British Journal of Radiology (2007) 80, e219-e221
© 2007 British Institute of Radiology
doi: 10.1259/bjr/24678934
Evidence of acute myocardial infarction on CT
J H Arnett, MD
K Mohajer, MD
and
S A Okon, MD
Departments of Radiology and Internal Medicine, Beth Israel Medical Center, First Avenue at 16th St., New York, NY 10003, USA
Correspondence: Dr John Arnett, 353 East 17th Street, Apartment 16E, New York, NY 10003, USA. E-mail: john.arnett{at}rcn.com
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Abstract
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Improvements in CT technology, specifically with respect to the development of multi-row detector CT, have increased the ability to detect acute myocardial ischaemia. This case report details the finding of decreased myocardial enhancement on CT in a patient who complained of acute chest symptomalogy and was diagnosed with acute myocardial infarction, which was subsequently confirmed by cardicac catheterization. Given the variability of the clinical presentation of acute myocardial infarction, greater attention should be paid by radiologists to myocardial enhancement in patients with significant coronary risk factors, as evidence of acute myocardial infarct or ischaemia may be detected.
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Case history
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The patient is a 66-year-old female with a past medical history of hypertension for several years, hypercholesterolemia, and a Type B aortic dissection. She presented to the Emergency Room (ER) with a history of vague pain in the anterior neck and throat extending to the chest, associated with shortness of breath. On the night of arrival to the ER, an electrocardiogram (ECG) demonstrated only non-specific T wave flattening and inversions in the inferior leads II, III, and aVF, not significantly changed from previously recorded ECGs. Her initial troponin level measured 0.00 ng mL–1 with no other abnormalities shown on initial laboratory results. The patient was kept overnight for observation. The next morning the patient complained of a mild (3/10) non-radiating pressure-like crescendo pain in the centre of the chest while resting in bed, which was relieved with sublingual nitroglycerin. An ECG done at that time showed new ST segment depressions and T wave inversions in leads II, III, aVF and V4-V6, indicating infero-lateral subendocardial ischaemia. Troponins drawn earlier that morning measured 0.33 ng mL–1 and subsequently 0.47 ng mL–1 when drawn at the time of chest pain. Owing to the patient's history of type B dissection, the patient was taken for a contrast-enhanced CT scan of the chest and abdomen to specifically evaluate for extension of aortic dissection. The CT scan did not show any interval change in the appearance of the Type B dissection, which was performed with the same protocol as a CT performed 2
months earlier. However, the scan showed decreased enhancement of the inferior subendocardial left ventricular wall when compared with the prior study, as shown in Figure 1
. The patient was transferred to the CCU with a subsequent troponin measurement that night of 1.24 ng mL–1. The patient underwent cardiac catherization the following morning, and was found to have a 95% stenosis in the mid right coronary artery (RCA) of a RCA dominant heart and a 70% stenosis in the mid left anterior descending artery. Successful percutaneous transluminal coronary angioplasty and stent placement of the RCA was performed. The patient was discharged from the hospital soon after the procedure, with routinely scheduled follow-up.
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Figure 1. (a) Axial image of contrast-enhanced CT performed 2 months prior to the patient's current presentation showing normal myocardial enhancement. (b–d) Axial, coronal and short-axis images of the contrast-enhanced CT performed during the period of acute symptomalogy, demonstrating decreased subendocardial enhancement predominantly in the inferior left ventricular wall.
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Discussion
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The initial diagnosis and evaluation of acute myocardial infarction is currently performed with the analysis of ECG changes and cardiac enzyme measurements. However, atypical presentations of acute myocardial infarction such as nausea, vomiting, syncope, or "tearing" chest pain generate a large differential diagnosis. Patients with these presentations are often evaluated with contrast-enhanced CT of the chest, sometimes with protocols specifically designed to evaluate for entities such as pulmonary embolism or aortic dissection, as in our patient. Improvements in CT technology have allowed better evaluation of the heart specifically by decreasing scan time and thus allowing more accurate timing of the intravenous contrast bolus and diminishing cardiac motion artifact [1]. Intravenous contrast-enhanced CT can readily identify the cardiac chambers, grossly assess their volumes and, using ECG-gating, can assess left ventricular wall motion and thickening [2]. Animal studies have demonstrated the ability of multi-detector row CT (MDCT) to permit the detection of acute myocardial infarction via lower measured CT attenuation in infarct areas relative to normal reference areas [3]. Earlier studies have also shown the ability of MDCT to demonstrate focal areas of decreased ventricular myocardial enhancement in a specific coronary arterial distribution consistent with the clinically diagnosed infarct in humans. Ischaemic changes in the myocardium after coronary arterial occlusion consist of disruption of cell membrane function and integrity and increased permeability of small vessel walls. The initial area of low attenuation primarily reflects myocardial oedema. Subsequently, necrotic myocardium is replaced by fibrous and/or fatty tissue [4]. Defects in myocardial perfusion are seen in the early phase of contrast enhancement in cases of acute myocardial infarction [5]. A perfusion defect, however, is not specific for infarction, because similar findings can occur in cases with severe local ischaemia (but no infarction) or other cardiac diseases causing perfusion inhomogeneities, such as hypertrophic cardiomyopathy. Also, myocardial contrast enhancement depends on a number of independent variables (e.g. contrast injection protocol and cardiac output). As a result, studies of myocardial enhancement in normal and infarcted tissue have shown significant variance in measured Hounsfield units (HU). This makes an absolute HU measurement of myocardium to determine the presence of infarcted tissue difficult. A relative change of enhancement seems more practical. Wall thinning in the left ventricle is an indirect finding associated with the healing process after myocardial infarction. It has been shown that, in patients with myocardial infarction, the wall thickness at the site of infarction decreased significantly over time [4]. Myocardial wall thinning was identified in the infarcted regions over 2–6 months as ventricular remodeling occurred [2]. MDCT has shown a moderate to high sensitivity for the detection of myocardial infarctions (85%). However, recent infarctions may be more difficult to detect given that the decrease in HU in the early arterial phase or the presence of wall thinning is not as pronounced as observed in chronic infarctions. Similarly, several studies have reported that CT underestimates the true extent of a myocardial infarction. This might be related to patchy and subendocardial infarctions given that collateral perfusion in the area of infracted myocardium may obscure foci of necrosis surrounded by normal myocardium. Thus, it has been suggested that infarct size assessed by MDCT should be used as an approximation of the true infarct size rather than an absolute measurement [4]. It also has been shown that delayed hyperenhancement also occurs in the infarcted region. In conjunction with decreased myocardial enhancement, these findings can be utilized to measure infarct size and progression [2]. Other recent studies have shown that MDCT, when evaluating for myocardial late enhancement in acute MI, is as reliable as delayed contrast-enhanced cardiac MRI in assessing infarct size [6]. With the advent of MDCT technology, true three-dimensional subsecond ECG gated imaging of the heart has become feasible. As a result, motion (cardiac and respiratory)-free imaging of the cardiac chambers, valves, coronary vessels and surrounding tissues can be accomplished within a single breath-hold period [7].
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Conclusion
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MDCT is able to identify acute myocardial infarction as a region of myocardium with lower attenuation than adjacent regions of normal enhanced myocardium. With contrast-enhanced MDCT-derived coronary CT angiograms and analysis of myocardial enhancement, and the ability to non-invasively provide information about the morphological and physiological significance of atherosclerotic coronary artery lesions, the initial method of diagnosis of myocardial infarction may change in the near future [7].
Received for publication January 21, 2006.
Revision received April 30, 2006.
Accepted for publication June 14, 2006.
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References
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