Non-Q-wave acute myocardial infarction: Body surface potential map and ventriculographic patterns

Terrence J. Montague, David E. Johnstone, C. Anne Spencer, Lucille D. Lalonde, Martin J. Gardner, Michael G. O'Reilly, B. Milan Horacek

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36 Citas (Scopus)

Resumen

Day 5 body surface map and radionuclide angiographic patterns were compared among 56 patients with first non-Q-wave or Q-wave acute myocardial infarction (AMI). Three radionuclide angiographic patterns were recognized in patients with non-Q infarction: no wall motion abnormalities (n = 8), single-segment wall motion abnormalities (n = 10) and multiple-segment wall motion abnormalities (n = 9). In contrast, only 2 radionuclide angiographic patterns were identified in patients with Q-wave infarction: multiple-segment wall motion abnormalities (n = 25) and single-segment wall motion abnormalities (n = 4). The Q-wave distributions of 14 of 18 patients with non-Q infarction with 0 or 1 wall motion abnormalities were normal; 2 patients had "missed" anterior; 1 patient had inferior; and 1 had posterior AMI patterns. Of 9 patients with non-Q infarction who had multiple-segment wall motion abnormalities, 8 had infarct Q waves on the posterior torso. Q-wave patterns in patients with anterior (n = 17) and inferior (n = 12) Q-wave infarctions were typical and homogeneous for each group. Quantitative analysis of minimum Q-zone integral, ΣQ-wave integrals, ST-integral maximum, wall motion abnormality score and ejection fraction revealed no differences between patients with non-Q-wave and those with inferior Q-wave infarction. In contrast, patients with anterior AMI had significantly more abnormal values of all variables than either of the other groups. Overall, the data support the concept of non-Q-wave AMI as a distinct, if heterogeneous, pathophysiologic entity. The variable body surface potential map and radionuclide angiographic patterns of the non-Q-wave AMI subgroups further suggest a variable prognosis. It remains to be determined, however, which patients are at greatest risk and why.

Idioma originalEnglish
Páginas (desde-hasta)1173-1180
Número de páginas8
PublicaciónAmerican Journal of Cardiology
Volumen58
N.º13
DOI
EstadoPublished - dic. 1 1986

Nota bibliográfica

Funding Information:
From the Dcpartmcnts of Medicine and Physiology and Biophysics. Dalhousie University and the Victoria General I lospi-tal, Halifax, Nova Scotia, Canada. This study was supported in part by grants from the Nova Scotia (Halifax] and New Brunswick (Saint John] Heart Foundations and the Medical Research Council of Canada, (Ottawa, PG-39). Manuscript received June 25. 1986; revised manuscript rcccivod July 28, 1986, acc;eplod July 29, 1986. Address for reprints: Tcrrcnce J, Montague. MD, h’KCP (C), Division of Cardiology, Room 3054-ACC, Victoria General I los-pital. Halifax, Nova Scotia, Canada B3H 2Y9.

ASJC Scopus Subject Areas

  • Cardiology and Cardiovascular Medicine

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