Wearables in Sports Cardiology.

The expanding array and adoption of consumer health wearables is creating a new dynamic to the patient-health-care provider relationship. Providers are increasingly tasked with integrating the biometric data collected from their patients into clinical care. Further, a growing body of evidence is supporting the provider-driven utility of wearables in the screening, diagnosis, and monitoring of cardiovascular disease.

Diagnosis, significance, and management of ventricular thrombi in patients referred for VT ablation.

Introduction: In patients with structural heart disease presenting with ventricular tachycardia (VT), detection of ventricular thrombi and subsequent management can be challenging. This study aimed to assess the value of multimodality imaging with cardiac magnetic resonance imaging (CMR), contrast-enhanced transthoracic echocardiography (TTE), and computed tomography (CT) for thrombus detection as well as a management algorithm geared towards anticoagulation and deferred ablation for patients referred for VT ablation.

Methods And Results: A total of 154 consecutive patients referred for VT ablation underwent preprocedural multimodality imaging with CMR, CT, and TTE.

Chiropractic Care in the Management of Inactive Ankylosing Spondylitis: A Case Series.

Objective: This report describes chiropractic management for 3 cases of inactive ankylosing spondylitis (AS).

Clinical Features: A 25-year-old woman presented with chronic, mechanical neck pain and stiffness that was ultimately diagnosed as AS. A 23-year-old man presented with chronic low back and left hip pain that was diagnosed as AS.

Novel junctophilin-2 mutation A405S is associated with basal septal hypertrophy and diastolic dysfunction.

Background: Hypertrophic cardiomyopathy (HCM), defined as asymmetric left ventricular hypertrophy, is a leading cause of cardiac death in the young. Perturbations in calcium (Ca) handling proteins have been implicated in the pathogenesis of HCM. -encoded junctophilin 2 is a major component of the junctional membrane complex, the subcellular microdomain involved in excitation-contraction coupling.

Junctophilin-2 gene therapy rescues heart failure by normalizing RyR2-mediated Ca release.

Background: Junctophilin-2 (JPH2) is the primary structural protein for the coupling of transverse (T)-tubule associated cardiac L-type Ca channels and type-2 ryanodine receptors on the sarcoplasmic reticulum within junctional membrane complexes (JMCs) in cardiomyocytes. Effective signaling between these channels ensures adequate Ca-induced Ca release required for normal cardiac contractility. Disruption of JMC subcellular domains, a common feature of failing hearts, has been attributed to JPH2 downregulation.

SPEG (Striated Muscle Preferentially Expressed Protein Kinase) Is Essential for Cardiac Function by Regulating Junctional Membrane Complex Activity.

Rationale: Junctional membrane complexes (JMCs) in myocytes are critical microdomains, in which excitation-contraction coupling occurs. Structural and functional disruption of JMCs underlies contractile dysfunction in failing hearts. However, the role of newly identified JMC protein SPEG (striated muscle preferentially expressed protein kinase) remains unclear.

Loss of microRNA-106b-25 cluster promotes atrial fibrillation by enhancing ryanodine receptor type-2 expression and calcium release.

Background: Enhanced sarcoplasmic reticulum Ca(2+)-leak via ryanodine receptor type-2 (RyR2) contributes to the pathogenesis of atrial fibrillation (AF). Recent studies have shown that the level of RyR2 protein is elevated in atria of patients with paroxysmal AF, suggesting that microRNA-mediated post-transcriptional regulation of RyR2 might be an underlying mechanism. Bioinformatic analysis suggests that miR-106b and miR-93, members of the miR-106b-25 cluster, could bind to RyR2-3'-untranslated region and suppress its translation.

Reduced junctional Na+/Ca2+-exchanger activity contributes to sarcoplasmic reticulum Ca2+ leak in junctophilin-2-deficient mice.

Expression silencing of junctophilin-2 (JPH2) in mouse heart leads to ryanodine receptor type 2 (RyR2)-mediated sarcoplasmic reticulum (SR) Ca(2+) leak and rapid development of heart failure. The mechanism and physiological significance of JPH2 in regulating RyR2-mediated SR Ca(2+) leak remains elusive. We sought to elucidate the role of JPH2 in regulating RyR2-mediated SR Ca(2+) release in the setting of cardiac failure.

Emerging roles of junctophilin-2 in the heart and implications for cardiac diseases.

Cardiomyocytes rely on a highly specialized subcellular architecture to maintain normal cardiac function. In a little over a decade, junctophilin-2 (JPH2) has become recognized as a cardiac structural protein critical in forming junctional membrane complexes (JMCs), which are subcellular domains essential for excitation-contraction coupling within the heart. While initial studies described the structure of JPH2 and its role in anchoring junctional sarcoplasmic reticulum and transverse-tubule (T-tubule) membrane invaginations, recent research has an expanded role of JPH2 in JMC structure and function.

The junctophilin family of proteins: from bench to bedside.

Excitable tissues rely on junctional membrane complexes to couple cell surface signals to intracellular channels. The junctophilins have emerged as a family of proteins critical in coordinating the maturation and maintenance of this cellular ultrastructure. Within skeletal and cardiac muscle, junctophilin 1 and junctophilin 2, respectively, couple sarcolemmal and intracellular calcium channels.

Mutation E169K in junctophilin-2 causes atrial fibrillation due to impaired RyR2 stabilization.

Objectives: This study sought to study the role of junctophilin-2 (JPH2) in atrial fibrillation (AF).

Background: JPH2 is believed to have an important role in sarcoplasmic reticulum (SR) Ca(2+) handling and modulation of ryanodine receptor Ca(2+) channels (RyR2). Whereas defective RyR2-mediated Ca(2+) release contributes to the pathogenesis of AF, nothing is known about the potential role of JPH2 in atrial arrhythmias.

Feasibility of using a standardized patient encounter for training chiropractic students in tobacco cessation counseling.

Objective : Although tobacco cessation training is included in many health profession programs, it is not yet routinely incorporated into chiropractic education. The purpose of this study was to assess the feasibility of incorporating a problem-based learning tobacco cessation activity into a lecture course for chiropractic students. Methods : Seventy-two students were assigned to participate in two 1-hour lectures on health promotion counseling and tobacco cessation followed by an experiential student-driven lab session using standardized patients at various stages of dependency and willingness to quit.

Junctophilin-2 is necessary for T-tubule maturation during mouse heart development.

Aims: Transverse tubules (TTs) provide the basic subcellular structures that facilitate excitation-contraction (EC) coupling, the essential process that underlies normal cardiac contractility. Previous studies have shown that TTs develop within the first few weeks of life in mammals but the molecular determinants of this development have remained elusive. This study aims to elucidate the role of junctophilin-2 (JPH2), a junctional membrane complex protein, in the maturation of TTs in cardiomyocytes.

Pathogenesis of lethal cardiac arrhythmias in Mecp2 mutant mice: implication for therapy in Rett syndrome.

Rett syndrome is a neurodevelopmental disorder typically caused by mutations in methyl-CpG-binding protein 2 (MECP2) in which 26% of deaths are sudden and of unknown cause. To explore the hypothesis that these deaths may be due to cardiac dysfunction, we characterized the electrocardiograms in 379 people with Rett syndrome and found that 18.5% show prolongation of the corrected QT interval (QTc), an indication of a repolarization abnormality that can predispose to the development of an unstable fatal cardiac rhythm.