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Advanced Molecular Research on Chronic Heart Failure
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Advanced Molecular Research on Chronic Heart Failure

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 1 January 2026 | Viewed by 3280

Special Issue Editor

Dr. Marco Tana

E-Mail Website
Guest Editor
Internal Medicine and Cardiovascular Ultrasound Unit, SS. Annunziata Hospital of Chieti, 66100 Chieti, Italy
Interests: heart failure; atrial fibrillation; cardiovascular medicine; cardiology; ultrasound; internal medicine; chronic heart failure; clinical practice
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic heart failure (CHF) is a complex clinical syndrome characterized by the heart's incapacity to effectively pump blood throughout the body to fulfill its metabolic requirements. It remains a significant challenge in cardiovascular medicine, affecting millions worldwide. Despite advances in treatment, the complex molecular mechanisms underlying CHF require further elucidation to develop targeted therapies and improve patient outcomes.

Moreover, various studies have suggested that almost 30–70% of HF patients have heart failure with preserved ejection fraction (HF-pEF), a complex clinical syndrome which is becoming a widespread challenge for daily clinical practice. In particular, amyloid infiltration of the myocardium, also called cardiac amyloidosis (CA), which has previously been considered a rare pathology, actually seems to be underestimated, resulting in approximately 15% of patients with HF-pEF.

This Special Issue aims to gather research on advanced molecular approaches to understanding and managing the disease. Submissions should address the intersection of molecular research with clinical practice, aiming to drive the field of cardiovascular medicine toward a more effective management of CHF. Topics of interest include, but are not limited to, the molecular pathways implicated in the pathogenesis of CHF disease, novel molecular imaging techniques for assessing cardiac function in CHF, biomarkers for early detection and prognosis of CHF, translational approaches of molecular research, clinical practice in CHF management and novel pharmacological treatment. Finally, extended consideration of CA should be made, a current emerging challenge in daily clinical practice and one of the most frequent causes of heart failure with preserved ejection fraction.

Dr. Marco Tana
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • chronic heart failure (CHF)
  • cardiovascular medicine
  • cardiac amyloidosis
  • biomarkers
  • translational ap-proaches
  • molecular approaches
  • pharmacological treatment
  • molecular mechanisms
  • molecular pathways
  • prognosis
  • clinical practice in CHF management

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Published Papers (2 papers)

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Research

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27 pages, 3427 KiB  
Article
Trimethylamine N-Oxide as a Biomarker for Left Ventricular Diastolic Dysfunction and Functional Remodeling After STEMI
by Tsung-Ying Tsai, Ali Aldujeli, Ayman Haq, Paddy Murphy, Ramunas Unikas, Faisal Sharif, Scot Garg, Emmanouil S. Brilakis, Yoshinobu Onuma and Patrick W. Serruys
Int. J. Mol. Sci. 2025, 26(7), 3400; https://doi.org/10.3390/ijms26073400 - 5 Apr 2025
Viewed by 367
Abstract
Despite successful primary percutaneous coronary intervention (PPCI), the incidence of heart failure (HF) following ST-elevation myocardial infarction (STEMI) remains high. We investigated using Trimethylamine N-oxide (TMAO), a gut microbiota-derived biomarker, to predict adverse functional left ventricular (LV) remodeling (FLVR) and/or diastolic dysfunction (DD), [...] Read more.
Despite successful primary percutaneous coronary intervention (PPCI), the incidence of heart failure (HF) following ST-elevation myocardial infarction (STEMI) remains high. We investigated using Trimethylamine N-oxide (TMAO), a gut microbiota-derived biomarker, to predict adverse functional left ventricular (LV) remodeling (FLVR) and/or diastolic dysfunction (DD), which are precursors of HF post-STEMI. This prospective, observational study enrolled 204 STEMI patients with multivessel coronary artery disease after PPCI. TMAO level was collected at the baseline and 3 months. An echocardiography was performed at the baseline and at 12 months. The primary endpoints were the number of patients developing Group 4 FLVR or ≥Grade II DD at 12 months. The median age was 65 [57.00, 76.00] and 39.7% were women. The primary endpoints occurred in 47 (23.0%) patients. Three months of TMAO can discriminate patients with/without ≥Grade II LV DD and FLVR Grade 4 with areas under the curve (AUC) of the ROC of 0.72 (95% CI: 0.63–0.81; p < 0.001) and 0.77 (95% CI: 0.63–0.91), respectively. Similar results were shown in the validation cohort of 31 patients. The addition of 3 months of TMAO to traditional risk factors significantly improved the AUCs from 0.675 to 0.736 for ≥Grade II DD and from 0.793 to 0.873 for FLVR Grade 4. In multivariable logistic regression, 3 months of TMAO was independently associated with ≥Grade II DD (OR: 1.29 (1.13–1.50), p < 0.001) and FLVR Grade 4 (OR: 1.28 (1.12–1.47), p < 0.001). Three months of TMAO is strongly associated with LV DD and adverse remodeling after STEMI and may help identifying such patients for early treatment. Full article
(This article belongs to the Special Issue Advanced Molecular Research on Chronic Heart Failure)
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Review

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13 pages, 710 KiB  
Review
Heart Failure with Preserved Ejection Fraction and Cardiac Amyloidosis in the Aging Heart
by Marco Tana, Rachele Piccinini, Livia Moffa and Claudio Tana
Int. J. Mol. Sci. 2024, 25(21), 11519; https://doi.org/10.3390/ijms252111519 - 26 Oct 2024
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Abstract
Heart Failure with Preserved Ejection Fraction (HFpEF) is one of the most frequent causes of heart failure in the world’s population (about 19–55%), and is commonly associated with a high rate of hospitalization (almost 70–80%) and with increased mortality (40–50% in a 5-year [...] Read more.
Heart Failure with Preserved Ejection Fraction (HFpEF) is one of the most frequent causes of heart failure in the world’s population (about 19–55%), and is commonly associated with a high rate of hospitalization (almost 70–80%) and with increased mortality (40–50% in a 5-year timeframe). The elderly are more often affected, with higher rates of hospitalizations than young people, and currently almost 70% of the population aged 65 years old has HFpEF. An increase in cardiomyocyte stiffness, thus resulting in diastolic dysfunction, increased filling pressures and heart failure with preserved ejection fraction are characteristics features of the disease. In addition, among the various causes of HFpEF, cardiac amyloidosis (CA) can provoke diastolic dysfunction and increased wall stiffness directly from intercellular deposition of insoluble proteic substances and their toxic activity. Totally, almost 30 different proteins are able to form deposits, but the most frequently involved are transthyretin and misfolded monoclonal immunoglobulin light chains, which bring to two clinical conditions called transthyretin amyloidosis (ATTR) and light-chain amyloidosis (AL). Although there has been increasing attention on ATTR-CA in recent years, the actual prevalence remains underestimated, especially in people of advanced age, as well as its real impact as a cause of HFpEF, and only data derived from autoptic exams are currently available. Moreover, CA itself often mimics HFpEF, and some conflicting data on the use of predictive scores are described in the literature. The close relationship between HFpEF and CA, especially in older population and the main pathophysiological mechanisms which bond these two conditions are described in this focused review. The need to screen red flags for ATTR-CA in elderly patients with HFpEF is urgently advised, because a prompt recognition of the disease can optimize the approach to the disease with an early therapeutic, life-saving choice. Full article
(This article belongs to the Special Issue Advanced Molecular Research on Chronic Heart Failure)
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