A serial changes of thallium-201 myocardial images in a patient with nontransmural myocardial infarction Takeshi Tanaka 1 , Yukiyoshi Itoh 1 , Yasuo Takayama 1 , Yohichi Shimizu 1 , Toshihide Tanaka 1 , Mitsuki Abe 1 , Mitsukazu Matsuda 1 , Shinji Hukuchi 1 , Takao Ida 1 , Takayuki Sakakibara 1 , Yoshio Obunai 1 , Shinichi Kimata 2 , Koshichiro Hirosawa 2 1Sakakibara Memorial Hospital 2Heart Institute of Japan, Tokyo Women's Medical College pp.89-96
Published Date 1986/1/15
DOI https://doi.org/10.11477/mf.1404204809
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A 66 year old man had suffered from inferior myocardial infarction one year ago and then suffered from effort angina. Recently rest angina attack frequently occurred and he was admitted because of angina attack refractory to TNG. After admission he was treated as nontransmural myo-cardial infarction, however he had repetitive non-transmural infarction. At last he developed severe ischemic attack accompanying pulmonary edema. Despite aggressive medical therapy hemodynamic deterioration increased and V3R decreased. IABP was instituted. After 24 hours hemodynamic stability was achieved and decreased V3R recovered to al-most preattack hight. Coronary angiography reveal-ed three vessels disease. Emergency coronary by-pass surgery to LAD and LCX was successfully performed. On 1 month postop left ventriculography revealed generalized hypokinetic movement and ejection fraction was 24%. After discharge he did well without ischemic events. Through the clinical course R decreased all over leads and new QS were noted only in V1~2. The patient was diagnosed as broad nontransmural infarction. A serial thal-lium-201 myocardial imagings at rest and thallium-201 lung uptake imagings were performed and some interesting findings were obtained as followings.

Myocardial imagings on 3rd day after admission showed no significant defect, however EF was 34%. Immediately after severe ischemic attack marked defect was noted at posterolateral region and ECG showed prominent precordial ST depression without accompanying significant ST change in II, III, aVF. On 3rd day after severe attack under hemody-namically and electrocardiographically stable state posterolateral defect improved, though still persisted. EF was 28%. On 3rd day postop no marked defects were noted in myocardial imagings, so posterolater-al defect at rest after severe ischemic attack was proved to be transient defect.

There were some reports about pathogenesis of precordial ST depression in acute inferior infarction. In this case marked precordial ST depression was noted, however no hypoperfusion area was noted in the anterior wall region. This indicated that the precordial ST depression did not reflect the anteri-or wall ischemia. There were no ST elevation in II, III, aVF, so the precordial ST depression was not thought to be reciprocal changes of ST changes of limb leads. Recently it was suggested that this ST depression reflected posterolateral or anteroseptal extension of inferior wall infarction. In acute phase improvement of hypoperfusion area in posterolateral region was noted and at the same time recovery of precordial ST depression also occurred. It was suggested that precordial ST depression in this case might correspond to posterolateral transient defect, not to posterolateral transmural infarction.

In this case thallium-201 lung uptake was not noted before attack. Immediately after severe attack thallium lung uptake increased and maximal uptake was noted at basal zone of lung, however in chest X-P typical butterfly shadow was noted at upper zone of lung. On 3rd day after severe attack hemo-dynamics improved and butterfly shadow ceased, though thallium lung uptake increased and noted at upper zone of lung. After operation thallium lung uptake improved.

Copyright © 1986, Igaku-Shoin Ltd. All rights reserved.


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