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Cells
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Understanding Biomarkers in Cardiology Volume II
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Understanding Biomarkers in Cardiology Volume II

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (21 October 2023) | Viewed by 7947

Special Issue Editors

Prof. Dr. Stephan Von Haehling

E-Mail Website
Guest Editor
Department of Cardiology & Pneumology, Universitätsmedizin Göttingen, D-37099 Göttingen, Germany
Interests: heart failure; comorbidities; biomarkers; pharmacotherapy; exercise capacity; quality of life
Special Issues, Collections and Topics in MDPI journals
Dr. Tania Garfias-Veitl

E-Mail Website
Guest Editor
Mathematisches Institut, Bunsenstraße 3-5, 37073 Göttingen, Germany
Interests: biostatistics; mathematics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Cardiovascular diseases are a major cause of mortality worldwide, causing more than 17 million deaths each year. Heart failure alone is affecting an estimated 26 million people worldwide. Biomarker support allows for prompt and accurate help in diagnosis and prognosis in several clinical settings in cardiology. For example, the diagnosis of heart failure with preserved ejection fraction requires additional findings beyond morphological signs of structural heart disease; in particular, elevated levels of B natriuretic peptides. The ruling-out of acute myocardial infarction is one of the major challenges in emergency departments. Electrocardiography and cardiac troponin form the standard diagnostic tools in approaching patients with suspected acute coronary syndrome, even though novel biomarker strategies may help in reaching a clinical decision faster than using troponin or in reaching prognostic assessments. Novel assays are steadily developed, improving the sensitivity, as in the case of N terminals pro BNP and high-sensitivity cardiac troponin. 

The first Special Issue showed the importance of a deeper comprehension of this topic. Accordingly, this second Special Issue aims to publish novel data from biomarker research in the broadest sense in populations of interest in cardiology, from coronary disease to cardio-oncology and heart failure over to genetic disorders and systemic diseases such as amyloidosis. We invite all scientists working on biomarkers in cardiology to participate in this Special Issue.

Prof. Dr. Stephan Von Haehling
Dr. Tania Garfias-Veitl
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. Cells 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 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

  • cardiology
  • biomarker
  • heart failure
  • acute coronary syndrome
  • acute myocardial infarction
  • cardiotoxicity

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Published Papers (4 papers)

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14 pages, 2909 KiB  
Article
CILP-1 Is a Biomarker for Backward Failure and Right Ventricular Dysfunction in HFrEF
by Annika Weidenhammer, Suriya Prausmüller, Clemens Partsch, Georg Spinka, Bianca Luckerbauer, Mirella Larch, Henrike Arfsten, Ramy Abdel Mawgoud, Philipp E. Bartko, Georg Goliasch, Stefan Kastl, Christian Hengstenberg, Martin Hülsmann and Noemi Pavo
Cells 2023, 12(24), 2832; https://doi.org/10.3390/cells12242832 - 13 Dec 2023
Cited by 2 | Viewed by 1263
Abstract
Background: CILP-1 regulates myocardial fibrotic response and remodeling and was reported to indicate right ventricular dysfunction (RVD) in pulmonary hypertension (PH) and heart failure (HF). This study examines CILP-1 as a potential biomarker for RVD and prognosis in heart failure with reduced ejection [...] Read more.
Background: CILP-1 regulates myocardial fibrotic response and remodeling and was reported to indicate right ventricular dysfunction (RVD) in pulmonary hypertension (PH) and heart failure (HF). This study examines CILP-1 as a potential biomarker for RVD and prognosis in heart failure with reduced ejection fraction (HFrEF) patients on guideline-directed medical therapy. Methods: CILP-1 levels were measured in 610 HFrEF patients from a prospective registry with biobanking (2016–2022). Correlations with echocardiographic and hemodynamic data and its association with RVD and prognosis were analyzed. Results: The median age was 62 years (Q1–Q3: 52–72), 77.7% of patients were male, and the median NT-proBNP was 1810 pg/mL (Q1–Q3: 712–3962). CILP-1 levels increased with HF severity, as indicated by NT-proBNP and NYHA class (p < 0.0001, for both). CILP-1 showed a weak–moderate direct association with increased left ventricular filling pressures and its sequalae, i.e., backward failure (LA diameter rs = 0.15, p = 0.001; sPAP rs = 0.28, p = 0.010; RVF rs = 0.218, p < 0.0001), but not with cardiac index (CI) and systemic vascular resistance (SVR). CILP-1 trended as a risk factor for all-cause mortality (crude HR for 500 pg/mL increase: 1.03 (95%CI: 1.00–1.06), p = 0.053) but lost significance when it was adjusted for NT-proBNP (adj. HR: 1.00 (95%CI: 1.00–1.00), p = 0.770). No association with cardiovascular hospitalization was observed. Conclusions: CILP-1 correlates with HFrEF severity and may indicate an elevated risk for all-cause mortality, though it is not independent from NT-proBNP. Increased CILP-1 is associated with backward failure and RVD rather than forward failure. Whether CILP-1 release in this context is based on elevated pulmonary pressures or is specific to RVD needs to be further investigated. Full article
(This article belongs to the Special Issue Understanding Biomarkers in Cardiology Volume II)
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12 pages, 2031 KiB  
Article
The Interleukin 6 Protein Level as well as a Genetic Variants, (rs1800795, rs1800797) Are Associated with Adverse Cardiovascular Outcomes within 10-Years Follow-Up
by Susanne Schulz, Selina Rehm, Axel Schlitt, Kerstin Bitter and Stefan Reichert
Cells 2023, 12(23), 2722; https://doi.org/10.3390/cells12232722 - 28 Nov 2023
Viewed by 1163
Abstract
Background: Worldwide, cardiovascular disease (CVD) is the leading cause of premature death. The proinflammatory cytokine interleukin 6 (IL-6) is a essential marker of innate immunity that is considered to play an important proatherogenic role for cardiovascular disease. The aim of this study (substudy [...] Read more.
Background: Worldwide, cardiovascular disease (CVD) is the leading cause of premature death. The proinflammatory cytokine interleukin 6 (IL-6) is a essential marker of innate immunity that is considered to play an important proatherogenic role for cardiovascular disease. The aim of this study (substudy of ClinTrials.gov identifier: NCT01045070) was to evaluate IL-6 protein level and genetic variants (rs1800795, rs1800797) with respect to CV outcome (combined endpoint: myocardial infarction, stroke/transient ischemic attack, cardiac death, death according to stroke) among patients CVD within 10-years follow-up. Material and methods: Overall 1002 in-patients with CVD were included. IL-6 protein level was determined by electrochemiluminescence immunoassay (fasting, between 7 and 8 a.m.). Genetic analyses were carried out by single specific primer-polymerase chain reaction. Results: In survival analyses, IL-6 protein levels of ≥6.4 pg/mL (log-rank test: p = 0.034; cox regression: p = 0.032, hazard ratio = 1.29) and CC genotype of rs1800795 (log-rank test: p < 0.001, cox regression: p < 0.001, hazard ratio = 1.72) and AA genotype of rs180797 (log-rank test: p = 0.002, cox regression: p < 0.001, hazard ratio = 1.62) were associated with a poorer CV prognosis considering combined CV endpoint. Conclusion: This study was the first to investigate both elevated IL-6 levels and genetic variants for their prognostic value for adverse CV outcomes in CVD patients within the 10-year follow-up period. Full article
(This article belongs to the Special Issue Understanding Biomarkers in Cardiology Volume II)
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13 pages, 1762 KiB  
Article
Role of Copeptin and hs-cTnT to Discriminate AHF from Uncomplicated NSTE-ACS with Baseline Elevated hs-cTnT—A Derivation and External Validation Study
by Stephan von Haehling, Matthias Müller-Hennessen, Tania Garfias-Veitl, Alina Goßling, Johannes T. Neumann, Nils A. Sörensen, Paul M. Haller, Tau Hartikainen, Jörn Ole Vollert, Martin Möckel, Stefan Blankenberg, Dirk Westermann and Evangelos Giannitsis
Cells 2023, 12(7), 1062; https://doi.org/10.3390/cells12071062 - 31 Mar 2023
Viewed by 1632
Abstract
Background: In light of overlapping symptoms, discrimination between non-ST-elevation (NSTE) acute coronary syndrome (ACS) and acute heart failure (HF) is challenging, particularly in patients with equivocal clinical presentation for suspected ACS. We sought to evaluate the diagnostic and prognostic properties of copeptin in [...] Read more.
Background: In light of overlapping symptoms, discrimination between non-ST-elevation (NSTE) acute coronary syndrome (ACS) and acute heart failure (HF) is challenging, particularly in patients with equivocal clinical presentation for suspected ACS. We sought to evaluate the diagnostic and prognostic properties of copeptin in this scenario. Methods: Data from 1088 patients from a single-center observational registry were used to test the ability of serial high sensitivity cardiac troponin T (hs-cTnT)—compared to copeptin, or a combination of copeptin with hs-cTnT—to discriminate acute HF from uncomplicated non-ST-elevation myocardial infarction (NSTEMI) and to evaluate all-cause mortality after 365 days. Patients with STEMI, those with unstable angina and either normal or undetectable hs-cTnT concentrations were excluded. The findings were validated in an independent external NSTE-ACS cohort. Results: A total of 219 patients were included in the analysis. The final diagnosis was acute HF in 56 and NSTE-ACS in 163, with NSTEMI in 78 and unstable angina having stable elevation of hs-cTnT >ULN in 85. The rate of all-cause death at 1 year was 9.6% and occurred significantly more often in acute HF than in NSTE-ACS (15 vs. 6%, p < 0.001). In the test cohort, the area under the receiver operator curve (AUC) for the discrimination of acute HF vs. NSTE-ACS without HF was 0.725 (95% confidence interval [CI] 0.625–0.798) for copeptin and significantly higher than for hs-cTnT at 0 h (AUC = 0.460, 0.370–0.550) or at 3 h (AUC = 0.441, 0.343–0.538). Copeptin and hs-cTnT used either as continuous values or at cutoffs optimized to yield 90% specificity for acute HF were associated with significantly higher age- and sex-adjusted risk for all-cause mortality at 365 days. The findings from the test cohort were consistently replicated in the independent external NSTE-ACS validation cohort. Conclusions: High concentrations of copeptin in patients with suspected NSTE-ACS and equivocal clinical presentation suggest the presence of acute HF compared to uncomplicated NSTE-ACS and are associated with higher rates of all-cause death at 365 days. Full article
(This article belongs to the Special Issue Understanding Biomarkers in Cardiology Volume II)
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Review

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22 pages, 1773 KiB  
Review
Cellular, Molecular and Clinical Aspects of Aortic Aneurysm—Vascular Physiology and Pathophysiology
by Dominika Domagała, Krzysztof Data, Hubert Szyller, Maryam Farzaneh, Paul Mozdziak, Sławomir Woźniak, Maciej Zabel, Piotr Dzięgiel and Bartosz Kempisty
Cells 2024, 13(3), 274; https://doi.org/10.3390/cells13030274 - 1 Feb 2024
Cited by 4 | Viewed by 3475
Abstract
A disturbance of the structure of the aortic wall results in the formation of aortic aneurysm, which is characterized by a significant bulge on the vessel surface that may have consequences, such as distention and finally rupture. Abdominal aortic aneurysm (AAA) is a [...] Read more.
A disturbance of the structure of the aortic wall results in the formation of aortic aneurysm, which is characterized by a significant bulge on the vessel surface that may have consequences, such as distention and finally rupture. Abdominal aortic aneurysm (AAA) is a major pathological condition because it affects approximately 8% of elderly men and 1.5% of elderly women. The pathogenesis of AAA involves multiple interlocking mechanisms, including inflammation, immune cell activation, protein degradation and cellular malalignments. The expression of inflammatory factors, such as cytokines and chemokines, induce the infiltration of inflammatory cells into the wall of the aorta, including macrophages, natural killer cells (NK cells) and T and B lymphocytes. Protein degradation occurs with a high expression not only of matrix metalloproteinases (MMPs) but also of neutrophil gelatinase-associated lipocalin (NGAL), interferon gamma (IFN-γ) and chymases. The loss of extracellular matrix (ECM) due to cell apoptosis and phenotype switching reduces tissue density and may contribute to AAA. It is important to consider the key mechanisms of initiating and promoting AAA to achieve better preventative and therapeutic outcomes. Full article
(This article belongs to the Special Issue Understanding Biomarkers in Cardiology Volume II)
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