Biomarkers of inflammation and fibrosis in young adults with history of Kawasaki disease <sup>☆</sup>

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Abstract

Background

Myocardial histology from autopsies of young adults with giant coronary artery aneurysms following Kawasaki disease (KD) shows bridging fibrosis beyond the territories supplied by the aneurysmal arteries. The etiology of this fibrosis is unknown, but persistent, low-level myocardial inflammation and microcirculatory ischemia are both possible contributing factors. To investigate the possibility of subclinical myocardial inflammation or fibrosis, we measured validated biomarkers in young adults with a remote history of KD.

Methods

We measured plasma calprotectin, galectin-3 (Gal-3), growth differentiation factor-15 (GDF-15), soluble ST2 (sST2), and serum procollagen type 1C-terminal propeptide (P1CP) in 91 otherwise healthy young adults with a remote history of KD and in 88 age-similar, healthy controls. KD subjects were stratified by coronary artery aneurysm (CAA) status and history of remote myocardial infarction (MI).

Results

After correction for multiple testing, calprotectin, Gal-3, and GDF-15 levels were significantly higher in subjects with persistent CAA (n = 26) compared with KD subjects with remodeled CAA (n = 20, p = 0.005, 0.001, 0.0036, respectively). In a multivariable regression model with CA status as the main predictor and adjusting for sex, MI history, and interval from KD onset, CA status was a significant predictor (Persistent CAA vs KD Normal CA) of calprotectin, Gal-3, GDF-15 and sST2 levels (p = 0.004, <0.001, 0.007, and 0.049, respectively).

Conclusions

These results suggest that ongoing inflammation and fibrosis may be occurring in individuals with persistent CAA. Longitudinal follow-up is needed to clarify the clinical significance of these elevated biomarker levels in this patient population that requires life-long monitoring.

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Most cited references 28

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Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Scientific Statement for Health Professionals From the American Heart Association

Jane C. Burns, Elfriede Pahl, Tsutomu T. Saji … (2017)

Kawasaki disease is an acute vasculitis of childhood that leads to coronary artery aneurysms in ≈25% of untreated cases. It has been reported worldwide and is the leading cause of acquired heart disease in children in developed countries.

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Kawasaki Disease.

Jane W Newburger, Masato Takahashi, Jane C. Burns (2016)

Kawasaki disease is an acute, self-limited vasculitis of unknown etiology that occurs predominantly in infants and children. If not treated early with high-dose intravenous immunoglobulin, 1 in 5 children develop coronary artery aneurysms; this risk is reduced 5-fold if intravenous immunoglobulin is administered within 10 days of fever onset. Coronary artery aneurysms evolve dynamically over time, usually reaching a peak dimension by 6 weeks after illness onset. Almost all the morbidity and mortality occur in patients with giant aneurysms. Risk of myocardial infarction from coronary artery thrombosis is greatest in the first 2 years after illness onset. However, stenosis and occlusion progress over years. Indeed, Kawasaki disease is no longer a rare cause of acute coronary syndrome presenting in young adults. Both coronary artery bypass surgery and percutaneous intervention have been used to treat Kawasaki disease patients who develop myocardial ischemia as a consequence of coronary artery aneurysms and stenosis.

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Circulating Biomarkers of Myocardial Fibrosis: The Need for a Reappraisal.

Begoña López, Arantxa González, Susana Ravassa … (2015)

Myocardial fibrosis impairs cardiac function, in addition to facilitating arrhythmias and ischemia, and thus influences the evolution and outcome of cardiac diseases. Its assessment is therefore clinically relevant. Although tissue biopsy is the gold standard for the diagnosis of myocardial fibrosis, a number of circulating biomarkers have been proposed for the noninvasive assessment of this lesion. A review of the published clinical data available on these biomarkers shows that most of them lack proof that they actually reflect the myocardial accumulation of fibrous tissue. In this "call to action" article, we propose that this absence of proof may lead to misinterpretations when considering the incremental value provided by the biomarkers with respect to traditional diagnostic tools in the clinical handling of patients. We thus argue that strategies are needed to more strictly validate whether a given circulating biomarker actually reflects histologically proven myocardial fibrosis before it is applied clinically.

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Author and article information

Contributors

Jane C. Burns

Journal

Journal ID (nlm-ta): Int J Cardiol Heart Vasc

Journal ID (iso-abbrev): Int J Cardiol Heart Vasc

Title: International Journal of Cardiology. Heart & Vasculature

Publisher: Elsevier

ISSN (Electronic): 2352-9067

Publication date PMC-release: 01 September 2021

Publication date Collection: October 2021

Publication date (Electronic): 01 September 2021

Volume: 36

Electronic Location Identifier: 100863

Affiliations

[a ]Dept. of Pediatrics, University of California San Diego, La Jolla, CA, United States

[b ]Dept. of Family Medicine and Public Health, University of California San Diego, La Jolla, CA, United States

[c ]Rady Children’s Hospital San Diego, San Diego, CA, United States

[d ]Dept. of Medicine, University of California San Diego, La Jolla, CA, United States

[e ]San Diego Cardiac Center, San Diego, CA, United States

Author notes

[* ]Corresponding author at: Dept. of Pediatrics, University of California San Diego, La Jolla, CA, United States. jcburns@ 123456ucsd.edu

Article

Publisher Item ID: S2352-9067(21)00151-2 Publisher ID: 100863

DOI: 10.1016/j.ijcha.2021.100863

PMC ID: 8413893

SO-VID: f984cdce-3a27-415c-b82d-cc1b860d76b6

License:

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).