Coronary Artery and Cardiac Disease in Patients With Type 2 Myocardial Infarction: A Prospective Cohort Study

Abstract

Background: Type 2 myocardial infarction is caused by myocardial oxygen supply-demand imbalance, and its diagnosis is increasingly common with the advent of high-sensitivity cardiac troponin assays. Although this diagnosis is associated with poor outcomes, widespread uncertainty and confusion remain among clinicians as to how to investigate and manage this heterogeneous group of patients with type 2 myocardial infarction.

Methods: In a prospective cohort study, 8064 consecutive patients with increased cardiac troponin concentrations were screened to identify patients with type 2 myocardial infarction. We excluded patients with frailty or renal or hepatic failure. All study participants underwent coronary (invasive or computed tomography angiography) and cardiac (magnetic resonance or echocardiography) imaging, and the underlying causes of infarction were independently adjudicated. The primary outcome was the prevalence of coronary artery disease.

Results: In 100 patients with a provisional diagnosis of type 2 myocardial infarction (median age, 65 years [interquartile range, 55-74 years]; 43% women), coronary and cardiac imaging reclassified the diagnosis in 7 patients: type 1 or 4b myocardial infarction in 5 and acute myocardial injury in 2 patients. In those with type 2 myocardial infarction, median cardiac troponin I concentrations were 195 ng/L (interquartile range, 62-760 ng/L) at presentation and 1165 ng/L (interquartile range, 277-3782 ng/L) on repeat testing. The prevalence of coronary artery disease was 68% (63 of 93), which was obstructive in 30% (28 of 93). Infarct-pattern late gadolinium enhancement or regional wall motion abnormalities were observed in 42% (39 of 93), and left ventricular systolic dysfunction was seen in 34% (32 of 93). Only 10 patients had both normal coronary and normal cardiac imaging. Coronary artery disease and left ventricular systolic dysfunction were previously unrecognized in 60% (38 of 63) and 84% (27 of 32), respectively, with only 33% (21 of 63) and 19% (6 of 32) on evidence-based treatments.

Conclusions: Systematic coronary and cardiac imaging of patients with type 2 myocardial infarction identified coronary artery disease in two-thirds and left ventricular systolic dysfunction in one-third of patients. Unrecognized and untreated coronary or cardiac disease is seen in most patients with type 2 myocardial infarction, presenting opportunities for initiation of evidence-based treatments with major potential to improve clinical outcomes.

Registration: URL: https://www.

Clinicaltrials: gov; Unique identifier: NCT03338504.

Keywords: cardiac imaging techniques; echocardiography; magnetic resonance imaging; myocardial infarction.

Figures

Figure 1.

Study population. Screening, enrollment, recruitment and final study population with an adjudicated diagnosis of type 2 myocardial infarction. CT indicates computed tomography; DEMAND-MI, Determining the Mechanism of Myocardial Injury and Role of Coronary Disease in Type 2 Myocardial Infarction; and MRI, magnetic resonance imaging.

Figure 2.

Imaging findings and diagnostic reclassification in patients with a clinical diagnosis of type 2 myocardial infarction. Alluvial plot illustrating the cause of supply-demand imbalance, presence of coronary disease on coronary imaging, and final adjudicated diagnosis according to the Fourth Universal Definition of Myocardial Infarction stratified according to evidence of myocardial infarction (MI) on cardiac imaging. The cause of supply-demand imbalance in type 2 myocardial infarction is categorized in 3 clinically relevant groups: coronary subgroup encompassing coronary artery dissection, coronary embolism, and vasospasm; systemic subgroup encompassing patients presenting for anemia, hypotension, severe hypertension, or hypoxemia; and arrhythmia subgroup encompassing supply-demand imbalance attributable to sustained bradyarrhythmia or tachyarrhythmia. MI indicates myocardial infarction.

Figure 3.

Exemplar cases and imaging studies according to cause of type 2 myocardial infarction. Patients with 3 differing causes of type 2 myocardial infarction showing clinical presentation data; study imaging, including invasive coronary angiogram; and cardiac magnetic resonance images. Coronary cause case: Invasive coronary angiogram (A) with evidence of coronary embolus with occlusion of the mid left anterior descending coronary artery (B). Cardiac magnetic resonance showed normal ventricular size and moderate impairment in left ventricular function (ejection fraction, 48%) with evidence of near-transmural late gadolinium enhancement in the anteroseptum (C). T2 value at the site of late gadolinium enhancement was elevated at 75.6 milliseconds, indicating an acute infarct (D). Systemic cause case: Invasive coronary angiogram showed evidence of 3-vessel obstructive coronary artery disease (A and B). Cardiac magnetic resonance showed normal ventricular size and function (ejection fraction, 64%) with evidence of subendocardial late gadolinium enhancement in the inferior wall (C). T2 value at the site of late gadolinium enhancement was elevated at 49.6 milliseconds, indicating an acute infarct (D). Arrhythmia cause case: Normal invasive coronary angiogram (A and B). Cardiac magnetic resonance showed normal ventricular size and function (ejection fraction, 62%) with evidence of basal subendocardial late gadolinium enhancement affecting the inferior, inferolateral, and anterior walls (C). T2 value at the site of late gadolinium enhancement was elevated at 51 milliseconds, indicating an acute infarct (D). BP indicates blood pressure; and HR, heart rate.

Figure 4.

Prior treatment in patients with coronary artery disease and left ventricular systolic impairment identified on coronary and cardiac imaging. Proportion of patients with coronary artery disease or left ventricular impairment identified on coronary and cardiac imaging, respectively, stratified by prior treatment with evidence-based medical therapy. ACE indicates angiotensin-converting enzyme.