Key result
Children with Kawasaki disease demonstrated significant global longitudinal strain depression compared with controls in both the acute (SMD 1.34; 95% CI 0.73-1.95) and chronic phases.
Why the study?
GLS can detect subclinical dysfunction missed by LVEF, but the magnitude of myocardial dysfunction across Kawasaki disease phases had not been quantified.
Does Kawasaki disease cause persistent myocardial dysfunction as measured by GLS compared to age-matched controls?
Systematic Review (n=1,671)
Does Kawasaki disease cause persistent myocardial dysfunction as measured by GLS compared to age-matched controls?
Despite LVEF normalization in the chronic phase of Kawasaki disease, subclinical myocardial dysfunction persists as detected by global longitudinal strain.
Answers are grounded in this paper and cite their sources.
GLS detects persistent subclinical dysfunction in chronic KD despite LVEF normalization; leaves open whether routine strain monitoring improves long-term outcomes.
Background Global longitudinal strain (GLS) can detect subclinical dysfunction missed by left ventricular ejection fraction (LVEF). We aim to quantify the magnitude of myocardial dysfunction using GLS across the phases of Kawasaki disease (KD). Method We systematically searched for studies comparing GLS measurements between children with KD and age‐matched controls. Effect sizes were pooled using a random‐effects model and reported as standardized mean differences (SMD) for the acute and chronic disease phases. SMDs were re‐expressed as mean differences (MDs) using pooled weighted standard deviations (SDs) of 2.75% and 1.89% for the control groups in the acute and chronic phases, respectively. Results We included 18 observational studies comprising 907 KD patients and 764 controls. KD patients demonstrated significant GLS depression compared with controls in both the acute (SMD: 1.34, 95% CI: 0.73, 1.95, p < 0.0001, I 2 = 93%; MD: 3.6%) and chronic (SMD: 0.72, 95% CI: 0.20, 1.25, p = 0.007, I 2 = 92%; MD: 1.9%) phases. LVEF was reduced in the acute phase (MD: −1.09%, 95% CI: −1.57, −0.61, I 2 = 0%), and normalized in the chronic phase (MD: −0.27%, 95% CI: −1.18, 0.64, I 2 = 36%). Multivariable meta‐regression in the acute phase identified CRP ( β = 0.02, p = 0.024) plus CAA patient proportion ( β = −1.13, p = 0.069) explaining 49.28% of heterogeneity, whereas vendor platform (GE vs. Philips) ( β = −1.02, p = 0.007) plus age at follow‐up ( β = 0.02, p = 0.019) explained 56.34% of heterogeneity in the chronic phase. Conclusions Despite LVEF normalization in the chronic phase of KD, myocardial dysfunction persists. This could be essential for long‐term monitoring algorithms.
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Danso et al. (2026) conducted a systematic review in Kawasaki disease (n=1,671). Kawasaki disease vs. Age-matched controls was evaluated on Global longitudinal strain (GLS) depression in the acute phase (SMD 1.34, 95% CI 0.73, 1.95, p=< 0.0001). Children with Kawasaki disease demonstrated significant global longitudinal strain depression compared with controls in both the acute (SMD 1.34; 95% CI 0.73-1.95) and chronic phases.
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