The past 3 decades have been characterized by an exponential growth in knowledge and advances in the clinical treatment of atrial fibrillation (AF). It is now known that AF genesis requires a vulnerable atrial substrate and that the formation and composition of this substrate may vary depending on comorbid conditions, genetics, sex, and other factors. Population-based studies have identified numerous factors that modify the atrial substrate and increase AF susceptibility. To date, genetic studies have reported 17 independent signals for AF at 14 genomic regions. Studies have established that advanced age, male sex, and European ancestry are prominent AF risk factors. Other modifiable risk factors include sedentary lifestyle, smoking, obesity, diabetes mellitus, obstructive sleep apnea, and elevated blood pressure predispose to AF, and each factor has been shown to induce structural and electric remodeling of the atria. Both heart failure and myocardial infarction increase risk of AF and vice versa creating a feed-forward loop that increases mortality. Other cardiovascular outcomes attributed to AF, including stroke and thromboembolism, are well established, and epidemiology studies have championed therapeutics that mitigate these adverse outcomes. However, the role of anticoagulation for preventing dementia attributed to AF is less established. Our review is a comprehensive examination of the epidemiological data associating unmodifiable and modifiable risk factors for AF and of the pathophysiological evidence supporting the mechanistic link between each risk factor and AF genesis. Our review also critically examines the epidemiological data on clinical outcomes attributed to AF and summarizes current evidence linking each outcome with AF.
Two new studies provide more evidence tilting the balance in favor of triglycerides, rather than HDL, playing a causative role in cardiovascular disease. But it is still too early to know whether the findings of any of the studies will point to useful new methods to prevent and treat disease.
There are links to other studies at the end of this Medpage article.
Take Home – Do not ignore triglycerides.
Heart failure death rates rising again after decade of decline
“Working 55 hours or more a week was associated with significant 33% increase in stroke risk and a more modest 13% increase in risk of developing coronary heart disease, compared to working 35 to 40 hours weekly, in the analysis of published and previously unpublished prospective cohort studies from the U.S., Europe, and Australia.”
One could argue for causation given the strength of association identified by this study. Common sense tells us that anyone working more than 60 hours a week is going to have considerably less time for other activities like exercise and time with family and friends. Long hours working also can lead to neglect of one’s health.
There are multiple links in the WP article to the original studies.