Hypertrophic cardiomyopathy patients with paroxysmal atrial fibrillation have a high burden of left atrial fibrosis by cardiac magnetic resonance imaging

OBJECTIVES This study hypothesized that paroxysmal atrial fibrillation (PAF) reflects the presence of a more severe cardiac hypertrophic cardiomyopathy (HCM) phenotype.BACKGROUND HCM is characterized by myocyte hypertrophy, fibrosis, and a high prevalence of PAF. It is currently unresolved whether atrial fibrillation (AF) is a marker or a mediator of adverse outcomes in HCM.METHODS This study retrospectively examined 45 HCM patients who underwent cardiovascular magnetic resonance (CMR) imaging in sinus rhythm. The function of all 4 cardiac chambers was assessed, as well as late gadolinium enhancement (LGE) in the left atrium (LA) and left ventricle (LV), as indicators of fibrosis. A fat-saturated, 3-dimensional inversion recovery-prepared, fast-spoiled, gradient-recalled echo sequence, and the image intensity ratio method were used to measure LA-LGE; LGE in the LV was quantified using a semi-automated threshold technique.RESULTS HCM patients (n = 45) were divided into 2 groups (PAF, no AF) based on history of PAF. All HCM patients had LGE in the LA posterior wall. The PAF group (n = 18) had higher LA volume, a lower LA ejection fraction, a lower global peak longitudinal LA strain (PLAS), and a higher amount of LA-LGE compared with the no AF group (n = 27). A modest inverse association was noted between the LA ejection fraction, PLAS, and LA-LGE; a positive association was present between LV-LGE and LA-LGE. The PAF group had lower ejection fractions in the LV, right atrium, and right ventricle compared with those in the no AF group.CONCLUSIONS PAF is associated with a greater degree of structural LA remodeling and global myopathy, which suggests a more severe cardiac HCM phenotype. (c) 2019 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Association of scar distribution with epicardial electrograms and surface ventricular tachycardia QRS duration in nonischemic cardiomyopathy

Introduction The association of late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) with epicardial and surface ventricular tachycardia (VT) electrogram features, in nonischemic cardiomyopathy (NICM), is unknown. We sought to define the association of LGE and viable wall thickness with epicardial electrogram features and exit site paced QRS duration in patients with NICM. Methods A total of 19 patients (age 53.5 +/- 11.5 years) with NICM (ejection fraction 40.2 +/- 13.2%) underwent CMR before VT ablation. LGE transmurality was quantified on CMR and coregistered with 2294 endocardial and 2724 epicardial map points. Results Both bipolar and unipolar voltage were associated with transmural signal intensity on CMR. Longer electrogram duration and fractionated potentials were associated with increased LGE transmurality, but late potentials or local abnormal ventricular activity were more prevalent in nontransmural versus transmural LGE regions (p < .05). Of all critical VT sites, 19% were located adjacent to regions with LGE but normal bipolar and unipolar voltage. Exit site QRS duration was affected by LGE transmurality and intramural scar location, but not by wall thickness, at the impulse origin. Conclusions In patients with NICM and VT, LGE is associated with epicardial electrogram features and may predict critical VT sites. Additionally, exit site QRS duration is affected by LGE transmurality and intramural location at the impulse origin or exit.Cardiovascular Aspects of Radiolog

Association of scar distribution with epicardial electrograms and surface ventricular tachycardia QRS duration in nonischemic cardiomyopathy

Introduction The association of late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) with epicardial and surface ventricular tachycardia (VT) electrogram features, in nonischemic cardiomyopathy (NICM), is unknown. We sought to define the association of LGE and viable wall thickness with epicardial electrogram features and exit site paced QRS duration in patients with NICM. Methods A total of 19 patients (age 53.5 +/- 11.5 years) with NICM (ejection fraction 40.2 +/- 13.2%) underwent CMR before VT ablation. LGE transmurality was quantified on CMR and coregistered with 2294 endocardial and 2724 epicardial map points. Results Both bipolar and unipolar voltage were associated with transmural signal intensity on CMR. Longer electrogram duration and fractionated potentials were associated with increased LGE transmurality, but late potentials or local abnormal ventricular activity were more prevalent in nontransmural versus transmural LGE regions (p < .05). Of all critical VT sites, 19% were located adjacent to regions with LGE but normal bipolar and unipolar voltage. Exit site QRS duration was affected by LGE transmurality and intramural scar location, but not by wall thickness, at the impulse origin. Conclusions In patients with NICM and VT, LGE is associated with epicardial electrogram features and may predict critical VT sites. Additionally, exit site QRS duration is affected by LGE transmurality and intramural location at the impulse origin or exit.Cardiovascular Aspects of Radiolog

Atrial Fibrillation and Epicardial Adipose Tissue

Atrial fibrillation (AF) is associated with increased cardiovascular morbidity and mortality with projections that it will affect 8–12 million people in the United States by 2050. Obesity has been identified as an important independent risk factor for AF, with weight loss leading to decreased AF burden and improved arrhythmia free survival. The precise mechanisms by which obesity contributes to AF remain poorly understood. However, it has recently been speculated that epicardial adipose tissue (EAT) may be a key mediator between obesity and AF. EAT is a visceral fat depot with anatomic contiguity to the myocardium. Under physiological conditions, EAT plays an important protective role via mechanical, metabolic, and thermogenic functions. However, under pathophysiological conditions, it may contribute to development of AF through various mechanisms including fatty infiltration, fibrosis, inflammation, oxidative stress, atrial remodelling, and genetic factors. EAT has been shown in multiple studies to be a risk factor for development of AF and predictor of recurrence after catheter ablation. The mechanisms directly linking EAT to the pathogenesis of AF also are uncertain. Multiple pharmacologic options have been proposed to target EAT; however, the efficacy of targeted reduction in EAT requires further investigation