Triggers of type 2 myocardial infarction: implications for long-term prognosis

Abstract Background Type 2 myocardial infarction (T2MI) is characterized by a mismatch between myocardial oxygen supply and demand, unrelated to acute coronary thrombosis. This discrepancy arises from triggers, which may or may not be of cardiac origin. Common cardiac triggers include coronary artery spasm, coronary embolism, and arrhythmias, whereas non-cardiac triggers encompass factors such as anemia, hypertension/hypotension, sepsis, renal damage, and respiratory failure. However, identifying these triggers isn't always straightforward. Aim Our study aimed to identify, whenever possible, the triggers contributing to the oxygen supply-demand mismatch in T2MI cases, as defined by the Fourth Universal Definition of Myocardial Infarction. Additionally, we sought to explore the correlation between these triggers and patient prognosis. Methods We enrolled all consecutive patients diagnosed with non-ST-segment elevation myocardial infarction (NSTEMI) who met the criteria for T2MI and underwent coronary angiography within 72 hours of diagnosis. Patients were categorized into three groups based on the trigger causing T2MI: cardiac, non-cardiac, and unidentified. The primary endpoint was the occurrence of major adverse cardiovascular events (MACEs), including all-cause mortality, new myocardial infarction, hospitalization for heart failure, and ischemic stroke, during long-term follow-up. We estimated MACE-free survival using Kaplan-Meier curves and compared it among the three groups using the log-rank test. Multivariable logistic regression analysis was performed to identify independent predictors of MACE. Results The final cohort comprised 598 T2MI patients, with 308 having a cardiac trigger, 147 having a non-cardiac trigger, and 143 with an unidentified trigger. The mean age of the overall population was 69.6±13.1 years, with a median follow-up time of 25 (13-49) months. Kaplan-Meier curves demonstrated statistically significant differences in MACEs based on the trigger causing T2MI (p<0.001). Specifically, patients with an unidentified trigger exhibited a better prognosis, while those with a non-cardiac trigger had a worse prognosis during long-term follow-up. Multivariable logistic regression analysis confirmed that not having an identified trigger is an independent protective factor for MACEs (HR 0.63, 95% CI 0.45-0.89, p=0.009, unidentified trigger vs cardiac + non-cardiac trigger). Conclusions T2MI is prevalent in clinical practice, yet reliable outcome predictors remain elusive. Our findings indicate a relationship between the type of trigger precipitating T2MI and patient prognosis, notably demonstrating that the absence of a specific identifiable trigger is linked to a more favorable long-term outcome. Further studies are needed to better define the prognostic stratification of these patients.MACE-free survival Kaplan Meier