title: Noncoronary inflammation in Kawasaki disease is associated with abnormal myocardial deformation in the acute phase.
abstract: BACKGROUND
  Patients with Kawasaki disease (KD) are at risk for developing coronary artery lesions, but the association of noncoronary changes such as mitral regurgitation (MR) and/or pericardial effusion (PE) with cardiac mechanics in the acute phase of KD has not been previously described. The aim of this study was to test the hypothesis that these noncoronary markers for carditis are associated with abnormalities in strain (ε) and strain rate (SR) in patients with MR or PE not appreciated by conventional echocardiography.
  
  
  METHODS
  Longitudinal and circumferential ε and SR analyses were retrospectively performed on patients with KD. Patients with and without MR or PE were compared. Strain values were also compared between patients with and without coronary artery lesions. Values for ejection fraction, shortening fraction, and clinical laboratory parameters were correlated with MR or PE. Follow-up echocardiographic outcomes were recorded at the first encounter after initial diagnosis. Follow-up ε and SR data were also obtained in the group with MR or PE and altered ventricular mechanics at diagnosis.
  
  
  RESULTS
  Of the 110 patients reviewed, 92 had appropriate image quality for either longitudinal ε and SR or circumferential ε and SR analysis. Twenty-eight patients (30%) had either MR or PE. Longitudinal ε and SR were significantly decreased in patients with MR or PE compared with patients without MR or PE (ε: -16.4 ± 4.0% vs -19.0 ± 3.7%, P = .004; SR: -1.3 ± 0.7 vs -1.6 ± 0.4 sec(-1), P = .03). No significant difference in longitudinal ε or SR was noted between patients with and without coronary artery lesions (ε: -17.9 ± 4.1% vs -17.8 ± 3.8%, P = .50; SR: -1.5 ± 0.3 vs -1.6 ± 0.8 sec(-1), P = .50). In the group with abnormal coronary arteries, presence of MR or PE was correlated with decreased longitudinal ε (-16.1 ± 3.6% vs -18.9 ± 3.4%, P = .02), without a significant difference in longitudinal SR (-1.6 ± 0.4 vs -1.5 ± 0.4 sec(-1), P = .20). At approximately 3-week follow-up (21.3 ± 15.8 days), longitudinal ε and SR for the group with MR or PE had increased significantly compared with diagnosis (ε: -16.4 ± 4.3% vs -18.6 ± 0.5%, P = .03; SR: -1.3 ± 0.6 vs -1.8 ± 0.4 sec(-1), P = .008), coincident with resolution of MR or PE. In both groups, erythrocyte sedimentation rate and C-reactive protein were elevated (85.3 ± 36.2 mm/h vs 75.1 ± 33.1 mm/h [P = .34] and 12.3 ± 6.7 vs 11.7 ± 8.2 mg/dL [P = .83]), but only modest correlations were noted between longitudinal ε and elevated erythrocyte sedimentation rate (r = 0.52, P = .01; confidence interval, 0.10-0.80) and C-reactive protein (r = 0.50, P = .02; confidence interval, 0.10-0.80) in patients with MR or PE. Shortening fraction and ejection fraction were within the normal range in both groups.
  
  
  CONCLUSIONS
  Patients presenting with KD with MR or PE at diagnosis are likely to have altered ventricular mechanics compared with patients with KD without MR or PE despite normal conventional echocardiographic measures of function. There is no significant difference in ventricular mechanics when comparing patients with KD with coronary ectasia or aneurysms and those without coronary lesions. Presence of abnormal ε in patients with KD with altered ventricular mechanics correlates modestly with laboratory inflammatory markers. Peak systolic longitudinal ε and SR increased significantly at 3-week follow-up compared with initial diagnosis, coincident with resolution of MR or PE.
authors.affiliation: Department of Cardiology, Children's National Medical Center, Washington, District of Columbia. Electronic address: lgaur1@jhmi.edu.
authors.forename: Lasya
authors.initials: L
authors.lastname: Gaur
authors.affiliation: Department of Cardiology, Children's National Medical Center, Washington, District of Columbia.
authors.forename: Kevin
authors.initials: K
authors.lastname: Waloff
authors.affiliation: Department of Cardiology, Children's National Medical Center, Washington, District of Columbia.
authors.forename: Ofer
authors.initials: O
authors.lastname: Schiller
authors.affiliation: Department of Cardiology, Children's National Medical Center, Washington, District of Columbia.
authors.forename: Craig A
authors.initials: CA
authors.lastname: Sable
authors.affiliation: Department of Cardiology, Children's National Medical Center, Washington, District of Columbia.
authors.forename: Lowell H
authors.initials: LH
authors.lastname: Frank
mesh_terms: D000208:Acute Disease; D002675:Child, Preschool; D015897:Comorbidity; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000503:physiopathology*; D004452:Echocardiography / Q000379:methods; D055119:Elastic Modulus; D054459:Elasticity Imaging Techniques / Q000379:methods; D005260:Female; D006801:Humans; D008297:Male; D008944:Mitral Valve Insufficiency / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000503:physiopathology*; D009080:Mucocutaneous Lymph Node Syndrome / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000503:physiopathology*; D010490:Pericardial Effusion / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000503:physiopathology*; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity; D033081:Shear Strength; D013314:Stress, Mechanical
keywords: Kawasaki disease; Mitral regurgitation; Pericardial effusion; Strain