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Acute and Chronic Heart Failure: Pathophysiology and New Therapeutic Developments,...
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Acute and Chronic Heart Failure: Pathophysiology and New Therapeutic Developments, 3rd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 July 2026 | Viewed by 4134

Editors

Dr. Serafino Fazio

E-Mail Website
Guest Editor
Department of Internal Medicine, School of Medicine, Federico II University, Via Sergio Pansini 5, 80135 Naples, Italy
Interests: hormones and heart; cardiac failure; insulin resistance; hyperinsulinism; metabolic syndrome; nutraceuticals; pulmonary arterial hypertension; COVID-19
Special Issues, Collections and Topics in MDPI journals
Dr. Valentina Mercurio

E-Mail Website
Guest Editor
Department of Translational Medical Sciences, Federico II University, Naples, Italy
Interests: heart failure; echocardiography; right ventricular function; pulmonary vascular disease; pulmonary arterial hypertension; cardio-oncology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Despite the considerable progress in the prevention and treatment of heart disease, heart failure is still a particularly important cause of recurring hospitalizations, with relevant social and healthcare costs, and it is burdened with significant mortality. Notably, while advances in the treatment of acute coronary syndromes with myocardial revascularization and the increased awareness in the management of cardiovascular risk factors have improved the survival of patients with ischemic heart disease, there has been a progressive increase in the number of patients with chronic heart failure.

Heart failure can result from alterations in both the left and right ventricles, which can be not only due to ischemic heart disease but also to other causes, such as valvular abnormalities, systemic hypertension, and pulmonary vascular disease. It is also noteworthy, not only for treatment purposes, to highlight the recent increase in the incidence of heart failure with reduced ejection fraction and that with preserved ejection fraction. Lately, there has also been an effort to improve the follow-up of patients with heart failure through telemedicine to reduce the number of hospital admissions and, thus, possibly, social and healthcare costs.

Therefore, we consider “Heart Failure” an extremely up-to-date and broad topic for which a Special Issue is relevant.

Dr. Serafino Fazio
Dr. Valentina Mercurio
Guest Editors

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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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly 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 failure with reduced ejection fraction
  • heart failure with preserved ejection fraction
  • pathophysiological novelties
  • treatment advances
  • pulmonary arterial hypertension
  • at-home follow-up of patients with heart failure

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Published Papers (5 papers)

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Research

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12 pages, 839 KB  
Article
Inflammation-Based C-Reactive Protein-to-Albumin Ratio for No-Reflow Prediction in STEMI
by Xhevdet Krasniqi, Altinë Spanca, Gresa Gojani, Josip Vincelj, Blerim Berisha and Aurora Bakalli
Biomedicines 2026, 14(6), 1383; https://doi.org/10.3390/biomedicines14061383 - 18 Jun 2026
Viewed by 270
Abstract
Background: The C-reactive protein/albumin ratio (CAR) has increasingly attracted attention as a reliable predictive marker in patients with acute myocardial infarction (AMI). Purpose: This study aimed to evaluate the predictive value of the CAR for no-reflow development. Methods: A total of 201 patients [...] Read more.
Background: The C-reactive protein/albumin ratio (CAR) has increasingly attracted attention as a reliable predictive marker in patients with acute myocardial infarction (AMI). Purpose: This study aimed to evaluate the predictive value of the CAR for no-reflow development. Methods: A total of 201 patients with STEMI who underwent PCI were included in the study. Admission laboratory tests included CRP, albumin, CK, CK-MB, troponin T, and other biochemical parameters. The CAR was calculated as CRP divided by albumin ×100, while the CUAR was calculated as the base-10 logarithm of CRP × UA divided by albumin. Patients were then divided into two groups based on CAR levels. Results: A total of 201 STEMI patients were included: 106 (52.7%) in the low-CAR group (≤48.4) and 95 (47.3%) in the high-CAR group (>48.4). Significant differences between groups were observed for smoking, albumin, cholesterol, CRP, CUAR, and TIMI flow grade ≤ 2. Logistic regression analysis identified albumin, cholesterol, CRP, BUN, uric acid, CK-MB, CAR, and CUAR as significant predictors of TIMI flow grade. A receiver operating characteristic (ROC) curve of CRP, albumin, CAR, and CUAR was used to plot the true positive rate against the false positive rate across various cut-off points; the area under the curve (AUC) was 0.87 (95% CI, 0.81–0.94, p < 0.0001) for CRP, 0.73 (95% CI, 0.65–0.81, p < 0.0001) for albumin, 0.9 (95% CI, 0.84–0.95, p < 0.0001) for the CAR, and 0.94 (95%, 0.89–0.99, p < 0.0001) for the CUAR. The cut-off values were 2.11 for the CUAR, 48.4 for the CAR, 18 for CRP, and 38 for albumin. Conclusions: The ratio of C-reactive protein to albumin (CAR) may serve as a reliable and clinically accessible marker associated with the no-reflow phenomenon in STEMI patients undergoing PCI. A defined CAR cut-off has been proposed to help stratify patients at increased risk of no-reflow. Full article
(This article belongs to the Special Issue Acute and Chronic Heart Failure: Pathophysiology and New Therapeutic Developments, 3rd Edition)
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13 pages, 3129 KB  
Article
Simvastatin Attenuates Doxorubicin-Induced Inflammation in Human Cardiomyocytes
by Roberta Vitale, Rosaria Margherita Rispoli, Maria Carmela Di Marcantonio, Barbara Pala, Stefania Marzocco, Gabriella Mincione and Ada Popolo
Biomedicines 2026, 14(5), 1071; https://doi.org/10.3390/biomedicines14051071 - 8 May 2026
Viewed by 890
Abstract
Background/Objectives: Clinical application of Doxorubicin (Doxo) is limited by cardiotoxicity, a process strongly associated with an interplay between oxidative stress and inflammatory signaling, particularly Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and Nucleotide oligomerization domain-like receptor family, pyrin domain containing [...] Read more.
Background/Objectives: Clinical application of Doxorubicin (Doxo) is limited by cardiotoxicity, a process strongly associated with an interplay between oxidative stress and inflammatory signaling, particularly Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and Nucleotide oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome engagement. Identifying strategies capable of mitigating these interconnected pathways is of critical importance in cardio-oncology. Simvastatin (SIM) is a promising option since it modulates oxidative stress, inflammation, and cell death through its pleiotropic effects, so this study aimed to evaluate whether SIM attenuates Doxo-induced inflammatory responses. Methods: Human Cardiomyocyte (HCM) cells were pre-treated with SIM (10 µM) for 4 h and then co-exposed to SIM and Doxo (1 µM) for 20 h. Cytofluorimetric analysis was used to evaluate inducible nitric oxide synthase (iNOS), Connexin 43 (Cx43), and Cx43 phosphorylated at Serine 368 (pS368Cx43) levels. Real-time qPCR was performed to evaluate iNOS gene expression, while Nitric oxide (NO) release was evaluated by spectrophotometric analysis. Interleukin (IL)-1β, IL-18, IL-6, tumor necrosis factor alpha (TNF-α) production, and NLRP3 levels were evaluated by means of ELISA assay. Expression levels of inhibitor of nuclear factor kappa B alpha (IκB-α), Caspase-1, and Gasdermin D (GSDMD) were evaluated by Western Blot analysis. Nuclear translocation of NF-κB was evaluated by immunofluorescence assay. Results: In our experimental model, SIM significantly (p < 0.01) reduced Doxo-induced nitrite release, as well as iNOS gene expression (p < 0.05) and protein levels (p < 0.01). SIM also markedly attenuated Doxo-induced NF-κB signaling, pro-inflammatory cytokines production (TNF-α and IL-6, p < 0.01), and inflammosome-related responses (cleaved caspase-1, IL-1β, N-terminal domain of GSDMD), and NLRP3 expression p < 0.05). Additionally, SIM significantly attenuated the overexpression of Cx43 and its phosphorylated form (pS368Cx43), which are responsible for impairing intercellular communication and electrical coupling in cardiomyocytes and contribute to arrhythmias and conduction abnormalities characteristic of acute Doxo-induced cardiotoxicity. Conclusions: Overall, these findings demonstrate that SIM exerts a multifaceted cardioprotective effect against Doxo-induced injury, thereby targeting interconnected inflammatory and pro-arrhythmic pathways implicated in Doxo cardiotoxicity. Full article
(This article belongs to the Special Issue Acute and Chronic Heart Failure: Pathophysiology and New Therapeutic Developments, 3rd Edition)
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30 pages, 85587 KB  
Article
Ferroptosis in Septic Cardiomyopathy Is Alleviated by Ondansetron: The Critical Role of the HTR3A-ATF3 Axis in Mitochondrial and Oxidative Homeostasis
by Xinyun Wang, Yangyi Lin, Wei Liu, Yufeng Wu, Boshen Yang, Yiming Qi, Yipeng Zhang, Yuanyuan Jin, Yuanlong Wang, Kaifan Niu and Xian Jin
Biomedicines 2026, 14(5), 1040; https://doi.org/10.3390/biomedicines14051040 - 3 May 2026
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Abstract
Background: Emerging evidence has established ferroptosis as a vital factor in the pathogenesis of cardiovascular diseases, especially in septic cardiomyopathy (SCM). Meanwhile, ondansetron (OND), a well-established 5-HT3 receptor antagonist, has gained increasing attention for its pleiotropic effects. However, its potential to modulate ferroptosis [...] Read more.
Background: Emerging evidence has established ferroptosis as a vital factor in the pathogenesis of cardiovascular diseases, especially in septic cardiomyopathy (SCM). Meanwhile, ondansetron (OND), a well-established 5-HT3 receptor antagonist, has gained increasing attention for its pleiotropic effects. However, its potential to modulate ferroptosis in the cardiovascular field remains unexplored. This study aims to fill this gap by exploring the potential of OND as an innovative therapeutic intervention for SCM. Methods: This study utilized both in vitro and in vivo models of septic cardiomyopathy (SCM), which was induced by lipopolysaccharide (LPS) stimulation in neonatal rat cardiomyocytes (NRCMs) and C57BL/6 mice. Through RNA sequencing, as well as molecular and functional assessments—including echocardiography and ferroptosis-related measurements—we revealed the anti-ferroptotic effect of ondansetron (OND). Mechanistically, ATF3 was identified as a pivotal regulator, with its overexpression via AAV9 in vivo and ADV in vitro confirming its role in OND-induced cardioprotection. Results: Ondansetron (OND) showed potent anti-ferroptotic effects in both cellular and murine models of septic cardiomyopathy (SCM). Treatment with OND not only improved cardiac performance but also reduced ferroptotic markers, mitigated lipid peroxidation and iron overload, and bolstered antioxidant defense. Notably, OND administration attenuated oxidative and endoplasmic reticulum (ER) stress while restoring mitochondrial integrity. Mechanistically, the anti-ferroptotic activity of OND was mediated through the HTR3A/ATF3 axis: ATF3 overexpression negated OND’s protective effects, while HTR3A antagonism with VUF10166 recapitulated its benefits. Conversely, HTR3A agonism with PBG attenuated ferroptosis resistance, further implicating this pathway as central to OND’s mechanism. Conclusions: This study demonstrated a novel pharmacological role for ondansetron (OND) in attenuating ferroptosis in septic cardiomyopathy (SCM) via the HTR3A/ATF3 signaling pathway. This finding delineates a novel therapeutic avenue and supports the repurposing of OND beyond its traditional antiemetic use to cardiovascular applications. Full article
(This article belongs to the Special Issue Acute and Chronic Heart Failure: Pathophysiology and New Therapeutic Developments, 3rd Edition)
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9 pages, 363 KB  
Article
Progressive Aortic Regurgitation After Impella Bridge-to-LVAD: A Two-Year Cohort Analysis
by Attila Nemeth, Aron Frederik Popov, Rodrigo Sandoval Boburg, Spiros Lukas Marinos, Helene Häberle, Christoph Salewski, Volker Steger, Christian Schlensak and Medhat Radwan
Biomedicines 2026, 14(3), 715; https://doi.org/10.3390/biomedicines14030715 - 19 Mar 2026
Viewed by 792
Abstract
Background/Objectives: Impella support is increasingly utilized as a crucial bridge to durable left ventricular assist device (LVAD) in patients with refractory cardiogenic shock. However, the transvalvular path of the Impella catheter raises concerns regarding mechanical trauma, potentially precipitating or accelerating aortic regurgitation [...] Read more.
Background/Objectives: Impella support is increasingly utilized as a crucial bridge to durable left ventricular assist device (LVAD) in patients with refractory cardiogenic shock. However, the transvalvular path of the Impella catheter raises concerns regarding mechanical trauma, potentially precipitating or accelerating aortic regurgitation (AR). We aimed to characterize the complete longitudinal trajectory of AR following Impella bridge-to-LVAD and to determine its association with clinical and hemodynamic sequelae. Methods: We conducted a single-center retrospective cohort study including all patients bridged from Impella to durable LVAD between 2013 and 2024 (n = 19). At Impella initiation, all patients met the retrospective SCAI shock stage D or worse criteria. At LVAD implantation, all patients were classified as INTERMACS 1–2 (INTERMACS 2, n = 13). The Impella models were 5.0 in 11 (axillary access), 2.5 in 5 (femoral access), and CP in 3 (femoral access); no periprocedural Impella complications were recorded. The implanted LVAD systems were HeartMate II (n = 7), HVAD (n = 3), and HeartMate III (n = 9). Patients undergoing concomitant aortic valve intervention were excluded. Transthoracic/TEE echocardiography was performed at prespecified time points (pre-Impella, pre-LVAD, post-LVAD discharge, 12 months, and 24 months) with standardized aortic regurgitation (AR) grading. Right ventricular (RV) function was assessed qualitatively when quantitative indices (TAPSE) were unavailable. Primary endpoints were new or progressive AR and AR severity at LVAD implantation. Secondary endpoints included survival, renal dysfunction, biomarkers, and rehospitalization. Univariate analyses were used to compare outcomes according to AR severity. Results: Nineteen patients (68% male, median age 57 years, IQR 47–60) underwent Impella support for 13.3 ± 9.9 days before HeartMate 3 (84%) or HVAD (16%) implantation. All patients had competent aortic valves (grade 0 AR) at the time of LVAD implantation. AR ≥ mild developed in 9/18 (50%) at discharge, 12/15 (80%) at 12 months, and 13/15 (87%) at 24 months, and 8/15 (53%) progressed to ≥ moderate AR by 24 months. Patients with moderate-to-severe AR had higher NT-proBNP levels at 12 months (median 6318 vs. 2336 pg/mL, p = 0.137). Thirty-day and 24-month survival rates were 95% and 79%, respectively. Conclusions: Aortic regurgitation frequently develops or progresses from the pre-LVAD period to follow-up in patients bridged from Impella to durable LVAD. Although limited by a small sample size and incomplete quantitative RV metrics, these observations support structured echocardiographic surveillance after Impella use and management strategies—routine valve inspection at LVAD implantation and post-LVAD speed/blood pressure targets that encourage aortic valve opening—to mitigate the risk and clinical impact of aortic regurgitation. Full article
(This article belongs to the Special Issue Acute and Chronic Heart Failure: Pathophysiology and New Therapeutic Developments, 3rd Edition)
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19 pages, 12935 KB  
Review
Across Clinical Profiles of Cardiorenal–Metabolic (CKM) Syndrome: A Phenotype-Driven Therapeutic Approach
by Irene Carlino, Sonia Di Franco, Nicola Colalillo, Stefania Bisogno, Luigi Gennari and Alberto Palazzuoli
Biomedicines 2026, 14(6), 1289; https://doi.org/10.3390/biomedicines14061289 - 5 Jun 2026
Viewed by 435
Abstract
Cardiorenal–metabolic (CKM) syndrome has emerged as a unifying condition describing the interplay between metabolic dysfunction, chronic kidney disease, and cardiovascular disease. To address this concept, the American Heart Association, in a 2023 Presidential Advisory, presented an official statement to capture the transition from [...] Read more.
Cardiorenal–metabolic (CKM) syndrome has emerged as a unifying condition describing the interplay between metabolic dysfunction, chronic kidney disease, and cardiovascular disease. To address this concept, the American Heart Association, in a 2023 Presidential Advisory, presented an official statement to capture the transition from metabolic risk and subtle cardiorenal dysfunction to overt cardiovascular and renal disease. Although this framework provides a structured representation of disease burden and facilitates risk stratification, emerging evidence suggests that it is primarily focused on the progressive nature, whereas high-risk patients may experience sudden cardiac or renal events. While staging systems provide important tools for risk stratification, they remain primarily descriptive and do not adequately reflect the dynamic and non-linear interactions underlying disease progression. Importantly, patients exhibit substantial heterogeneity in dominant pathophysiological drivers, related to various baseline risk factors and primitive cardio–kidney disorders, that is not fully captured by stage-based classifications. Notably, we propose a phenotype-oriented approach to CKM syndrome based on the recognition that its clinical expression reflects heterogeneous and evolving pathophysiological mechanisms rather than a uniform disease trajectory. According to this strategy, the paradigm of management shifts from an evolutive concept to a more appropriate use of disease modifying agents with cross-organ effects. Sodium–glucose cotransporter-2 inhibitors (SGLT2i), glucagon-like peptide-1 receptor agonists (GLP-1a), and non-steroidal mineralocorticoid receptor antagonists (MRA) have demonstrated the ability to modulate key biological pathways across the cardiovascular, renal, and metabolic axes. Therefore, personalized management that identifies a specific strategy according to CKM phenotypes must be assessed. Full article
(This article belongs to the Special Issue Acute and Chronic Heart Failure: Pathophysiology and New Therapeutic Developments, 3rd Edition)
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