Type 2 Myocardial Infarction: A Geriatric Population-based Model of Pathogenesis

Distinction between type 2 myocardial infarction (T2MI), defined as an imbalance between oxygen supply and demand without atherothrombosis, and type 1 myocardial infarction (T1MI), due to plaque disruption, is often a clinical challenge in frail elderly patients. We aimed to identify the characteristics and underlying causes of T2MI using a comprehensive geriatric approach. From a multicentre population-based prospective study in coronary care units, we adjudicated 4572 consecutive patients hospitalized for an acute T1MI or T2MI, according to the 3rd universal definition and a prespecified geriatric model of T2MI pathogenesis. In total, 3710 (81%) had T1MI and 862 (19%) T2MI. Patients with T2MI were 10 y older (77 vs 67 y, p<0.001), more frequently female (44 vs 26%, p<0.001) and had more frequent comorbidities. In multivariate analysis, acute heart failure, tachycardia and C-reactive protein elevation at admission were associated with a higher risk of T2MI vs T1MI, whereas chest pain, troponin I peak > 10 µg/L and ST-segment elevation were associated with a lower risk. Underlying mechanisms leading to T2MI highlighted 3 main patterns: 1) Age-related physiological cardiovascular decline 2) chronic predisposing factors including chronic anaemia (10%) and severe aortic stenosis (7%), 3) acute triggering factors, the most common being acute infection (39%), mainly respiratory tract infection, followed by tachyarrhythmia (13%) and acute heart failure (10%). 122 (14%) patients had combined predisposing and triggering conditions for T2MI. In our large population-based survey of T2MI, chronic anaemia and severe aortic stenosis increased predisposition to T2MI and acute respiratory infection was by far the most frequent trigger. Our data shed new light on the age-related pathophysiological basis for discrepancies in oxygen supply and demand leading to MI.