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Myocardial function in infarcted and remote regions early after infarction in man: Assessment by magnetic resonance tagging and strain analysis
Author(s) -
Marcus J. Tim,
Götte Marco J. W.,
van Rossum Albert C.,
Kuijer Joost P. A.,
Heethaar Robert M.,
Axel Leon,
Visser Cees A.
Publication year - 1997
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.1910380517
Subject(s) - infarction , magnetic resonance imaging , cardiology , medicine , basal (medicine) , perfusion , diastole , myocardial infarction , artery , systole , contraction (grammar) , cardiac function curve , radiology , heart failure , insulin , blood pressure
Early after infarction in the perfusion bed of the left anterior descending coronary artery, cine MRI with spatial modulation of magnetization (SPAMM) tagging (7‐mm grid) was used for short‐ and long‐axis cardiac imaging. Two‐dimensional strain analysis of triangular finite elements was performed between end‐diastole and end‐systole. Patients ( n = 10) were compared with age‐matched healthy subjects ( n = 8). The anteroseptal region at midventricular level was considered representative for “infarcted” and the posterolateral region at basal level was considered “remote”. The left ventricular end‐diastolic volume index was larger in the patients (69 ± 15 ml/m 2 versus 56 ± 4 ml/m 2 , P < 0.05). Short‐axis images showed in the infarcted region a decrease of first principal strain (greatest systolic lengthening: 1.10 ±. 06 versus 1.27 ± 0.04, P < 0.0001), and in the remote region an increase (1.48 ± 0.11 versus 1.36 ± 0.07, P < 0.025). The lateral and inferior ventricular regions at mid‐ and basal levels were found to function normally. Long‐axis images yielded similar results. Early after infarction, regions with dysfunction, normal function, and hyperfunction can be delineated with MR tagging. The compensatory increased contraction in the remote region is possibly triggered by the Frank‐Starling mechanism.