Research Area
Heart failure, the common end-point in cardiac disease of diverse etiologies, is a major cause of morbidity and mortality in affluent societies. Indeed, the incidence and prevalence of heart failure in these countries are increasing due to altered demographics with increased proportion of the elderly, as well as increased survival of myocardial infarction. Despite implementation of several new treatment modalities during the last 20 years, heart failure is still a progressive and ominous disease indicating that important pathogenic mechanisms remain unmodified by the most current treatment modalities.
In evolving heart failure multiple compensatory actions are triggered in order to maintain cardiac output, among which are activation of the sympathetic nervous system, the renin-angiotensin system, as well as a number of autocrine/paracrine factors synthesized in myocardial tissue. The compensatory actions also reflect alterations in of cardiac structure, collectively called cardiac remodeling. These structural alterations comprise, dilatation of the ventricular chambers, myocardial hypertrophy and fibrosis. Although cardiac remodeling may initially balance loss of contractile force, the continuum of these structural alterations often engages in vicious circles leading to progression of cardiac dysfunction and overt heart failure. Increasing evidence points to myocardial hypertrophy, fibrosis, and dilatation of the ventricular cavities as independent risk factors of heart failure. Indeed, recognition of these structural alterations of the heart is implemented in the new recommendations for the evaluation and management of chronic heart failure recently published by the American College of Cardiology/American Heart Association Task Force. According to these recommendations, which are meant to complement the New York Heart Association (NYHA) functional classification, patients are to be stratified according to risk factors for developing heart failure, including the absence or presence of structural alterations of the heart.
Despite substantial new insights into the mechanisms of myocardial hypertrophy and fibrosis, many of the nodal points that orchestrate these structural alterations still remain to be identified. Furthermore, current knowledge largely precludes from deciphering of adaptive versus maladaptive cellular responses to insufficient cardiac output. Thus, the focus of our research group is to unravel the signal transduction mechanisms leading to dysfunctional signaling responses and pathologic remodeling of the heart. The urpose of these investigations is to provide new knowledge of disease mechanisms enabling development of novel pharmacological interventions for heart failure.
Our research group is a multidisciplinary team of experts in gene technology, molecular and cellular biology, as well as experimental and clinical medicine. The research efforts comprise studies of isolated cardiac myocytes, integrated physiology in transgenic animal models, as well as clinical investigations. Our research group is member of Center for Heart Failure Research, University of Oslo (www.heartfailure.no), a thematic research initiative and focus area of research selected by the Faculty of Medicine. The Institute for Surgical Research provides infrastructure with state-of-the-art equipment for high-resolution echocardiography and integrated physiologic assessment of cardiac function in transgenic mice. (Fig. 1 & 2).
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| Fig. 1: M-mode (bottom panel) and 2D-mode (upper panel) image acquisition of left ventricle of adult mouse heart using VisualSonics high resolution ulstrasonograpy system for small animal research. |
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| Fig.2: 2D-mode image acquisition of left ventricle of mouse heart catheterized with combined conductance/micromanometer-tip catheter for simultaneous pressure volume analysis. |
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