Distinguishing Type 1 from Type 2 Myocardial Infarction by Using CT Coronary Angiography

Abstract

Purpose: To determine whether quantitative plaque characterization by using CT coronary angiography (CTCA) can discriminate between type 1 and type 2 myocardial infarction.

Materials and methods: This was a secondary analysis of two prospective studies (ClinicalTrials.gov registration nos. NCT03338504 [2014-2019] and NCT02284191 [2018-2020]) that performed blinded quantitative plaque analysis on findings from CTCA in participants with type 1 myocardial infarction, type 2 myocardial infarction, and chest pain without myocardial infarction. Logistic regression analyses were performed to identify predictors of type 1 myocardial infarction.

Results: Overall, 155 participants (mean age, 64 years ± 12 [SD]; 114 men) and 36 participants (mean age, 67 years ± 12; 19 men) had type 1 and type 2 myocardial infarction, respectively, and 136 participants (62 years ± 12; 78 men) had chest pain without myocardial infarction. Participants with type 1 myocardial infarction had greater total (median, 44% [IQR: 35%-50%] vs 35% [IQR: 29%-46%]), noncalcified (39% [IQR: 31%-46%] vs 34% [IQR: 29%-40%]), and low-attenuation (4.15% [IQR: 1.88%-5.79%] vs 1.64% [IQR: 0.89%-2.28%]) plaque burdens (P < .05 for all) than those with type 2. Participants with type 2 myocardial infarction had similar low-attenuation plaque burden to those with chest pain without myocardial infarction (P = .4). Low-attenuation plaque was an independent predictor of type 1 myocardial infarction (adjusted odds ratio, 3.44 [95% CI: 1.84, 6.96]; P < .001), with better discrimination than noncalcified plaque burden and maximal area of coronary stenosis (C statistic, 0.75 [95% CI: 0.67, 0.83] vs 0.62 [95% CI: 0.53, 0.71] and 0.61 [95% CI: 0.51, 0.70] respectively; P ≤ .001 for both).

Conclusion: Higher low-attenuation coronary plaque burden in patients with type 1 myocardial infarction may help distinguish these patients from those with type 2 myocardial infarction.Keywords: Ischemia/Infarction, CT Angiography, Quantitative CTClinical trial registration nos. NCT03338504 and NCT02284191 Supplemental material is available for this article. © RSNA, 2022.

Keywords: CT Angiography; Ischemia/Infarction; Quantitative CT.

Conflict of interest statement

Disclosures of conflicts of interest: M.M. Author is a British Heart Foundation (BHF) clinical research fellow at the University of Edinburgh, a BHF grant (grant no. FS/19/46/34445) has supported author’s work since November 2019. A.B. Support for the present manuscript from the BHF (grant no. FS/16/75/32533). E.T. No relevant relationships. A.R.C. No relevant relationships. M.D. No relevant relationships. J.D.H. No relevant relationships. J.C. No relevant relationships. C.T. No relevant relationships. R.W. Clinical training research fellowship from the Medical Research Council UK (no. MR/V007017/1). A.G. Participation on advisory board for Abbott for brain and cardiac biomarkers, fees paid to author’s institution. M.R.D. No relevant relationships. C.R. No relevant relationships. N.C. Unrestricted research grants from Boston Scientific, Haemonetics, Beckmann Coulter, and HeartFlow; speakers fees from Abbott and Boston Scientific; travel sponsorship from Biosensors, Abbott, Edwards, and Medtronic. A.K. No relevant relationships. D.F. No relevant relationships. N.L.M. BHF grants (grant nos. CH/F/21/90010, RG/20/10/34966, and RE/18/5/34216) paid to author’s institution; payment or honoraria for lectures from Abbott Diagnostics and Siemens Healthineers; payment for participation on advisory boards for LumiraDX, Roche Diagnostics, and Siemens Healthineers; receipt of reagent from Siemens Healthineers to support research. P.J.S. Grants from Siemens Medical Systems and National Institutes of Health, paid to author’s institution; royalties or licenses from Cedars-Sinai Medical Systems, paid to author and author’s institution; consulting fees from IBA; several patents planned and pending, not related to this field of work, via Cedars-Sinai; vice-president of Society of Nuclear Medicine. D.E.N. Supported by the BHF (grant nos. CH/09/002, RG/16/10/32375, and RE/18/5/34216) and is the recipient of a Wellcome Trust Senior Investigator award (no. WT103782AIA); author is a co-applicant and co-author on the RAPID-CTA trial funded by the National Institute for Health (NIH) Research Health Technology Assessment Programme (no. 13/04/108) and the DEMAND-MI study funded by the BHF (FS/16/75/32533). D.D. NIH/National Heart, Lung, and Blood Institute grants (nos. 1R01HL148787-01A1 and 1R01HL151266); software royalties from Cedars-Sinai Medical Center, outside the current work. M.C.W. Supported by the BHF (grant no. FS/ICRF/20/26002); author has given talks for Canon Medical Systems and Siemens Healthineers; member of the board of directors of Society of Cardiovascular Computed Tomography; president-elect of the education committee of the British Society of Cardiovascular Imaging; president-elect of the European Society of Cardiovascular Radiology; Radiology: Cardiothoracic Imaging editorial board member.

© 2022 by the Radiological Society of North America, Inc.

Figures

Graphical abstract

Figure 1:

Substudy diagram shows the screening and final study participants. DEMAND-MI = Determining the Mechanism of Myocardial Injury and Role of Coronary Disease in Type 2 Myocardial Infarction, RAPID-CTCA = Rapid Assessment of Potential Ischemic Heart Disease with CT Coronary Angiography.

Figure 2:

Comparison of plaque burden subtypes in patients with type 1 myocardial infarction, type 2 myocardial infarction, and acute chest pain without myocardial infarction. Histograms (medians ± IQRs) comparing burden of plaque subtypes demonstrate that participants with type 1 myocardial infarction had higher burdens of total, noncalcified, and low-attenuation plaque burden. MI = myocardial infarction, ns = not significant, * = P < .05, ** = P < .01, *** = P < .001, **** = P < .0001.

Figure 3:

Predictors of type 1 myocardial infarction. Receiver operating characteristic curves compare ability of low-attenuation plaque (LAP; black) burden, noncalcified plaque (NCP; green) burden, and maximal area stenosis (blue) to discriminate between type 1 and type 2 myocardial infarction. There was a low-attenuation plaque burden C statistic of 0.75 (95% CI: 0.67, 0.83), noncalcified plaque burden C statistic of 0.62 (95% CI: 0.53, 0.71), and maximal area stenosis C statistic of 0.61 (95% CI: 0.51, 0.70). AUC = area under the receiver operating characteristic curve.

Figure 4:

Representative images of CT plaque analysis demonstrate differences between type 1 and type 2 myocardial infarction. Left panel: Images in a 42-year-old man diagnosed with type 1 myocardial infarction. (A) Image from invasive angiography demonstrates severe stenosis in the distal left anterior descending artery. (B) CT coronary angiogram, curved planar reformation, (C) quantitative plaque analysis, and(D) three-dimensional quantitative plaque analysis demonstrate a high burden of low-attenuation plaque. Right panel: Images in a 74-year-old man diagnosed with type 2 myocardial infarction.(E) Electrocardiogram demonstrates broad-complex tachycardia consistent with ventricular tachycardia. (F) CT coronary angiogram, curved planar reformation, (G) quantitative plaque analysis, and (H) three-dimensional quantitative plaque analysis demonstrate a low burden of low-attenuation plaque. Both participants have obstructive coronary artery disease detected with CT coronary angiography. Quantitative plaque analysis demonstrates clear differences, with a much higher burden of low-attenuation plaque in the participant presenting with type 1 myocardial infarction compared with the participant presenting with type 2.