Coronary Reperfusion in Primates SERIAL ELECTROCARDIOGRAPHIC AND HISTOLOGIC ASSESSMENT

Smith, Gregory T.; Soeter, John R.; Haston, Harold H.; McNamara, J. Judson

doi:10.1172/jci107889

Cited by 68 publications

(7 citation statements)

References 11 publications

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“…Our finding that reperfusion causes abnormalities in hemodynamics during the first hours ofrecanalization is consistent with the findings of other investigators (25,26,32,33). Heyndrickx (34) reported that in dogs subjected to only 15-min periods of occlusion followed by reperfusion, regional function in the ischemic zone may take up to 6 h to normalize.…”

Section: Discussionsupporting

confidence: 94%

“…This agrees with the results of Geary (25), who found an infarct size of 50% in baboons reperfused after 2 h of LAD occlusion, in contrast with 94% in a control group with permanent occlusion. Smith et al (26) also showed that 50% of acutely injured myocardium was salvaged with reperfusion after 2 h of LAD occlusion in monkeys. These authors observed large areas of patchy necrosis surrounding a central infarct.…”

Section: Discussionmentioning

confidence: 97%

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Coronary thrombolysis and infarct size reduction after intravenous infusion of recombinant tissue-type plasminogen activator in nonhuman primates.

Flameng¹,

Werf²,

Vanhaecke³

et al. 1985

J. Clin. Invest.

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Occlusive thrombus was produced by thrombin-induced coagulation in the left anterior descending coronary artery (LAD) of 16 open-chest baboons. In six control animals, occlusive thrombosis persisting over a period of 4 h as evidenced by coronary arteriography resulted in large transmural infarction (63.1±3.5% of the perfusion area). In 10 animals, tissue-type plasminogen activator obtained by recombinant DNA technology (rt-PA) was infused systemically at a rate of 1,000 IU (10 isg)/kg per min for 30 min after 30-80 min of coronary thrombosis. Reperfusion occurred within 30 min in nine animals. In one animal, intravenous infusion was followed by an intracoronary infusion at the same rate, which resulted in thrombolysis within 8 min. In the rt-PA group, mean duration of occlusion before reperfusion was 77±24 min. Reocclusion occurred in one animal. Recanalization resulted in an overall reduction of infarct size (37.8±5.9%, P < 0.05 versus controls). Residual infarction was related to the duration of occlusion (r = 0.80, P < 0.01). Reperfusion was associated with reduced reflow. Myocardial blood flow in the perfusion area of the LAD was only 70% of normal after 4 h despite perfect angiographic refilling.The infusion of rt-PA was not associated with systemic activation of the fibrinolytic system, fibrinogen breakdown, or clinically evident bleeding.It is concluded that intravenous infusion of rt-PA may recanalize thrombosed coronary vessels without inducing systemic lysis. The extent of residual infarction is closely related to the duration of coronary artery occlusion before thrombolysis.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 97%

Coronary thrombolysis and infarct size reduction after intravenous infusion of recombinant tissue-type plasminogen activator in nonhuman primates.

Flameng¹,

Werf²,

Vanhaecke³

et al. 1985

J. Clin. Invest.

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“…Reperfusion has been shown to protect ischemic myocardium from necrosis even when it is delayed for 6 hr (16,17). However, with prolonged myocardial ischemia, hemorrhagic infarcts may occur (18) and postreperfusion mechanical dysfunction, which may persist for prolonged periods, occurs (19).…”

Section: Methodsmentioning

confidence: 99%

Prolonged derangements of canine myocardial purine metabolism after a brief coronary artery occlusion not associated with anatomic evidence of necrosis

DeBoer

Ingwall

Kloner

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

216

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Changes in myocardial purine metabolism were studied after temporary coronary artery occlusion and subsequent reperfusion in the dog. Sequential myocardial biopsies were performed to allow for measurements of ATP, adenine nucleotide, nucleoside, and base concentrations after 15 min of ischemia, and after 90 min and 72 hr of reperfusion following this period of ischemia. Control, nonischemic sites were also sampled. After 15 min of coronary occlusion, subendocardial ATP concentrations (reported in nmol/mg of protein; mean + SEM) were depressed in the ischemic zone at 19.9 + 3.5 compared to 38.1 ± 2.8 in the nonischemic zone (P < 0.001). Subepicardial ATP concentrations also were depressed at 27.0 ± 2.2 in ischemic sites compared to subepicardial nonischemic sites (40.0 + 4.0, P < 0.005). After 90 min of reperfusion ATP concentrations remained depressed in the previously ischemic subendocardium 26.8 b 4.2 (P < 0.025 vs. nonischemic sites). After 72 hr of reperfusion, ATP was still depressed in the previously ischemic subendocardium at 29.2 ± 2.5 (P < 0.025 vs. nonischemic) and subepicardium (27.9 + 3.3, P < 0.05 vs. nonischemic). Total purines were determined as the sum of ATP, ADP, AMP, adenosine, inosine, and hypoxanthine. After 15 min of occlusion, the total purine pool in the ischemic subendocardium tended towards being lower than in the nonischemic zone (42.0 + 5.9 vs. 53.8 + 5.2, not significant) but in the ischemic subepicardium the total purine pool was similar to that in the nonischemic zone. After 90 min of reperfusion the previously ischemic subendocardial purine pool was reduced compared to the nonischemic zone (39.0 + 4.8, P < 0.025). Total purines were also depleted in both the subendocardium and subepicardium of previously ischemic zones after 72 hr of reperfusion (44.5 + 2.9 and 40.0 + 4.4, respectively, P < 0.05). Histologic analysis of the previously ischemic tissue revealed no evidence of necrosis. Therefore, brief temporary coronary artery occlusions not associated with anatomic evidence of necrosis may result in prolonged abnormalities of ATP concentration and significant depletion of the total purine pool. It is generally assumed that the myocardium of patients who experience temporary myocardial ischemia, such as occurs in angina pectoris, and who recover from this event without developing electrocardiographic, enzymatic, or radioisotopic evidence of myocardial infarction, rapidly returns to normal. There are experimental studies that support this assumption. Thus, after temporary coronary artery occlusion in animals in which the myocardium is ischemic for less than 20 min, no necrosis develops when the coronary artery is released. Hence this myocardium has been considered to be reversibly injured (1). On the other hand, when the temporary coronary occlusion is maintained for a longer period of time (40-60 min), histologic evidence of necrosis develops in the subendocardium and, by definition, these cells may be considered to be irreversibly injured (1). Although brief coronary arter...

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“…The significance of these changes is difficult to evaluate, but the fact that transmural infarction is a complication of aortocoronary bypass operation suggests that subendocardial infarction can be incriminated in some cases. However, pericarditis resulting from surgery causes identical changes, and changes in repolarisation which follow sudden reperfusion of ischaemic myocardium may be the result of relief of ischaemia rather than of infarction (Smith et al, 1974). It is possible that this may have contributed to the increased incidence of T loop changes in patients showing previous infarction.…”

Section: Discussionmentioning

confidence: 99%

Myocardial infarction after aortocoronary saphenous vein bypass. Vectorcardiographic study.

Mcneill¹,

Poirier²,

Morin³

et al. 1977

Heart

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Since aortocoronary bypass by saphenous vein graft was first reported (Favaloro, 1968), the operation has gained widespread acceptance as a means of relieving angina pectoris in a large majority of patients. However, the procedure is frequently associated with electrocardiographic features of myocardial infarction. The limitations ofthe electrocardiogram in diagnosing infarction are well known and it has been frequently shown that the vectorcardiogram can diagnose infarction which is not apparent on the electrocardiogram (Hugenholtz et al., 1961;Wolff et al., 1961;Simonson et al., 1966;Gunnar et al., 1967 (Frank, 1956).Conventional electrocardiographic criteria (Perloff, 1964;Schrank et al., 1974) and vectorcardiographic criteria (Chou and Helm, 1967;Gunnar et al., 1967;McConahay et al., 1970;Starr et al., 1974) of known value in the diagnosis of transmural myocardial infarction were employed. T loop changes were not considered diagnostic of infarction and were examined separately. Conduction disturbances were also sought.In evaluating the incidence of perioperative

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Coronary Reperfusion in Primates SERIAL ELECTROCARDIOGRAPHIC AND HISTOLOGIC ASSESSMENT

Cited by 68 publications

References 11 publications

Coronary thrombolysis and infarct size reduction after intravenous infusion of recombinant tissue-type plasminogen activator in nonhuman primates.

Coronary thrombolysis and infarct size reduction after intravenous infusion of recombinant tissue-type plasminogen activator in nonhuman primates.

Prolonged derangements of canine myocardial purine metabolism after a brief coronary artery occlusion not associated with anatomic evidence of necrosis

Myocardial infarction after aortocoronary saphenous vein bypass. Vectorcardiographic study.

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