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Advances in Cardiovascular Diseases (CVD)

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

Deadline for manuscript submissions: closed (15 October 2023) | Viewed by 22201

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Special Issue Editor

Dr. Adrian Wlodarczak

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Guest Editor

Department of Cardiology, Miedziowe Centrum Zdrowia, 59-300 Lubin, Poland
Interests: cardiovascular diseases; endothelial dysfunction; diagnostic tools; coronary artery diseases; high-risk interventions; structural interventions; peripheral interventions; bioresorbable materials

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVD) are the most common cause of death worldwide, and despite undeniable progress in prevention and therapeutics protocols, they still remain a relevant clinical issue. Therefore, numerous studies focused on etiopathogenesis, risk factors, diagnostic methods, and therapeutic efforts have recently been conducted. This Special Issue will highlight the latest findings in the field of Cardiovascular Diseases involving the pathogenesis and mechanisms of development of CVD, with particular emphasis on endothelial disorders and the potential role of oxidative stress. Studies investigating novel invasive and non-invasive diagnostic tools are also welcomed. The topic of this Special Issue will additionally expand on novel treatment methods in CVD (involving CAD especially high-risk interventions (CHIP), PAD, structural interventions in Heart Diseases, and cardio-renal interventions). Recently, advances in the field of Cardiovascular Diseases have been inextricably linked with the use of bioresorbables; therefore, articles relating to this topic are also highly recommended as a part of this Special Issue. Authors are invited to contribute reviews, original papers.

We look forward to receiving your contributions.

Dr. Adrian Wlodarczak
Guest Editor

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Keywords

cardiovascular diseases
endothelial dysfunction
diagnostic tools
coronary artery diseases
high-risk interventions
structural interventions
peripheral interventions
bioresorbable materials

Published Papers (14 papers)

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Research

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12 pages, 2390 KiB

Open AccessArticle

Association between the Use of Proton Pump Inhibitors and Cardiovascular Diseases: A Nested Case-Control Study Using a National Health Screening Cohort

by Sarang Jang, Hyo Geun Choi, Mi Jung Kwon, Ji Hee Kim, Joo-Hee Kim, Yoonjoong Kim and So Young Kim

Biomedicines 2024, 12(1), 170; https://doi.org/10.3390/biomedicines12010170 - 12 Jan 2024

Viewed by 755

Abstract

We investigated the association of proton pump inhibitor (PPI) use with the risk of stroke and ischemic heart disease (IHD). The Korean National Health Insurance Service-Health Screening cohort from 2002 to 2003, the participants of which were followed up until 2019, was used. In study I, 45,905 participants who were diagnosed with stroke were matched with 91,810 control I participants. The history of PPI medication was examined. In study II, 40,928 participants who were diagnosed with IHD were matched with 81,856 control II participants. In both study I and study II, the previous history of PPI medication was examined. A propensity score overlap-weighted multivariable logistic regression analysis was conducted to estimate the overlap-weighted odds ratios (ORs) of PPI use for stroke (study I) and IHD (study II). Current PPI use was linked with higher odds for stroke in study I. The odds for stroke were higher in groups with a longer duration of PPI use (OR = 0.96 [95% CI = 0.92–1.00] < 1.55 [1.50–1.61] < 1.62 [1.57–1.68] for < 30 days, 30 to 180 days, and ≥180 days of PPI use). Previous PPI use was linked with higher odds for IHD in study II. The odds for stroke were higher in groups with a longer duration of PPI use (OR = 1.13 [95% CI = 1.08–1.18] < 2.12 [2.04–2.21] < 2.60 [2.51–2.69] for <30 days, 30 to 180 days, and ≥180 days of PPI use). Current PPI medication is associated with a high risk of stroke and IHD. A longer duration of PPI medication was related to a higher risk of stroke and IHD. However, a prior history of PPI medication was not linked with a high risk of stroke or IHD. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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10 pages, 668 KiB

Open AccessArticle

Low Plasma Levels of Soluble Endoglin and Cardiovascular Events in Patients Undergoing Coronary Angiography

by Emi Saita, Yoshimi Kishimoto, Masayuki Aoyama, Reiko Ohmori, Kazuo Kondo and Yukihiko Momiyama

Biomedicines 2023, 11(11), 2975; https://doi.org/10.3390/biomedicines11112975 - 04 Nov 2023

Viewed by 821

Abstract

TGF-β is recognized as playing a protective role against atherosclerosis. Endoglin is a receptor for TGF-β, and its expression is upregulated in atherosclerotic plaques. Endoglin is secreted from the cell membrane into the circulation as a soluble form (sEng). We previously reported that plasma sEng levels were low in patients with coronary artery disease (CAD). However, the prognostic value of sEng levels has not been clarified. We investigated the association between plasma sEng levels and cardiovascular events in 403 patients who had an elective coronary angiography and were then followed up. Cardiovascular events were defined as cardiovascular death, myocardial infarction, unstable angina, heart failure, stroke, or coronary revascularization. Of the 403 patients, 209 (52%) had CAD. Plasma sEng levels were lower in patients with CAD than in those without CAD (median 4.26 vs. 4.41 ng/mL, p < 0.025). During a mean follow-up period of 7.5 ± 4.5 years, cardiovascular events occurred in 79 patients. Compared with 324 patients without events, 79 with events had lower sEng levels (3.95 vs. 4.39 ng/mL) and more often had an sEng level < 3.9 ng/mL (47% vs. 28%) (p < 0.02). A Kaplan–Meier analysis showed lower event-free survival in patients with sEng < 3.9 ng/mL than in those with ≥3.9 ng/mL (p < 0.02). In a multivariate Cox proportional hazards analysis, the sEng level (<3.9 ng/mL) was an independent predictor of cardiovascular events (hazard ratio: 1.59; 95%CI: 1.01–2.49). Furthermore, only among the 209 patients with CAD, the sEng level was also a predictor of further cardiovascular events (hazard ratio: 2.07; 95%CI: 1.24–3.45). Thus, low plasma sEng levels were found to be associated with an increased risk of cardiovascular events in patients with CAD and patients undergoing coronary angiography. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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18 pages, 5742 KiB

Open AccessArticle

High Fidelity Pressure Wires Provide Accurate Validation of Non-Invasive Central Blood Pressure and Pulse Wave Velocity Measurements

by Alessandro Scalia, Chadi Ghafari, Wivine Navarre, Philippe Delmotte, Rob Phillips and Stéphane Carlier

Biomedicines 2023, 11(4), 1235; https://doi.org/10.3390/biomedicines11041235 - 21 Apr 2023

Viewed by 1430

Abstract

Central blood pressure (cBP) is known to be a better predictor of the damage caused by hypertension in comparison with peripheral blood pressure. During cardiac catheterization, we measured cBP in the ascending aorta with a fluid-filled guiding catheter (FF) in 75 patients and with a high-fidelity micromanometer tipped wire (FFR) in 20 patients. The wire was withdrawn into the brachial artery and aorto-brachial pulse wave velocity (abPWV) was calculated from the length of the pullback and the time delay between the ascending aorta and the brachial artery pulse waves by gating to the R-wave of the ECG for both measurements. In 23 patients, a cuff was inflated around the calf and an aorta-tibial pulse wave velocity (atPWV) was calculated from the distance between the cuff around the leg and the axillary notch and the time delay between the ascending aorta and the tibial pulse waves. Brachial BP was measured non-invasively and cBP was estimated using a new suprasystolic oscillometric technology. The mean differences between invasively measured cBP by FFR and non-invasive estimation were −0.4 ± 5.7 mmHg and by FF 5.4 ± 9.4 mmHg in 52 patients. Diastolic and mean cBP were both overestimated by oscillometry, with mean differences of −8.9 ± 5.5 mmHg and −6.4 ± 5.1 mmHg compared with the FFR and −10.6 ± 6.3 mmHg and −5.9 ± 6.2 mmHg with the FF. Non-invasive systolic cBP compared accurately with the high-fidelity FFR measurements, demonstrating a low bias (≤5 mmHg) and high precision (SD ≤ 8 mmHg). These criteria were not met when using the FF measurements. Invasively derived average Ao-brachial abPWV was 7.0 ± 1.4 m/s and that of Ao-tibial atPWV was 9.1 ± 1.8 m/s. Non-invasively estimated PWV based on the reflected wave transit time did not correlate with abPWV or with atPWV. In conclusion, we demonstrate the advantages of a novel method of validation for non-invasive cBP monitoring devices using acknowledged gold standard FFR wire transducers and the possibility to easily measure PWV during coronary angiography with the impact of cardiovascular risk factors. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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11 pages, 1594 KiB

Open AccessArticle

SDF-1α-Releasing Microspheres Effectively Extend Stem Cell Homing after Myocardial Infarction

by Karolina Bajdak-Rusinek, Agnieszka Fus-Kujawa, Piotr Buszman, Dorota Żyła-Uklejewicz, Katarzyna Jelonek, Monika Musiał-Kulik, Carlos Fernandez, Magdalena Michalak, Kurian George, Janusz Kasperczyk and Paweł Buszman

Biomedicines 2023, 11(2), 343; https://doi.org/10.3390/biomedicines11020343 - 25 Jan 2023

Cited by 1 | Viewed by 1521

Abstract

Ischemic heart disease (IHD) is one of the main focuses in today’s healthcare due to its implications and complications, and it is predicted to be increasing in prevalence due to the ageing population. Although the conventional pharmacological and interventional methods for the treatment of IHD presents with success in the clinical setting, the long-term complications of cardiac insufficiency are on a continual incline as a result of post-infarction remodeling of the cardiac tissue. The migration and involvement of stem cells to the cardiac muscle, followed by differentiation into cardiac myocytes, has been proven to be the natural process, though at a slow rate. SDF-1α is a novel candidate to mobilize stem cells homing to the ischemic heart. Endogenous SDF-1α levels are elevated after myocardial infarction, but their presence gradually decreases after approximately seven days. Additional administration of SDF-1α-releasing microspheres could be a tool for the extension of the time the stem cells are in the cardiac tissue after myocardial infarction. This, in turn, could constitute a novel therapy for more efficient regeneration of the heart muscle after injury. Through this practical study, it has been shown that the controlled release of SDF-1α from biodegradable microspheres into the pericardial sac fourteen days after myocardial infarction increases the concentration of exogenous SDF-1α, which persists in the tissue much longer than the level of endogenous SDF-1α. In addition, administration of SDF-1α-releasing microspheres increased the expression of the factors potentially involved in the involvement and retention of myocardial stem cells, which constitutes vascular endothelial growth factor A (VEGFA), stem cell factor (SCF), and vascular cell adhesion molecules (VCAMs) at the site of damaged tissue. This exhibits the possibility of combating the basic limitations of cell therapy, including ineffective stem cell implantation and the ability to induce the migration of endogenous stem cells to the ischemic cardiac tissue and promote heart repair. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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16 pages, 5299 KiB

Open AccessArticle

Accuracy and Clinical Impact of Estimating Low-Density Lipoprotein-Cholesterol at High and Low Levels by Different Equations

by Maureen Sampson, Anna Wolska, Justine Cole, Rafael Zubirán, James D. Otvos, Jeff W. Meeusen, Leslie J. Donato, Allan S. Jaffe and Alan T. Remaley

Biomedicines 2022, 10(12), 3156; https://doi.org/10.3390/biomedicines10123156 - 06 Dec 2022

Cited by 11 | Viewed by 1794

Abstract

New more effective lipid-lowering therapies have made it important to accurately determine Low-density lipoprotein-cholesterol (LDL-C) at both high and low levels. LDL-C was measured by the β-quantification reference method (BQ) (N = 40,346) and compared to Friedewald (F-LDL-C), Martin (M-LDL-C), extended Martin (eM-LDL-C) and Sampson (S-LDL-C) equations by regression analysis, error-grid analysis, and concordance with the BQ method for classification into different LDL-C treatment intervals. For triglycerides (TG) < 175 mg/dL, the four LDL-C equations yielded similarly accurate results, but for TG between 175 and 800 mg/dL, the S-LDL-C equation when compared to the BQ method had a lower mean absolute difference (mg/dL) (MAD = 10.66) than F-LDL-C (MAD = 13.09), M-LDL-C (MAD = 13.16) or eM-LDL-C (MAD = 12.70) equations. By error-grid analysis, the S-LDL-C equation for TG > 400 mg/dL not only had the least analytical errors but also the lowest frequency of clinically relevant errors at the low (<70 mg/dL) and high (>190 mg/dL) LDL-C cut-points (S-LDL-C: 13.5%, F-LDL-C: 23.0%, M-LDL-C: 20.5%) and eM-LDL-C: 20.0%) equations. The S-LDL-C equation also had the best overall concordance to the BQ reference method for classifying patients into different LDL-C treatment intervals. The S-LDL-C equation is both more analytically accurate than alternative equations and results in less clinically relevant errors at high and low LDL-C levels. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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18 pages, 3871 KiB

Open AccessArticle

Physical Exercise Promotes DNase Activity Enhancing the Capacity to Degrade Neutrophil Extracellular Traps

by Anna S. Ondracek, Adrienne Aszlan, Martin Schmid, Max Lenz, Andreas Mangold, Tyler Artner, Michael Emich, Monika Fritzer-Szekeres, Jeanette Strametz-Juranek, Irene M. Lang and Michael Sponder

Biomedicines 2022, 10(11), 2849; https://doi.org/10.3390/biomedicines10112849 - 08 Nov 2022

Cited by 3 | Viewed by 1433

Abstract

(1) Background: An unhealthy lifestyle is a significant contributor to the development of chronic diseases. Physical activity can benefit primary and secondary prevention. Higher DNase activity is associated with favourable outcomes after cardiovascular (CV) events. In this study, we aimed to investigate the influence of consequent endurance exercise on DNase activity. (2) Methods: 98 subjects with at least one CV risk factor but the physical ability to perform endurance training were included. Individuals performed a bicycle stress test at the beginning and after 8 months to assess physical performance. In between, all participants were instructed to engage in guideline-directed physical activity. Blood samples were drawn in two-month intervals to assess routine laboratory parameters, cell-free DNA (cfDNA), and DNase activity. (3) Results: Prevailing CV risk factors were overweight (65.9%), a positive family history (44.9%), hypertension (32.7%) and smoking (20.4%). Performance changed by 7.8 ± 9.1% after 8 months. Comparison of baseline to 8 months revealed a decrease in cfDNA and an increase in DNase activity. This effect was driven by participants who achieved a performance gain. (4) Conclusions: Regular physical activity might improve CV health by increasing DNase activity and thereby, the capacity to lower pro-inflammatory signalling, complementing measures of primary and secondary prevention. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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12 pages, 1521 KiB

Open AccessArticle

Rota-Lithotripsy as a Novel Bail-Out Strategy for Highly Calcified Coronary Lesions in Acute Coronary Syndrome

by Piotr Rola, Łukasz Furtan, Szymon Włodarczak, Jan Jakub Kulczycki, Mateusz Barycki, Marek Szudrowicz, Michalina Kędzierska, Anna Pszonka, Justyna Korus, Adrian Doroszko, Maciej Lesiak and Adrian Włodarczak

Biomedicines 2022, 10(11), 2795; https://doi.org/10.3390/biomedicines10112795 - 03 Nov 2022

Cited by 3 | Viewed by 1359

Abstract

Background: Heavily calcified lesions in acute coronary syndrome (ACS) still represent a challenging subset for percutaneous coronary intervention (PCI). Rota-lithotripsy—a marriage of rotational atherectomy and intravascular lithotripsy—has recently been introduced to clinical practice as a novel therapeutic option. Methods: This study is among the to present the 6-month clinical outcomes of rota-lithotripsy when performed in the ACS setting. The study cohort consisted of 15 consecutive ACS patients who underwent a rota-lithotripsy-PCI due to the presence of a highly calcified, undilatable lesion. Results: The procedural success ratio reached 100%. During the 6-month follow-up, in two of the patients, instances of MACE (major adverse cardiac events) occurred, including one fatal event. Additionally, during the observation period, one target lesion failure, due to subacute stent thrombosis, was identified. Conclusions: Rotational atherectomy with the subsequent use of shockwave intravascular lithotripsy appears to be a safe and effective therapeutic bail-out option for the management of highly calcified coronary artery lesions. Despite, these initial favorable outcomes, carrying out a large number of studies with long-term observations is still necessary in order to establish the potential benefits and shortcomings of rota-lithotripsy. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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12 pages, 1143 KiB

Open AccessArticle

Retinal Microvascular Abnormalities and Systemic Arterial Stiffness Are the First Manifestation of Cardiovascular Abnormalities in Patients with Untreated Moderate to Severe Obstructive Sleep Apnoea and with Low to Intermediate Cardiovascular Risk—A Pilot Study

by Swathi Seshadri, Hala Shokr and Doina Gherghel

Biomedicines 2022, 10(10), 2669; https://doi.org/10.3390/biomedicines10102669 - 21 Oct 2022

Cited by 4 | Viewed by 1405

Abstract

This study aimed to investigate macro- and microvascular function parameters and their relationship with known markers of cardiovascular risk in patients with untreated moderate to severe obstructive sleep apnoea (OSA). Fourteen patients with moderate to severe OSA and fourteen controls were included in the present study. General assessments included BMI, systemic blood pressure (BP) and circulating markers for oxidative stress and endothelial function. Additional assessments included 24 h BP and heart rate monitoring, as well as the assessment of heart rate variability. Macro- and microvascular assessments included augmentation index, carotid intima-media thickness, brachial artery flow-mediated dilation, as well as various retinal microvascular function assessments, using the Dynamic Retinal Vessel Analyzer. All participants completed the Short Form Health Survey, Functional Outcomes of Sleep Questionnaire, and Epworth Sleepiness Scale. The results show that, in comparison to controls, BMI (p = 0.003) and AIx (p = 0.025) were significantly higher in the OSA group. There was, however, no significant difference between groups with regard to other measured systemic general, vascular and circulatory parameters (all p > 0.05). Nevertheless, the retinal microvascular function showed various alterations in the OSA patients, including a delayed reaction time in response to flicker (p = 0.047), as well as a decreased dilation amplitude (p = 0.004), dilation slope (p = 0.004), and post-flicker constriction (p = 0.015). In addition, the observed Slope_AD alterations correlated negatively with BMI values only in the OSA group (r = −0.46, p = 0.045). In conclusion, individuals with untreated moderate to severe OSA but without overt CVD, exhibit signs of increased arterial stiffness and retinal microvascular dysfunction, which can be early indicators for future vascular complications. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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13 pages, 279 KiB

Open AccessArticle

SELL and GUCY1A1 Gene Polymorphisms in Patients with Unstable Angina

by Damian Malinowski, Magda Zawadzka, Krzysztof Safranow, Marek Droździk and Andrzej Pawlik

Biomedicines 2022, 10(10), 2494; https://doi.org/10.3390/biomedicines10102494 - 06 Oct 2022

Cited by 5 | Viewed by 1226

Abstract

Acute ischaemia is mostly caused by the rupture of an unstable atherosclerotic plaque in a coronary artery, resulting in platelet accumulation and thrombus formation, which closes the lumen of the coronary vessel. Many different factors can cause atherosclerotic plaques to occlude the lumen of a coronary artery, including factors that increase vascular inflammation and blood platelet aggregation, as well as genetic factors. L-selectin is an adhesion molecule encoded by the human SELL gene, playing an important role in leukocyte adhesion to the endothelium and the development of inflammation. Guanylate cyclase 1 soluble subunit alpha 1 (GUCY1A1) is a gene that affects vasoreactivity and platelet function, thereby influencing thrombotic processes and the risk of developing thrombotic lesions in the coronary vessels. In SELL and GUCY1A1 genes, several polymorphisms have been detected, which may affect gene expression. The aim of our study was to assess the association between the SELL rs2205849 and rs2229569 and GUCY1A1 rs7692387 polymorphisms with the risk of acute coronary syndromes in the form of unstable angina pectoris, and the association between these polymorphisms and selected clinical parameters affecting the risk of developing ischemic heart disease. The study included 232 patients with unstable angina. The diagnosis of unstable angina was achieved by a typical clinical presentation and confirmation of significant coronary artery lumen stenosis (>70%) during coronary angiography. There were no statistically significant differences in GUCY1A1 rs7692387 and SELL rs2205849 and rs2229569 polymorphism distribution between the total study and the control groups. However, when only analysing patients over 55 years of age, we found a decreased frequency of the GUCY1A1 rs7692387AA genotype (AA vs. GA + GG, OR: 0.07; 95% CI: 0.01–0.78) and an increased frequency of the SELL rs2205849 CC genotype (CC vs. TC + TT p = 0.022) and SELL rs2229569 AA genotype (AA vs. GA + GG p = 0.022) in patients with unstable angina. Our results suggest that the SELL rs2205849 and rs2229569 and GUCY1A1 rs7692387 polymorphisms are not risk factors for unstable angina in the Polish population. The GUCY1A1 rs7692387 polymorphism may increase the risk of unstable angina in patients younger than 55 years, while the SELL polymorphisms rs2205849 and rs2229569 may increase the risk of unstable angina in patients older than 55 years in the Polish population. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

Review

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15 pages, 1305 KiB

Open AccessReview

Role of Helicobacter pylori Infection in Pathogenesis, Evolution, and Complication of Atherosclerotic Plaque

by Tiziana Ciarambino, Pietro Crispino, Giovanni Minervini and Mauro Giordano

Biomedicines 2024, 12(2), 400; https://doi.org/10.3390/biomedicines12020400 - 08 Feb 2024

Viewed by 585

Abstract

The therapeutic management of atherosclerosis focuses almost exclusively on the reduction of plasma cholesterol levels. An important role in the genesis and evolution of atherosclerosis is played by chronic inflammation in promoting thrombosis phenomena after atheroma rupture. This review aims to take stock of the knowledge so far accumulated on the role of endemic HP infection in atherosclerosis. The studies produced so far have demonstrated a causal relationship between Helicobacter pylori (HP) and CVD. In a previous study, we demonstrated in HP-positive patients that thrombin and plasma fragment 1 + 2 production was proportionally related to tumor necrosis factor-alpha levels and that eradication of the infection resulted in a reduction of inflammation. At the end of our review, we can state that HP slightly affects the risk of CVD, particularly if the infection is associated with cytotoxic damage, and HP screening could have a clinically significant role in patients with a high risk of CVD. Considering the high prevalence of HP infection, an infection screening could be of great clinical utility in patients at high risk of CVD. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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14 pages, 1723 KiB

Open AccessReview

Vitamin K and Calcium Chelation in Vascular Health

by Jan O. Aaseth, Urban Alehagen, Trine Baur Opstad and Jan Alexander

Biomedicines 2023, 11(12), 3154; https://doi.org/10.3390/biomedicines11123154 - 27 Nov 2023

Cited by 1 | Viewed by 1852

Abstract

The observation that the extent of artery calcification correlates with the degree of atherosclerosis was the background for the alternative treatment of cardiovascular disease with chelator ethylenediamine tetraacetate (EDTA). Recent studies have indicated that such chelation treatment has only marginal impact on the course of vascular disease. In contrast, endogenous calcium chelation with removal of calcium from the cardiovascular system paralleled by improved bone mineralization exerted, i.e., by matrix Gla protein (MGP) and osteocalcin, appears to significantly delay the development of cardiovascular diseases. After post-translational vitamin-K-dependent carboxylation of glutamic acid residues, MGP and other vitamin-K-dependent proteins (VKDPs) can chelate calcium through vicinal carboxyl groups. Dietary vitamin K is mainly provided in the form of phylloquinone from green leafy vegetables and as menaquinones from fermented foods. Here, we provide a review of clinical studies, addressing the role of vitamin K in cardiovascular diseases, and an overview of vitamin K kinetics and biological actions, including vitamin-K-dependent carboxylation and calcium chelation, as compared with the action of the exogenous (therapeutic) chelator EDTA. Consumption of vitamin-K-rich foods and/or use of vitamin K supplements appear to be a better preventive strategy than EDTA chelation for maintaining vascular health. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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16 pages, 1450 KiB

Open AccessReview

New Insights into the Use of Liraglutide—Impact on Cardiovascular Risk and Microvascular Outcomes

by Magdalena Wronka, Julia Krzemińska, Ewelina Młynarska, Jacek Rysz and Beata Franczyk

Biomedicines 2023, 11(4), 1159; https://doi.org/10.3390/biomedicines11041159 - 12 Apr 2023

Cited by 1 | Viewed by 1968

Abstract

Despite the availability of many glucose-lowering drugs, patients with type 2 diabetes mellitus (T2DM) often do not achieve the desired effect, and cardiovascular complications remain the leading cause of death in this group of patients. Recently, more and more attention has been paid to the properties of drugs, with particular emphasis on the possibility of reducing cardiovascular risk. One of them is liraglutide, which belongs to long-acting analogs of glucagon-like peptides-1 (GLP-1); it imitates incretins and causes an increase in insulin secretion. The current study focused on analyzing the efficacy and safety of liraglutide, as well as its impact on microvascular and cardiovascular outcomes in the treatment of patients with T2DM. Hyperglycemia-induced endothelial dysfunction, which is known to play a key role in maintaining cardiovascular homeostasis, is common in diabetes. Liraglutide reduces endothelial dysfunction by reversing damage to endothelial cells. By reducing the generation of reactive oxygen species (ROS), thereby affecting Bax, Bcl-2 protein levels, and restoring signaling pathways, Liraglutide reduces oxidative stress, inflammation, and prevents endothelial cell apoptosis. Liraglutide has beneficial effects on the cardiovascular system; patients with high cardiovascular risk particularly benefit from treatment, as it reduces their major adverse cardiovascular event (MACE) rate, which takes into account cardiovascular death, stroke, and non-fatal myocardial infarction. Liraglutide reduces the occurrence and progression of nephropathy, which is one of the most common microvascular complications of diabetes. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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12 pages, 304 KiB

Open AccessReview

Hyperuricemia and Endothelial Function: Is It a Simple Association or Do Gender Differences Play a Role in This Binomial?

by Tiziana Ciarambino, Pietro Crispino and Mauro Giordano

Biomedicines 2022, 10(12), 3067; https://doi.org/10.3390/biomedicines10123067 - 29 Nov 2022

Cited by 10 | Viewed by 1622

Abstract

The endothelium plays a fundamental role in the biological processes that ensure physiological vessel integrity, synthesizing numerous substances that are capable of modulating the tone of vessels, inflammation and the immune system, and platelet function. Endothelial dysfunction refers to an anomaly that develops at the level of the tunica that lines the internal surface of arterial and venous vessels, or, more precisely, an alteration to normal endothelial function, which involves the loss of some structural and/or functional characteristics. Studies on sex differences in endothelial function are conflicting, with some showing an earlier decline in endothelial function in men compared to women, while others show a similar age of onset between the sexes. Since increased cardiovascular risk coincides with menopause, female hormones, particularly estrogen, are generally believed to be cardioprotective. Furthermore, it is often proposed that androgens are harmful. In truth, these relationships are more complex than one might think and are not just dependent on fluctuations in circulating hormones. An increase in serum uric acid is widely regarded as a possible risk factor for cardiovascular disease; however, its role in the occurrence of endothelial dysfunction has not yet been elucidated. Several studies in the literature have evaluated sex-related differences in the association between elevated uric acid levels and cardiovascular events, with conflicting results. The association between uric acid and cardiovascular disease is still controversial, and it is not yet clear how gender differences affect the serum concentration of these substances. This review was primarily aimed at clarifying the effects of uric acid at the level of the vascular endothelium and describing how it could theoretically cause damage to endothelial integrity. The second aim was to determine if there are gender differences in uric acid metabolism and how these differences interact with the vascular endothelium. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

19 pages, 2642 KiB

Open AccessReview

Dirty Jobs: Macrophages at the Heart of Cardiovascular Disease

by Travis W. Stevens, Fatimah K. Khalaf, Sophia Soehnlen, Prajwal Hegde, Kyle Storm, Chandramohan Meenakshisundaram, Lance D. Dworkin, Deepak Malhotra, Steven T. Haller, David J. Kennedy and Prabhatchandra Dube

Biomedicines 2022, 10(7), 1579; https://doi.org/10.3390/biomedicines10071579 - 02 Jul 2022

Cited by 4 | Viewed by 3107

Abstract

Cardiovascular disease (CVD) is one of the greatest public health concerns and is the leading cause of morbidity and mortality in the United States and worldwide. CVD is a broad yet complex term referring to numerous heart and vascular conditions, all with varying pathologies. Macrophages are one of the key factors in the development of these conditions. Macrophages play diverse roles in the maintenance of cardiovascular homeostasis, and an imbalance of these mechanisms contributes to the development of CVD. In the current review, we provide an in-depth analysis of the diversity of macrophages, their roles in maintaining tissue homeostasis within the heart and vasculature, and the mechanisms through which imbalances in homeostasis may lead to CVD. Through this review, we aim to highlight the potential importance of macrophages in the identification of preventative, diagnostic, and therapeutic strategies for patients with CVD. Full article

(This article belongs to the Special Issue Advances in Cardiovascular Diseases (CVD))

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