Coronary artery reperfusion in acute myocardial infarction: Assessment by pre- and postintervention thallium-201 myocardial perfusion imaging

Coster, Patrick M. De; Detry, Jean-Marie R.; Brasseur, L.; Beckers, Christian; Col, Jacques

doi:10.1016/0002-9149(85)90712-x

Cited by 73 publications

(5 citation statements)

References 37 publications

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“…1025,27. 28 The time course pattern with a significant improvement in function during the initial 48 to 72 h and maintenance of this improved function during the rest of the study period, is similar to the improvement reported in the experimental modelz9 and also is in accordance with the early and follow-up improvement in the myocardial thallium uptake in patients as reported by de Coster et al 30 This improvement is then probably due to the recovery of the stunned myocardium.z2…”

Section: Discussionsupporting

confidence: 83%

Daily serial evaluation of left ventricular function with equilibrium radionuclide ventriculography following thrombolysis during acute myocardial infarction

Marx

Aswegen

Kleynhans

et al. 1988

Clinical Cardiology

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Summary:The changes in ventricular function after reperfusion by coronary thrombolysis are important when deciding about further definitive treatment necessary to ensure long-term vessel patency. The purpose of this study was to evaluate the early changes in left ventricular function after reperfusion. Left ventricular function was serially evaluated for 10 days in a group of 18 patients receiving intracoronary thrombolytic therapy for an acute myocardial infarction. Comparison of the global ventricular function in the successfully and unsuccessfully reperfused groups of patients showed significantly better function in the successful group than the unsuccessful group after the first day, which was maintained for the entire study period. Global and regional ventricular function in the successfully reperfused patients showed significant early improvement during the initial 72 h with maintenance'of this improvement for the study period of 10 days. In the patients in whom reperfusion was unsuccessful, regional ventricular function showed no change, while the global function declined from day 5 to day 8 of the study period. This study then confirms the significant improvement in ventricular function after successful reperfusion. The time course pattern of the change in ventricular function indicates that the most significant improvement occurs within the first 72 h after reperfusion. These changes are similar to those previously reported in experimental animals.

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Section: Discussionsupporting

confidence: 83%

Daily serial evaluation of left ventricular function with equilibrium radionuclide ventriculography following thrombolysis during acute myocardial infarction

Marx

Aswegen

Kleynhans

et al. 1988

Clinical Cardiology

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“…Myocardial thallium-201 (Tl-201) imaging has been used to evaluate the efficacy of thrombolytic therapy in acute myocardial infarction. [3][4][5][6] In patients demonstrating successful reperfusion, improved Tl-201 uptake compared with prethrombolysis images are observed. [3][4][5] Patients with a persistently occluded infarct-related vessel show little change in defect size.45 There are some significant limitations to the use of rest Tl-201 scintigraphy for evaluating myocardial salvage after coronary reperfusion.7 First, because of prominent redistribution, it is necessary to obtain pretreatment images that may delay for up to 20-30 minutes the institution of thrombolytic therapy.…”

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confidence: 99%

Quantification of area at risk during coronary occlusion and degree of myocardial salvage after reperfusion with technetium-99m methoxyisobutyl isonitrile.

et al. 1990

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Serial myocardial imaging with technetium-99m methoxyisobutyl isonitrile (9'Tc-MIBI) has been proposed for evaluating myocardial salvage after reperfusion. To define 'mTc-MIBI uptake before and after reperfusion, 17 open-chest dogs underwent 3 hours of left anterior descending artery occlusion and 3 hours of reperfusion. 9'Tc-MIBI was injected during occlusion (group 1) or after 90 minutes of reperfusion (group 2). Myocardial 99'Tc-MIBI activity was correlated with microsphere flow during occlusion and reperfusion. Anatomic risk area and infarct area were defined by postmortem vital staining and correlated with the perfusion defects defined by analysis of 99mTc-MIBI macroautoradiographs and gamma camera images of myocardial slices. The left ventricle was divided into 96 segments for gamma well counting. Flow and '9"Tc-MIBI activity were normalized to nonischemic values. Myocardial segments were grouped, based on occlusion flow, into zones: severely ischemic (<30% nonischemic), moderately ischemic (>30%o, .60%o nonischemic), mildly ischemic (>60%o, <90%1 nonischemic), and nonischemic (>90%o, < 120% nonischemic). Among dogs injected with "'Tc-MIBI during coronary occlusion (group 1), myocardial 99'Tc-MIBI activity correlated linearly with occlusion flow for both endocardial (r=0.91) and transmural (r=0.91) segments. The risk area defined by '9mTc-MIBI autoradiography (group 1) correlated with the postmortem risk area (p=0.94) but was 29O smaller than the anatomic risk area (p=0.03), reflecting the contribution of collateral flow. Among dogs injected with "'Tc-MIBI after reperfusion (group 2), myocardial 99"Tc-MIBI did not correlate with reperfusion flow in either endocardial or transmural segments. Among group 2 dogs, myocardial 9'Tc-MIBI activity was significantly less than reperfusion flow at the time of injection in the severely ischemic (25 ±5% versus 74±24% nonischemic,p=0.002), moderately ischemic (54±12% versus 96+15% nonischemic, p=0.001), and mildly ischemic (84±6% versus 93±3% nonischemic, p=0.002) zones. The defect area defined by 'mTc-MIBI autoradiography (group 2) correlated very closely with the postmortem infarct area (p=0.98). Thus, the myocardial uptake of 99mTc-MIBI during coronary occlusion correlates with occlusion flow and reflects the "area at risk." When 99mTc-MIBI was given after 90 minutes of reperfusion following 3 hours of coronary occlusion, the myocardial activity was significantly reduced compared with reperfusion flow in both necrotic and perinecrotic regions, reflecting myocardial viability more than the degree of reperfusion. (Circulation 1990;82:1424-1437 T X ahe current management of myocardial infarcinfarction, the extent of myocardial necrosis is detertion focuses on the application of acute mined by the "area at risk," collateral flow, and the interventional reperfusion techniques to duration of coronary occlusion.2 A noninvasive imagreduce myocardial necrosis.1 During myocardial ing technique that could 1) assess the area at risk, 2)

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“…The injection of the same tracer after reperfusion provides us with an estimate of myocardial infarct size, and hence of salvaged myocardium. In contrast to the earlier studies involving thallium-201, 12 technetium99m-based perfusion tracers undergo minimal redistribution, allowing image acquisition several hours after injection. [13][14][15] Another advantage of Tc-99m over Tl-201 is the higher peak energy window, which allows a more accurate identification of the boundaries of a perfusion defect and increases accuracy of gated images.…”

Section: How To Measure the Extent Of Myocardium At Riskmentioning

confidence: 97%

Myocardium at risk: Reasons and methods for measuring the extent

Gimelli

Rovai

2013

Journal of Nuclear Cardiology

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See related article, pp. 99-110 MYOCARDIUM AT RISKIf a coronary artery is acutely occluded, the downstream myocardium becomes severely under-perfused and at risk of necrosis. The area of myocardium at jeopardy of infarction is usually referred to as area at risk. It is intuitive that the extent of myocardium at risk downstream from an occluded coronary artery does not have the dimension of an area, but rather that of a volume or a mass. Indeed, the extent of myocardium at risk is usually expressed in grams or in percentage of ventricular myocardium. However, because the initial experiments were carried out by injecting dyes or radionuclide-labeled microspheres upstream from the occluded coronary artery, and because the myocardium at risk was defined postmortem as the non-stained or non-labeled area in cross-sectional slices of the heart, the term area at risk has become common and hence entered the medical dictionary. 1,2 If a flow tracer is injected into a coronary artery proximal to its occlusion, and a second flow tracer is injected after the occlusion upstream the occluded artery, it becomes evident that the extent of myocardium perfused by a given open artery is larger than the myocardium at risk when the same vessel is occluded ( Figure 1A, B). This difference is on average 20% in the canine heart, and is due to the collateral circulation. 3 It has been traditionally assumed that coronary arteries are functional end-arteries under physiological conditions. However, even in the absence of coronary stenoses or in entirely normal hearts, brief periods of coronary occlusion produced by balloon inflation are not followed by electrocardiographic signs of myocardial ischemia in 20%-25% of patients. This is attributed to collateral circulation. 4 This phenomenon is more prominent in the case of preexisting collaterals, as observed in patients with chronic coronary artery disease. Thus, the extent of the area at risk after coronary occlusion is influenced both by an anatomical factor (the size and hierarchy of the occluded vessel) and by a series of functional factors (largely related to the collateral circulation). For this reason, an acute coronary occlusion causes a smaller infarction and a less severe hemodynamic impairment in an older patient with extensive coronary atherosclerosis and well-developed collaterals than in a younger patient without preexisting collaterals. Another functional factor is how rapid is the occlusion. If the occlusion is very slow (as it can be obtained in experimental animals and as it occurs in patients with coronary lesions slowly evolving toward total occlusion), collaterals have the time to develop and to minimize the extent of myocardium at risk. This goes in parallel with the common observation of patients with even complete occlusion of a proximal coronary artery and absence of myocardial infarction. Finally, if the perfusion territory is small, as when a secondary branch is occluded, collateral vessels can totally obscure the area of myocardium at risk. WHY MEASURE THE EXTENT ...

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Coronary artery reperfusion in acute myocardial infarction: Assessment by pre- and postintervention thallium-201 myocardial perfusion imaging

Cited by 73 publications

References 37 publications

Daily serial evaluation of left ventricular function with equilibrium radionuclide ventriculography following thrombolysis during acute myocardial infarction

Daily serial evaluation of left ventricular function with equilibrium radionuclide ventriculography following thrombolysis during acute myocardial infarction

Quantification of area at risk during coronary occlusion and degree of myocardial salvage after reperfusion with technetium-99m methoxyisobutyl isonitrile.

Myocardium at risk: Reasons and methods for measuring the extent

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