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European Heart Journal· 2026Q1

Beyond the lifestyle paradigm: environmental triggers and susceptible cardiovascular phenotypes

Shazina Saeed, Priyadarshini Arambam, Upendra Kaul

Short summary

Fine particulate matter (PM2.5) exposure differentially affected risk for myocardial infarction with non-obstructive coronary arteries (MINOCA) versus obstructive coronary disease during the COVID-19 pandemic, suggesting environmental triggers can selectively impact cardiovascular phenotypes based on individual susceptibility.

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Key points

  • PM2.5 exposure risk for MINOCA decreased during the COVID-19 pandemic, unlike infarction with obstructive coronary disease.
  • This selective change suggests environmental triggers can differentially impact cardiovascular phenotypes.
  • MINOCA encompasses various mechanisms (e.g., vasospasm, microvascular dysfunction) that may respond uniquely to pollution-induced inflammation and endothelial dysfunction.
  • The findings support a susceptibility-trigger-phenotype model where individual vascular health dictates the clinical outcome.

AI-generated from the title and abstract; the full text is not read.

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 clinical phenotypes: endotype-specific environmental cardiovascular susceptibility’, by M. Ishii et al., https://doi.org/10.1093/eurheartj/ehag814. We read with interest the nationwide study by Ishii et al.1 on short-term fine particulate matter (PM2.5) exposure and acute myocardial infarction (AMI) before and during the COVID-19 pandemic. The most striking finding, in our view, was not the pollution–AMI association itself but how it behaved across phenotypes: PM2.5-associated risk of myocardial infarction with non-obstructive coronary arteries (MINOCA) fell during the pandemic, while no comparable change was seen for infarction with obstructive coronary disease.1 This selective attenuation raises a question that extends well beyond this dataset: can a single environmental exposure preferentially trigger different cardiovascular phenotypes, depending on the susceptibility of the individual exposed? MINOCA is not one disease but several—coronary vasospasm, microvascular dysfunction, thromboembolism, spontaneous coronary dissection, and other mechanisms.2 Each pathway could plausibly respond differently to the inflammation, endothelial dysfunction, autonomic imbalance, and prothrombotic tendency that air pollution is known to provoke.3 Read this way, the data from Ishii et al.1 support a susceptibility–trigger–phenotype model: pollution supplies the trigger, an individual's vascular or coronary substrate determines the susceptibility, and the clinical event is the resulting phenotype—a different starting point from treating PM2.5 as a generic risk factor that simply raises AMI incidence across the board.

The authors' abstract, as published at the source. European Heart Journal, 2026 · DOI ↗

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Field: Cardiology and Cardiovascular Medicine

Cardiology and Cardiovascular MedicineMedicine