Circulation. 2008;118:e89-e92
doi: 10.1161/CIRCULATIONAHA.107.747691
(Circulation. 2008;118:e89-e92.)
© 2008 American Heart Association, Inc.
Images in Cardiovascular Medicine |
The Complex Pathophysiology of Acute Myocardial Infarction Imaged by Cardiovascular Magnetic Resonance
Infarction, Edema, Microvascular Obstruction, and Inducible Ischemia
Chiara Bucciarelli-Ducci, MD;
Fu Siong Ng, BSc(Hons), MRCP;
Karen Symmonds, DCR(R);
Eliana Reyes, MD;
Carl Schultz, MD;
Sam Kaddoura, MD, FRCP;
Sanjay K. Prasad, MD, FRCP
From the Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital (C.B.-D., K.S., S.K.P.), Imperial College, National Heart and Lung Institute (C.B.-D., S.K., S.K.P.), Nuclear Medicine Department, Royal Brompton Hospital (E.R.), Cardiology Department, Chelsea and Westminster Hospital (F.S.N., E.R., S.K.), and Catheterization Laboratory, Royal Brompton Hospital (C.S.), London, United Kingdom.
Correspondence to C. Bucciarelli-Ducci, Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, Sydney St, London, SW36NP UK, E-mail c.bucciarelli-ducci{at}rbht.nhs.uk
A 61-year-old man, an ex-smoker with a history of hypercholesterolemia, presented with crushing central chest pain radiating to the left arm, nausea, and cold sweat after consuming up to 2 g of recreational cocaine. ECG revealed Q waves in V1 through V3 with associated marginal ST-segment elevation of <1 mm (Figure 1). His troponin I level was 13.7 µg/L (normal range 0 to 0.04 µg/L). The patient was treated with dual antiplatelet therapy in addition to low-molecular-weight heparin and a calcium antagonist. He was referred for invasive coronary angiography, which demonstrated proximal occlusion of the left anterior descending artery (Figure 2) associated with anterior akinesia on ventriculography. To assess viability in this territory, myocardial perfusion scintigraphy and cardiovascular magnetic resonance (CMR) were requested. The myocardial perfusion scintigraphy images showed extensive full-thickness, anterior myocardial infarction involving the apex and the adjacent septum with evidence of peri-infarct ischemia in the basal anteroseptal segment (Figure 3). Gadolinium contrast-enhanced CMR imaging confirmed the anterior wall and septal akinesia (Movies I and II) and the presence of transmural myocardial infarction of the mid-cavity and apical portions of the anterior wall and septum with superimposed perfusion defect during adenosine infusion; no inducible peri-infarct ischemia was identified. CMR demonstrated the presence of both transmural myocardial edema and microvascular obstruction of the infarcted segments and thereby provided a more detailed myocardial tissue characterization of the damaged myocardium (Figures 4, 5, and 6
and Movie III). Repeat ECG 2 weeks after the acute event showed ST-segment elevation in the anterior leads suggesting evolution toward left ventricular remodeling (Figure 7).

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Figure 1. Twelve-lead electrocardiographic tracing shows Q waves in V1 through V3 with associated marginal ST-segment elevation of <1 mm.
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Figure 2. Invasive coronary angiography shows occlusion of the proximal segment of the left anterior descending artery (black arrows).
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Figure 3. Thallium-201 myocardial perfusion scintigraphy demonstrates a large, fixed defect that involves most of the anterior wall, the apex, and adjacent septum, consistent with full-thickness myocardial infarction of the left anterior descending coronary artery territory (arrowheads). There is mild peri-infarct ischemia in the remaining basal anteroseptal segment (arrows). SA indicates short-axis; VLA, vertical long-axis; and HLA, horizontal long-axis views.
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Figure 4. Cardiovascular magnetic resonance imaging, short-axis orientation. A, T2-weighted image shows increased signal intensity in the septum and anterior wall indicating myocardial edema (white arrows). B, Corresponding T1-weighted image after gadolinium-contrast administration demonstrates the presence of transmural infarction (white arrows) and areas of microvascular obstruction (black arrows). C and D, Adenosine perfusion images obtained at stress and rest show the myocardial perfusion defect superimposed with the infarct zone with no areas of inducible perfusion defect. The perfusion defect that is present at stress and persists in the rest image (asterisks) represents microvascular obstruction (also observed in B).
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Figure 5. Cardiovascular magnetic resonance imaging, 4-chamber orientation. A, T2-weighted image shows increased signal intensity in the septum and apex, indicating myocardial edema (white arrows). B, Corresponding T1-weighted image obtained after gadolinium-contrast administration demonstrates the presence of transmural infarction (white arrows) and areas of microvascular obstruction (black arrows).
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Figure 6. First-pass hybrid echo-planar short-axis perfusion images obtained during adenosine infusion (top) and corresponding images obtained at rest (bottom). There is inducible perfusion defect in the mid- and apical anterior wall and septum (white arrows).
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Figure 7. Repeat ECG performed 2 weeks after the acute event shows up to 4 mm of ST-segment elevation in leads V2 through V5, which indicates left ventricular remodeling.
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Irreversible myocardial damage in the anterior wall and septum, demonstrated by both myocardial perfusion scintigraphy and CMR, suggested that reopening of the occluded left anterior descending artery would be unfruitful.
In humans, cocaine has a deleterious effect on myocardial oxygen supply and demand by increasing the hearts metabolic needs and reducing coronary blood flow1 through intense and diffuse vasoconstrictive stimulation of both normal and atherosclerotic coronary arteries.2 Cocaine triggers myocardial infarction in patients with normal coronary arteries (who would otherwise be at relatively low risk), but it can also precipitate underlying coronary artery disease, as in the patient described.3,4
The pathophysiological processes that occur after acute myocardial infarction are complex. CMR provides noninvasive in vivo myocardial tissue characterization. This is achieved by exploiting different pulse sequences, including the inversion-recovery sequence, after the administration of gadolinium-chelate contrast media. Increased myocardial signal intensity depicted by T2-weighted imaging identifies areas of increased water content consistent with active myocardial inflammation and edema, which are distinctive aspects of acute myocardial infarction.5 Late myocardial enhancement obtained from T1-weighted imaging after contrast administration reveals irreversible myocardial injury (ie, myocardial necrosis), and the spatial resolution of the technique is such that the transmurality of damage can be assessed accurately.6 In addition, CMR identifies the presence of microvascular obstruction (poor contrast penetration due to vascular damage), which is considered an independent predictor of left ventricular remodeling with long-term prognostic impact.7
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Sources of Funding
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Funding has been received from CORDA and the British Heart Foundation.
Disclosures
None.
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Footnotes
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The online-only Data Supplement, which contains Movies I through III, can be found at http://circ.ahajournals.org/cgi/content/full/118/5/e89/DC1.
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References
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N Eng J Med. 1994; 330: 454–459.
[Abstract/Free Full Text]2. Flores ED, Lange RA, Cigarroa RG, Hillis LD. Effect of cocaine on coronary artery dimensions in atherosclerotic coronary artery disease: enhanced vasoconstriction at sites of significant stenosis. J Am Coll Cardiol. 1990; 16: 74–79.[Abstract]
3. Minor RL Jr, Scott BD, Brown DD, Winniford MD. Cocaine-induced myocardial infarction in patients with normal coronary arteries. Ann Intern Med. 1991; 115: 797–806.[Abstract/Free Full Text]
4. Mittleman MA, Mintzer D, Maclure M, Tofler GH, Sherwood JB, Muller JE. Triggering of myocardial infarction by cocaine. Circulation. 1999; 99: 2737–2741.[Abstract/Free Full Text]
5. Abdel-Aty H, Zagrosek A, Shulz-Menger J, Taylor AJ, Messroghli D, Kumar A, Gross M, Dietz R, Friedrich MG. Delayed enhancement and T2-weighted cardiovascular magnetic resonance imaging differentiate acute from chronic myocardial infarction. Circulation. 2004; 109: 2411–2416.[Abstract/Free Full Text]
6. Wagner A, Mahrholdt H, Holly TA, Elliott MD, Regenfus M, Parker M, Klocke FJ, Bonow RO, Kim RJ, Judd RM. Contrast-enhanced MRI and routine single photon emission tomography (SPECT) perfusion imaging for detection of subendocardial myocardial infarcts: an imaging study. Lancet. 2003; 361: 374–379.[CrossRef][Medline]
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7. Wu KC, Zerhouni EA, Judd RM, Lugo-Olivier CH, Barouch LA, Schulman SP, Blumenthal RS, Lima JA. Prognostic significance of microvascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. Circulation. 1998; 97: 765–772.[Abstract/Free Full Text]
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