Characteristics and Outcomes of Type 2 Myocardial Infarction - Coscia, T.; Nestelberger, T.; Boeddinghaus, J.; Lopez-Ayala, P.; Koechlin, L.; Miro, O.; Keller, D. I.; Strebel, I.; Yufera Sanchez, A.; Okamura, B.; Wussler, D.; Shrestha, S.; et al. (JAMA Cardiol, 2022)
IMPORTANCE: In contrast to type 1 myocardial infarction (T1MI) caused by atherothrombosis, characteristics and outcomes of type 2 myocardial infarction (T2MI) caused by supply-demand mismatch are incompletely understood. OBJECTIVE: To explore the characteristics and outcomes of patients with T2MI compared with those with T1MI. DESIGN, SETTING, AND PARTICIPANTS: In a prospective, international, multicenter cohort study including 12 emergency departments (EDs) in 5 European countries, unselected patients presenting with acute chest discomfort were enrolled from April 2006 to April 2018. Follow-up was done by telephone or in written form 3, 12, and 24 months after hospital discharge. Data were analyzed from April 2006 to April 2020. INTERVENTIONS: The final diagnoses of T2MI and T1MI were centrally adjudicated according to the Fourth Universal Definition of Myocardial Infarction by 2 independent cardiologists, including the pathophysiological trigger of T2MI. MAIN OUTCOMES AND MEASURES: Patient characteristics and outcomes, including 2-year all-cause and cardiovascular mortality and future T2MI and T1MI events. RESULTS: Of 6253 included patients, 2078 (33.2%) were women, and the median (IQR) age was 61 (48-74) years. Among 6253 patients with acute chest discomfort, the final adjudicated diagnosis was T2MI in 251 patients (4.0%), with tachyarrhythmia and hypertension responsible for two-thirds of cases, and T1MI in 1027 patients (16.4%). All-cause and cardiovascular mortality were comparable at 2 years (T2MI: adjusted hazard ratio, 1.0; 95% CI, 0.7-1.5; T1MI: adjusted hazard ratio, 0.7; 95% CI, 0.4-1.1). Patients with tachyarrhythmia or hypertension as their underlying trigger of T2MI had a lower mortality compared with patients with hypotension, hypoxemia, or anemia. Future T2MI was more likely among patients with index T2MI compared with patients with index T1MI (hazard ratio, 3.2; 95% CI, 1.4-7.5). Similarly, future T1MI was more likely to occur among patients with index T1MI (hazard ratio, 3.0; 95% CI, 1.2-7.4). CONCLUSIONS AND RELEVANCE: Among patients with T2MI, tachyarrhythmia and hypertension were responsible for more than two-thirds of T2MI cases. While T2MI and T1MI had comparable all-cause and cardiovascular mortality at 2 years, patients with tachyarrhythmia or hypertension as their underlying trigger of T2MI had a lower mortality compared with patients with hypotension, hypoxemia, or anemia. Future T2MI occurred 3-fold more frequently among patients with T2MI vs T1MI as the index event. Improved understanding of the specifics of patients with T2MI should help improve management strategies. QUESTION: What are the characteristics and outcomes of type 2 myocardial infarction (T2MI) compared with type 1 myocardial infarction (T1MI) in patients presenting to the emergency department (ED) with acute chest discomfort? FINDINGS: In this cohort study 6253 patients, 251 patients (4.0%) and 1027 patients (16.4%) were diagnosed with T2MI and T1MI, respectively, and had comparable all-cause and cardiovascular mortality at 2 years. Tachyarrhythmia and hypertension were responsible for more than two-thirds of patients with T2MI and had lower mortality compared with patients with hypotension, hypoxemia, or anemia. MEANING: Improved understanding of the specifics of patients with T2MI should help improve management strategies. eng This cohort study explores the characteristics and outcomes of patients with type 2 myocardial infarction compared with those with type 1 myocardial infarction. eng from the Swiss National Science Foundation, the Prof Dr Max Cloetta Foundation, the Margarete und Walter Lichtenstein-Stiftung, and the University Hospital Basel as well as personal fees from Beckman Coulter, Bayer, Ortho Clinical Diagnostics, and Orion Pharma outside the submitted work. Dr Boeddinghaus received research grants from the University of Basel, the University Hospital of Basel and the Division of Internal Medicine, the Swiss Academy of Medical Sciences, and the Gottfried and Julia Bangerter-Rhyner-Foundation and personal fees from Siemens, Roche Diagnostics, Ortho Clinical Diagnostics, and Quidel Corporation outside of the submitted work. Dr Lopez-Ayala has received research support from the Swiss Heart Foundation and personal fees from Quidel paid to his institution outside the submitted work. Dr Koechlin received a research grant from the University of Basel, the Swiss Academy of Medical Sciences and the Gottfried and Julia Bangerter-Rhyner Foundation as well as the Freiwillige Akademische Gesellschaft Basel. Dr Martin-Sanchez has received personal fees from Novartis, Merck Sharp & Dohme, Bristol Myers Squibb, Pfizer, The Medicines Company, Otsuka, Thermo Fisher, Cardiorentis, and Sanofi and research grants from the Spanish Ministry of Health and Fondo Europeo de Desarrollo Regional, Mapfre, Novartis, Bayer, Merck Sharp & Dohme, Abbott, and Orion Pharma outside the submitted work. Dr Twerenbold has received research support from the Swiss National Science Foundation, the Swiss Heart Foundation, the Swiss Society of Cardiology, the Cardiovascular Research Foundation Basel, the University of Basel and the University Hospital Basel and personl fees from Abbott, Amgen, AstraZeneca, Roche, Siemens, Singulex, and Thermo Scientific BRAHMS outside the submitted work. Dr Rubini Gimenez has received research grants from the Swiss Heart Foundation and Swiss National Science Foundation as well as personal fees from Abbott, Ortho Clinical Diagnostics, Roche, and Siemens outside the submitted work. Dr Wildi has received research funding from the Freiwillige Akademische Gesellschaft Basel, the Julia und Gottfried Bangerter-Rhyner-Stiftung, the Prince Charles Hospital Foundation, The Wesley Medical Research Foundation, and the CRE Action fund as well as a PhD scholarship from the University of Queensland. Dr Mueller has received research support from the Swiss National Science Foundation, the Swiss Heart Foundation, the Kommission fur Technologie und Innovation (KTI), the European Union, the University of Basel, the University Hospital Basel, Abbott, Beckman Coulter, Idorsia, Ortho Cinical Diagnostics, Quidel, Roche, Siemens, Singulex, and Sphingotec as well as personal fees from Acon, Amgen, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Idorsia, Novartis, Osler, Roche, and Sanofi outside of the submitted work. No other disclosures were reported.
Keywords: journalArticle; *Myocardial Infarction/therapy; Humans; Risk Factors