Atrial Fibrillation Clinics in Canada: A Nationwide Project Report

The increased prevalence of atrial fibrillation (AF) has led to specialized AF clinics (AFCs) to facilitate management of AF patients. In this article we report on outpatient AFCs in Canada, which is essential to health policies required to standardize the performance of existing AFCs and help design new AFCs. We surveyed 14 clinics in 5 provinces; 100% provided responses to a detailed questionnaire on clinic processes and care practices. Fourteen care maps were analyzed, and 5 models of care were identified; 4 were specific to AFCs. An online survey with 49 questions included items on: (1) process before visit; (2) process at visit; (3) patient education provided; (4) outreach; and (5) specific clinic information. Clinicians’ advice to patients on self-care items such as: (1) amount of alcohol and (2) caffeine intake; (3) exercise activity; (4) stressful events; (5) “when to go to the emergency department”; and (6) lifestyle changes, were evaluated to assess consistency in practice. There were moderate variances in clinicians’ advice to patients in 5 of 6 self-care items. The 1 item that had 100% consistent practice recommendation was when to go to the emergency department. A guideline-based clinical assessment checklist (CAC) was piloted to obtain feedback on its usability in real-world practice; revisions finalized the “simplified CAC” for AF care encompassing 35 data points with rationale. There was 100% positive feedback on its ability to provide baseline elements in AF care. When validated, a “simplified CAC” can facilitate a standardized clinical assessment tool in clinical practice.     

Can We Eliminate Low-Density Lipoprotein Cholesterol-Related Cardiovascular Events Through More Aggressive Primary Prevention Therapy?

Intravascular levels of low-density lipoprotein cholesterol (LDL-C) at approximately ≤ 0.6 mmol/L are likely to minimize, and perhaps eliminate, LDL-C-related vascular toxicity while having no effect on essential, intracellular cholesterol homeostatic pathways, according to accumulated knowledge from basic science. Randomized clinical trials, observational reports, and Mendelian randomization trials are also forcing a reconsideration of what “normal” LDL-C means. Recent trials of secondary prevention have substantiated that such levels are safe and associated with a decreased risk of cardiovascular events (CVEs) compared with patients with higher levels of LDL-C. Similarly, treatment to this low range is associated with regression and stabilization of established atherosclerosis. Primary prevention trials also show that low levels of LDL-C are safe and associated with decreased risk of CVEs through cholesterol-lowering in adults with LDL-C ≥ 3.5 mmol/L or when levels are < 3.5 mmol/L in association with other cardiovascular risks. Although there are no randomized clinical outcome trials of familial hypercholesterolemia patients, such patients have very high, lifetime risk of CVE, and registry studies show that LDL-C reduction has nearly normalized their CVE rates. The possibility of familial hypercholesterolemia should be considered if LDL-C is > 4.5 and > 4.0 mmol/L at ages 18-39 years and younger than 18 years, respectively. On the basis of these convergent and internally consistent lines of evidence, in this article we speculate on a translational paradigm aimed at eliminating LDL-C-related CVEs through aggressive primary prevention strategies that are already proven and well accepted in principle.     

Age as a Critical Determinant of Atrial Fibrillation: A Two-sided Relationship

The incidence of atrial fibrillation (AF), the most common sustained arrhythmia and a major public health burden, increases exponentially with age. However, mechanisms underlying this long-recognized association remain incompletely understood. Experimental and human studies have demonstrated the involvement of aging in several arrhythmogenic processes, including atrial electrical and structural remodelling, disturbed calcium homeostasis, and enhanced atrial ectopic activity/increased vulnerability to re-entry induction. Given this wide range of putative mechanisms, the task of delineating the specific effects of aging responsible for AF promotion is not simple, as aging is itself associated with increasing prevalence of a host of AF-predisposing conditions, including heart failure, coronary artery disease, and hypertension. Although we usually think of old age promoting AF, there is also evidence that young age may actually have a protective effect against AF occurrence. For example, the low AF incidence among populations of young patients with significant structural congenital heart disease and substantial atrial enlargement/remodelling suggests that younger age might protect against fibrillation in the diseased atrium; efforts at understating how younger age may prevent AF might be helpful in elucidating missing mechanistic links between AF and age. The goal of this paper is to review the epidemiologic and pathophysiologic evidence regarding mechanisms underlying age-related AF. Although the therapeutic options for AF have recently improved, major gaps still remain and a better understanding of the special relationship between age and AF may be important for the identification of new targets for therapeutic innovation.