Despite the long belief that the role of the adipose tissue was restricted to that of a passive store of triglycerides and a rich source of fatty acids, accumulating data demonstrates that the adipose tissue acts as an endocrine organ, capable of producing a large number of cytokines incriminated in generating a systemic inflammatory status. At its turn, this adiposity-related pro-inflammatory status appears to promote a large range of cardiovascular disorders, including atrial fibrillation (AF). Recent studies suggest that, in addition to systemic adiposity, the volume of the pericardial fat of the entire heart, and particularly of that overlying the atria, may represent an even more important risk factor for AF. This review focuses on the most relevant clinical and experimental data that bridge adiposity-induced inflammation and AF, and provides, through a multidisciplinary approach, a discussion that integrates both the current knowledge regarding the prolific activity of systemic and pericardial adipose tissue as sources of inflammatory mediators and the main effects of adiposity-induced inflammation on the most relevant electrophysiological, structural, and autonomic mechanisms responsible for AF.

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A 55-year-old hypertensive patient presents atrial fibrillation after vasovagal syncope. Non-invasive cardiac workup is normal. Without antiarrhythmic therapy, the patient has no recurrence for the next 3years, then presents with a stroke. Echocardiography eventually reveals left atrial dilation. This sequence of events illustrates the well-known links between age, arterial hypertension, atrial fibrillation, atrial neuromyopathy and stroke. A frequently neglected common denominator in this equation is impaired sympathovagal balance. Contrary to what is often stated, autonomic imbalance is not a simple modulation factor of atrial fibrillation; both the trigger and the substrate of atrial fibrillation can be influenced by abnormal cardiac innervation. Here, we review the neurogenic theory of atrial fibrillation, based on literature and original data. We also provide evidence that this concept may help to improve atrial fibrillation prediction, early diagnosis and therapy.

Despite important advancements in acute myocardial infarction (AMI) management, it continues to represent a leading cause of mortality worldwide. Fast and reliable AMI diagnosis can significantly reduce mortality in this high-risk population. Diagnosis of AMI has relied on biomarker evaluation for more than 50 years. The upturn of high-sensitivity cardiac troponin testing provided extremely sensitive means to detect cardiac myocyte necrosis, but this increased sensitivity came at the cost of a decrease in diagnostic specificity. In addition, although cardiac troponins increase relatively early after the onset of AMI, they still leave a time gap between the onset of myocardial ischemia and our ability to detect it, thus precluding very early management of AMI. Newer biomarkers detected in processes such as inflammation, neurohormonal activation, or myocardial stress occur much earlier than myocyte necrosis and the diagnostic rise of cardiac troponins, allowing us to expand biomarker research in these areas. Increased understanding of the complex AMI pathophysiology has spurred the search of new biomarkers that could overcome these shortcomings, whereas multi-omic and multi-biomarker approaches promise to be game changers in AMI biomarker assessment. In this review, we discuss the evolution, current application, and emerging blood biomarkers for the diagnosis of AMI; we address their advantages and promises to improve patient care, as well as their challenges, limitations, and technical and diagnostic pitfalls. Questions that remain to be answered and hotspots for future research are also emphasized.

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