Implications of a new clinical classification of acute myocardial infarction

Abstract

Aims: The diagnostic criteria for Type 2 myocardial infarction identify a heterogeneous group of patients with variable outcomes and no clear treatment implications. We aimed to determine the implications of a new clinical classification for myocardial infarction with more objective diagnostic criteria using cardiac imaging.

Methods and results: In a prospective cohort study, patients with Type 2 myocardial infarction underwent coronary angiography and cardiac magnetic resonance imaging or echocardiography. The new classification was applied to identify (i) spontaneous myocardial infarction due to acute coronary pathology, (ii) secondary myocardial infarction precipitated by acute illness in the presence of obstructive coronary artery disease, a new regional wall motion abnormality, or infarct-pattern scarring, and (iii) no myocardial infarction in the absence of obstructive disease or new myocardial abnormality. In 100 patients (65 years, 43% women) with Type 2 myocardial infarction, the new classification identified 25 and 31 patients with spontaneous and secondary myocardial infarction, respectively, and 44 without myocardial infarction. Compared with patients without myocardial infarction, those with secondary myocardial infarction were older, had more risk factors, and had higher troponin concentrations (P < 0.05 for all). During a median follow-up of 4.4 years, death, myocardial infarction, or heart failure hospitalization was more common in secondary myocardial infarction compared with those without myocardial infarction [55% (17/31) vs. 16% (7/44), P < 0.001].

Conclusion: A new clinical classification of myocardial infarction informed by cardiac imaging would reduce the diagnosis of myocardial infarction in acute illness and identify those patients at highest risk who are most likely to benefit from treatment.

Clinical trial registration: https://clinicaltrials.gov/ct2/show/NCT03338504.

Keywords: Cardiac troponin; Coronary artery disease; Imaging; Myocardial infarction.

Figure 1

Alluvial plot illustrating the reclassification of patients with a diagnosis of Type 2 myocardial infarction into spontaneous and secondary myocardial infarction or no myocardial infarction. Patients with spontaneous myocardial infarction had evidence of acute coronary pathology (acute atherothrombosis, coronary embolism, spontaneous coronary dissection, and coronary vasospasm). Patients with secondary myocardial infarction had either evidence of obstructive coronary artery disease or functional consequences of myocardial injury with new left ventricular systolic impairment or evidence of infarct pattern late gadolinium enhancement on cardiac magnetic resonance imaging with or without regional wall motion abnormality. Two patients classified as no myocardial infarction had evidence of previous infarction with late gadolinium enhancement.

Figure 2

Case of spontaneous myocardial infarction (A), secondary myocardial infarction (B), and no myocardial infarction (C). (A) A 65-year-old patient with a recent diagnosis of atrial fibrillation and prior history of hypertension, Type 2 diabetes mellitus, and chronic obstructive pulmonary disease presented with chest pain at rest. They were found to be in sinus rhythm with ST-segment elevation across the anterior leads. Coronary angiography demonstrated abrupt occlusion of the left anterior descending artery, and thrombectomy was performed to restore coronary perfusion. Optical coherence tomography imaging demonstrated minimal atherosclerosis with no evidence of plaque rupture, and the patient was anticoagulated with apixaban. The peak cardiac troponin I concentration was 32 201 ng/L. Cardiac magnetic resonance imaging revealed near transmural late gadolinium enhancement in the mid-to-apical antero-septum with evidence of left ventricular systolic impairment (ejection fraction 48%). The final diagnosis was spontaneous myocardial infarction secondary to coronary embolism. (B) An 82-year-old patient with a history of angina and peripheral vascular disease presented with sudden onset palpitation and chest pain. The electrocardiogram demonstrated rapid atrial fibrillation with left bundle brunch block. Peak cardiac troponin I concentration was 3500 ng/L. Coronary angiography demonstrated diffuse coronary artery disease with a severe ostial lesion of the left anterior descending coronary artery. Optical coherence tomography revealed no evidence of plaque rupture or thrombosis. Pressure wire assessment showed marked gradient across the lesion (fractional flow reserve 0.99–0.56). Cardiac magnetic resonance imaging revealed severe left ventricular systolic impairment (ejection fraction 16%). The scan was stopped early on patient request and late gadolinium enhancement sequences were not obtained. The final diagnosis was secondary myocardial infarction due to atrial fibrillation with obstructive coronary artery disease and significant left ventricular impairment. (C) A 72-year-old patient with hypertension and hypercholesterolaemia presented with a 2 day history of chest tightness, left arm pain, and palpitations. The electrocardiogram demonstrated ventricular tachycardia, and the patient required cardioversion on arrival. The peak cardiac troponin I concentration was 1637 ng/L. Coronary angiography demonstrated normal coronary arteries with evidence of marked calcification of the aortic valve and aortic root dilatation. The patient underwent an echocardiogram which showed evidence of severe bicuspid aortic stenosis. Cardiac magnetic resonance imaging identified normal left ventricular systolic function (ejection fraction 67%) with no late gadolinium enhancement. Myocardial infarction was excluded. The final diagnosis was ventricular tachycardia secondary to severe aortic stenosis.

Figure 3

Survival free from death, myocardial infarction, or heart failure hospitalization in patients with spontaneous and secondary myocardial infarction and those without myocardial infarction. Kaplan–Meier curves illustrating survival free from all-cause death, myocardial infarction, or hospitalization with heart failure in patients with a clinical diagnosis of Type 2 myocardial infarction reclassified following cardiac imaging as having spontaneous, secondary, or no myocardial infarction according to the new clinical classification.