Type 2 myocardial infarction: challenges in diagnosis and treatment

Abstract

The Fourth Universal Definition of Myocardial Infarction recommends a classification based on aetiology, in recognition that the underlying pathophysiology of myocardial infarction influences the approach to investigation and treatment. Type 1 myocardial infarction occurs due to atherosclerotic plaque rupture with thrombosis, whereas type 2 myocardial infarction occurs due to an imbalance in myocardial oxygen supply or unmet need in myocardial oxygen demand, without atherothrombosis, usually in the context of another acute illness. In this state-of-the-art review, the diagnosis, investigation, and treatment of patients with type 2 myocardial infarction are considered, with general advice for clinical practice and a consideration of future research directions.

Keywords: Fourth Universal Definition; Troponin; Type 2 myocardial infarction.

Graphical Abstract

Challenges in the diagnosis and treatment of type 2 myocardial infarction relate to the multiple, often competing aetiologies and underlying disease susceptibility—both of which contribute to an integrated risk of future cardiovascular events. MI, myocardial infarction.

Figure 1

Aetiology of type 2 myocardial infarction. Type 2 myocardial infarction is a descriptive term encompassing a number of different aetiologies. Aetiologies may be stratified as systemic, cardiac, or coronary mechanisms. Patients with these mechanisms may share characteristics, and this might be helpful to guide further investigation and treatment

Figure 2

Distribution of type 2 myocardial infarction by aetiology. Density plot illustrating prevalence of type 2 myocardial infarction by aetiology with individual data point for each study cohort and area under the curve representing total number of patients

Figure 3

Evaluation of the ischaemic threshold. The magnitude of haemodynamic stress and burden of coronary atheroma influence the likelihood of supply–demand ischaemia and type 2 myocardial infarction. A patient without coronary artery disease requires a significant haemodynamic stressor to result in supply or demand imbalance compared to a patient with obstructive coronary artery disease. This illustration considers coronary disease in isolation for simplicity, but in practice, multiple competing aetiologies contribute

Figure 4

Susceptibility to type 2 myocardial infarction. Multiple factors contribute to an individual patient’s susceptibility to myocardial oxygen supply or demand imbalance. Patient, coronary, and structural factors are all important, some of which may be modifiable and could plausibly reduce the likelihood of recurrent events

Figure 5

Diagnostic algorithm for the evaluation of patients with myocardial ischaemia in clinical practice. The clinician determines if a patient has evidence of myocardial ischaemia, either based on symptoms or electrocardiogram criteria. Where electrocardiogram evidence of ST-segment elevation exists, established pathways are followed. In patients without a rise and/or fall in cardiac troponin, differential diagnoses are considered. In those with evidence of supply or demand imbalance, this is corrected where possible. A reassessment is undertaken to identify if symptoms or signs of ischaemia persist, and the diagnosis of type 1 myocardial infarction considered. A clinical assessment of the mechanism of type 2 myocardial infarction is made, and additional investigations considered on the basis of risk profile, mechanism, and likelihood of cardiac disease to guide immediate treatment and secondary prevention. STEMI, ST-segment elevation myocardial infarction; CMRI, cardiac MRI; CT, computed tomography

Figure 6

Evaluation of the patient with type 1 or type 2 myocardial infarction. Several factors may guide the clinician in determining whether an initial invasive or non-invasive assessment is appropriate to guide diagnosis and treatment. Where the balance favours a diagnosis of type 1 myocardial infarction, where atherothrombosis has resulted in oxygen imbalance, initial invasive assessment is proposed. MI, myocardial infarction; ECG, electrocardiogram

Figure 7

Illustrative case example of patient with clinical diagnosis of type 2 myocardial infarction where the use of invasive coronary angiography and optical coherence tomography led to diagnostic reclassification. A 64-year-old presents with increasing ischaemic sounding chest pain, with fever, breathlessness, and cough for 2 days. The admission observations were heart rate 114, oxygen saturations 93% on 4L, respiratory rate 34, temperature 38.9 °C, and blood pressure 156/78. The electrocardiogram demonstrates a presumed new left bundle branch block. A chest X-ray demonstrates right lower lobe consolidation with a C-reactive protein 160 ng/L. The peak high-sensitivity cardiac troponin I was 6451 ng/L. This was treated as type 2 myocardial infarction. Coronary angiography demonstrated a severe lesion in the proximal left anterior descending artery with collaterals to an occluded right coronary artery (A and B) with intracoronary plaque rupture and thrombosis in the left anterior descending artery on optical coherence tomography (C), and corresponding basal anteroseptal late gadolinium enhancement on cardiac magnetic resonance imaging scan (D). The diagnosis was reclassified as type 1 myocardial infarction. Reproduced with permission from the DEMAND-MI educational resource with identifiable features changed