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Cardiovascular Diseases: Biomarker-Guided Therapy and Clinical Management
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Cardiovascular Diseases: Biomarker-Guided Therapy and Clinical Management

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

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 3426

Special Issue Editors

Dr. Jianmin Yang

E-Mail Website
Guest Editor
Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China
Interests: molecular mechanism and intervention target of cardiovascular remodeling
Dr. Chuanbao Li

E-Mail Website
Guest Editor
Department of Emergency Medicine, Qilu Hospital of Shandong University, Jinan 250012, China
Interests: basic and clinical study of acute and critical cardiovascular disease including acute myocardial infarction, valvular heart disease, heart failure, aortic dissection and arrhythmia
Dr. Weidong Qin

E-Mail Website
Guest Editor
Department of Critical Care Medicine, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250012, China
Interests: basic research in the inflammation and immunity, and the pathogenesis of vascular diseases, such as atherosclerosis and abdominal aortic aneurysm

Special Issue Information

Dear Colleagues,

We invite you to participate in this Special Issue of JCM on “Cardiovascular Diseases: Biomarker-Guided Therapy and Clinical Management”. As is well-known, despite ongoing advances in prevention, diagnosis and treatment, cardiovascular disease (CVD) is the leading cause of death worldwide. Thus, it is necessary to find sensitive and specific biomarkers to promote early diagnostic and prognostic evaluation of CVD. Several biomarkers have been investigated as potential predictors of CVD, such as CRP, troponin and BNP. Numerous other biomarkers pertaining to diagnosis, prognosis, and risk prediction have been identified, but few have been used in clinical practice. In this Special Issue of JCM, we aim to better interpret the role of currently available biomarkers and discover other candidate biomarkers. Both original research papers and comprehensive review papers in the following areas are welcome:
1) The use of biomarkers in CVD severity.
2) The use of biomarkers for monitoring the progression of CVD.
3) The role of biomarkers in risk stratification.
4) The role of biomarkers in therapeutic management.
5) The use of biomarkers in postoperative outcome prediction.

Dr. Jianmin Yang
Dr. Chuanbao Li
Dr. Weidong Qin
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

  • cardiovascular disease
  • biomarker
  • therapy
  • risk stratification
  • diagnosis
  • prognosis

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Published Papers (2 papers)

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Research

16 pages, 711 KiB  
Article
Guideline-Optimised Treatment in Heart Failure—Do Higher Doses Reduce Systemic Inflammation More Significantly?
by Alexandru Mircea Arvunescu, Ruxandra Florentina Ionescu, Silviu Ionel Dumitrescu, Ondin Zaharia and Tiberiu Ioan Nanea
J. Clin. Med. 2024, 13(11), 3056; https://doi.org/10.3390/jcm13113056 - 23 May 2024
Cited by 2 | Viewed by 1477
Abstract
Background: Chronic inflammation is a constant phenomenon which accompanies the heart failure pathophysiology. In all phenotypes of heart failure, irrespective of the ejection fraction, there is a permanent low-grade activation and synthesis of proinflammatory cytokines. Many classes of anti-remodelling medication used in the [...] Read more.
Background: Chronic inflammation is a constant phenomenon which accompanies the heart failure pathophysiology. In all phenotypes of heart failure, irrespective of the ejection fraction, there is a permanent low-grade activation and synthesis of proinflammatory cytokines. Many classes of anti-remodelling medication used in the treatment of chronic heart failure have been postulated to have an anti-inflammatory effect. Methods: This retrospective study enrolled 220 patients and focused on evaluating the effect of the most used active substances from these classes in reducing the level of inflammatory biomarkers (C reactive protein, erythrocyte sedimentation rate and fibrinogen) after initiation or up-titration. Our research is evaluating if this anti-inflammatory effect intensifies while raising the dose. The evaluation was performed at two visits with an interval between them of 6 months. Results: From the beta-blockers class, carvedilol showed a reduction in erythrocyte sedimentation rate (ESR), in low (6.25 mg, bi daily) and medium (12.5 mg, bi daily) doses. At the same time, sacubitril/valsartan showed a reduction in CRP levels. This effect was obtained only in the medium (49/51 mg, bi daily) and high (97/103 mg, bi daily) doses, with the maximum reduction being observed in the high dose. Conclusions: From the classes of medication evaluated, the study showed a significant reduction in ESR levels in the low and medium doses of carvedilol and a reduction in CRP values in the cases of medium and high doses of ARNI. Full article
(This article belongs to the Special Issue Cardiovascular Diseases: Biomarker-Guided Therapy and Clinical Management)
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8 pages, 918 KiB  
Communication
Soluble Suppression of Tumorigenicity 2 (sST2) in Patients with Predominantly Decompensated Right Heart Failure—A Prospective Observational Study
by Victoria Dworok, Valentin Hähnel, Marwin Bannehr, Vera Paar, Christoph Edlinger, Michael Lichtenauer, Christian Butter and Anja Haase-Fielitz
J. Clin. Med. 2023, 12(23), 7200; https://doi.org/10.3390/jcm12237200 - 21 Nov 2023
Cited by 1 | Viewed by 1276
Abstract
Right heart failure is a major challenge in clinical practice. Soluble Suppression of Tumorigenicity-2 (sST2), a member of the interleukin-1-receptor family, may have clinical prognostic value. The aim of this study was to analyze whether sST2 correlates with signs of acute right heart [...] Read more.
Right heart failure is a major challenge in clinical practice. Soluble Suppression of Tumorigenicity-2 (sST2), a member of the interleukin-1-receptor family, may have clinical prognostic value. The aim of this study was to analyze whether sST2 correlates with signs of acute right heart decompensation. This prospective single-center study included 50 patients admitted for clinical signs of predominant right heart decompensation. Signs of reduced blood supply to other organs (e.g., renal function parameter, troponin T, NT-proBNP), diuretics, and signs of venous congestion (inferior vena cava (IVC) diameter) with fluid retention (weight gain, peripheral edema) resulting from reduced RV function were analyzed. The degree of peripheral edema was defined as none, mild (5–6 mm depressible, regression in 15–60 s) or severe (>7 mm depressible, regression in 2–3 min). sST2 levels were measured at the day of hospitalization. A total of 78.7% showed severe peripheral edema. The median concentration of sST2 was 35.2 ng/mL (25.–75. percentiles 17.2–46.7). sST2 is correlated with the peripheral edema degree (rSpearman = 0.427, p = 0.004) and the diameter of IVC (r = 0.786, p = 0.036), while NT-proBNP (r = 0.114, p = 0.456), troponin T (r = 0.123, p = 0.430), creatinine-based eGFR (r = −0.207, p = 0.195), or cystatin C-based eGFR (r = −0.032, p = 0.839) did not. sST2, but no other established marker, is correlated with peripheral and central fluid status in patients with decompensated right heart failure. Full article
(This article belongs to the Special Issue Cardiovascular Diseases: Biomarker-Guided Therapy and Clinical Management)
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