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Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Promoting excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
Working Groups goals is to stimulate and disseminate scientific knowledge in different fields of cardiology.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Ole Johan Kemi,
This morning saw several important and informative sessions dedicated to the topic of exercise training in the management of heart disease and failure. In an earlier session, we had learned that exercise training has the power to prolong life and to some degree also mend dysfunction; several classic trials conducted over the last few decades back this claim, but although some effort was made to tailor the exercise training to specific patient populations, there is still scope for more specificity. This is true in order to both differentiate between heart failure patients as well as between types and modalities of exercise training into appropriate and stratifiable sub-populations and –categories. The session “From Bench to Bedside: Benefits of Exercise Training in Chronic Heart Failure” provided expert views on this from selected perspectives.
Systolic heart failure has received more scientific attention than diastolic heart failure, perhaps partly as an unintentional result of the availability of appropriate animal models. Thus, Drs Nicolle Kraenkel from the University of Zurich, Switzerland, and Oyvind Ellingsen from the Norwegian University of Science and Technology in Trondheim, Norway, highlighted the evidence that aerobic exercise training improves a number of different outcomes that all contribute to improve exercise capacity and quality of life; the former focusing on the more moderate-intensity endurance exercise training, and the latter on the more high-intensity interval exercise training. Importantly, the intensity of each bout of the latter form of exercise training is so high that after 3-5 minutes, a break or an active recovery is needed so as to allow for continued exercise; hence the term interval training. Taken together, Drs Kraenkel and Ellingsen showed that the benefits come as a result of activated systemic anti-inflammatory, anti-oxidative and neurohormonal mechanisms, but also as a result of improved function in skeletal muscle, vasculature, and the myocardium and the heart itself. This evidence comes from an increasing number of animal studies involving mouse and rat models exercise trained after the induction of a myocardial infarction due to a coronary artery ligation that leads to heart failure with reduced systolic function, and it comes from smaller human clinical trials of heart failure patients also with systolic dysfunction.
Does the outcome depend on exercise intensity, or in other words whether moderate-intensity endurance exercise training or high-intensity interval exercise training is carried out? In most studies, this is not controlled for, but in those that have controlled for it, the indication is that yes – the outcome does seem to improve when the exercise intensity is ramped up by high-intensity intervals. Especially in the heart, this is explained by improved systolic pump function that again is explained by the contractile and electrophysiological apparatus of the cardiac muscle cell responding accordingly; that is, responding to a greater extent than after moderate-intensity exercise training. How can this be? Two genes known to regulate myocardial contraction and remodelling are the sarcoplasmic reticulum calcium ATPase (SERCA2a) and atrial natriuretic peptide (ANP), and both respond in an intensity-dependent manner. These are genes that have both received recent attention, SERCA2a as a potential gene therapy target and ANP for its role in modulating reverse remodelling (a reversal of the pathologic remodelling observed in heart failure). Now, these mechanisms may also beneficially be targeted by focused exercise training programs.
Other promising targets covered in the session that are thought to modulate systolic dysfunction and that respond to exercise training, but have yet to be studied with respect to different exercise training intensities or modalities, include capillary density, anabolic/catabolic balance regulators, and coronary blood vessel function. Thus, more is to come on this frontier.
Does exercise training benefit patients with diastolic heart failure or those with heart failure with preserved ejection fraction; in other words, characterized by increased left ventricular end-diastolic filling pressure but with close-to-normal systolic function? Dr Frank Edelman from the University of Goettingen, Germany, showed us that this group of patients also improve exercise capacity and quality of life after completing a program of exercise training, and that this correlates with increased diastolic function. Unfortunately, a lack of mechanistic studies and a lack of an appropriate animal model for now means that we do not yet know exactly how and why this is.
Finally, Dr Jean-Paul Schmid from the University of Berne, Switzerland, presented data that show us that patients with heart failure including those with moderate hypertension also may benefit from resistance or strength training; it improves strength and muscular endurance, and it appears to do so without also leading to a disproportionate increase in blood pressure while carrying out the exercise, which has been raised as a counterargument in the past. However, resistance or strength training does not come without drawbacks; for some unknown reason it seems to counteract some of the positive reverse remodelling effects that come with aerobic endurance exercise training, if both are undertaken concomitantly. However, this should not deter us from also prescribing this type of training, where appropriate.
All speakers highlighted an important point, namely that data on safety aspects are sparse, but we still lack the data to conclude with sufficient statistical power, exercise training including high-intensity endurance and resistance training does appear to be safe in patients with chronic heart failure; at least safer than the alternative of not engaging in exercise training.
Clearly, the topic has not yet been exhausted, and much work lies ahead of us before we are in a position to prescribe the optimal exercise training program to specific heart failure patients, the session showed us that we have begun on the path of finding this out. Evidence is gathering that exercise is not only a generic term and therefore that we in the future should reconsider our advice from “stay active” to providing specific evidence-based guidelines that are very specific as to how, in which form, and how often it is carried out. Perhaps then will the real power of exercise training come forth.
From bench to practice: benefits of exercise training in chronic heart failure