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Endothelial Dysfunction—Clinical Implications of Novel Findings
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Endothelial Dysfunction—Clinical Implications of Novel Findings

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

Deadline for manuscript submissions: closed (20 November 2021) | Viewed by 6436

Special Issue Editors

Prof. Dr. Andrzej Surdacki

E-Mail Website
Guest Editor
Second Department of Cardiology, Jagiellonian University Medical College, 2 Jakubowskiego Street, 30-688 Krakow, Poland
Interests: endothelial dysfunction; nitric oxide; asymmetric dimethylarginine; homoarginine; coronary artery disease; atherogenesis; nontraditional cardiovascular risk factors; chronic kidney disease; cardionephrology; metabolic syndrome; insulin resistance; cardiodiabetology; cardiooncology; adult childhood cancer survivors; cardiorheumatology; echocardiography; aortic valve stenosis; myocardial hemodynamics; left ventricular hypertrophy; diastolic dysfunction; heart failure with preserved ejection fraction; arterial compliance; platelet reactivity; antiplatelet drugs; proton pump inhibitors
Special Issues, Collections and Topics in MDPI journals
Dr. Olga Kruszelnicka

E-Mail Website
Guest Editor
Department of Coronary Artery Disease and Heart Failure, Jagiellonian University Medical College, 80 Prądnicka Street, 31-202 Cracow, Poland
Interests: endothelium dysfunction in 2 type diabetes; coronary artery disease and valvular disease
Special Issues, Collections and Topics in MDPI journals
Dr. Bernadeta Chyrchel

E-Mail Website
Guest Editor
Second Department of Cardiology, Jagiellonian University Medical College, 2 Jakubowskiego Street, 30-688 Cracow, Poland
Interests: clinical cardiology; echocardiography; aortic valve disease; left ventricular hypertrophy; cardiac hemodynamics; heart failure; systemic arterial compliance; platelet reactivity; antiplatelet drugs; endothelial dysfunction; biomarkers; atherogenesis; coronary artery disease

Special Issue Information

Dear Colleagues,

Endothelial mediators modulate multiple interwoven regulatory pathways implicated in the development and outcome of cardiovascular diseases. Endothelial dysfunction is not only an antecedent of atherosclerotic plaques in large and medium-sized arteries, but also affects coronary microvessels, thereby predisposing to left ventricular (LV) constrictive remodeling and diastolic dysfunction, well-recognized predecessors of heart failure with preserved ejection fraction. Further, nitric oxide regulates myocardial energy metabolism and reduced cardiac mechanical energetic efficiency frequently accompanies hypertension, obesity and diabetes, common cardiovascular risk factors. Additionally, endothelial dysfunction enhances large artery stiffening, which increases LV afterload and may accelerate symptom onset in patients with coexistent coronary artery disease, subclinical LV damage or aortic valve disease. Endothelial dysfunction was also linked to future deterioration of glucose tolerance and progressive renal function decline which – in turn – can lead to a subsequent rise in the risk of major adverse cardiovascular events. Moreover, endothelial effects may contribute to clinical benefits of cardiovascular drugs. Notably, the blockade of platelet P2Y12 receptors strongly potentiates antiplatelet effects of key endothelial mediators, nitric oxide and prostacyclin.

With this Special Issue, we would like to encourage submissions of original articles and reviews focused on potential clinical implications of novel findings in the field of endothelial function and related cardiovascular regulatory mechanisms.

We look forward to receiving your submission.

Prof. Dr. Andrzej Surdacki
Dr. Olga Kruszelnicka
Dr. Bernadeta Chyrchel
Guest Editors

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

  • endothelial dysfunction
  • cardiovascular remodeling
  • heart failure
  • cardiac hemodynamics
  • systemic arterial compliance
  • atherogenesis
  • metabolic diseases
  • insulin resistance
  • chronic kidney disease
  • aortic valve disease
  • ischemic heart disease
  • antiplatelet drugs

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Published Papers (3 papers)

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Research

12 pages, 877 KiB  
Article
8-Isoprostanes and Asymmetric Dimethylarginine as Predictors of Mortality in Patients Following Coronary Bypass Surgery: A Long-Term Follow-Up Study
by Aleksandra Gołąb, Dariusz Plicner, Anna Rzucidło-Hymczak, Lidia Tomkiewicz-Pająk, Bogusław Gawęda, Bogusław Kapelak and Anetta Undas
J. Clin. Med. 2022, 11(1), 246; https://doi.org/10.3390/jcm11010246 - 4 Jan 2022
Cited by 3 | Viewed by 1474
Abstract
Background: We previously demonstrated that enhanced oxidative stress and reduced nitric oxide bioavailability are associated with unfavorable outcomes early after coronary artery bypass grafting. It is not known whether these processes may impact long-term results. We sought to assess whether during long-term follow-up, [...] Read more.
Background: We previously demonstrated that enhanced oxidative stress and reduced nitric oxide bioavailability are associated with unfavorable outcomes early after coronary artery bypass grafting. It is not known whether these processes may impact long-term results. We sought to assess whether during long-term follow-up, markers of oxidative stress and nitric oxide bioavailability may predict cardiovascular mortality following bypass surgery. Methods: We studied 152 consecutive patients (118 men, age 65.2 ± 8.3 years) who underwent elective, primary, isolated on-pump bypass surgery. We measured plasma 8-iso-prostaglandin F2α and asymmetric dimethylarginine before surgery and twice after surgery (18–36 h and 5–7 days). We assessed all-cause and cardiovascular death in relation to these two biomarkers during a mean follow-up time of 11.7 years. Results: The overall mortality was 44.7% (4.7 per 100 patient-years) and cardiovascular mortality was 21.0% (2.2 per 100 patient-years). Baseline 8-iso-prostaglandin F2α was associated with cardiovascular mortality (HR 1 pg/mL 1.010, 95% CI 1.001–1.021, p = 0.036) with the optimal cut-off ≤ 364 pg/mL for higher survival rate (HR 0.460, 95% CI 0.224–0.942, p = 0.030). Asymmetric dimethylarginine > 1.01 μmol/L measured 18–36 h after surgery also predicted cardiovascular death (HR 2.467, 95% CI 1.140–5.340, p = 0.020). Additionally, elevated 8-iso-prostaglandin F2α measured at the same time point associated with all-cause mortality (HR 1 pg/mL 1.007, 95% CI 1.000–1.014, p = 0.048). Conclusions: Our findings indicate that in advanced coronary disease, increased oxidative stress, reflected by 8-iso-prostaglandin F2α before bypass surgery and enhanced asymmetric dimethylarginine accumulation just after the surgery are associated with cardiovascular death during long-term follow-up Full article
(This article belongs to the Special Issue Endothelial Dysfunction—Clinical Implications of Novel Findings)
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13 pages, 548 KiB  
Article
Properties of Plasma Clots in Adult Patients Following Fontan Procedure: Relation to Clot Permeability and Lysis Time—Multicenter Study
by Maciej Skubera, Aleksandra Gołąb, Dariusz Plicner, Joanna Natorska, Michał Ząbczyk, Olga Trojnarska, Anna Mazurek-Kula, Monika Smaś-Suska, Agnieszka Bartczak-Rutkowska, Piotr Podolec and Lidia Tomkiewicz-Pająk
J. Clin. Med. 2021, 10(24), 5976; https://doi.org/10.3390/jcm10245976 - 20 Dec 2021
Cited by 5 | Viewed by 2109
Abstract
Objectives: thromboembolic complications are a major cause of morbidity and mortality following Fontan (FO) surgery. It is also well established that altered FO circulation results in systemic complications, including liver and endothelium damage. We sought to evaluate whether dysfunctions of these sources of [...] Read more.
Objectives: thromboembolic complications are a major cause of morbidity and mortality following Fontan (FO) surgery. It is also well established that altered FO circulation results in systemic complications, including liver and endothelium damage. We sought to evaluate whether dysfunctions of these sources of hemostatic factors may result in changes of fibrin clot properties. Methods: a permeation coefficient (Ks) and clot lysis time (CLT) were assessed in 66 FO patients, aged 23.0 years [IQR 19.3–27.0], and 59 controls, aged 24.0 years [IQR 19.0–29.0]. Ks was determined using a pressure-driven system. CLT value was measured according to assay described by Pieters et al. Endothelium and liver-derived hemostatic factors along with liver function parameters were evaluated. The median time between FO operation and investigation was 20.5 years [IQR 16.3–22.0]. Results: FO patients had lower Ks (p = 0.005) and prolonged CLT (p < 0.001) compared to that of controls. Ks correlated with CLT (r = −0.28), FVIII (r = −0.30), FIX (r = −0.38), fibrinogen (r = −0.41), ALT (r = −0.25), AST (r = −0.26), GGTP (r = −0.27) and vWF antigen (r = −0.30), (all p < 0.05). CLT correlated with the time between FO operation and investigation (r = 0.29) and FIX (r = 0.25), (all p < 0.05). After adjustment for potential cofounders, TAFI antigen and GGTP were independent predictors of reduced Ks (OR 1.041 per 1% increase, 95% CI 1.009–1.081, p = 0.011 and OR 1.025 per 1 U/L increase, 95% CI 1.005–1.053, p = 0.033, respectively). Protein C and LDL cholesterol predicted prolonged CLT (OR 1.078 per 1% increase, 95% CI 1.027–1.153, p = 0.001 and OR 6.360 per 1 μmol/L increase, 95% CI 1.492–39.894, p = 0.011, respectively). Whereas elevated tPA was associated with lower risk of prolonged CLT (OR 0.550 per 1 ng/mL, 95% CI 0.314–0.854, p = 0.004). GGTP correlated positively with time between FO surgery and investigation (r = 0.25, p = 0.045) and patients with abnormal elevated GGTP activity (n = 28, 42.4%) had decreased Ks, compared to that of the others (5.9 × 10−9 cm2 vs. 6.8 × 10−9 cm2, p = 0.042). Conclusion: our study shows that cellular liver damage and endothelial injury were associated with prothrombotic clot phenotype reflected by Ks and CLT. Full article
(This article belongs to the Special Issue Endothelial Dysfunction—Clinical Implications of Novel Findings)
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12 pages, 2062 KiB  
Article
Effect of Hyperbaric Oxygenation on Blood Cytokines and Arginine Derivatives; No Evidence for Induction of Inflammation or Endothelial Injury
by Jacek Siewiera, Michał Smoleński, Natalia Jermakow, Jacek Kot, Klaudia Brodaczewska, Jacek Turyn, Magdalena A. Zabielska-Kaczorowska, Nils Ludwig and Mirosław J. Szczepański
J. Clin. Med. 2021, 10(23), 5488; https://doi.org/10.3390/jcm10235488 - 23 Nov 2021
Cited by 1 | Viewed by 2144
Abstract
(1) Background: Hyperbaric oxygen therapy (HBOT) uses 100% oxygen delivered at 1.5–3 times the atmospheric pressure in a specialised chamber to achieve supraphysiological oxygen tension in blood and tissues. Besides its target, HBOT may affect inflammation, endothelial function or angiogenesis. This study analysed [...] Read more.
(1) Background: Hyperbaric oxygen therapy (HBOT) uses 100% oxygen delivered at 1.5–3 times the atmospheric pressure in a specialised chamber to achieve supraphysiological oxygen tension in blood and tissues. Besides its target, HBOT may affect inflammation, endothelial function or angiogenesis. This study analysed the effect of HBOT on blood concentrations of factors that may affect these processes in patients with necrotizing soft-tissue infections (NSTI), aseptic bone necrosis (ABN) and idiopathic sudden sensory neural hearing loss (ISSNHL). (2) Methods: Concentrations asymmetric dimethylarginine (ADMA) and other arginine derivatives were measured with liquid chromatography/mass spectrometry, whereas ELISA was used to quantitate vascular endothelial growth factor (VEGF) and cytokines (IL-1, IL-4, IL-6, IL-10, TGF-β) before and after HBOT in 80 patients (NSTI n = 21, ISSNHL n = 53, ABN n = 6). (3) Results: While some differences were noted between patient groups in ADMA and other arginine derivatives as well as in cytokine concentrations, HBOT did not affect any of these parameters. (4) Conclusions: While cytokines and arginine derivatives concentrations were modified by underlying pathology, hyperbaric oxygenation did not immediately modify it suggesting that it is neutral for inflammation and is not inducing endothelial injury. Full article
(This article belongs to the Special Issue Endothelial Dysfunction—Clinical Implications of Novel Findings)
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