The Complex Pathophysiology of Acute Myocardial Infarction Imaged by Cardiovascular Magnetic Resonance
Infarction, Edema, Microvascular Obstruction, and Inducible Ischemia
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).
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 heart’s 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
Sources of Funding
Funding has been received from CORDA and the British Heart Foundation.
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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