Cardiovascular Diseases: From Pathophysiology to Novel Therapeutic Approaches, 2nd 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 August 2026 | Viewed by 1439

Special Issue Editors

Special Issue Information

Dear Colleagues,

Despite the considerable progress made over recent decades in the treatment and prevention of cardiovascular diseases, they still remain the leading cause of hospitalizations and deaths in developed and developing countries. Hence, it is likely that we are missing something. We have therefore developed a Special Issue, entitled "Cardiovascular Diseases: From Pathophysiology to Novel Therapeutic Approaches, 2nd Edition", which addresses this problem in depth, collecting manuscripts that can contribute to the in-depth study of the topic and attempt to clarify what has been done and what can still be done to reduce the risks related to cardiovascular diseases, from both therapeutic and preventive point of views. For example, a condition that has considerable scientific literature to support it but is still rather neglected is insulin resistance with associated hyperinsulinemia. This condition, which in itself should already be considered an independent risk factor for the development of cardiovascular diseases, when elevated to a risk factor, is often treated only too late, namely when it transforms into type 2 diabetes mellitus. It is very likely that if we intervened earlier with screening and therapy, we could obtain a notable prognostic improvement.

Dr. Serafino Fazio
Dr. Valentina Mercurio
Guest Editors

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Keywords

  • cardiovascular diseases
  • heart failure
  • cardiac arrhythmias
  • metabolic syndrome
  • stroke
  • pulmonary hypertension
  • peripheral artery disease (PAD)
  • acute coronary syndrome
  • myocarditis
  • pericarditis
  • valvulopathies

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Published Papers (2 papers)

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Research

21 pages, 1284 KB  
Article
Disentangling Uric Acid and Renal Pathways in SGLT2 Inhibitor Effects After Acute Myocardial Infarction: A Retrospective Mediation Analysis
by Ioana Maria Suciu, Călin Muntean, Laura Gaiță, Teodora Mateoc-Sîrb, Daliborca Cristina Vlad, Bogdan Timar and Dan Gaiță
Biomedicines 2026, 14(4), 842; https://doi.org/10.3390/biomedicines14040842 - 7 Apr 2026
Viewed by 591
Abstract
Background/Objectives: Sodium–glucose cotransporter-2 (SGLT2) inhibitors have demonstrated cardiovascular benefits beyond glycemic control, yet the specific biological pathways potentially linking SGLT2 inhibitor exposure to cardiovascular outcomes after acute myocardial infarction (AMI) remain incompletely characterized. Two biologically plausible pathways, serum uric acid (SUA) reduction and [...] Read more.
Background/Objectives: Sodium–glucose cotransporter-2 (SGLT2) inhibitors have demonstrated cardiovascular benefits beyond glycemic control, yet the specific biological pathways potentially linking SGLT2 inhibitor exposure to cardiovascular outcomes after acute myocardial infarction (AMI) remain incompletely characterized. Two biologically plausible pathways, serum uric acid (SUA) reduction and renal functional preservation, have been proposed, but not directly compared in a unified analytical framework. This study aimed to explore whether associations between SGLT2 inhibitor exposure and recurrent post-AMI outcomes may be more strongly linked to SUA reduction and to renal functional changes, using a hypothesis-generating causal mediation analysis. Methods: This retrospective observational cohort study included 142 consecutive patients hospitalized for AMI who underwent percutaneous coronary intervention (PCI) during the index hospitalization, reflecting standard-of-care management for AMI in this tertiary center. Patients were categorized by SGLT2 inhibitor exposure (n = 57) vs. controls (n = 85). Both diabetic (47.2%) and non-diabetic (52.8%) patients were included. The primary endpoint was change in SUA (ΔUA); the secondary endpoint was myocardial infarction (MI) recurrence. Causal mediation analysis with nonparametric bootstrap simulation tested both mechanistic pathways. Results: SGLT2 inhibitor therapy was associated with significant SUA reduction (ΔUA = −0.99 mg/dL vs. +0.56 mg/dL in controls; p < 0.001), consistent across diabetic and non-diabetic subgroups and independent of AMI recurrence. Each 1 mg/dL decrease in SUA was associated with lower odds of recurrent MI in the initial model (β = −0.25; p = 0.041). However, after incorporation of renal functional change, the uric acid-mediated pathway lost significance (ACME p = 0.462), whereas the renal-mediated pathway remained significant (ACME p = 0.038). Serum creatinine change emerged as the strongest independent predictor of MI recurrence (β = 2.22; p = 0.015). Conclusions: The findings are more consistent with a renal-mediated pathway than with an independent uric acid-mediated pathway in explaining the observed associations between SGLT2 inhibitor exposure and recurrent post-AMI outcomes. These hypothesis-generating results from a retrospective design warrant prospective validation. Full article
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17 pages, 321 KB  
Article
Association of Genetic Polymorphisms with Ischemic Sudden Cardiac Death: A Comparative Case–Control Study in North-Western Transylvania (Romania)
by Daniela Cristina Pavel (Mironescu), Costel Siserman, Mihaela Laura Vică Matei, Gheorghe Zsolt Nicula, Ștefana Bâlici, Bogdan-Alexandru Gheban, Ioana-Andreea Gheban-Roșca, Alexandra Șonfălean, Denisa Jurje, Denisa Lucian, Andrei Marușca, Daniel-Corneliu Leucuța and Horea-Vladi Matei
Biomedicines 2026, 14(3), 618; https://doi.org/10.3390/biomedicines14030618 - 10 Mar 2026
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Abstract
Background/Objectives: Ischemic sudden cardiac death (SCD) is a devastating event that often occurs in apparently healthy individuals. Genetic susceptibility may play a key role in the pathogenesis of such ischemic events. This study aimed to investigate the correlations between Human Leukocyte Antigen [...] Read more.
Background/Objectives: Ischemic sudden cardiac death (SCD) is a devastating event that often occurs in apparently healthy individuals. Genetic susceptibility may play a key role in the pathogenesis of such ischemic events. This study aimed to investigate the correlations between Human Leukocyte Antigen (HLA) alleles, genotypes, and haplotypes and SCD to identify potential risk factors. This study also investigated three Single-Nucleotide Polymorphisms (SNPs) in the MYBPC3 gene and their association with SCD. Methods: We conducted an exploratory study between 2022 and 2024 in North-Western Transylvania (Romania) on 81 autopsy-confirmed SCD cases, compared with 162 controls for HLA typing, and with 96 controls for SNPs. HLA analysis of the HLA-DRB1 and HLA-DQB1 genes was performed using low-resolution SSP-PCR. The three SNPs in the MYBPC3 gene: rs142317339 (C > T), rs148808089 (G > A), and rs11570076 (G > A) were performed using a Real-Time PCR System. Results: The HLA-DRB1*07 allele has reduced odds of SCD, after adjustment for age and sex, and the HLA-DRB1*08 allele showed a trend toward increased odds. No statistically significant associations were detected at the allele or genotype level for HLA-DQB1. Haplotype-based analyses further revealed that genetic susceptibility is driven predominantly by low-frequency protective haplotypes rather than by common risk haplotypes, with several combinations conferring strong or moderate protection (HLA-DRB1*07~HLA-DQB1*03, HLA-DRB1*07~HLA-DQB1*02, and HLA-DRB1*15~HLA-DQB1*05). No statistically significant association was found between the three SNPs studied in the two groups, and their frequencies were very low. Conclusions: Specific HLA-DRB1 and HLA-DQB1 alleles and haplotypes may be associated with protection against SCD, supporting a possible immunogenetic role in SCD and the identification of genetic risk markers. Full article
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