Type 2 Myocardial Infarction: Clinical Characteristics and Outcomes

Quick Takes

  • In this European cohort of patients presenting to emergency departments with chest pain, type 1 myocardial infarction (MI) was diagnosed in 16.4% of patients, and type 2 MI in 4.0%.
  • All-cause and cardiovascular mortality were similar in the type 1 and type 2 MI groups. However, among patients with type 2 MI, those with hypoxemia, hypotension, or anemia as the ischemic trigger had higher mortality than those with underlying tachycardia or hypertension.

Study Questions:

What are the clinical characteristics and outcomes of myocardial infarction caused by supply-demand mismatch, or type 2 myocardial infarction (T2MI)?

Methods:

This prospective cohort study, conducted at 12 emergency departments in five European countries, enrolled patients who presented with acute chest discomfort from 2006–2018. Treatment was at the discretion of the attending physician. High-sensitivity cardiac troponin (hs-cTn) levels were measured at a core laboratory, and final diagnoses of type I MI (T1MI) and T2MI were centrally adjudicated by two independent cardiologists, according to the Fourth Universal Definition of Myocardial Infarction. The diagnosis of T2MI required dynamic changes in hs-cTn level (as also seen in T1MI) and a clear trigger for ischemia (e.g., arrhythmia, hypoxemia, hypotension). Patients with non-atherosclerotic coronary artery dissection or embolism, as well as coronary vasospasm, were also included in the T2MI group. Outcomes of interest included 2-year all-cause and cardiovascular mortality and subsequent T1MI and T2MI events.

Results:

A total of 6,253 patients (33.2% women, mean age 61 years) were included in the analysis. T1MI was diagnosed in 1,027 patients (16.4%), and T2MI in 251 patients (4.0%). Patients with T2MI were more likely to be female (35.9% vs. 26.0%, p = 0.002). Coronary angiography was performed in 86% of T1MI patients and 27.5% of T2MI patients (p < 0.001). Pathophysiologic mechanisms for T2MI included tachyarrhythmia (53.8%), hypertension (18.7%), anemia (4.4%), bradyarrhythmia (4.0%), hypoxemia (3.6%), and hypotension (1.6%), as well as coronary vasospasm (5.6%), coronary dissection (1.2%), and coronary embolism (0.8%).

Treatment for T1MI was more likely to include revascularization (75.2% for T1MI vs. 3.6% for T2MI, p < 0.001), dual antiplatelet therapy at discharge (76.3% vs. 13.9%, p < 0.001), and statin therapy at discharge (89.8% vs. 53.8%, p < 0.001), while fewer patients with T1MI were prescribed oral anticoagulation (13.5% vs. 30.7%, p < 0.001). Two-year all-cause mortality was similar between T1MI and T2MI patients (13.9% vs. 11.7%, p = 0.39), as was 2-year cardiovascular mortality (7.6% vs. 9.3%, p = 0.39). Among patients with T2MI, those with hypoxemia, hypotension, or anemia as the ischemic trigger had higher mortality than those with underlying tachycardia or hypertension. Recurrent events were likely to be of the same type as the index event (adjusted hazard ratio for future T2MI in patients with index T2MI vs. T1MI, 3.20; 95% confidence interval, 1.37-7.50; p = 0.007).

Conclusions:

In this European cohort of patients presenting to emergency departments with chest pain, T1MI was more common than T2MI. Although all-cause and cardiovascular mortality were similar in the T1MI and T2MI groups, patients with T2MI due to hypoxemia, hypotension, or anemia had higher mortality.

Perspective:

Patients presenting with T2MI are heterogenous, particularly with regard to the fact that underlying coronary atherosclerosis may or may not be present. Those who have multiple chronic medical conditions such as kidney disease, diabetes, and heart failure are at particularly high risk for poor outcomes. One limitation of this study is that most patients diagnosed with T2MI did not undergo coronary angiography, so it is possible that some of them had atherosclerotic coronary events that were mislabeled as supply-demand mismatch events. The findings of this study cannot be extrapolated to patients with asymptomatic troponin elevation in the setting of medical stressors (i.e., nonischemic myocardial injury) or to critically ill patients.

Clinical Topics: Acute Coronary Syndromes, Anticoagulation Management, Arrhythmias and Clinical EP, Cardiac Surgery, Dyslipidemia, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Prevention, Stable Ischemic Heart Disease, Vascular Medicine, Atherosclerotic Disease (CAD/PAD), Anticoagulation Management and ACS, Implantable Devices, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Cardiac Surgery and Arrhythmias, Cardiac Surgery and SIHD, Nonstatins, Novel Agents, Statins, Interventions and ACS, Interventions and Coronary Artery Disease, Interventions and Imaging, Interventions and Vascular Medicine, Angiography, Nuclear Imaging, Hypertension, Chronic Angina

Keywords: Acute Coronary Syndrome, Anemia, Hypoxia, Anticoagulants, Arrhythmias, Cardiac, Bradycardia, Chest Pain, Coronary Angiography, Coronary Artery Disease, Coronary Vasospasm, Dissection, Embolism, Emergency Service, Hospital, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hypertension, Hypotension, Hypoxia-Ischemia, Brain, Myocardial Infarction, Myocardial Ischemia, Myocardial Revascularization, Patient Discharge, Platelet Aggregation Inhibitors, Secondary Prevention, Tachycardia, Troponin


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