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Articles by Maurits A. Sikking
Immunomodulation of Myocardial Fibrosis:
Introduction Myocardial damage may cause myocardial fibrosis, which ultimately predisposes the heart to cardiac arrhythmias and heart failure. Contrarily, myocardial fibrosis is also a process that is necessary to maintain the integrity of cardiac tissue after a myocardial insult (eg, infarction, viral infection, or cluster of differentiation [CD]4+ T-cell–mediated damage).
Cardiac Inflammation in Adult-Onset Genetic Dilated Cardiomyopathy
Abstract : Dilated cardiomyopathy (DCM) has a genetic cause in up to 40% of cases, with differences in disease penetrance and clinical presentation, due to different exogeneous triggers and implicated genes. Cardiac inflammation can be the consequence of an exogeneous trigger, subsequently unveiling a phenotype. The study aimed to determine cardiac inflammation in a cohort of genetic DCM patients and investigate whether it associated with a younger disease onset.
Clonal Hematopoiesis Has Prognostic Value in Dilated Cardiomyopathy Independent of Age and Clone Size:
References 1. "Clonal hematopoiesis and risk of atherosclerotic cardiovascular disease". N Engl J Med . 2017;377:111-121. 2. "Clonal hematopoiesis associated with TET2 deficiency accelerates atherosclerosis development in mice". Science . 2017;355:842-847. 3. "Clonal hematopoiesis-driver DNMT3A mutations alter immune cells in heart failure". Circ Res . 2021;128:216-228. 4. "Association of mutations contributing to clonal hematopoiesis with prognosis in chronic ischemic heart failure". JAMA Cardiol .
Diagnostic and prognostic relevance of using large gene panels in the genetic testing of patients with dilated cardiomyopathy - European Journal of Human Genetics
Abstract It was previously suggested that increasing the number of genes on diagnostic gene panels could increase the genetic yield in patient with dilated cardiomyopathy (DCM). We explored the diagnostic and prognostic relevance of testing DCM patients with an expanded gene panel. The current study included 225 consecutive DCM patients who had no genetic diagnosis after a 48-gene cardiomyopathy-panel. These were then evaluated using an expanded gene panel of 299 cardiac-associated genes.
Inflammation and Syndecan-4 Shedding from Cardiac Cells in Ischemic and Non-Ischemic Heart Disease
Open AccessArticle by Mari E. Strand 1, Maarten Vanhaverbeke 2, Michiel T. H. M. Henkens 3,4,5, Maurits A. Sikking 5, Karoline B. Rypdal 6,7,8,*, Bjørn Braathen 9, Vibeke M. Almaas 10, Theis Tønnessen 1,9, Geir Christensen 1, Stephane Heymans 11 and Ida G.
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