•  EN 
  • Employee login

CardioVascular Center (CVC)

Print 
​​

The CardioVascular Center (CVC) is dedicated to preserve cardiac function over time. Cardiovascular (CV) disease is still the major cause for morbidity and mortality, and is strongly age-related, so prevalence will increase. In recent years, CVC has shifted its main focus from solving the pathophysiological mechanisms of systolic heart failure (HF) or Heart Failure with reduced Ejection Fraction (HFrEF) towards other emerging diseases in the CV spectrum: early structural heart disease, diastolic HF (or Heart Failure with preserved Ejection Fraction, HFpEF), and atrial fibrillation (AF).  
First goals are optimal therapy of these disorders, which often but not always coincide with the goals to preserve cardiac function, and to prevent other associated morbidities, including stroke and mortality. Ultimately, prevention of HFpEF, HFrEF and AF is our goal, i.e. healthy aging. Interestingly, these disorders are related to vascular dysfunction and are strongly age-related, although they start to occur at younger ages. High quality research with strong translational focus could help reducing the burden of CV-related loss of lives and productive years and contribute to healthy ageing. The CVC has embraced as its central mission to generate new insights into the mechanisms that drive both epidemics of HF and AF, and translate these insights in new targets, new treatments, and develop patient tailored therapy in order to preserve cardiac function and prevent adverse outcomes (figure 1.)

Scientific and Societal output    Dissertations   Principal Investigators   Programme Leaders   Description of the Programme  

To enable the preservation of cardiac function through the lifetime, several research lines work closely together within CVC (historically organized as CVC-1: clinical heart failure; CVC-2: experimental heart failure; CVC-2: atrial fibrillation). The central theme is safeguarded by including a temporal interaction and translational focus in all research activities. The program of CVC includes the following main aspects:

Standing research lines

1. To study the dynamics of heart disease and its development, our research group makes use of large biobanks, comprising several cohorts of subjects from the general population (PREVEND, LifeLines) with long-term follow-up. These databases often are coupled to other large databases (see Section 7.5 on collaborations), which together will enable the study of components and risk factors for heart disease development. Additionally, we have created and continuously build new large databases of both low-risk and high-risk patients, e.g. patients with new onset HF (PREVEND), and new onset AF (AF risk, RACE 3 and 5) that allow early intervention studies, as well as patient at risk to develop HF (carriers of pathogenic mutations, and post-MI patients (CardioLines), and they are sampled at multiple stages during the CV disease continuum. 

2. CVC has a longstanding history of elucidating specific pathophysiological mechanisms that contribute to the onset and progression of HF, which we aim to discover, unravel and describe in a preclinical research program (CVC program 2), situated in the division of experimental cardiology. In recent decades, this has resulted in several new clinical insights, which have been successfully translated into clinical research lines. Several of those were followed by clinical targeted randomized intervention studies. Examples of characteristic, collaborative and world-leading research lines in HF, initiated in experimental studies, with their respective clinical trials are: erythropoietin in HF (RCTs: HEBE, RED-HF), cardiorenal mechanisms (RCT: ARIANE-HF, diuretic resistance studies in PROTECT), diabetes and the use of metformin (GIPS-III), galectin-3, microvascular function (thrombosuction), and genetics in HF. For AF, we are world opinion leaders in mechanisms associated with AF progression and optimal therapy, including rate versus rhythm control (RACE 1&2), optimal pharmacological therapy to prevent AF (VERDICT, CONVERT), and the role of microvascular function and genetics in AF (AF Risk, RACE V).  

3. During the last decade, CVC has devoted considerable efforts to establishing genetic consortia that have resulted in much larger databases that have had major impact due to their such stronger power, not only on initiation of both epidemics but also at progression of HF and AF and their associated morbidities and mortality. Furthermore, CVC has successfully obtained funding for national study groups of monogenetic inheritable cardiomyopathies (PREDICT, DOSIS), that ensure strong national embedding. Using detailed phenotyping in combination with genotyping and advanced system biology analyses we will gain better understanding of mechanisms of both initiation and progression of both HF and AF. For specific collaborations and consortia: see the section on national and international collaboration. We will continue to develop and expand these experimental and clinical research lines in clinical HF and AF, but will also expand to pulmonary hypertension, pregnancy and heart disease, and consequences of acute myocardial infarction. These lines will entail pharmacological studies, disease management studies, imaging studies and device therapy.

Newest developments

4. HF and AF are typical diseases of the elderly patient. However, both diseases develop nowadays at younger ages in part due to adverse lifestyle changes, such as obesity and sedentary lifestyle. Our research group will continue to conduct research on the prevalence, predictive value, and cause of co-morbidities in elderly, but also at younger ages, and thereby contribute to healthy ageing of the aging population and the population as a whole. Examples of programs in HF research are HF and diabetes, liver function abnormalities, renal dysfunction, and cognitive dysfunction, with experimental and clinical research lines. For AF, lifestyle changes including physical activity and weight reduction are and will be strongly incorporated in our treatment strategy as currently investigated in RACE 3 (data expected in 2018) and our atrial ablation studies (Cryo and hybrid ablation registries). 

5. We lead several large scale HF biomarker studies that are expected to uncover promising novel markers (COACH, BIOSTAT-CHF, CVON-ARENA, PREVEND, PROTECT, CTMM MARC, CardioLines), allowing the study of genetic and plasma biomarkers. We aim to use these to study underlying pathophysiological mechanisms, to predict response both to pharmacological and non-pharmacological therapies, as well as to identify patients at higher risk. We envision working along the translational axis, i.e. from experimental work into the clinic or the reverse (from clinical observations back to mechanistic insights). Also for AF, through the study of genetic and plasma biomarkers, including systems biology analyses, we aim to identify novel targets for atrial fibrillation treatment. Furthermore, RACE V will study the presence and importance of vascular dysfunction and thrombosis in AF in a large cohort of early onset AF patients who will be continuously monitored by a miniaturized implantable loop recorder.  

6. We have initiated several large scale AF studies to uncover mechanisms of AF progression, with a special focus on the association between HF and AF, and the discovery of new therapies directed at the underlying mechanisms. The latest trial is VIP-HF, which studies arrhythmogenesis and causes of death in patients with HFpEF and AF. 

7. In patients with congenital heart disease, abnormal loading conditions commonly result in heart failure. The Center of Congenital Heart Disease of the CVC conducts research in children and adults with congenital heart disease, focusing on lifetime myocardial and pulmonary vascular adaptation to abnormal loading conditions. Major research subjects are pulmonary hypertension and pulmonary vascular remodeling; right ventricular adaptation and failure; and pregnancy in women with congenital heart disease. We strive to synchronize and merge these efforts with the main research lines, and they are executed in shared laboratory spaces.

Mission  

The CardioVascular Center (CVC) is dedicated to preserving cardiac function over time, aiming at healthy ageing. CV diseases remain a major killer in Western society, and we see it as our mission to minimize this burden to our patients and society as a whole.  Our main tools to meet our ambitions are:

  • Provide ongoing education and a continuous flow of innovative experimental and clinical studies. This has positioned CVC at the forefront of the CV research in Europe. We believe this has helped to attract excellent young researchers, and we have prepared our junior research staff and doctors to also make a difference in their field of expertise.
  • Improve the outcome, quality of life, and care for patients suffering from CV disease
  • Putting together a group of dedicated, ambitious and skilled researchers
  • Making constant improvements in the financial,
    organizational and ethical infrastructure of our research work.
Relevance to Healthy Ageing  

"The heart is a tough organ: a marvelous mechanism that, mostly without repairs, will give valiant pumping service up to a hundred years." Willis John Potts, MD, 1895-1968

Our mission to preserve cardiac function over time has important relevance to the general theme healthy aging. Heart disease is a disease primarily of the elderly, and therefore the study of heart disease will involve mostly elderly patients. The CVC has participated and initiated several projects with a primary focus on aging: telomeres in cardiovascular disease (which has led to the discovery of two genes that accelerate biological aging); the SENIORS study (Study of the Effects of Nebivolol Intervention on OUtcomes and Rehospitalisation in Seniors With Heart Failure), the first heart failure trial exclusively aimed to study the elderly. We have an interest in the study of heart failure patients with co-morbidities, which by default involves elderly. This has resulted in well recognized research lines on cardiorenal interaction, heart failure and anemia, and atrial fibrillation and cerebrovascular morbidity. 
Furthermore, it should be noted that the treatment of congenital and acquired cardiovascular disease has contributed to an increased life span, more so than treatment of any other disease. Patients with congenital heart disease nowadays survive well into adult age, but the majority faces lifetime abnormal loading conditions which often result in heart failure. The research of the congenital heart centre contributes to increased knowledge on risk factors and treatment outcomes in pulmonary hypertension. 
All of this should be regarded as clear valorisation of research money and has directly benefited the population as a whole. Several key publications from the CVC have changed the global guidelines, e.g. the treatment of atrial fibrillation (RACE1&2, NEJM 2002/2010),  acute myocardial infarction (TAPAS, NEJM 2009) and pediatric pulmonary hypertension (TOPP, Lancet 2012),  helping to further lower morbidity and mortality and to better utilize scarce resources.