TY - JOUR
T1 - Ischemic myocardial injury in rapidly paced dogs
T2 - Contribution to ventricular dysfunction
AU - Radio, Stanley J.
AU - Zucker, Irving H.
AU - Chen, Jwo Sheng
AU - Caruso, Rhonda M.
AU - Wang, Wei
AU - McManus, Bruce M.
N1 - Funding Information:
Supported in part by a grant from the National Institutes of Health (HL-39690). Manuscript received September 25, 1991; accepted December 2, 1991. Address for reprints: Stanley J. Radio, MD, Department of Pathology and Microbiology, University of Nebraska Medical Center, 600 S. 42nd Street, Omaha, NE 68198-3135.
PY - 1992
Y1 - 1992
N2 - Chronic rapid ventricular pacing in the dog has been shown to provide a predictable and stable model of heart failure for which the operative pathomechanism remains in question. In a group of 20 dogs with congestive failure induced by rapid ventricular pacing for a mean duration of 29.5 ± 13.1 days (range 7 to 55 days), mean left ventricular end diastolic pressure (LVEDP) was elevated as compared with unpaced controls (23.2 ± 2.7 mmHg vs. 2.0 ± 0 mmHg, p < 0.001). Gross myocardial hemorrhage was present at autopsy in 9 of 20 (45%) paced animals, and necrosis was present in 5 of 20 (25%). Histologic findings included acute ischemic myocardial injury with contraction band necrosis, wavy myofibers, and coagulation necrosis ranging from 0 to 4 lesions per paced animal (1.4 ± 1.4, mean ± SD), compared with none in unpaced animals (p < 0.03). Healed ischemic lesions ranged from 0 to 10 per animal (mean 3.2 ± 2.9) versus none in control animals (p < 0.0001). Total injury score (acute plus healed) for each paced animal ranged from 0 to 12 (mean 4.6 ± 2.9), compared with no injury in nonpaced controls (p < 0.0001). Thus ischemic injury reflected by multiple foci of acute and healed myocardial injury is a prominent and common feature in the canine rapid ventricular pacing model of heart failure.
AB - Chronic rapid ventricular pacing in the dog has been shown to provide a predictable and stable model of heart failure for which the operative pathomechanism remains in question. In a group of 20 dogs with congestive failure induced by rapid ventricular pacing for a mean duration of 29.5 ± 13.1 days (range 7 to 55 days), mean left ventricular end diastolic pressure (LVEDP) was elevated as compared with unpaced controls (23.2 ± 2.7 mmHg vs. 2.0 ± 0 mmHg, p < 0.001). Gross myocardial hemorrhage was present at autopsy in 9 of 20 (45%) paced animals, and necrosis was present in 5 of 20 (25%). Histologic findings included acute ischemic myocardial injury with contraction band necrosis, wavy myofibers, and coagulation necrosis ranging from 0 to 4 lesions per paced animal (1.4 ± 1.4, mean ± SD), compared with none in unpaced animals (p < 0.03). Healed ischemic lesions ranged from 0 to 10 per animal (mean 3.2 ± 2.9) versus none in control animals (p < 0.0001). Total injury score (acute plus healed) for each paced animal ranged from 0 to 12 (mean 4.6 ± 2.9), compared with no injury in nonpaced controls (p < 0.0001). Thus ischemic injury reflected by multiple foci of acute and healed myocardial injury is a prominent and common feature in the canine rapid ventricular pacing model of heart failure.
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U2 - 10.1016/1054-8807(92)90016-H
DO - 10.1016/1054-8807(92)90016-H
M3 - Article
C2 - 25990124
AN - SCOPUS:38249014802
SN - 1054-8807
VL - 1
SP - 131
EP - 139
JO - Cardiovascular Pathology
JF - Cardiovascular Pathology
IS - 2
ER -