Abstract
Ventricular arrhythmia and subsequent sudden cardiac death (SCD) due to acute myocardial infarction (AMI) is one of the most frequent causes of death in humans. Lethal ventricular arrhythmias like ventricular fibrillation (VF) prior to hospitalization have been reported to occur in more than 10% of all AMI cases and survival in these patients is poor. Identification of risk factors and mechanisms for VF following AMI as well as implementing new risk stratification models and therapeutic approaches is therefore an important step to reduce mortality in people with high cardiovascular risk. Studying spontaneous VF following AMI in humans is challenging as it often occurs unexpectedly in a low risk subgroup. Large animal models of AMI can help to bridge this knowledge gap and are utilized to investigate occurrence of arrhythmias, involved mechanisms and therapeutic options. Comparable anatomy and physiology allow for this translational approach. Through experimental focus, using state-of-the-art technologies, including refined electrical mapping equipment and novel pharmacological investigations, valuable insights into arrhythmia mechanisms and possible interventions for arrhythmia-induced SCD during the early phase of AMI are now beginning to emerge. This review describes large experimental animal models of AMI with focus on first AMI-associated ventricular arrhythmias. In this context, epidemiology of first AMI, arrhythmogenic mechanisms and various potential therapeutic pharmacological targets will be discussed.
Highlights
Despite a decrease in overall cardiovascular mortality over the past decades, ∼17 million deaths a year occur worldwide as a result of cardiovascular disease [1] and ∼50% of these are reported to be sudden cardiac deaths (SCD) [2]
For a successful translation into clinical studies it is of importance to adjust the experimental design according to human situation
Summary
Despite a decrease in overall cardiovascular mortality over the past decades, ∼17 million deaths a year occur worldwide as a result of cardiovascular disease [1] and ∼50% of these are reported to be sudden cardiac deaths (SCD) [2]. To understand the mechanisms of ventricular arrhythmias developing during AMI and to discover new treatment modalities for these patients, investigations through translational experimental models, mimicking the clinical situation, are needed. A relatively limited number of studies focus on the acute arrhythmogenic risk of AMI. This in spite of the fact, that there is a critical need for fast acting acute antiarrhythmic treatments in AMI patients. There is an unmet medical need for such therapeutic options, which calls for investigations of novel pharmacological targets in clinical and preclinical antiarrhythmic research. This review will present the published literature on experimental large animal models of AMI with focus on translatability to the epidemiology of first AMI-associated ventricular arrhythmias. A brief overview of the involved arrhythmogenic mechanisms leading to VF during AMI is given
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