Lone Atrial Fibrillation Is Associated With Impaired Left Ventricular Energetics That Persists Despite Successful Catheter Ablation

Background: Lone atrial fibrillation (AF) may reflect a subclinical cardiomyopathy that persists after sinus rhythm (SR) restoration, providing a substrate for AF recurrence. To test this hypothesis, we investigated the effect of restoring SR by catheter ablation on left ventricular (LV) function and energetics in patients with AF but no significant comorbidities. Methods: Fifty-three patients with symptomatic paroxysmal or persistent AF and without significant valvular disease, uncontrolled hypertension, coronary artery disease, uncontrolled thyroid disease, systemic inflammatory disease, diabetes mellitus, or obstructive sleep apnea (ie, lone AF) undergoing ablation and 25 matched control subjects in SR were investigated. Magnetic resonance imaging quantified LV ejection fraction (LVEF), peak systolic circumferential strain (PSCS), and left atrial volumes and function, whereas phosphorus-31 magnetic resonance spectroscopy evaluated ventricular energetics (ratio of phosphocreatine to ATP). AF burden was determined before and after ablation by 7-day Holter monitoring; intermittent ECG event monitoring was also undertaken after ablation to investigate for asymptomatic AF recurrence. Results: Before ablation, both LV function and energetics were significantly impaired in patients compared with control subjects (LVEF, 61% [interquartile range (IQR), 52%–65%] versus 71% [IQR, 69%–73%], P<0.001; PSCS, –15% [IQR, –11 to –18%] versus −18% [IQR, –17% to –19%], P=0.002; ratio of phosphocreatine to ATP, 1.81±0.35 versus 2.05±0.29, P=0.004). As expected, patients also had dilated and impaired left atria compared with control subjects (all P<0.001). Early after ablation (1–4 days), LVEF and PSCS improved in patients recovering SR from AF (LVEF, 7.0±10%, P=0.005; PSCS, –3.5±4.3%, P=0.001) but were unchanged in those in SR during both assessments (both P=NS). At 6 to 9 months after ablation, AF burden reduced significantly (from 54% [IQR, 1.5%–100%] to 0% [IQR 0%–0.1%]; P<0.001). However, LVEF and PSCS did not improve further (both P=NS) and remained impaired compared with control subjects (P<0.001 and P=0.003, respectively). Similarly, there was no significant improvement in atrial function from before ablation (P=NS), and this remained lower than in control subjects (P<0.001). The ratio of phosphocreatine to ATP was unaffected by heart rhythm during assessment and AF burden before ablation (both P=NS). It was unchanged after ablation (P=0.57), remaining lower than in control subjects regardless of both recovery of SR and freedom from recurrent AF (P=0.006 and P=0.002, respectively). Conclusions: Patients with lone AF have impaired myocardial energetics and subtle LV dysfunction, which do not normalize after ablation. These findings suggest that AF may be the consequence (rather than the cause) of an occult cardiomyopathy, which persists despite a significant reduction in AF burden after ablation

Seek and ye shall find… subclinical atrial fibrillation in high-risk elderly patients.

Atrial fibrillation (AF) is a rapidly growing public health and economic burden. The global number of individuals with clinically diagnosed AF was estimated to be 33 million in 2010 and is expected to double by 2050 due to demographic changes and the rising prevalence of risk factors for AF, such as obesity, diabetes and hypertension. AF is associated with substantial morbidity and mortality (mostly secondary to an increased risk of stroke), reduced quality of life, and considerable costs. Yet, these figures are likely to underestimate the true prevalence of AF, as prolonged ECG monitoring detects clinically silent subclinical AF (SCAF) in a variable proportion of subjects presenting in sinus rhythm, depending on the type and duration of monitoring, the characteristics of the study population (in particular, age and medical history), and the definition of A

Mechanisms of atrial fibrillation

Atrial fibrillation (AF) is the most common sustained arrhythmia, currently affecting over 33 million individuals worldwide, and its prevalence is expected to more than double over the next 40 years. AF is associated with a twofold increase in premature mortality, and important major adverse cardiovascular events such as heart failure, severe stroke and myocardial infarction. Significant effort has been made over a number of years to define the underlying cellular, molecular and electrophysiological changes that predispose to the induction and maintenance of AF in patients. Progress has been limited by the realisation that AF is a complex arrhythmia that can be the end result of various different pathophysiological processes, with significant heterogeneity between individual patients (and between species). In this focused Review article, we aim to succinctly summarise for the non-specialist the current state of knowledge regarding the mechanisms of AF. We address all aspects of pathophysiology, including the basic electrophysiological and structural changes within the left atrium, the genetics of AF and the links to comorbidities and wider systemic and metabolic perturbations that may be upstream contributors to development of AF. Finally, we outline the translational implications for current and future rhythm control strategies in patients with AF

Rivaroxaban in stable cardiovascular disease

A response to "Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease" N Engl J Med 2017; 377:1319-1330

Target: ligand interactions of the vascular endothelium. Implications for molecular imaging in inflammation.

Molecular imaging refers to the non-invasive visualisation of biological processes at the molecular and cellular levels within a living organism, and offers a wide range of potential benefits to both clinical medicine and research into novel therapeutic agents. Inflammation plays an important role in a wide variety of pathological processes and imaging the molecular and cellular machinery that underlies chronic inflammation is attractive and feasible. In this review, we present an overview of molecular imaging of inflammation. We start by characterising molecular and cellular events in early inflammation, identifying current and potential future imaging targets. We focus on the imaging of endothelial cells, which mediate the important first steps in inflammation in any tissue, are readily accessible to imaging probes and which present an approach that can be applied across multiple modalities. We then review the generic requirements for imaging contrast agents and focus on the important considerations in respect of ligands, ligand-target interactions and contrast vehicles. We aim to provide an integrated view of current progress with a focus on promising recent developments in experimental and translational molecular imaging