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Special Issue "(Cardio-)Vascular System in Health and Disease: Current Update and Perspectives—Volume II"

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

Deadline for manuscript submissions: 31 December 2023 | Viewed by 1618

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Prof. Dr. Nandu Goswami

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Division of Physiology, Otto Loewi Research Center for Vascular Biology, Immunology and Inflammation, Medical University of Graz, Auenbruggerpl. 2, 8036 Graz, Austria
Interests: cardiovascular system; heart rate variability; gravitational adaptation
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Dear Colleagues,

We are thrilled to announce the release of the second volume of our Special Issue, "(Cardio-)Vascular System in Health and Disease: Current Update and Perspectives—Volume II". As we all know, cardiovascular disease is a major public health concern and a leading cause of death worldwide. Therefore, we have assembled a diverse collection of research articles that explore this system from a variety of perspectives, including pathogenesis, diagnosis, treatment, and prevention of cardiovascular disease.

This Special Issue features contributions from esteemed scholars and researchers from around the world, whose work represents a broad range of disciplines and approaches. Our contributors have provided unique perspectives on the latest research in the field, which offers valuable insights into the current understanding of cardiovascular disease and its management.

In this volume, we have included articles that discuss current trends in the management of cardiovascular disease, including the use of novel therapies and approaches to prevention. We have also included articles that explore the pathogenesis of the cardiovascular disease, providing insights into the underlying mechanisms of the disease and potential new targets for therapy.

It is worth noting that this Special Issue is a continuation of the successful first volume, which saw nearly 30 articles published on the topic. We are confident that this second volume will continue to advance the field of cardiovascular research and provide valuable insights to practitioners, scholars, and researchers alike.

We invite you to visit our website to access the first volume of our Special Issue, which is available at the following link:

https://www.mdpi.com/journal/jcm/topical_collections/cardiovascular_system_health_disease.

Thank you for your continued support of our Special Issue. We look forward to your contributions to future volumes and to the ongoing advancement of cardiovascular research.

Prof. Dr. Nandu Goswami
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

heart rate
blood pressure
autonomic function
orthostatic intolerance
tilt table
preeclampsia
sex
children
older adults
coagulation

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(Cardio-)Vascular System in Health and Disease: Current Update and Perspectives in Journal of Clinical Medicine (26 articles)

Published Papers (3 papers)

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Research

Open AccessArticle

The Mechanism of Effort Intolerance in Patients with Peripheral Arterial Disease: A Combined Stress Echocardiography and Cardiopulmonary Exercise Test

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J. Clin. Med. 2023, 12(18), 5817; https://doi.org/10.3390/jcm12185817 - 07 Sep 2023

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Abstract

Aim: We used a combined stress echocardiography and cardiopulmonary exercise test (CPET) to explore effort intolerance in peripheral arterial disease (PAD) patients. Methods: Twenty-three patients who had both PAD and coronary artery disease (CAD) were compared with twenty-four sex- and age-matched CAD patients and fifteen normal controls using a symptom-limited ramp bicycle CPET on a tilting dedicated ergometer. Echocardiographic images were obtained concurrently with gas exchange measurements along predefined stages of exercise. Oxygen extraction was calculated using the Fick equation at each activity level. Results: Along the stages of exercise (unloaded; anaerobic threshold; peak), in PAD + CAD patients compared with CAD or controls, diastolic function worsened (p = 0.051 and p = 0.013, respectively), and oxygen consumption (p < 0.001 and p < 0.001, respectively) and oxygen pulse (p = 0.0024 and p = 0.0027, respectively) were reduced. Notably, oxygen pulse was blunted due to an insufficient increase in both stroke volume (p = 0.025 and p = 0.028, respectively) and peripheral oxygen extraction (p = 0.031 and p = 0.038, respectively). Chronotropic incompetence was more prevalent in PAD patients and persisted after correction for beta-blocker use (62% vs. 42% and 11%, respectively). Conclusions: In PAD patients, exercise limitation is associated with diastolic dysfunction, chronotropic incompetence and peripheral factors. Full article

(This article belongs to the Special Issue (Cardio-)Vascular System in Health and Disease: Current Update and Perspectives—Volume II)

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Open AccessArticle

Defining Peri-Operative Myocardial Injury during Cardiac Surgery Using High-Sensitivity Troponin T

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J. Clin. Med. 2023, 12(13), 4291; https://doi.org/10.3390/jcm12134291 - 26 Jun 2023

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Objective: Cut-offs for high-sensitivity troponin (hs-Tn) elevations to define prognostically significant peri-operative myocardial injury (PMI) in cardiac surgery is not well-established. We evaluated the associations between peri-operative high-sensitivity troponin T (hs-TnT) elevations and 1-year all-cause mortality in patients undergoing cardiac surgery. Methods: The prognostic significance of baseline hs-TnT and various thresholds for post-operative hs-TnT elevation at different time-points on 1-year all-cause mortality following cardiac surgery were assessed after adjusting for baseline hs-TnT and EuroSCORE in a post-hoc analysis of the ERICCA trial. Results: 1206 patients met the inclusion criteria. Baseline elevation in hs-TnT >x1 99th percentile upper reference limit (URL) was significantly associated with 1-year all-cause mortality (adjusted hazard ratio 1.90, 95% confidence interval 1.15–3.13). In the subgroup with normal baseline hs-TnT (n = 517), elevation in hs-TnT at all post-operative time points was associated with higher 1-year mortality, reaching statistical significance for elevations above: ≥100 × URL at 6 h; ≥50 × URL at 12 and 24 h; ≥35 × URL at 48 h; and ≥30 × URL at 72 h post-surgery. Elevation in hs-TnT at 24 h ≥ 50 × URL had the optimal sensitivity and specificity (73% and 75% respectively). When the whole cohort of patients was analysed, including those with abnormal baseline hs-TnT (up to 10 × URL), the same threshold had optimal sensitivity and specificity (66% and 70%). Conclusions: Both baseline and post-operative hs-TnT elevations are independently associated with 1-year all-cause mortality in patients undergoing cardiac surgery. The optimal threshold to define a prognostically significant PMI in our study was ≥50 × URL elevation in hs-TnT at 24 h. Full article

(This article belongs to the Special Issue (Cardio-)Vascular System in Health and Disease: Current Update and Perspectives—Volume II)

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Open AccessArticle

Deep Vein Thrombosis Is Facilitated by Endothelial-Derived Extracellular Vesicles via the PDI–GRP94–GPIIb/IIIa Pathway in Mice

and

J. Clin. Med. 2023, 12(13), 4265; https://doi.org/10.3390/jcm12134265 - 26 Jun 2023

Viewed by 714

Abstract

Aims: Deep vein thrombosis (DVT) is a prevalent cardiovascular condition. Endothelial-derived extracellular vesicles (EVs) may play a crucial role in platelet-dependent DVT development via platelet activation, but the mechanism is not clear yet. This research aims to understand how platelets and endothelial-derived EVs work in DVT. Methods: The interaction between protein disulfide isomerase (PDI) and glucose-regulated protein 94 (GRP94) was founded by molecular docking. Inferior vena cava stasis–induced mice received PDI and GRP94 inhibitor treatments. Platelet activation, endothelial-derived EVs, and PDI were measured using flow cytometry. The expression of PDI and dimetric GRP94 in platelets co-cultured with hypoxic endothelial cells was confirmed by Western blot or native PAGE. The fluorescence resonance energy transfer assay shows conformational changes in GPIIb/IIIa on platelet surfaces. A tracking experiment was performed using PKH26, which labelled endothelial-derived EVs, and the endocytosis of EVs by platelets was tracked by confocal microscope. Results: In a DVT mouse model, platelets enhance venous thrombus formation in a coagulation-independent manner, instead, platelet activation and the length of the thrombus are related to PDI and GRP94 activity. Next, we found that the expression level of endothelial-derived EVs carrying PDI is significantly increased in plasma. Endothelial-derived EVs carrying PDI are endocytosed by platelets, in which the content of GRP94 dimer is elevated, and consequently increases the expression of surface GPIIb/IIIa. In addition, PDI allosterically interacts with GPIIb/IIIa, which is re-configurated into an activated form. Conclusion: Endothelial-derived EVs carrying PDI induce DVT via interplay with GRP94 and GPIIb/IIIa in platelets. These findings emphasize the significance of platelets in DVT formation, and PDI may be a suitable target in DVT prevention. Full article

(This article belongs to the Special Issue (Cardio-)Vascular System in Health and Disease: Current Update and Perspectives—Volume II)

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Special Issue "(Cardio-)Vascular System in Health and Disease: Current Update and Perspectives—Volume II"

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