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• LATE CORONARY ANEURYSM FORMATION IN KAWASAKI DISEASE: A SUBTLE PHENOMENON WITH POTENTIAL IMPLICATIONS
  KENAN YALTA, MUHAMMET GURDOGAN and GOKAY TAYLAN
  Published on: 25 February 2020

• Published on: 25 February 2020

  LATE CORONARY ANEURYSM FORMATION IN KAWASAKI DISEASE: A SUBTLE PHENOMENON WITH POTENTIAL IMPLICATIONS

  • KENAN YALTA, cardiologist trakya university
  • Other Contributors:
    • MUHAMMET GURDOGAN, cardiologist
    • GOKAY TAYLAN, cardiologist

  LATE CORONARY ANEURYSM FORMATION IN KAWASAKI DISEASE: A SUBTLE PHENOMENON WITH POTENTIAL IMPLICATIONS

  Kenan YALTA, MD
  Muhammet GURDOGAN, MD
  Gokay TAYLAN, MD

  a,Trakya University, Cardiology Department, Edirne, TURKEY

  Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
  Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856

  In clinical practice, coronary artery aneurysms (CAAs) in the setting of Kawasaki disease (KD) mostly evolve in the earlier stages, and generally reach their maximum size by 6 weeks after disease onset (1). Importantly, they are mostly encountered in untreated cases, and are strongly associated with the disease severity (and in particular; the degree of acute necrotizing vasculitis) (1). In their recently published enlightening report (2), Brogan P have discussed long-term management of KD patients with a particular emphasis on CAAs in this setting (2). However, we would like to comment on a specific phenomenon, namely ‘late CAA’ formation that might emerge even several months to years after the index KD:
  Firstly, late CAAs were previously defined as new CAAs emerging at the same location of a previously regressed CAA, and were attributed to hemodynamic and residual pathological abnormalities along the arterial wal...

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  LATE CORONARY ANEURYSM FORMATION IN KAWASAKI DISEASE: A SUBTLE PHENOMENON WITH POTENTIAL IMPLICATIONS

  Kenan YALTA, MD
  Muhammet GURDOGAN, MD
  Gokay TAYLAN, MD

  a,Trakya University, Cardiology Department, Edirne, TURKEY

  Corresponding Author: Kenan YALTA Trakya University, Cardiology Department, Edirne, TURKEY
  Email- kyalta@gmail.com, akenanyalta@trakya.edu.tr Phone: 00905056579856

  In clinical practice, coronary artery aneurysms (CAAs) in the setting of Kawasaki disease (KD) mostly evolve in the earlier stages, and generally reach their maximum size by 6 weeks after disease onset (1). Importantly, they are mostly encountered in untreated cases, and are strongly associated with the disease severity (and in particular; the degree of acute necrotizing vasculitis) (1). In their recently published enlightening report (2), Brogan P have discussed long-term management of KD patients with a particular emphasis on CAAs in this setting (2). However, we would like to comment on a specific phenomenon, namely ‘late CAA’ formation that might emerge even several months to years after the index KD:
  Firstly, late CAAs were previously defined as new CAAs emerging at the same location of a previously regressed CAA, and were attributed to hemodynamic and residual pathological abnormalities along the arterial wall (3). However, we hold the opinion that these aneurysms mostly arise as a ‘de novo’ phenomenon in apparently normal or mildly affected coronary segments (and hence not associated with severe necrotizing vasculitis at the onset), and might potentially be associated with dysfunctional vascular healing in the long-term (potential under-healing due to prolonged steroid use for KD or other purposes, diabetes, etc).
  Secondly, as analogous to progressive aortic remodeling in connective tissue disease, an over-healing process leading to excessive vascular remodeling in the long-term (largely through genetically determined and enhanced actions of certain profibrotic substances including transforming growth factor-beta (TGF-ß) (1), ,etc.and certain enzymes including matrix metalloproteinase-9 (MMP-9)) has been previously reported in KD, and might also serve as an alternative mechanism of late CAA evolution (4-6) particularly in coronary segments with pre-existing mild vasculitis as well.
  Thirdly, based on potential favorable impact of captopril on prevention of classical early CAA formation (through inhibition of MMP-9) (5), blockade of renin-angiotensin system might also be indicated indefinitely in the presence of high-risk features (persistently high levels of profibrotic mediators and MMP-9, etc.) for prevention of late CAA evolution.
  Lastly, even though late CAA, reportedly appears to have a more favorable prognosis (3) (due to its smaller size and low incidence of intramural thrombus formation, etc as compared with classical CAA), close supervision of long-term changes in coronary morphology (even in the presence of normal or near-normal coronary arteries at 6 weeks) may also be indicated in high-risk patients for timely initiation of further management strategies (anticoagulation, etc.). Interestingly, since late CAAs might be associated with progressive arterial remodeling involving intima and media layers (4,6), they may possibly be more prone to specific complications including spontaneous coronary artery dissection (SCAD) in comparison to classical CAAs with substantial multi-layer necrosis.
  In conclusion, late CAA formation in KD might be regarded as an under-recognized phenomenon with important implications, and might constitute a significant portion of idiopathic coronary aneurysms on routine coronary imaging regardless of confirmed KD history. However, further insights of this phenomenon still remain to be established.

  Conflict of interest: None

  REFERENCES:
  1- Newburger JW, Takahashi M, Burns JC. Kawasaki Disease. J Am Coll Cardiol. 2016 ;67(14):1738-49.
  2- Brogan P, Burns JC, Cornish J, et al. Lifetime cardiovascular management of patients with previous Kawasaki disease. Heart 2019;0:1–10. doi:10.1136/heartjnl-2019-315925
  3- Tsuda E, Kamiya T, Ono Y, et al. Dilated coronary arterial lesions in the late period after Kawasaki disease. Heart. 2005; 91(2): 177-82.
  4- Suzuki A, Miyagawa-Tomita S, et al. Remodeling of coronary artery lesions due to Kawasaki disease: comparison of arteriographic and immunohistochemical findings. Jpn Heart J. 2000 ;41(3):245-56.
  5- Inoue N, Takai S, Jin D, et al. Effect of angiotensin-converting enzyme inhibitor on matrix metalloproteinase-9 activity in patients with Kawasaki disease. Clin Chim Acta. 2010; 411(3-4): 267-9.
  6- Toyono M, Shimada S, Aoki-Okazaki M, et al. Expanding coronary aneurysm in the late phase of Kawasaki disease. Pediatr Int. 2012; 54(1): 155-8.

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  Conflict of Interest:
  None declared.

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