Early Estimation of Myocardial Damage in Conscious Dogs and Patients with Evolving Acute Myocardial Infarction

Shell, William E.; Lavelle, John F.; Covell, James W.; Sobel, Burton E.

doi:10.1172/jci107450

Cited by 173 publications

(41 citation statements)

References 17 publications

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“…After coronary artery occlusion, the speed at which acutely ischemic cells become irreversibly injured is not uniform and depends on their location as well as on a number of other factors (3)(4)(5). However, the fate of these cells can be modified, at least in the short term, by various therapeutic interventions, as was shown indirectly by epicardial ST segment (4,5) and QRS (6) mapping, by the relationship between epicardial ST segment elevation and the creatine kinase (CK)1 content ofthe sibjacent myocarditum (4,5), and by serial changes in serum CK activity (7,8). These experiments involved the uise of the indirect techniques mentioned above and the examination of the effects of interventions 24 h after the occluision, when the process of infaretion is still incomplete.…”

Section: Introductionmentioning

confidence: 99%

Long-Term Preservation of Ischemic Myocardium after Experimental Coronary Artery Occlusion

Maclean¹,

Fishbein²,

Braunwald³

et al. 1978

J. Clin. Invest.

170

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A B S T R A C T The results of experiments with indirect methods have suggested that various interventions reduce infarct size after coronary artery occlusion. To determine and quantify directly both the shortand long-term effects of several interventions on myocardial salvage without relying on indirect methods, the left coronary artery was occluded in 880 rats; they were then given either no treatment or one of the following interventions: (a) hyaluronidase, an enzyme that hydrolyzes interstitial glycoproteins, 1,500 National Formulary (NF) U/kg i.v. 5 min and 24 h after occlusion; (b) cobra venom factor, a protein that depletes the third component of complement, 20 U/kg i.v. 5 min after occlusion; (c) a glucocorticoid: hydrocortisone, 50 mg/kg i.v. 5 min after occlusion; or the fivefold more potent methylprednisolone (MP): (i) 50 mg/kg i.v. 5 min after occlusion or (ii) 50 mg/kg i.v. 5 min after occlusion followed by 50 mg/kg i.m. 3, 6, and 24 h after occlusion; or (d) reserpine, an agent that depletes the heart of catecholamines, 0.5 mg/kg i.m. once on each of the 3 days before occlusion. The animals were sacrificed either 2 days after occlusion, i.e., at the time of peak necrosis, or after 3 wk, i.e., after the infarct was completely healed. The amount of preserved myocardium was then assessed by two independent techniques: planimetric measurement of serial histologic sections and creatine kinase activity of the whole left ventricle. The amount of normal myocardium preserved at 21 days postocclusion was significantly increased, by 22.3±7.8% (P < 0.025) after the administration of hyaluronidase, by 25.3 ±5.8% (P < 0.005) after cobra venom factor, by 14.5 ±6.9% (P < 0.05) after hydrocortisone, by 20.8±8.2% (P < 0.025) after the single dose of MP, by 20.9±3.9% (P < 0

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Section: Introductionmentioning

confidence: 99%

Long-Term Preservation of Ischemic Myocardium after Experimental Coronary Artery Occlusion

Maclean¹,

Fishbein²,

Braunwald³

et al. 1978

J. Clin. Invest.

170

View full text Add to dashboard Cite

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“…For example, measurement of serum creatine phosphokinase and lactate dehydrogenase isoenzymes after suspected myocardial infarction both confirms the diagnosis and may be used to estimate the volume of infarcted muscle (15,16). In 1975, Lieberman (17) first reported that angiotensin-converting enzyme (ACE; EC 3.415.1, peptidyl dipeptidase)l is elevated in sera of patients with active pulmonary sarcoidosis.…”

mentioning

confidence: 99%

Release of angiotensin converting enzyme by the lung after Pseudomonas bacteremia in sheep.

Gorin¹,

Hasagawa²,

Hollinger³

et al. 1981

J. Clin. Invest.

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A B S T R A C T We studied release of angiotensin-converting enzyme (ACE) by the lung after acute injury associated with an increase in pulmonary vascular permeability. In eight adult sheep with chronic lung lymph fistulas, we measured lymph flow (QL), and both ACE activity and total protein content in lymph and plasma under base-line conditions and during 24 h after an infusion of live pseudomonas organisms.Under base-line conditions, ACE activity in plasma was 4.93+0.43 U/ml (mean±SEM ml/h before pseudomonas bacteremia, and rose to 6.7 ± 1.2 ml/h by 2 h after onset of the infusion (mean ±SEM, P < 0.05). CTP remained significantly elevated for at least 10 h after the infusion. Release of ACE into lung lymph doubled after acute lung injury and equaled 22.3 ± 13.8 U/h at 4 h after onset of the infusion. ACE secretion into lung lymph had returned to baseline levels by 24 h after bacteremia. We did not observe a significant rise in plasma ACE activity after acute lung injury.Pseudomonas bacteremia in sheep results in acute, reversible lung injury associated with increased pulmonary vascular permeability, and increased release of Address reprint requests to Dr.

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“…13 CK is released in skeleton muscles, hence the quantitative relation between serum CK depletion attack, which are responsible for many of the false positive enzymes elevation reported particularly in early studies, when iso-enzymes study were not available. [14][15][16] Several studies have shown the elevated relation between peak serum enzyme activities after myocardial infarction. [17][18][19] Lindsay et al 20 are argued that the metabolic effect that leads to increase in flux may fully and partially reversible, therefore the elevation of CK-MB could signify the adverse effect on the myocardial cell resulting from something other than necrosis or ischemia.…”

Section: Discussionmentioning

confidence: 99%

Serum enzymes markers in myocardial infarction: A study of rural area

Pochhi¹,

2017

Asian J Med Sci

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Background: Acute Myocardial Infarction is the reduction of coronary flow to such an extent that supply of oxygen to the myocardium do not need the oxygen demand of myocardial tissues. The diagnosis of AMI cannot be fulfilled unless the elevated levels of serum cardiac enzymes particularly CK-MB iso-enzyme activity. The rate of release of cardiac enzymes is highly diagnostic. Aims and Objectives: Therefore, the present thesis aim is-in evaluating, whether the elevated levels of cardiac marker enzymes can be compared to the extent of the Myocardial infarction. Material and Methods: Therefore the present study was undertaken on 50 patients of MI and 50 patients of control. They were group according to the age and sex. The activity of different cardiac enzymes were studied. Result: The AMI patients had significantly elevated levels of 90% patients of high LDH values and 86% patients have elevated levels of AST. The significant elevation of serum enzymes as compared to the control. Conclusion: The magnitude of the elevated levels of enzymes can be compared to the extent of the myocardial infarction. Serum GGT can also be useful marker of oxidative stress in myocardial infarction.

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Early Estimation of Myocardial Damage in Conscious Dogs and Patients with Evolving Acute Myocardial Infarction

Abstract: A B S T R A C T

Cited by 173 publications

References 17 publications

Long-Term Preservation of Ischemic Myocardium after Experimental Coronary Artery Occlusion

Long-Term Preservation of Ischemic Myocardium after Experimental Coronary Artery Occlusion

Release of angiotensin converting enzyme by the lung after Pseudomonas bacteremia in sheep.

Serum enzymes markers in myocardial infarction: A study of rural area

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