmural infarction. Transmural injury was produced by combining coronary ligation with distal embolization of a rubber polymer. Dogs were anesthetized and studied before and 1 h, 24 h and 1 week after infarction. Marker positions were recorded by rapid biplane cineradiography, and three-dimensional coordinates were reconstructed by a computer-assisted tracking system. Regional deformation was expressed by a local surface area equal to the sum of multiple (three to four) triangles generated by marker triplets.
As early as 1 h after infarction, end-diastolic area in the infarct region increased by 20.3 ± 3.1%, while that in the remote region increased by only 7.9 ± 3.5%. Both changes and the difference between them were significant. At 24 h after infarction, both territories continued to undergo dilation, this time to a similar extent (additional +10.3% in the remote region and +10.1% in the infarct region), thus maintaining the significant disproportionate infarct dilation. At 1 week, however, the infarct territory remained dilated with a mean end-diastolic area 31.4 ± 3.1% above control, while that in the remote region returned to a net mean 8.5 ± 4.7% increase.
Thus, the major extent of disproportionate infarct dilation occurs within 1 h after transmural injury and is accompanied by remote dilation as a compensatory response. The extent of further infarct dilation achieved by 24 h is maintained in the chronic infarct, and compensatory mechanisms enable noninjured myocardium to become less dilated. This is an even earlier time course than previously demonstrated, which suggests that attempts to limit infarct dilation should target the acute phase of injury.
↵2 Dr. Kass is a recipient of Physician Scientist Award HL-01820.
↵3 Dr. Maughan is a recipient of Research Career Development Award HL-01610-01 from the National Institutes of Health.
↵1 Dr. Healy's present address is: Research Division, The Cleveland Clinics, Cleveland, Ohio 44106.
☆ This study was supported by National Health Service Grants HL-4529, HL-4903 and HL-33243 from the National Institutes of Health, Bethesda, Maryland.
- Received April 21, 1987.
- Revision received July 23, 1987.
- Accepted August 7, 1987.