October 19, 2026European Heart Journal
Beyond clinical phenotypes: endotype-specific environmental cardiovascular susceptibility
Key Points
- To examine how short-term fine particulate matter exposure differentially affects acute myocardial infarction subtypes and to propose assessing mechanistic endotypes rather than broad clinical phenotypes.
- Evaluated observational data analyzing associations between short-term fine particulate matter (PM2.5) exposure and acute myocardial infarction before and during the COVID-19 pandemic.
- Assessed differences in susceptibility across myocardial infarction with non-obstructive coronary arteries (MINOCA) and myocardial infarction with obstructive coronary artery disease.
- Short-term PM2.5-associated risk showed attenuation during the COVID-19 pandemic specifically for MINOCA, whereas no significant temporal change occurred for obstructive coronary artery disease.
- The findings demonstrated that MINOCA functions as an umbrella syndrome encompassing distinct pathophysiological mechanisms, including epicardial spasm, microvascular spasm, spontaneous coronary artery dissection, and coronary thromboembolism.
PICO
P
Population
Acute myocardial infarction
E
Exposure / Comparator
PM2.5 exposure
O
Primary Outcome
Acute myocardial infarction
Limitations
- Observational data cannot establish causality between changes in PM2.5 exposure and temporal differences in risk.
- Data cannot identify the specific mechanisms underlying the heterogeneous MINOCA syndrome.
Key expert perspectives
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“However, these observational data do not indicate that changes in PM2.5 exposure cause the temporal difference, nor can they identify the mechanisms underlying MINOCA. This distinction is important because MINOCA is an umbrella syndrome encompassing heterogeneous coronary mechanisms, including epicardial spasm, microvascular spasm, spontaneous coronary artery dissection, coronary thromboembolism, and other mechanisms.”
Implication
Emphasizes the heterogeneity of acute myocardial infarction phenotypes (such as MINOCA vs obstructive CAD) in response to environmental triggers like PM2.5 exposure.
Abstract
This commentary refers to ‘Air pollution before and during the COVID-19 pandemic: changes in risk of acute myocardial infarction’, by M. Ishii et al., https://doi.org/10.1093/eurheartj/ehag102 and the discussion piece ‘Beyond the lifestyle paradigm: environmental triggers and susceptible cardiovascular phenotypes’, by S. Saeed et al., https://doi.org/10.1093/eurheartj/ehag813. We thank Saeed et al.1 for their thoughtful commentary on our study and for proposing a susceptibility–trigger–phenotype framework for environmental cardio vascular risk. We agree that this perspective may help move the field beyond viewing fine particulate matter (PM2.5) as a uniform cardiovascular risk factor. Our study showed that the association between short-term PM2.5 exposure and acute myocardial infarction varied according to clinical phenotype. Attenuation of the PM2.5-associated risk for myocardial infarction with non-obstructive coronary arteries (MINOCA) during the COVID-19 pandemic was observed, whereas no significant change was observed in myocardial infarction with obstructive coronary artery disease.2 However, these observational data do not indicate that changes in PM2.5 exposure cause the temporal difference, nor can they identify the mechanisms underlying MINOCA. This distinction is important because MINOCA is an umbrella syndrome encompassing heterogeneous coronary mechanisms, including epicardial spasm, microvascular spasm, spontaneous coronary artery dissection, coronary thromboembolism, and other mechanisms.3
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Cite This Study
Ishii et al. (2026) conducted a letter in Acute myocardial infarction. PM2.5 exposure was evaluated on Acute myocardial infarction.