Theis Tønnessen

Cardiothoracic Surgery, Cardiology

MD, PhD
37.87
Theis Tønnessen has

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  • [Show abstract] [Hide abstract] ABSTRACT: Inflammation is central to heart failure progression. Innate immune signaling increases expression of the transmembrane proteoglycan syndecan-4 in cardiac myocytes and fibroblasts, followed by shedding of its ectodomain. Circulating shed syndecan-4 is increased in heart failure patients, however the pathophysiological and molecular consequences associated with syndecan-4 shedding remain poorly understood. Here we used lipopolysaccharide (LPS) challenge to investigate the effects of syndecan-4 shedding in the heart.
    Full-text available · Article · Oct 2015 · Journal of Molecular and Cellular Cardiology
    3Citations 93Reads
  • [Show abstract] [Hide abstract] ABSTRACT: Penetrating cardiac injuries in Europe have been poorly studied. We present a 10-year outcome for patients with penetrating heart injuries at Oslo University Hospital. Data from 01.01.2001 until 31.12.2010 was collected from the Oslo University Hospital Trauma Registry and from the patients' records. Thirty-one patients were admitted with a penetrating cardiac injury. Fourteen patients survived (45 %). Four out of 8 patients (50 %) with gunshot wounds survived compared to 10 out of 23 (44 %) with stab wounds. Median (quartiles) for the following values were: Injury Severity Score 25 (21-35), Revised Trauma Score 0 (0-6,9), Probability of Survival 0,015 (0,004-0,956), Glasgow Coma Scale 3 (3-13). Thirteen patients had signs of life on admission and survived. Eighteen patients were admitted without signs of life and received emergency department thoracotomy. Eight of these had no signs of life at the scene of injury and did not survive. Out of the remaining 10 patients, one survived. The outcome of patients with penetrating cardiac injury reaching the emergency department with signs of life was excellent. Hemodynamic instability indicates immediate surgery. Stable patients with penetrating thoracic trauma and possible cardiac injury detected by imaging should be considered for conservative treatment.
    Full-text available · Article · Jun 2015 · Scandinavian Journal of Trauma Resuscitation and Emergency Medicine
    10Citations 68Reads
  • [Show abstract] [Hide abstract] ABSTRACT: In pressure overload, left ventricular (LV) dilatation is a key step in transition to heart failure (HF). We recently found that collagen VIII (colVIII), a non-fibrillar collagen and extracellular matrix (ECM) constituent, was reduced in hearts of mice with HF and correlated to degree of dilatation. A reduction in colVIII might be involved in LV dilatation, and we here examined the role of reduced colVIII in pressure overload-induced remodeling using colVIII knock-out (col8KO) mice. Col8KO mice exhibited increased mortality 3-9 days after aortic banding (AB) and increased LV dilatation from day one after AB, compared to wild type (WT). LV dilatation remained increased over 56 days. Forty eight hours after AB, LV expression of main structural collagens (I and III) was threefold increased in WT mice, but these collagens were unaltered in the LV of col8KO mice together with reduced expression of the pro-fibrotic cytokine TGF-β, SMAD2 signaling and the myofibroblast markers Pxn, α-SMA and SM22. Six weeks after AB, LV collagen mRNA expression and protein were increased in col8KO mice, although less pronounced than in WT. In vitro, neonatal cardiac fibroblasts from col8KO mice showed lower expression of TGF-β, Pxn, α-SMA and SM22 and reduced migratory ability possibly due to increased RhoA activity and reduced MMP2 expression. Stimulation with recombinant colVIIIα1 increased TGF-β expression and fibroblast migration. Lack of colVIII reduces myofibroblast differentiation and fibrosis and promotes early mortality and LV dilatation in response to pressure overload in mice. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.
    Full-text available · Article · Feb 2015 · Cardiovascular Research
    4Citations 82Reads

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