Left ventricular remodelling and dysfunction. Can the process be prevented?

Due to continuous remodelling myocardial dysfunction is a progressive condition. Even if the initial event is so mild that it causes no immediate cardiac dysfunction (e.g. a small myocardial infarction), the remodelling process is triggered. Although the remodelling process can be adaptive, the process becomes maladaptive when the stimuli are continuous and pathological. A similar remodelling process is seen in most primary myocardial disorders, suggesting common mechanisms for the development of heart failure. Although clinical heart failure may develop acutely, for example, after an acute myocardial infarction, the progressive changes in myocardial structure and deterioration of myocardial function can go on silently for a very long time and overt heart failure may develop several years after an initial insult, even if there are no further events. In order to fundamentally improve prognosis in cardiac failure it is necessary to identify patients with an ongoing remodelling process and to effectively counteract this process as early as possible.     

Large-scale screening studies for atrial fibrillation – is it worth the effort?

Atrial fibrillation (AF) is a common disease with increasing prevalence, approximately 3.2% in the adult population. In addition, about one third of AF cases are considered asymptomatic. Due to increased longevity, increased detection and increased prevalence of risk factors, the prevalence of AF is expected to at least double by the year 2060. Patients with AF have an increased risk for ischaemic stroke, heart failure, death and cognitive decline. Treatment with oral anticoagulation reduces the risk of ischaemic stroke and mortality, and the effect on cognitive decline is being studied. Based on the increasing prevalence of AF, its often asymptomatic and paroxysmal presentation and the efficacy of oral anticoagulation treatment, screening for AF has been proposed. AF seems to fulfil most of the Wilson–Jungner criteria for screening issued by the World Health Organization, but some knowledge gaps remain, gaps that will be addressed by several ongoing studies. The knowledge gaps in AF screening consist of the magnitude of the net benefit or net harm inflicted by AF screening because the oral anticoagulation treatment will also increase the risk of bleeding, and the psychological effects of AF screening are not very well studied. So far, the AF screening recommendations issued by the European Society of Cardiology have had limited impact on national and regional AF screening activities. Several large-scale AF screening studies will report results on hard endpoints within the next few years, and these results will hopefully manifest AF as a cardiovascular disease which we need to pay more attention to.     

Non-antiarrhythmic drug therapy for the prevention of atrial fibrillation?

In atrial fibrillation (AF), the absence of a clear benefit of a rhythm-control strategy over a rate-control strategy seen in recent trials may be due to the fact that many of the usual antiarrhythmic strategy have significant weaknesses. Besides research efforts to improve the efficacy and safety of conventional antiarrhythmic agents, therapies directed 'upstream'of the electrical aspects of AF, towards the underlying anatomical substrate and atrial remodelling, have been proposed as new pharmacological therapeutic approaches. Potential upstream therapies for AF comprise a variety of agents such as angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB), statins, N-3 polyunsaturated fatty acids and steroids. On the basis of experimental data, clinical studies have provided information on the potential of upstream therapy for the prevention of AF across a broad spectrum of cardiovascular patient groups. In patients with heart failure or hypertension, data are sufficient to support the use of ACEI or ARB as treatment that may decrease the risk of AF beyond their other beneficial effects. Similarly, it is highly possible that the use of statin in patients with a recognized indication may be associated with a benefit against AF. However, in most clinical settings, the evidence appears to be insufficient to drive changes in therapy management per se, and large-scale, randomized controlled trials with adequately defined endpoints are still needed. The results from these trials may help to understand the complex mechanisms that lead to AF, and may clarify the benefit-to-risk ratio of these new therapeutic approaches.