In vivo assessment by computed tomography of the natural progression of infarct size, left ventricular muscle mass and function after acute myocardial infarction in the dog

Wallace W. Peck, G. B.John Mancini, Robert A. Slutsky, Robert F. Mattrey, Charles B. Higgins

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Quantification of myocardial infarct (MI) size is of prognostic importance in patients with acute ischemic damage. Evaluation of the efficacy of interventions for salvage of ischemic myocardium depends on the accurate estimation of the ischemic area and a knowledge of the natural progression of the infarct. Computerized transmission tomography (CTT) is a reliable in vivo technique for estimating infarct size. We serially studied 8 dogs over approximately 1 month after occlusion of the left anterior descending coronary artery using both ungated and prospectively electrocardiogram-gated CTT. Scans were obtained 20 minutes after occlusion and then several more times until the dogs were killed. Using the ungated CTT scans, infarct size increased from 0 to 4 days (+65 ± 20%, mean ± standard error of the mean, p <0.05), then progressively decreased. The initial perfusion defect overestimated the eventual MI size at 1 month by 33 ± 15% (p <0.05). The MI size at necropsy correlated well (r = 0.98, p <0.001) with CTT MI size determined just before sacrifice. Noninfarcted left ventricular (LV) muscle mass increased significantly (27 ± 7% greater at 1 month compared with day 0, p <0.01) over time, presumably representing compensatory LV hypertrophy. The LV muscle mass at necropsy correlated well (r = 0.94, p <0.001) with CTT LV muscle mass just before sacrifice. Using gated scans we found that wall thickening after occlusion became virtually akinetic and at times dyskinetic in the infarcted region (anterior wall), but did not change or increase in the 2 normal regions (septum and lateral wall) compared with control values. The percent change in the mid-LV area decreased acutely with occlusion, then gradually returned toward control values. The percent change in the mid-LV area decreased acutely with occlusion (37.2 ± 3.3% at control to 27.3 ± 2.9% after acute left anterior descending occlusion on day 0, P <0.005), then gradually returned toward control values. Thus, it is concluded that CTT is an accurate technique for measuring and following MI size, LV muscle mass and LV function over time. Canine infarcts increase in size and then progressively get smaller, making the design of intervention studies particularly important if changes in infarct size are to be related to specific therapies.

Original languageEnglish (US)
Pages (from-to)929-935
Number of pages7
JournalThe American Journal of Cardiology
Volume53
Issue number7
DOIs
StatePublished - Mar 15 1984

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X Ray Tomography
Myocardial Infarction
Tomography
Dogs
Muscles
Left Ventricular Hypertrophy
Left Ventricular Function
Canidae
Coronary Vessels
Myocardium
Electrocardiography
Perfusion

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

In vivo assessment by computed tomography of the natural progression of infarct size, left ventricular muscle mass and function after acute myocardial infarction in the dog. / Peck, Wallace W.; Mancini, G. B.John; Slutsky, Robert A.; Mattrey, Robert F.; Higgins, Charles B.

In: The American Journal of Cardiology, Vol. 53, No. 7, 15.03.1984, p. 929-935.

Research output: Contribution to journalArticle

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abstract = "Quantification of myocardial infarct (MI) size is of prognostic importance in patients with acute ischemic damage. Evaluation of the efficacy of interventions for salvage of ischemic myocardium depends on the accurate estimation of the ischemic area and a knowledge of the natural progression of the infarct. Computerized transmission tomography (CTT) is a reliable in vivo technique for estimating infarct size. We serially studied 8 dogs over approximately 1 month after occlusion of the left anterior descending coronary artery using both ungated and prospectively electrocardiogram-gated CTT. Scans were obtained 20 minutes after occlusion and then several more times until the dogs were killed. Using the ungated CTT scans, infarct size increased from 0 to 4 days (+65 ± 20{\%}, mean ± standard error of the mean, p <0.05), then progressively decreased. The initial perfusion defect overestimated the eventual MI size at 1 month by 33 ± 15{\%} (p <0.05). The MI size at necropsy correlated well (r = 0.98, p <0.001) with CTT MI size determined just before sacrifice. Noninfarcted left ventricular (LV) muscle mass increased significantly (27 ± 7{\%} greater at 1 month compared with day 0, p <0.01) over time, presumably representing compensatory LV hypertrophy. The LV muscle mass at necropsy correlated well (r = 0.94, p <0.001) with CTT LV muscle mass just before sacrifice. Using gated scans we found that wall thickening after occlusion became virtually akinetic and at times dyskinetic in the infarcted region (anterior wall), but did not change or increase in the 2 normal regions (septum and lateral wall) compared with control values. The percent change in the mid-LV area decreased acutely with occlusion, then gradually returned toward control values. The percent change in the mid-LV area decreased acutely with occlusion (37.2 ± 3.3{\%} at control to 27.3 ± 2.9{\%} after acute left anterior descending occlusion on day 0, P <0.005), then gradually returned toward control values. Thus, it is concluded that CTT is an accurate technique for measuring and following MI size, LV muscle mass and LV function over time. Canine infarcts increase in size and then progressively get smaller, making the design of intervention studies particularly important if changes in infarct size are to be related to specific therapies.",
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N2 - Quantification of myocardial infarct (MI) size is of prognostic importance in patients with acute ischemic damage. Evaluation of the efficacy of interventions for salvage of ischemic myocardium depends on the accurate estimation of the ischemic area and a knowledge of the natural progression of the infarct. Computerized transmission tomography (CTT) is a reliable in vivo technique for estimating infarct size. We serially studied 8 dogs over approximately 1 month after occlusion of the left anterior descending coronary artery using both ungated and prospectively electrocardiogram-gated CTT. Scans were obtained 20 minutes after occlusion and then several more times until the dogs were killed. Using the ungated CTT scans, infarct size increased from 0 to 4 days (+65 ± 20%, mean ± standard error of the mean, p <0.05), then progressively decreased. The initial perfusion defect overestimated the eventual MI size at 1 month by 33 ± 15% (p <0.05). The MI size at necropsy correlated well (r = 0.98, p <0.001) with CTT MI size determined just before sacrifice. Noninfarcted left ventricular (LV) muscle mass increased significantly (27 ± 7% greater at 1 month compared with day 0, p <0.01) over time, presumably representing compensatory LV hypertrophy. The LV muscle mass at necropsy correlated well (r = 0.94, p <0.001) with CTT LV muscle mass just before sacrifice. Using gated scans we found that wall thickening after occlusion became virtually akinetic and at times dyskinetic in the infarcted region (anterior wall), but did not change or increase in the 2 normal regions (septum and lateral wall) compared with control values. The percent change in the mid-LV area decreased acutely with occlusion, then gradually returned toward control values. The percent change in the mid-LV area decreased acutely with occlusion (37.2 ± 3.3% at control to 27.3 ± 2.9% after acute left anterior descending occlusion on day 0, P <0.005), then gradually returned toward control values. Thus, it is concluded that CTT is an accurate technique for measuring and following MI size, LV muscle mass and LV function over time. Canine infarcts increase in size and then progressively get smaller, making the design of intervention studies particularly important if changes in infarct size are to be related to specific therapies.

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