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Cardiac Arrhythmias in Autoimmune Diseases
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Cardiac Arrhythmias in Autoimmune Diseases

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Cardiology".

Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 23960

Special Issue Editor

Dr. Krzysztof Kaczmarek

E-Mail Website
Guest Editor
Department of Electrocardiology, Central University Hospital, Medical University of Lodz, Lodz, Poland
Interests: cardiac arrhythmias; invasive cardiology; catheter ablation; cardiac implantable electronic devices

Special Issue Information

Dear Colleagues,

I have the great pleasure and honor to announce this Special Issue on “Cardiac Arrhythmias in Autoimmune Diseases”. Autoimmune diseases are often complicated with cardiovascular disorders predominantly cardiomyopathies and/or cardiac arrhythmias. Pathophysiological mechanisms underlying the rhythm disorders concomitant to autoimmune disease mostly include myocardial inflammation and fibrosis. Additionally, antibody-mediated and drug-induced arrhythmias, as well as inflammatory impairment of the autonomic nervous system, are to be taken into consideration. For arrhythmic patients suffering from autoimmunological diseases, the dynamically developing novel pharmacotherapy of autoimmune disorders and augmented facilities for invasive cardiac electrophysiology are changing the landscape of therapeutic management. The reduction of the risk of cardiac fibrosis through contemporary rheumatological therapy might prevent the development of arrhythmia substrates. However, if arrhythmia does occur, there are many possibilities to treat dysrhythmia with advanced electrophysiological techniques.

Therefore, this Special Issue on “Cardiac Arrhythmias in Autoimmune Diseases” will demonstrate contemporary research in this interesting field that requires a broad interdisciplinary perspective. Scientific papers containing evidence on actual arrhythmic problems of patients with autoimmune disorders, especially therapeutic solutions, are of the utmost interest. We are very much looking forward to receiving your original research and review articles.

Dr. Krzysztof Kaczmarek
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • autoimmune disease
  • connective-tissue disease
  • immunosuppression
  • monoclonal antibody
  • arrhythmia
  • tachycardia
  • catheter ablation
  • cardiac pacemaker
  • implantable cardioverter-defibrillator

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Published Papers (2 papers)

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Research

15 pages, 2977 KiB  
Article
Inflammatory Biomarkers in Postural Orthostatic Tachycardia Syndrome with Elevated G-Protein-Coupled Receptor Autoantibodies
by William T. Gunning III, Stanislaw M. Stepkowski, Paula M. Kramer, Beverly L. Karabin and Blair P. Grubb
J. Clin. Med. 2021, 10(4), 623; https://doi.org/10.3390/jcm10040623 - 6 Feb 2021
Cited by 24 | Viewed by 19598
Abstract
A growing body of evidence suggests that postural orthostatic tachycardia syndrome (POTS) may be an autoimmune disorder. We have reported in a previous manuscript that 89% of POTS patients (n = 55) had elevations in G-protein-coupled adrenergic A1 receptor autoantibodies and 53% [...] Read more.
A growing body of evidence suggests that postural orthostatic tachycardia syndrome (POTS) may be an autoimmune disorder. We have reported in a previous manuscript that 89% of POTS patients (n = 55) had elevations in G-protein-coupled adrenergic A1 receptor autoantibodies and 53% had elevations in muscarinic acetylcholine M4 receptor autoantibodies, as assessed by ELISA. Patients with autoimmune disorders have been reported with a variety of elevated cytokines and cytokines (such as rheumatoid arthritis); thus, we evaluated a limited number of cytokines/chemokines in POTS patients with elevated adrenergic and muscarinic receptor autoantibodies. We utilized the plasma of 34 patients from a previous study; all of the patients (100%) had autoantibodies against the A1 adrenergic receptor and 55.9% (19/34) had autoantibodies against the M4 muscarinic acetylcholine receptor. In particular, the plasma cytokine/chemokine levels were measured as biomarkers of inflammation by Quantibody® technology (Raybiotech, Peachtree Corners, GA, USA). We also evaluated the platelet dense granule numbers, as these patients frequently complain of symptoms related to platelet dysfunction. Patients were predominantly young females who displayed a multitude of co-morbidities but generally reported viral-like symptoms preceding episodes of syncope. Eighty five percent (29/34) had platelet storage pool deficiency. Patients had elevations in five of ten cytokine/chemokines biomarkers (IL1β, IL21, TNFα, INFγ, and CD30), whereas two biomarkers had decreased levels (CD40L and RANTES). Our observations demonstrate that POTS patients known to have autoantibodies against the G-protein-coupled adrenergic A1 receptor have abnormal plasma concentrations of inflammatory cytokines. Full article
(This article belongs to the Special Issue Cardiac Arrhythmias in Autoimmune Diseases)
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15 pages, 2075 KiB  
Article
Left Ventricular Contraction Duration Is the Most Powerful Predictor of Cardiac Events in LQTS: A Systematic Review and Meta-Analysis
by Mena Abdelsayed, Ibadete Bytyçi, Annika Rydberg and Michael Y. Henein
J. Clin. Med. 2020, 9(9), 2820; https://doi.org/10.3390/jcm9092820 - 31 Aug 2020
Cited by 4 | Viewed by 3881
Abstract
Background: Long-QT syndrome (LQTS) is primarily an electrical disorder characterized by a prolonged myocardial action potential. The delay in cardiac repolarization leads to electromechanical (EM) abnormalities, which adds a diagnostic value for LQTS. Prolonged left ventricular (LV) contraction was identified as a potential [...] Read more.
Background: Long-QT syndrome (LQTS) is primarily an electrical disorder characterized by a prolonged myocardial action potential. The delay in cardiac repolarization leads to electromechanical (EM) abnormalities, which adds a diagnostic value for LQTS. Prolonged left ventricular (LV) contraction was identified as a potential risk for arrhythmia. The aim of this meta-analysis was to assess the best predictor of all EM parameters for cardiac events (CEs) in LQTS patients. Methods: We systematically searched all electronic databases up to March 2020, to select studies that assessed the relationship between echocardiographic indices—contraction duration (CD), mechanical dispersion (MD), QRS onset to peak systolic strain (QAoC), and the EM window (EMW); and electrical indices— corrected QT interval (QTC), QTC dispersion, RR interval in relation to CEs in LQTS. This meta-analysis included a total of 1041 patients and 373 controls recruited from 12 studies. Results: The meta-analysis showed that LQTS patients had electrical and mechanical abnormalities as compared to controls—QTC, WMD 72.8; QTC dispersion, WMD 31.7; RR interval, WMD 91.5; CD, WMD 49.2; MD, WMD 15.9; QAoC, WMD 27.8; and EMW, WMD −62.4. These mechanical abnormalities were more profound in symptomatic compared to asymptomatic patients in whom disturbances were already manifest, compared to controls. A CD ≥430 ms had a summary sensitivity (SS) of 71%, specificity of 84%, and diagnostic odds ratio (DOR) >19.5 in predicting CEs. EMW and QTC had a lower accuracy. Conclusions: LQTS is associated with pronounced EM abnormalities, particularly prolonged LV myocardial CD, which is profound in symptomatic patients. These findings highlight the significant role of EM indices like CD in managing LQTS patients. Full article
(This article belongs to the Special Issue Cardiac Arrhythmias in Autoimmune Diseases)
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