Coronary Spastic Angina Causing Myocardial Stunning Associated with Reversible Wall Thinning and Motion Abnormality of the Left Ventricle: A Case Report

Abstract

A 70-year-old woman presented to our emergency department with sudden resting angina at 8 p.m. Although she had experienced similar episodes over the previous 2 years, she had not previously sought medical attention, as these episodes had not been severe. She was a non-smoker with a prior history of untreated hypertension. On admission, her blood pressure was high (systolic/diastolic blood pressure, 173/109 mmHg), but findings of physical examination were otherwise unremarkable. A 12-lead electrocardiogram (ECG) showed ST-segment elevation in leads I, aVL, and V2-V6 and reciprocal ST-segment depression in leads II, III, and aVF (Fig. 1A). The symptoms were resolved with an intravenous injection of isosorbide dinitrate. To investigate the myocardial damage in detail, we performed cardiac magnetic resonance imaging (MRI) on hospitalization day 2. Although cardiac MRI showed anterior wall thinning, late gadolinium enhancement (LGE) was not detected (Fig. 4). We also examined the cardiac single photon emission computed tomography (SPECT) using 123 iodine beta methyl-iodophenyl pentadecanoic acid ( 123 I-BMIPP) and 201 thallium ( 201 Tl) on hospitalization day 5. The dual cardiac SPECT revealed a mismatch from the apex to the mid-anterior LV; 123 I-BMIPP images showed that the defect was ischemic memory (Fig. 5). Thus, cardiac MRI and SPECT were able to differentiate between infarcted and stunned myocardium. Coronary Spastic Angina Causing Myocardial Stunning Associated with Reversible Wall Thinning and Motion Abnormality of the Left Ventricle: a Case ReportToshiaki Isogai, Hiroyuki Tanaka, Motohiro Asaki, Tetsuro Ueda We describe a rare case of coronary spastic angina (CSA) causing myocardial stunning with reversible wall thinning and motion abnormality of the left ventricle (LV). A 70-year-old woman presented with sudden resting angina. A 12-lead electrocardiogram showed typical ST-T changes of acute myocardial infarction. Although left ventriculography revealed akinesis from the apex to the mid-anterior LV, urgent coronary angiography did not show an obstructed coronary artery. Cardiac magnetic resonance imaging (MRI) identified thinning of the anterior wall in the akinetic region, without any late gadolinium enhancement. Cardiac single photon emission computed tomography (SPECT), using 123 iodine beta methyl-iodophenyl pentadecanoic acid ( 123 I-BMIPP) and 201 thallium ( 201 Tl), showed a mismatch congruent with the akinetic region. An acetylcholine provocation test performed during hospitalization revealed multivessel coronary spasms in all 3 epicardial arteries. After initiation of treatment with coronary vasodilators, the wall thinning and motion abnormality gradually recovered to the normal range. In the present case, CSA caused myocardial stunning associated with reversible wall thinning and motion abnormality in the acute phase. CSA can occasionally lead to two conditions associated with LV wall abnormalities: myocardial infarction and stunning. Although the findings of the 2 conditions are similar in the a...