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Myocyte Vacuolization in Infarct Border Zones is Reversible

Overview
Journal Am J Pathol
Publisher Elsevier
Specialty Pathology
Date 1985 Dec 1
PMID 4073219
Citations 5
Authors
Affiliations
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Abstract

The nature of the changes occurring in the border zone of myocardial infarcts is uncertain. To study this question, the authors analyzed a number of morphologic features in hearts studied after postmortem arteriography and fixation in distention from 204 patients with single myocardial infarcts autopsied at The Johns Hopkins Hospital. Vacuolization of myocytes was observed in 53 (26%) cases, predominantly in surviving subendocardium and trabecular myocardium within the infarct. Lateral myocardium seldom and subepicardial myocardium almost never showed vacuolar change. Myocyte vacuolization progressively developed and then decreased with time: 1/20 (5%) hearts with infarcts less than 2 days old, 17/48 (35%) infarcts 2-14 days old, 13/27 (48%) infarcts 15-60 days old, 4/12 (33%) infarcts 61-365 days old, and 18/97 (19%) infarcts greater than 365 days old. Reduction in vacuolization with time was not explained by necrosis of vacuolated cells; rather, the myocardium showed normal morphology. Presence of vacuolization in old infarcts was associated with severe multivessel coronary artery disease and endocardial fibroelastosis. The results suggest that infarct border zone myocyte vacuolization may be correctable by reversal of regional ischemia; however, only a trivial amount of myocardium, relative to infarct size, undergoes vacuolar change.

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References
1.
Hutchins G, Bannayan G . Development of endocardial fibroelastosis following myocardial infarction. Arch Pathol. 1971; 91(2):113-8. View

2.
Hutchins G, Anaya O . Measurements of cardiac size, chamber volumes and valve orifices at autopsy. Johns Hopkins Med J. 1973; 133(2):96-106. View

3.
Ridolfi R, Hutchins G . The relationship between coronary artery lesions and myocardial infarcts: ulceration of atherosclerotic plaques precipitating coronary thrombosis. Am Heart J. 1977; 93(4):468-86. DOI: 10.1016/s0002-8703(77)80410-9. View

4.
Hutchins G, Miner M, Bulkley B . Tortuosity as an index of the age and diameter increase of coronary collateral vessels in patients after acute myocardial infarction. Am J Cardiol. 1978; 41(2):210-5. DOI: 10.1016/0002-9149(78)90158-3. View

5.
Prizel K, Hutchins G, Bulkley B . Coronary artery embolism and myocardial infarction. Ann Intern Med. 1978; 88(2):155-61. DOI: 10.7326/0003-4819-88-2-155. View