Echocardiography in acute myocardial infarction

Corya, Betty C.; Rasmussen, S; Knoebel, Suzanne B.; Feigenbaum, Harvey

doi:10.1016/0002-9149(75)90859-0

Cited by 132 publications

(15 citation statements)

References 21 publications

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“…Body surface potential mapping could increase STEMI detection by 27.5% over that obtained with standard ECG [24]. Moreover, transthoracic echocardiography might be helpful, particularly for patients with non-evident changes in ECG and isolated lateral or posterior ischaemia [25]. It has previously been described that hypokinesis or akinesis of the ventricular myocardium appears before the development of ST-segment changes on the ECG [26].…”

Section: Discussionmentioning

confidence: 99%

Total coronary occlusion of infarct-related arteries in patients with non-ST-elevation myocardial infarction undergoing percutaneous coronary revascularisation

et al. 2017

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A b s t r a c t Background:The prevalence and impact of total coronary occlusion of an infarct-related artery (IRA) on outcomes in patients with non-ST-elevation myocardial infarction (NSTEMI) remain unclear. Aim:We evaluated the clinical significance of total coronary occlusion in NSTEMI patients. Methods:A total of 2767 patients with NSTEMI enrolled in the Polish Registry of Acute Coronary Syndromes, who underwent percutaneous coronary interventions, were analysed. The patients were divided into two groups according to preprocedural culprit vessel thrombolysis in myocardial infarction (TIMI) flows (TIMI flow 0 -total coronary occlusion [TO]: 728, 26.3% of the patients, and TIMI flow 1-3 -non-total occlusion [non-TO]: 2039, 73.7% of the patients).Results: Patients with total occlusion were younger, were more often current smokers, and had lower incidence of hypertension and diabetes mellitus. The left circumflex artery (LCx) was the major IRA in the TO group (48.1%), whereas the left anterior descending artery (LAD) was more commonly the IRA in the non-TO group (38.8%). Multivariate analysis revealed that LCx as the culprit lesion (OR ± 95 CI 1.54 [1.26-1.89], p < 0.0001) was an independent predictor of TIMI flow 0 in IRA. In-hospital and one-month mortality occurred more frequently in the TO group (4.0% vs. 1.7%, p = 0.0005 and 5.5% vs. 3.5%, p = 0.0175, respectively), no differences in the 12-, 24-, or 36-month mortalities were observed between these groups. Conclusions:Only LCx as a culprit lesion was an independent predictor of total occlusion in IRAs. The NSTEMI patients with TO had higher in-hospital and one-month mortalities, but their long-term outcomes were similar to those of non-TO patients.

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Section: Discussionmentioning

confidence: 99%

Total coronary occlusion of infarct-related arteries in patients with non-ST-elevation myocardial infarction undergoing percutaneous coronary revascularisation

et al. 2017

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“…Some studies using epicardial strain gauges did not find an apparent hyperfunction of nonischemic areas (Banka and Helfant, 1974;Vokonas et al, 1976;Wyatt et al, 1976), indicating that the effects may not always be reflected transmurally. An increase in systolic motion in nonischemic areas has been noted in patients by echocardiography (Corya et al, 1975;Nieminen and Heikkila, 1976) and angiography (Rigaud et al, 1979;Stack et al, 1983;Sheehan et al, 1983).…”

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confidence: 95%

Mechanisms of augmented segment shortening in nonischemic areas during acute ischemia of the canine left ventricle.

Lew¹,

Chen²,

Guth³

et al. 1985

Circulation Research

122

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SUMMARY. To examine the interaction between normal and nonischemic areas of the left ventricle during acute ischemia, we implanted midwall ultrasonic segment length gauges in the ischemic zone and in nonischemic areas of the canine left ventricle. During acute ischemia, enddiastolic pressure and segment length in the nonischemic areas increased. There was no change from control in the segment length at the time of aortic valve opening and closure. Thus, in nonischemic areas, total segment shortening, as measured by the percent change in segment length from the time of end-diastole to aortic valve closure, increased. This was due to an increase in isovolumic shortening (end-diastole to aortic valve opening) with no change in ejection shortening (aortic valve opening to closure). The progressive increase in isovolumic shortening in nonischemic areas over time was directly paralleled by the progressive development of the isovolumic lengthening or bulge in the ischemic zone. Nonischemic areas, whether adjacent, on the opposite wall, or distant to the ischemic zone, all behaved similarly. Adrenergic blockade did not qualitatively alter these findings. We conclude that acute ischemia induces a mechanical disadvantage which is greater than just the loss of contractile function by the ischemic segment. Despite the apparent hyperfunction of nonischemic areas, the increased total segment shortening is expended in stretching the ischemic zone during isovolumic systole. As a result, there is no significant "compensatory' increase in ejection shortening in nonischemic areas. The results from the present study indicate that augmented total segment shortening in nonischemic areas is due ' to a combination of the Frank-Starling mechanism and regional intraventricular unloading of the nonischemic into the ischemic areas. (Circ Res 56: 351-358, 1985)

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“…[1][2][3][4][5][6] The application of two-dimensional echocardiography (2-D echo) to the problem of acute myocardial infarction (AMI) poses an important challenge to the clinical cardiologist. Reports have emerged that infarcted areas can be detected from left ventricular (LV) wall motion abnormalities present by 2-D echo.7 I Most recently, several investigations suggest further that infarct size can be predicted, based on a comparison of the extent of wall motion abnormality to thallium-201 perfusion defects9 or to peak CK-MB serum enzyme activities.…”

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confidence: 99%

Serial evaluation of myocardial thickening and thinning in acute experimental infarction: identification and quantification using two-dimensional echocardiography.

Nieminen¹,

Parisi²,

O'Boyle³

et al. 1982

Circulation

110

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SUMMARY Regional left ventricular function was studied serially by quantitative two-dimensional echocardiography (2-D echo) We conclude that there is considerable heterogeneity to myocardial thickening by 2-D echo, but failure to thicken is not seen in the normal dog heart. In many dogs, the extent of myocardial dysfunction 2 hours after coronary ligation exceeds that seen later. Tissue IS is difficult to predict accurately from ACS. Since the amount of muscle dysfunction is not necessarily equivalent to the amount of tissue necrosis in acute myocardial infarction, ACS may be more appropriately used to track the course of infarction rather than to predict IS.USING M-MODE echocardiography, several investigators have shown the potential of ultrasonic examination of the heart in patients with myocardial infarction, preparing the way for advances in instrumentation. [1][2][3][4][5][6] The application of two-dimensional echocardiography (2-D echo) to the problem of acute myocardial infarction (AMI) poses an important challenge to the clinical cardiologist. Reports have emerged that infarcted areas can be detected from left ventricular (LV) wall motion abnormalities present by 2-D echo.7 I Most recently, several investigations suggest further that infarct size can be predicted, based on a comparison of the extent of wall motion abnormality to thallium-201 perfusion defects9 or to peak CK-MB serum enzyme activities.'0 In a postmortem study the circumferential extent of infarct size correlated well with 2-D echo findings, even though infarct size was systematically overpredicted. " Reports of using 2-D echo to size infarction in animal models have been more circum- et al. 2 reported that the transmural extent of infarction has a nonlinear relationship to the extent of wall motion abnormality determined at 48 hours after coronary ligation. This was characterized by a "threshold"I phenomenon, i.e., various degrees of transmural infarction in excess of 20% almost always produced 100% dysfunction.'2 Pandian et al.'3 made a preliminary report that 2-D echo overpredicts infarct size but underpredicts the total amount of tissue at risk. The problem of infarct size determination is even more complicated in a clinical setting because early dysfunction (i.e., in the first 2-4 hours), rather than late dysfunction (after 24-48 hours), will be the focus of inquiry and possibly intervention. To simulate this sequence of clinical events, we produced AMI by coronary artery ligation in a series of experimental animals and performed serial closed-chest 2-D echo observations of regional myocardial function at 2, 24 and 48 hours after coronary occlusion. While tissue infarct size may be difficult to predict accurately, serial changes in regional myocardial performance assessed by thickening and thinning must be evaluated for their relevance to managing patients with AMI. All 2-D echo analyses were performed quantitatively using an extension of applications recently developed in our laboratory.'4 '5 Methods Experimental ProceduresMongrel ...

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Echocardiography in acute myocardial infarction

Cited by 132 publications

References 21 publications

Total coronary occlusion of infarct-related arteries in patients with non-ST-elevation myocardial infarction undergoing percutaneous coronary revascularisation

Total coronary occlusion of infarct-related arteries in patients with non-ST-elevation myocardial infarction undergoing percutaneous coronary revascularisation

Mechanisms of augmented segment shortening in nonischemic areas during acute ischemia of the canine left ventricle.

Serial evaluation of myocardial thickening and thinning in acute experimental infarction: identification and quantification using two-dimensional echocardiography.

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