Assessment of non–ST-segment elevation acute coronary syndromes with cardiac magnetic resonance imaging
Sven Plein, MD*,*,
John P. Greenwood, PhD*,
John P. Ridgway, PhD ,
Gillian Cranny, MSc ,
Stephen G. Ball, PhD and
Mohan U. Sivananthan, MD*
BHF-Cardiac Magnetic Resonance Unit, the General Infirmary at Leeds, Leeds, United Kingdom
Department of Medical Physics, the General Infirmary at Leeds, Leeds, United Kingdom
Clinical Trials Research Unit, University of Leeds, Leeds, United Kingdom
BHF Heart Research Centre, University of Leeds, Leeds, United Kingdom
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Figure 1 Cardiac magnetic resonance (CMR) imaging protocol. Times are approximations; gaps between imaging blocks indicate time for planning of subsequent CMR images. The protocol commences with localizer images and a reference scan that is required to utilize sensitivity encoding (SENSE). A resting myocardial perfusion acquisition is then performed using 0.05 mmol/kg body weight of dimeglumine gadopentetate. Next, a coronary scout image is acquired, followed by a high-resolution angiogram aligned along the course of the right coronary artery (RCA). An adenosine-stress perfusion acquisition is then performed, immediately followed by injection of a further 0.1 mmol/kg of contrast in preparation for viability imaging. An angiogram targeted on the left coronary vessels is then acquired, followed by viability images using a late contrast-enhanced technique.
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Figure 2 Selected cardiac magnetic resonance (CMR) images from one study patient. Cardiac magnetic resonance findings in a 49-year-old male patient (presented with anterolateral ST-segment depression, troponin 0.2 mg/l). Only one short-axis image of selected CMR acquisitions is shown. Cine images demonstrate anteroseptal hypokinesia, diastolic frame at midventricular level in (a), systolic frame in (b), white arrows. Stress perfusion imaging (c) shows an anteroseptal perfusion defect. Late contrast-enhanced images (d) show no hyperenhancement, indicating that the entire myocardium is viable. Coronary CMR shows a lesion in the mid-left anterior descending coronary artery (LAD) (e, dotted arrow), with normal left circumflex coronary artery (LCX) and right coronary artery (RCA) (f). The combined CMR analysis thus suggested significant coronary artery disease with a stenosis of the LAD and a large area of viable myocardium at ischemic risk. X-ray angiography, (g and h), confirmed a proximal high-grade lesion in the LAD (dotted arrow), with a normal LCX and RCA. LV = left ventricle; RV = right ventricle.
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Figure 3 Cardiac magnetic resonance imaging examples from three study patients with a variety of myocardial perfusion deficits. All examples show only one midventricular slice of the stress images. (a) Inducible anteroseptal subendocardial perfusion defect (white arrow). X-ray angiography showed subtotal occlusion of the proximal left anterior descending coronary artery (LAD). (b) Inducible lateral perfusion defect in a thinned lateral wall (white arrow) and further small transmural septal perfusion defect (black arrow). X-ray angiography showed significant stenosis of the mid-LAD and an occluded left circumflex coronary artery. (c) Inferior transmural perfusion defect (white arrow). X-ray angiography showed a significant stenosis in the mid-right coronary artery.
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Figure 4 Cardiac magnetic resonance imaging examples from three study patients with a variety of abnormalities on late contrast-enhanced images. (a) A small area of hyperenhancement at the inferolateral junction (arrow) in a patient with transient inferior ST-segment depression on the presenting electrocardiogram (ECG) (serum troponin level 7.5 mg/l). (b) Subendocardial hyperenhancement of the inferior wall, which appears to involve the posterior papillary muscle, in a patient who had no significant electrocardiographic changes (serum troponin level 0.7 mg/l). (c) Lateral full thickness hyperenhancement with a central hypoenhancing zone indicating no-reflow in the infarct core (arrow). Clinically, this patient presented with a non–ST-segment elevation myocardial infarction, and a standard 12-lead ECG showed only minimal ST-segment depression in the lateral leads. Peak creatinine kinase was 1,910 IU and troponin 12.3 mg/l.
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Figure 5 Cardiac magnetic resonance (CMR) imaging examples from three study patients showing abnormalities of coronary CMR angiograms compared with corresponding X-ray angiograms. The CMR angiograms in the top row, corresponding X-ray angiograms in bottom row. (a and d) Stenosis (dotted arrows) of the mid-left anterior descending artery (LAD). (b and e) Stenosis (dotted arrows) in the proximal circumflex artery (LCX). (c and f) Stenosis (dotted arrows) of the mid-right coronary artery (RCA).
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Figure 6 Prediction of significant coronary artery disease by comprehensive analysis of all cardiac magnetic resonance data by separate analysis of the four cardiac magnetic resonance components, and by a Thrombolysis In Myocardial Infarction (TIMI) risk score of  3. Coros = coronary magnetic resonance angiography; LeMRI = late contrast-enhanced magnetic resonance imaging; WM = wall motion analysis. Solid bars = sensitivity; open bars = specificity.
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