Experimental coronary artery occlusion

Schäper, Wolfgang; Frenzel, H; Hort, W

doi:10.1007/bf01907684

Cited by 152 publications

(56 citation statements)

References 8 publications

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“…The boundaries of the involved vascular bed were determined from x-rays of serial cross sections of the ventricles after postmortem coronary injection with barium sulfate suspensions. Similar techniques have been used by others.7 [24][25][26][27] The study demonstrated a close linear correlation between infarct size and the size of the vascular bed. Thus, in humans as in dogs, ischemic bed size is a major determinant of infarct size.…”

Section: Variation Of Infarct Size Within the Vascular Bed At Risksupporting

confidence: 53%

Myocardial infarct size and location in relation to the coronary vascular bed at risk in man.

Lee¹,

Ideker²,

Reimer³

1981

Circulation

146

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SUMMARY Recent infarcts were compared with the anatomic boundaries of the involved vascular bed in human hearts to determine the amount and location of necrosis in relation to the myocardium at risk. The coronary arteries were injected with BaSo4 in 18 human hearts with 3-16-day-old infarcts. Thin (3-4-mm) slices were cut at 10-15-mm intervals, photographed, x-rayed and used for histologic analysis. Infarct outlines were traced from gross photographs using histologic confirmation of infarct boundaries, and the vascular bed was independently traced from the x-rays. Ischemic bed size and infarct size were then calculated by computerized planimetry. Infarct size ranged from 13-72% of the left ventricle (mean 30 ± 3.6%) and was linearly related to the size of the occluded vascular bed (r = 0.93). However, the infarcts were always smaller than the occluded beds. They involved 50-88% of the ischemic bed (mean 69 ± 3.0%) due to variation in the transmural extent of necrosis. A lateral zone of viable muscle within the ischemic bed was present but consistently narrow (mean 1.7 ± 0.3 mm) so that the infarcts involved 93 ± 2.3% of the width of the bed at risk. Thus, ischemic bed size is a major determinant of infarct size in fatal human infarcts. When natural limitation of infarct size occurs, it is due primarily to limitation of the transmural extent of necrosis.INTERVENTIONS designed to limit infarct size after coronary occlusion are being closely examined. Fundamental to this goal is the presence of ischemic but reversibly injured cells that would eventually die without therapy. The exact location of these cells within the distribution of an occluded coronary artery in animal models remains controversial.'-"' Classically, this myocardium at risk for infarction has been considered to be in a concentric peripheral zone of intermediate ischemia surrounding a severely ischemic core.' Recent studies in dogs suggest, however, that at the subendocardial lateral border of an infarct the transition from well-perfused to severely ischemic tissue is sharp.2 3 Reimer et al.4' have demonstrated that cell death in an evolving acute canine myocardial infarct progresses in a transmural wave front over a period of 3-6 hours, but that the subendocardial, lateral boundaries of the infarct are established within the first 40 minutes. Variation among dogs in the size of completed infarcts after permanent coronary occlusion is a function of the size of the anatomic vascular bed and of the transmural extent of the infarct within this area at risk. Variation among dogs in the transmural extent of infarction is primarily a function of the amount of collateral blood flow supplying the subepicardial myocardium.5Although other authors concluded that human infarcts are usually smaller than the ischemic area at risk,'7 the anatomic relationship between an infarct and the vascular bed at risk in man has not been well studied.2' The present study was done to compare, by detailed postmortem gross, histologic and radiographic analysis, the size and loca...

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Section: Variation Of Infarct Size Within the Vascular Bed At Risksupporting

confidence: 53%

Myocardial infarct size and location in relation to the coronary vascular bed at risk in man.

Lee¹,

Ideker²,

Reimer³

1981

Circulation

146

View full text Add to dashboard Cite

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“…Accordingly, the primary therapeutic strategy to reduce cardiovascular mortality is reduction of infarct size (IS). IS increases with coronary artery occlusion time, myocardial area at risk for infarction (AR), lack of collateral supply, absence of preconditioning, and myocardial demand for O 2 (i.e., the product of contractility, heart rate, and ventricular wall stress) (16,18).…”

mentioning

confidence: 99%

Variable ECG signs of ischemia during controlled occlusion of the left and right coronary artery in humans

Marchi

Meier²,

Oswald³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Variable ECG signs of ischemia during controlled occlusion of the left and right coronary artery in humans. Am J Physiol Heart Circ Physiol 290: H351-H356, 2006. First published January 20, 2006 doi:10.1152/ajpheart.00992.2005.-Infarct size (IS) increases with vascular occlusion time, area at risk for infarction, lack of collateral supply, absence of preconditioning, and myocardial demand for O2 supply. ECG S-T segment elevation is used as a measure of severity of ischemia and a surrogate for IS. This study in 50 patients with coronary artery disease undergoing a first 120-s balloon occlusion of a stenosis sought to determine whether S-T segment elevation, corrected for the above-mentioned variables, in the left coronary artery (LCA group, n ϭ 36) is different from that in the right coronary artery (RCA group, n ϭ 14) territory. After consideration of all known determinants of IS, particularly mass at risk and collateral supply, the LCA territory is more sensitive than the RCA region to a 2-min period of myocardial ischemia. coronary disease; collateral circulation ANNUAL MORTALITY RATE from all causes across Europe amounts to 11 per 1,000 inhabitants, with 5.4 per 1,000 (49%) due to cardiovascular disease and 2.4 per 1,000 (22%) due to ischemic heart disease (3). In patients suffering from coronary artery disease (CAD), the size of the myocardial infarction is the most important determinant of the outcome after such an event (22). Accordingly, the primary therapeutic strategy to reduce cardiovascular mortality is reduction of infarct size (IS). IS increases with coronary artery occlusion time, myocardial area at risk for infarction (AR), lack of collateral supply, absence of preconditioning, and myocardial demand for O 2 (i.e., the product of contractility, heart rate, and ventricular wall stress) (16, 18).As a surrogate for IS, clinical studies on the effect of various procedures on myocardial salvage have ubiquitously employed the magnitude of ECG changes during artificial coronary occlusion (2). In this context, the following unresolved clinical question has been raised (2): Does ischemia induced by balloon inflation in different coronary artery segments result in the same magnitude of ECG S-T segment shift? There has been evidence from experimental studies of 1) regional differences in infarct development and protection from within the left anterior descending coronary artery (LAD) territory (19) and 2) augmented coronary collateral conductance in small apical vs. large basal ARs (12). In humans, investigations on regional differences in myocardial ischemia have allowed little more than speculation that the territory of ischemia might be another determinant of IS. For example, during acute myocardial infarction, "tombstone" ECG S-T segment elevation is tightly associated with a large infarct in the LAD region, which could be explained by the large AR in this territory and/or sitespecific myocardial vulnerability to ischemia (13). Quantitative collateral flow index (CFI) measurements in 450 patients with ...

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“…[1][2][3] Similarly, for a given RA size and duration of coronary occlusion, IS depends on the magnitude and spatial extent of residual collateral-derived MBF. [1][2][3] Currently, IS can be measured by myocardial contrast echocardiography (MCE) only after reperfusion, by exploiting the "no-reflow" state of necrotic tissue. 4 -8 In this setting, fewer microbubbles enter the necrotic zone because of functional and/or structural damage to the capillaries.…”

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confidence: 99%

Noninvasive Prediction of Ultimate Infarct Size at the Time of Acute Coronary Occlusion Based on the Extent and Magnitude of Collateral-Derived Myocardial Blood Flow

et al. 2001

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Background We hypothesized that by detecting regions with adequate collateral-derived myocardial blood flow (MBF) within the risk area (RA), we could predict ultimate infarct size (IS) at the time of coronary occlusion. Methods and Results Group 1 dogs (n=15) underwent coronary occlusion without reperfusion, whereas group 2 dogs (n=6) underwent both occlusion and reperfusion. RA was measured with aortic root injections of microbubbles. Myocardial contrast echocardiography (MCE) was performed with high mechanical index intermittent harmonic imaging at pulsing intervals (PIs) of <1 to 30 cardiac cycles during an intravenous infusion of microbubbles (Sonozoid). MBF was measured with radiolabeled microspheres, and postmortem tissue staining was used to determine IS. Perfusion defect size (PDS) on MCE varied with the PI and was largest at a PI of 2.6±0.4 seconds, where it correlated well with RA ( r =0.82). PDS was smallest at a PI of ≥10.6±1.5 seconds, where it correlated closely with IS ( r ≥0.92). Areas that underwent necrosis could be identified early after coronary occlusion as having the lowest microvascular flow velocity (β) and MCE-derived MBF (A×β). The results were similar with or without reperfusion. Because of variability in collateral-derived MBF, there was no correlation between RA and ultimate IS ( P =0.37). The extent of regional dysfunction also correlated poorly with IS ( r =0.31). Conclusions MCE can be used immediately after coronary occlusion to define ultimate IS by measuring the magnitude and spatial extent of collateral-derived residual MBF within the RA. Thus, it could help individualize risk and management in acute myocardial infarction.

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Experimental coronary artery occlusion

Cited by 152 publications

References 8 publications

Myocardial infarct size and location in relation to the coronary vascular bed at risk in man.

Myocardial infarct size and location in relation to the coronary vascular bed at risk in man.

Variable ECG signs of ischemia during controlled occlusion of the left and right coronary artery in humans

Noninvasive Prediction of Ultimate Infarct Size at the Time of Acute Coronary Occlusion Based on the Extent and Magnitude of Collateral-Derived Myocardial Blood Flow

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