Key result
Inducible perfusion defects on spCMR linked to ~4-fold higher major event risk in Kawasaki disease.
Why the study?
Does the presence of inducible perfusion defects on spCMR predict major cardiac events in Kawasaki disease patients with coronary artery aneurysms?
Cohort (n=62)
No
Does the presence of inducible perfusion defects on spCMR predict major cardiac events in Kawasaki disease patients with coronary artery aneurysms?
Inducible perfusion defects on spCMR strongly predict major cardiac events in high-risk Kawasaki disease patients with coronary artery aneurysms, supporting its use in longitudinal surveillance.
Answers are grounded in this paper and cite their sources.
Supports spCMR for risk-adapted surveillance in high-risk KD with CAA; extends prognostic value of functional testing in this population.
BACKGROUND: Kawasaki disease (KD) with coronary artery aneurysms (CAA) places patients at risk for myocardial ischemia and major cardiac events (MCE). While stress perfusion cardiac magnetic resonance imaging (spCMR) is used for surveillance, its prognostic value has not been established. METHODS: We conducted a retrospective cohort study of KD patients (AHA risk levels 3-5) who underwent clinically indicated vasodilator spCMR at a tertiary pediatric center between October 2014 and December 2024. We evaluated inducible perfusion defects, late gadolinium enhancement (LGE), ventricular function, and MCE (myocardial infarction, ventricular dysfunction, arrhythmia, revascularization, transplant, or death). We performed Cox regression and Kaplan-Meier analyses to evaluate risk factors associated with MCE. RESULTS: About 62 patients underwent 107 spCMR examinations. Over a median follow-up of 8.6 years (IQR 5.9-12.1) from KD diagnosis, 18 patients (29.0%) experienced an MCE, all of whom were AHA risk level 5. Nine patients developed MCEs after their first spCMR, and inducible perfusion defects on that initial study were associated with higher risk of subsequent events (HR 4.2, 95% CI 1.1-15.6; p=0.03). Among the 44 AHA risk level 5 patients, inducible perfusion defects occurred in 13 (29.5%), who had a higher incidence of subsequent MCE (44.4% vs. 14.3%, p = 0.045); among those with both significant luminal narrowing and positive spCMR, 64% developed MCE. Serial spCMR identified new inducible defects in patients who later experienced MCE. In six patients, post-operative spCMR helped assess revascularization adequacy and return-to-activity decisions. CONCLUSIONS: In KD patients with CAA, inducible perfusion defects on spCMR were associated with increased MCE risk, whereas a normal spCMR in AHA risk levels 3-4 was reassuring. Serial spCMR identified evolving ischemia, guided revascularization decisions, and informed post-intervention management. These findings support the incorporating spCMR into longitudinal surveillance pathway for high-risk KD patients.
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Kiener et al. (2026) conducted a cohort in Kawasaki disease with coronary artery aneurysms (n=62). Inducible perfusion defects on spCMR vs. No inducible perfusion defects was evaluated on Major cardiac events (MCE) (HR 4.2, 95% CI 1.1-15.6, p=0.03). In Kawasaki disease patients with coronary artery aneurysms, inducible perfusion defects on spCMR were associated with a higher risk of subsequent major cardiac events (HR 4.2; 95% CI 1.1-15.6; p=0.03).
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