Molecular and Technological Advances in the Diagnosis and Therapy of Cardiovascular Diseases

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

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 3774

Special Issue Editor

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality in the Western world. The escalating global prevalence of CVDs necessitates modern advancements in molecular diagnostics and technology. Primary prevention strategy should tailor the early identification of atherosclerosis. This is a very demanding process requiring genetic, biochemical, pathophysiological, and cardiovascular imaging studies that will enable personalized treatment approaches. Similarly, the secondary prevention of CVDs should follow the principles of precision medicine, determining the extent of follow-up and the intensity of therapy. Up to now, multiple and complex pathophysiologic mechanisms are involved in the progression of a wide spectrum of CVDs. Hence, there is still an increasing need to develop and apply more personalized diagnostic tests (molecular and imaging) and therapeutic regimen for CVDs.

We invite research submissions and narrative reviews focusing on CVDs to advance prevention, diagnosis, risk assessment, and treatment through personalized medicine. This Special Issue aims to acquaint medical professionals and researchers with recent strides in CVDs within the context of personalized medicine.

Original research and reviews are encouraged for this Special Issue.

Relevant topics include, but are not confined to, the following:

  • Atherosclerosis research;
  • Novel biomarkers in CVDs;
  • Genomics, GWAS, and population genetics;
  • Atherosclerosis epigenetics and microRNAs;
  • Lipids, lipoproteins, and apolipoproteins;
  • Proteomic and metabolomic exploration of atherosclerosis;
  • Heart failure management;
  • Significant valvular diseases;
  • Emerging therapies in valvular diseases;
  • Arrhythmia management;
  • Advances in cardiovascular imaging;
  • Novel therapies in CVDs;
  • Novel therapies for cardiomyopathies.

Dr. Nikolaos Kadoglou
Guest Editor

Manuscript Submission Information

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Keywords

  • cardiovascular diseases

  • personalized medicine
  • molecular diagnostics
  • biomarkers
  • cardiovascular imaging
  • atherosclerosis
  • basic research
  • clinical trials
  • gene therapy
  • precision medicine for diagnosis and treatment
  • heart failure
  • valvular diseases
  • arrhythmias

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Published Papers (4 papers)

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Research

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16 pages, 2285 KiB  
Article
Apolipoprotein B and Glycemic Dysregulation: New Predictors of Type 2 Diabetes in High-Cardiovascular-Risk Populations
by Makhabbat Bekbossynova, Tatyana Ivanova-Razumova, Aknur Kali, Aliya Sailybayeva, Sadyk Khamitov, Gulnur Daniyarova, Kamila Akzholova and Timur Saliev
J. Pers. Med. 2025, 15(5), 163; https://doi.org/10.3390/jpm15050163 - 23 Apr 2025
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Abstract
Background: Apolipoprotein B (ApoB), a key component of atherogenic lipoproteins, has been increasingly implicated in cardiometabolic disorders beyond dyslipidemia. However, its role in glycemic dysregulation remains unclear. This study aimed to investigate the association between ApoB levels and glycemic parameters, including fasting glucose, [...] Read more.
Background: Apolipoprotein B (ApoB), a key component of atherogenic lipoproteins, has been increasingly implicated in cardiometabolic disorders beyond dyslipidemia. However, its role in glycemic dysregulation remains unclear. This study aimed to investigate the association between ApoB levels and glycemic parameters, including fasting glucose, insulin resistance, and glycated hemoglobin (HbA1c), in individuals without diagnosed diabetes. Methods: This study was conducted at the National Research Cardiac Surgery Center (Kazakhstan) over the period between 2023 and 2024 as a cross-sectional analysis. Adults aged ≥ 20 years without diagnosed diabetes and with complete data on their ApoB and glycemic markers were included. Associations between ApoB and fasting plasma glucose (FPG), HbA1c, and HOMA-IR were assessed using multivariable linear and logistic regression models adjusted for demographic, lifestyle, and metabolic covariates. Results: Higher ApoB levels were significantly associated with increased fasting glucose (β = 2.07 mg/dL per 1-SD increase in ApoB, p < 0.001), higher HbA1c (β = 0.06%, p < 0.001), and elevated HOMA-IR (β = 0.54, p < 0.001). Participants in the highest ApoB quartile had 53% higher odds of prediabetes (adjusted OR = 1.53; 95% CI: 1.22–1.91; p < 0.001) compared to the lowest quartile. These associations remained significant after adjusting for BMI, lipid levels, and other confounders. Conclusions: Elevated ApoB is independently associated with adverse glycemic profiles in nondiabetic individuals, suggesting its potential role in early glucose metabolism disturbances. Full article
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15 pages, 1196 KiB  
Article
Associations Between Plasma Levels of NLRP3 Protein, Interleukin-1 Beta and Features of Acute ST-Elevation Myocardial Infarction
by Vyacheslav Ryabov, Yulia Samoilova, Aleksandra Gombozhapova, Anastasiia Nesova and Irina Kologrivova
J. Pers. Med. 2024, 14(11), 1103; https://doi.org/10.3390/jpm14111103 - 13 Nov 2024
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Abstract
Background. Phenotyping inflammation in ST-elevation myocardial infarction (STEMI) is a challenge for modern cardiology. NLRP3 inflammasome is a proven predictor of adverse outcomes in cardiovascular disease, but its specificity in stratifying inflammatory activity in patients with myocardial infarction (MI) has not been demonstrated. [...] Read more.
Background. Phenotyping inflammation in ST-elevation myocardial infarction (STEMI) is a challenge for modern cardiology. NLRP3 inflammasome is a proven predictor of adverse outcomes in cardiovascular disease, but its specificity in stratifying inflammatory activity in patients with myocardial infarction (MI) has not been demonstrated. The aim of this paper is to describe the levels of NLRP3 protein and IL-1β concentrations and their changes in dynamics and associations with clinical, laboratory and instrumental characteristics of patients with STEMI. Methods. A total of 45 patients with STEMI were enrolled. Concentrations of NLRP3 and IL-1β were evaluated in arterial and venous EDTA blood from the infarct-related coronary and peripheral arteries and veins on days 1, 3 and 7 after MI. Results and Conclusions. The concentrations of markers were higher on the first day after MI with a maximum decrease on the third day. The levels of both markers in venous plasma correlated with those in arterial blood, allowing their routine determination in venous plasma on the first day after MI. IL-1β levels correlated directly with the wall motion index and inversely with left ventricular ejection fraction and stroke volume, which characterize the potential contribution to adverse myocardial remodeling. There were two multidirectional trends in changes in NLRP3 and IL-1β levels during hospitalization. Initially higher levels with a gradual decrease by day 7 were associated with a longer duration of myocardial ischemia and higher plasma troponin I levels. Further evaluation of the long-term outcomes of MI will allow identifying inflammatory factors that input to the development of secondary major adverse cardiac events and will provide a new step in the understanding of inflammatory phenotyping. Full article
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12 pages, 3829 KiB  
Article
The Prognostic Role of Global Longitudinal Strain and NT-proBNP in Heart Failure Patients Receiving Cardiac Resynchronization Therapy
by Nikolaos P. E. Kadoglou, Sjoerd Bouwmeester, Anouk G. W. de Lepper, Marloes C. de Kleijn, Ingeborg H. F. Herold, Arthur R. A. Bouwman, Ioannis Korakianitis, Tim Simmers, Franke A. L. E. Bracke and Patrick Houthuizen
J. Pers. Med. 2024, 14(2), 188; https://doi.org/10.3390/jpm14020188 - 8 Feb 2024
Cited by 5 | Viewed by 1419
Abstract
Background: We aimed to evaluate whether baseline GLS (global longitudinal strain), NT-proBNP, and changes in these after cardiac resynchronization therapy (CRT) can predict long-term clinical outcomes and the echocardiographic-based response to CRT (defined by 15% relative reduction in left ventricular end-systolic volume). Methods: [...] Read more.
Background: We aimed to evaluate whether baseline GLS (global longitudinal strain), NT-proBNP, and changes in these after cardiac resynchronization therapy (CRT) can predict long-term clinical outcomes and the echocardiographic-based response to CRT (defined by 15% relative reduction in left ventricular end-systolic volume). Methods: We enrolled 143 patients with stable ischemic heart failure (HF) undergoing CRT-D implantation. NT-proBNP and echocardiography were obtained before and 6 months after. The patients were followed up (median: 58 months) for HF-related deaths and/or HF hospitalizations (primary endpoint) or HF-related deaths (secondary endpoint). Results: A total of 84 patients achieved the primary and 53 the secondary endpoint, while 104 patients were considered CRT responders and 39 non-responders. At baseline, event-free patients had higher absolute GLS values (p < 0.001) and lower NT-proBNP serum levels (p < 0001) than those achieving the primary endpoint. A similar pattern was observed in favor of CRT responders vs. non-responders. On Cox regression analysis, baseline absolute GLS value (HR = 0.77; 95% CI, 0.51–1.91; p = 0.002) was beneficially associated with lower primary endpoint incidence, while baseline NT-proBNP levels (HR = 1.55; 95% CI, 1.43–2.01; p = 0.002) and diabetes presence (HR = 1.27; 95% CI, 1.12–1.98; p = 0.003) were related to higher primary endpoint incidence. Conclusions: In HF patients undergoing CRT-D, baseline GLS and NT-proBNP concentrations may serve as prognostic factors, while they may predict the echocardiographic-based response to CRT. Full article
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Review

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17 pages, 1366 KiB  
Review
The Uncommon Phenomenon of Short QT Syndrome: A Scoping Review of the Literature
by Aristi Boulmpou, Andreas Giannopoulos, Christodoulos Papadopoulos, Georgios Giannopoulos, Ioannis Papagiannis, Georgios Zormpas, Anastasia Keivanidou, Liana Fidani and Vassilios Vassilikos
J. Pers. Med. 2025, 15(3), 105; https://doi.org/10.3390/jpm15030105 - 8 Mar 2025
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Abstract
Background: Short QT syndrome (SQTS) is a rare inheritable channelopathy characterized by a shortened corrected QT interval on an electrocardiogram and a significant risk of atrial and ventricular arrhythmias, potentially leading to sudden cardiac death. Despite advancements in our understanding of SQTS, knowledge [...] Read more.
Background: Short QT syndrome (SQTS) is a rare inheritable channelopathy characterized by a shortened corrected QT interval on an electrocardiogram and a significant risk of atrial and ventricular arrhythmias, potentially leading to sudden cardiac death. Despite advancements in our understanding of SQTS, knowledge gaps persist due to its extreme rarity. This scoping review aims to summarize the available knowledge on its clinical presentations, genetic mutations, and management strategies, while identifying areas for further investigation. Methods: This scoping review was conducted across the PubMed, Scopus, and Cochrane databases and identified relevant case reports, case series, and available studies on SQTS. We focused on articles that reported clinical outcomes, genetic mutations, diagnostic criteria, and management strategies, while excluding studies on the secondary causes of short QT intervals. Results: SQTS is present across a wide age range, from asymptomatic individuals to those experiencing syncope, palpitations, or sudden cardiac arrest. Common genetic mutations include KCNQ1, KCNH2, and KCNJ2. Management strategies vary, with some patients receiving implantable cardioverter defibrillators for secondary prevention and others treated pharmacologically, primarily with hydroquinidine. Our findings highlight the rarity and clinical variability of SQTS, underscoring the need for optimized diagnostic criteria and individualized management strategies. Conclusions: This review emphasizes the need for continued research to better understand the genetic basis of SQTS, optimize diagnostic tools, and improve treatment approaches. Large-scale studies and the integration of genetic and clinical data are critical to addressing the gaps in SQTS management and improving outcomes for patients with this potentially life-threatening arrhythmic disorder. Full article
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