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Identifying Mechanisms and Patterns in Cardiovascular Disease
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Identifying Mechanisms and Patterns in Cardiovascular Disease

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425). This special issue belongs to the section "Cardiovascular Clinical Research".

Deadline for manuscript submissions: closed (15 February 2024) | Viewed by 4946

Special Issue Editor

Prof. Dr. Craig Steven McLachlan

E-Mail Website
Guest Editor
Centre for Healthy Futures, Torrens University Australia, Surry Hills, NSW 2010, Australia
Interests: cardiac devices; cardiac hypertrophy; aortic stiffening; gene pathways; atrial fibrillation; ventricular tachycardia; HRV; COVID-19

Special Issue Information

Dear Colleagues,

Despite significant progress in the prevention and management of heart disease, there are always new emerging concepts, mechanistic understanding in atrial fibrillation, cardiomyopathy, cardiac hypertrophy, heart failure, and aortic and carotid stiffness. These new targets, biomarkers, or pathology processes may challenge or complement current or existing therapies. Future identification of device and therapeutic targets requires clinical insights as to how they may benefit the individual patient and align with current therapies. Holistically, we have rarely considered the immune system and its role in sustaining or driving cardiac disease. COVID has certainly been an interesting case for how immune dysregulation may also increase the burden of heart disease. This focused series considers emerging cardiovascular mechanistic pathways and associations, as well as how any newly identified target or mechanism of disease may fit into the realm of future clinical practice with particular emphasis on the individual patient.

Prof. Dr. Craig Steven McLachlan
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 Cardiovascular Development and Disease is an international peer-reviewed open access monthly 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 2700 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

  • COVID
  • atrial fibrillation
  • immune system
  • aortic stiffness
  • carotid stiffness
  • molecular targets
  • cardiac hypertrophy
  • bioengineering
  • medical devices
  • gene pathway analysis
  • heart failure

Published Papers (3 papers)

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Research

13 pages, 479 KiB  
Article
Changing Face of Inflammatory Activation in Complex Coronary Artery Disease during the COVID-19 Pandemic
by Tomasz Urbanowicz, Paweł Czub, Anna Olasińska-Wiśniewska, Michał Michalak, Zuzanna Fryska, Jakub Zieliński, Krzysztof Jerzy Filipiak, Krzysztof Wróbel, Andrzej Tykarski and Marek Jemielity
J. Cardiovasc. Dev. Dis. 2023, 10(5), 199; https://doi.org/10.3390/jcdd10050199 - 30 Apr 2023
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Abstract
Introduction: The COVID-19 pandemic has changed the immunological status of the population, indicating increased activation. The aim of the study was to compare the degree of inflammatory activation in patients admitted for surgical revascularization in the period before and during the COVID-19 pandemic. [...] Read more.
Introduction: The COVID-19 pandemic has changed the immunological status of the population, indicating increased activation. The aim of the study was to compare the degree of inflammatory activation in patients admitted for surgical revascularization in the period before and during the COVID-19 pandemic. Materials and methods: This retrospective analysis included an analysis of inflammatory activation assessed on the basis of whole blood counts in 533 patients (435 (82%) male and 98 (18%) female) with a median age of 66 (61–71) years who underwent surgical revascularization, including 343 and 190 patients operated on in 2018 and 2022, respectively. Results: The compared groups were matched by propensity score matching analysis, obtaining 190 patients in each group. Significantly higher values of preoperative monocyte count (p = 0.015), monocyte-to-lymphocyte ratio (p = 0.004) and systemic inflammatory response index (p = 0.022) were found in the during-COVID subgroup. The perioperative and 12-month mortality rates were comparable, with 1% (n = 4) in 2018 vs. 1% (n = 2) in 2022 (p = 0.911), and 5.6 % (n = 11 patients) vs. 7% (n = 13 patients) (p = 0.413), in the pre-COVID and during-COVID subgroups, respectively. Conclusions: Simple whole blood analysis in patients with complex coronary artery disease performed before and during the COVID-19 pandemic indicates excessive inflammatory activation. However, the immune variation did not interfere with one-year mortality rate after surgical revascularization. Full article
(This article belongs to the Special Issue Identifying Mechanisms and Patterns in Cardiovascular Disease)
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17 pages, 3764 KiB  
Article
Transcriptomic Comparison of Human Peripartum and Dilated Cardiomyopathy Identifies Differences in Key Disease Pathways
by Jude Taylor, Anna C. Y. Yeung, Anthony Ashton, Alen Faiz, Victor Guryev, Bernard Fang, Sean Lal, Mark Grosser, Cristobal G. dos Remedios, Filip Braet, Craig S. McLachlan and Amy Li
J. Cardiovasc. Dev. Dis. 2023, 10(5), 188; https://doi.org/10.3390/jcdd10050188 - 23 Apr 2023
Viewed by 1450
Abstract
Peripartum cardiomyopathy (PPCM) is a rare form of acute onset heart failure that presents in otherwise healthy pregnant women around the time of delivery. While most of these women respond to early intervention, about 20% progress to end-stage heart failure that symptomatically resembles [...] Read more.
Peripartum cardiomyopathy (PPCM) is a rare form of acute onset heart failure that presents in otherwise healthy pregnant women around the time of delivery. While most of these women respond to early intervention, about 20% progress to end-stage heart failure that symptomatically resembles dilated cardiomyopathy (DCM). In this study, we examined two independent RNAseq datasets from the left ventricle of end-stage PPCM patients and compared gene expression profiles to female DCM and non-failing donors. Differential gene expression, enrichment analysis and cellular deconvolution were performed to identify key processes in disease pathology. PPCM and DCM display similar enrichment in metabolic pathways and extracellular matrix remodeling suggesting these are similar processes across end-stage systolic heart failure. Genes involved in golgi vesicles biogenesis and budding were enriched in PPCM left ventricles compared to healthy donors but were not found in DCM. Furthermore, changes in immune cell populations are evident in PPCM but to a lesser extent compared to DCM, where the latter is associated with pronounced pro-inflammatory and cytotoxic T cell activity. This study reveals several pathways that are common to end-stage heart failure but also identifies potential targets of disease that may be unique to PPCM and DCM. Full article
(This article belongs to the Special Issue Identifying Mechanisms and Patterns in Cardiovascular Disease)
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10 pages, 267 KiB  
Article
Genetic Basis of Early Onset Atrial Fibrillation in Patients without Risk Factors
by Irina Rudaka, Baiba Vilne, Jekaterina Isakova, Oskars Kalejs, Linda Gailite and Dmitrijs Rots
J. Cardiovasc. Dev. Dis. 2023, 10(3), 104; https://doi.org/10.3390/jcdd10030104 - 28 Feb 2023
Viewed by 1611
Abstract
Background: Atrial fibrillation (AF) is the most common arrhythmia and typically occurs in elderly patients with other cardiovascular and extracardiac diseases. However, up to 15% of AF develops without any related risk factors. Recently, the role of genetic factors has been highlighted in [...] Read more.
Background: Atrial fibrillation (AF) is the most common arrhythmia and typically occurs in elderly patients with other cardiovascular and extracardiac diseases. However, up to 15% of AF develops without any related risk factors. Recently, the role of genetic factors has been highlighted in this particular form of AF. Aims: The aims of this study were to determine the prevalence of pathogenic variants in early-onset AF in patients without known disease-related risk factors and to identify any structural cardiac abnormalities in these patients. Materials and Methods: We conducted exome sequencing and interpretation in 54 risk factor-free early-onset AF patients and further validated our findings in a similar AF patient cohort from the UK Biobank. Results: Pathogenic/likely pathogenic variants were found in 13/54 (24%) patients. The variants were identified in cardiomyopathy-related and not arrhythmia-related genes. The majority of the identified variants were TTN gene truncating variants (TTNtvs) (9/13 (69%) patients). We also observed two TTNtvs founder variants in the analysed population—c.13696C>T p.(Gln4566Ter) and c.82240C>T p.(Arg27414Ter). Pathogenic/likely pathogenic variants were found in 9/107 (8%) individuals from an independent similar AF patient cohort from the UK Biobank. In correspondence with our Latvian patients, only variants in cardiomyopathy-associated genes were identified. In five (38%) of the thirteen Latvian patients with pathogenic/likely pathogenic variants, dilation of one or both ventricles was identified on a follow-up cardiac magnetic resonance scan. Conclusions: We observed a high prevalence of pathogenic/likely pathogenic variants in cardiomyopathy-associated genes in patients with risk factor-free early-onset AF. Moreover, our follow-up imaging data indicate that these types of patients are at risk of developing ventricular dilation. Furthermore, we identified two TTNtvs founder variants in our Latvian study population. Full article
(This article belongs to the Special Issue Identifying Mechanisms and Patterns in Cardiovascular Disease)
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