The Challenges and Therapeutic Prospects in Cardiovascular Disease

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Mechanisms of Diseases".

Deadline for manuscript submissions: closed (20 February 2025) | Viewed by 3414

Special Issue Editor


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Guest Editor
Department of ProMISE, University Hospital Paolo Giaccone, University of Palermo, Palermo, Italy
Interests: cardiovascular disease; coronary artery disease; coronary microvascular dysfunction; percutaneous coronary intervention; cardiovascular prevention; hypercholesterolemia
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Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVD) are a leading global cause of mortality and are primarily driven by atherosclerotic coronary artery disease. Their pathogenesis involves multi-factorial mechanisms, among which coronary artery disease plays a causative role. Cardiology represents an area of highly innovative medicine based on new diagnostic strategies, new therapies, and cutting-edge pharmacological and interventional technologies. Today, pathologies such as heart failure, arterial hypertension, and hypercholesterolemia have increasingly effective therapies. This Special Issue aims to provide an overview of the latest challenges in diagnosis and new therapeutic prospects in cardiovascular disease.

In this Special Issue, we welcome original research and review articles regarding new challenges and therapies for cardiovascular diseases.

Dr. Vincenzo Sucato
Guest Editor

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Keywords

  • cardiovascular disease
  • coronary artery disease
  • coronary microvascular dysfunction
  • percutaneous coronary intervention
  • cardiomyopathy
  • cardiovascular prevention
  • heart failure
  • hypercholesterolemia
  • residual cardiovascular risk
  • cardioncology

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Published Papers (2 papers)

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Research

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12 pages, 519 KiB  
Article
Effect of Flecainide in Idiopathic Premature Ventricular Contractions and the Induced Cardiomyopathy—UNIFLECA: A Single Arm, Non-Randomized Trial: Review of the Literature and Initial Results
by Sotirios Kotoulas, Dimitrios Tsiachris, Michail Botis, Athanasios Kordalis, Dimitrios Varvarousis, Georgios Leventopoulos, Eleftherios Kallergis, Ioannis Doundoulakis, Leonidas E. Poulimenos and Konstantinos Tsioufis
J. Pers. Med. 2025, 15(4), 132; https://doi.org/10.3390/jpm15040132 - 29 Mar 2025
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Abstract
Background/Objectives: Persistent high Premature Ventricular Contraction (PVC) burden (>10%) may result in PVC-induced cardiomyopathy. Current guidelines, supported by limited evidence, recommend flecainide for PVCs originating from the ventricular outflow tract (Class IIa). UNIFLECA is a prospective cohort study, aiming to assess the [...] Read more.
Background/Objectives: Persistent high Premature Ventricular Contraction (PVC) burden (>10%) may result in PVC-induced cardiomyopathy. Current guidelines, supported by limited evidence, recommend flecainide for PVCs originating from the ventricular outflow tract (Class IIa). UNIFLECA is a prospective cohort study, aiming to assess the efficacy and safety of flecainide in PVC burden reduction in adults, irrespective of PVC origin, focusing secondarily on symptom relief and improvement of left ventricular ejection fraction (LVEF) in patients suffering from PVC-induced cardiomyopathy. Methods: Participants were adults with frequent PVCs, defined as PVC burden > 5%, confirmed by two 24 h Holter recordings taken at least one month apart, who denied catheter ablation treatment. Patients who were deemed ineligible for catheter ablation were also included. A total of 50 patients were screened and 35 were administered Flecainide, with dosage adjustment based on follow-up Holter results and QRS increases. Changes in PVC burden, LVEF, symptomatic status, along with treatment adherence, were evaluated. Results: In adults with frequent PVCs, flecainide led to a significant reduction in PVC burden, with a mean decrease of 76.2% in the first month, and 63.1% of patients achieving a PVC burden reduction greater than 80%. Conclusions: UNIFLECA contributes to the understanding of how personalized, non-interventional therapeutic modalities can be employed to manage PVCs, especially for patients unwilling to have or ineligible for ablation procedures. Full article
(This article belongs to the Special Issue The Challenges and Therapeutic Prospects in Cardiovascular Disease)
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Review

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10 pages, 726 KiB  
Review
Dysfunctional High-Density Lipoprotein Cholesterol and Coronary Artery Disease: A Narrative Review
by Cristina Madaudo, Giada Bono, Antonella Ortello, Giuseppe Astuti, Giulia Mingoia, Alfredo Ruggero Galassi and Vincenzo Sucato
J. Pers. Med. 2024, 14(9), 996; https://doi.org/10.3390/jpm14090996 - 19 Sep 2024
Cited by 3 | Viewed by 2304
Abstract
High-density lipoprotein (HDL) cholesterol is traditionally viewed as protective against cardiovascular disease (CVD). However, emerging evidence reveals that dysfunctional HDL, characterized by impaired reverse cholesterol transport (RCT), reduced anti-inflammatory and antioxidant activities and increased endothelial dysfunction, which can contribute to coronary artery disease [...] Read more.
High-density lipoprotein (HDL) cholesterol is traditionally viewed as protective against cardiovascular disease (CVD). However, emerging evidence reveals that dysfunctional HDL, characterized by impaired reverse cholesterol transport (RCT), reduced anti-inflammatory and antioxidant activities and increased endothelial dysfunction, which can contribute to coronary artery disease (CAD). Dysfunctional HDL, resulting from oxidative modifications of Apolipoprotein A-1 (Apo A-1) and enzyme inactivation, fails to effectively remove cholesterol from peripheral tissues and may promote inflammation and atherosclerosis. Genetic mutations affecting HDL metabolism further complicate its role in cardiovascular health. Studies have shown that conventional therapies aimed at raising HDL-C levels do not necessarily reduce cardiovascular events, highlighting the need for new approaches that improve HDL functionality. Therapeutic strategies such as Apo A-1 mimetic peptides, reconstituted HDL infusions, and drugs targeting specific HDL metabolic pathways are being explored. Additionally, weight loss, statin therapy, and niacin have shown potential in enhancing HDL function. The pathophysiology of dysfunctional HDL involves complex mechanisms, including oxidative stress, inflammation, and genetic mutations, which alter its structure and function, diminishing its cardioprotective effects. New functional assays, such as the cholesterol efflux capacity (CEC) and HDL inflammatory index, provide more accurate predictions of cardiovascular risk by assessing HDL quality rather than quantity. As research progresses, the focus is shifting towards therapeutic strategies that enhance HDL function and address the root causes of its dysfunction, offering a more effective approach to reducing cardiovascular risk and preventing CAD. Full article
(This article belongs to the Special Issue The Challenges and Therapeutic Prospects in Cardiovascular Disease)
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