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- Volume 22, Issue 6, 2024
Current Vascular Pharmacology - Volume 22, Issue 6, 2024
Volume 22, Issue 6, 2024
- Medicine, Cardiology, Pharmacology, Peripheral Vascular Disease
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Neovascularization as a Leading Mechanism of Intraplaque Hemorrhage and Carotid Plaque Destabilization: A Narrative Review
Authors: Arkadiusz Migdalski and Arkadiusz JawienIntraplaque neovascularization (IPN) is considered a leading mechanism causing carotid plaque destabilization. We provide an objective and comprehensive summary of the biology, imaging techniques, and treatment options related to carotid IPN. Plaque neovascularization has been reported to originate mainly from the adventitial vasa vasorum as a response to hypoxia. The leakage and rupture of neovessels lead to the formation of extravasations and foci of inflammation that destabilize the plaque. Vascular endothelial growth factor and its receptors are key regulators of neoangiogenesis. Neovascularization can be analyzed by advanced computed tomography and magnetic resonance imaging. The basic tools for the ultrasound assessment of IPN are contrast-enhanced ultrasound, superb microvascular imaging, and ultrasound molecular imaging. A promising direction of research seems to be the identification of patients with advanced plaque neovascularization. A simple test assessing low-velocity flow in the IPN can detect patients at risk of stroke before they experience rupture of defective neovessels and intracerebral embolism. In addition to surgical treatment, the stabilization of carotid atherosclerotic plaque can be supported pharmacologically. Statins have the best-documented role in this respect. The ideal moment of intensified therapeutic intervention in patients with previously stable carotid plaque is its increased neovascularization. However, the time frame in which intracerebral embolization may occur is unknown, and therapeutic intervention may be too late. The formation of deficient neovessels can currently be non-invasively evaluated with ultrasound. Superb microvascular imaging may change the clinical approach for asymptomatic patients at risk of cerebral ischemia.
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Comparison of Amiodarone Loading Dosage in the Treatment of Postoperative Atrial Fibrillation: High Versus Standard Dose Treatment
Authors: Ersin Sarıçam, Arslan Öcal, Murat Doğan İşcanlı, Engin Bozkurt, Erdoğan İlkay and Ömer Faruk CantekinBackgroundPostoperative atrial fibrillation (POAF) is associated with poor outcomes, including hemodynamic instability, stroke, myocardial infarction, and death. In hemodynamic stable patients, the rhythm-control strategy is more advantageous than rate control. Current standard intravenous amiodarone administration has limited success and a delayed effect; the acute success rate is 44% (8-12 h to several days).
PurposeThe aim of this study was to evaluate the effectiveness of higher amiodarone loading dosage to restore sinus rhythm in patients with POAF after noncardiac surgery.
MethodsThis is a prospective, randomized, controlled single-center study. The study included 39 patients with POAF, divided into group I (n=27) (intravenous 600 mg amiodarone loading dosage over 2 h and infusion of 50 mg/h over a 24-h period) and group II (n=12) (standard protocol; 300 mg of bolus intravenously in 30 min and infusion of 50 mg/h over a 24-h period). The primary endpoint of the study was a restoration of sinus rhythm at the 24th hour.
ResultsBaseline clinical, laboratory and echocardiographic characteristics of both groups were similar. The patients with higher loading amiodarone dosage had earlier restoration of sinus rhythm (2.38 ± 1.41 vs 8.66 ± 2.87 h, respectively; p=0.015). There was no significant difference in achieving sinus rhythm at the 24th hour between both groups.
ConclusionHigher loading amiodarone dosage increased early conversions to sinus rhythm compared with standard amiodarone protocol in patients with POAF.
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Association between Dietary Vitamin E Intake and the Risk of Hypertension in US Adults
More LessBackgroundMany studies have shown that Vitamin E (VitE) intake has beneficial effects on human health, but the relationship between VitE intake and Blood Pressure (BP) is not well understood. Thus, our present study aimed to assess the relationship between VitE intake and hypertension, systolic and diastolic BP in US (United States) adults.
MethodsWe used data from the 2003-2018 National Health and Nutrition Examination Survey (NHANES). Weighted multivariate regression analysis, subgroup analysis, and Restricted Cubic Splines (RCS) were used to explore the independent associations between VitE intake and hypertension, systolic and diastolic BP. A total of 32,371 participants were included in this study. The mean VitE intake of participants was 8.50 ± 0.08 mg/d. The prevalence of hypertension in subjects was 37.76% and it decreased with increasing VitE intake quartiles (quartile 1: 40.97%, quartile 2: 37.60%, quartile 3: 37.47%, quartile 4: 35.66%). A significant negative correlation was found between VitE intake and hypertension.
ResultsWe also observed a significant negative association between VitE intake and systolic BP (model 1: β = -0.11, 95% CI: -0.15 ~ -0.07; model 2: β = -0.09, 95% CI: -0.12 ~ -0.05; and model 3: β = -0.05, 95% CI: -0.10 ~ -0.01). Quartile 2 of dietary VitE intake significantly correlated to a lower diastolic BP compared to the lowest quartile of VitE intake (model 3: β = -0.72, 95%CI: -1.26~-0.18).
ConclusionIn US adults, VitE intake has not been significantly found to be associated with hypertension, but it has been found to exhibit a negative association with both systolic and diastolic BP in US adults.
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Identification of Vascular Genes Differentially Expressed in the Brain of Patients with Alzheimer's Disease
BackgroundAlzheimer's disease (AD) plays a prominent role as the most common form of dementia. Moreover, the traditional mechanism of AD does not explain the microvascular damage observed in about 25-30 years between the onset of AD, which results in late application treatment that inhibits or delays neurodegeneration.
ObjectiveOur objective was to identify differentially expressed genes in human brain samples associated with vascular disruption in AD.
MethodsWe analyzed 1633 post-mortem brain samples in the GEO database and, after applying clinical and bioinformatic exclusion criteria, worked with 581 prefrontal and frontal samples. All datasets were analyzed using GEO2R from NCBI. We identified common genes using the Venny tool, and their metabolic relevance associated with AD and the vascular system was analyzed using MetaboAnalyst tools.
ResultsOur bioinformatic analysis identified PRKCB, MAP2K2, ADCY1, GNA11, GNAQ, PRKACB, KCNMB4, CALD1, and GNAS as potentially involved in AD pathogenesis. These genes are associated with signal transductions, cell death signaling, and cytoskeleton, suggesting potential modulation of cellular physiology, including endoplasmic reticulum and mitochondrial activity.
ConclusionThis study generates hypotheses regarding the roles of novel genes over critical pathways relevant to AD and its relation with vascular dysfunction. These findings suggest potential new targets for further investigation into the pathogenesis of dementia and AD.
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Assessment of Early Vascular Aging Ambulatory Score (EVAAs): A Large Population-based External Validation Study
Authors: Christina Antza, Victoria Potoupni, Evangelos Akrivos, Stella Stabouli and Vasilios KotsisBackgroundPulse Wave Velocity (PWV) remains the gold-standard method to assess Early Vascular Aging (EVA) defined by arterial stiffness. However, its high cost, time-consuming process, and need for qualified medical staff shows the importance of identifying alternative methods for the EVA evaluation.
ObjectiveIn order to simplify the process of assessing patient's EVA, we recently developed the Early Vascular Aging Ambulatory score (EVAAs), a simple tool to predict the risk of EVA. The aim of the present study was the external validation of EVAAs in an independent population.
MethodsEight hundred seventy-nine (46.3% men) patients who were referred to our Hypertension ESH Excellence Center were included in this study. The mean age was 46.43 ± 22.87 years. EVA was evaluated in two different ways. The first assessment included c-f PWV values, whereas the second one included EVAAs without the direct measurement of carotid-femoral PWV.
ResultsThe null hypothesis was that the prediction of EVA based on EVAAs does not present any statistically significant difference compared to the prediction based on the calculation from c-f PWV. Mean squared error (MSE) was used for the assessment of the null hypothesis, which was found to be 0.40. The results revealed that the EVAAs shows the probability of EVA with 0.98 sensitivity and 0.75 specificity. The EVAAs present 95% positive predictive value and 92% negative predictive value.
ConclusionOur study revealed that EVAAs could be as reliable as the carotid-femoral PWV to identify patients with EVA. Hence, we hope that EVAAs will be a useful tool in clinical practice.
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Burden of Ischemic Heart Diseases among US States from 1990-2019
BackgroundIschemic Heart Disease (IHD) is a leading cause of global mortality, including in the United States. Understanding the burden of IHD in the United States is crucial for informed decision-making and targeted interventions aimed at reducing morbidity and mortality associated with this leading cause of death. This study aimed to understand the burden of IHD, identify gender disparities and risk factors, explore the relationship between socioeconomic growth and IHD, and analyze risk factor distribution across the states of the United States.
MethodsThis study utilized data from the Global Burden of Diseases Study 2019, which provided comprehensive information on IHD from 1990 to 2019. Data related to IHD from these years were extracted using a query tool from the Institute for Health Metrics and Evaluation (IHME) website. The study assessed the relationship between IHD and socioeconomic development using the Socio-demographic Index (SDI) and measured the overall impact of IHD using Disability-adjusted Life Years (DALYs), considering premature death and disability. Additionally, the study analyzed the burden of IHD attributed to six main risk factors. Data analysis involved comparing prevalence, mortality, SDI, DALYs, attributable burden, and risk estimation among the states.
ResultsBetween 1990 and 2019, there was an improvement in socioeconomic development in all states. Age-standardized rates of disease burden for IHD decreased by 50% [ASDR 3278.3 to 1629.4 (95% UI: 1539.9-1712.3) per 100,000] with the most significant decline observed in Minnesota. Males had higher burden rates than females in all states, and the southeast region had the highest mortality rates. The prevalence of IHD showed a declining trend, with approximately 8.9 million cases (95% UI: 8.0 million to 9.8 million) in 2019, representing a 37.1% decrease in the Age-standardized Prevalence Rate (ASPR) from 1990. Metabolic risks were the leading contributors to the disease burden, accounting for 50% of cases, with Mississippi having the highest attributable risk. Arkansas had the highest attributable risk for high cholesterol and smoking. Conversely, Minnesota had the lowest burden of IHD among all the states.
ConclusionThis study highlights variations in the burden of IHD across US states and emphasizes the need for tailored prevention programs to address specific risk factors and gender differences. Understanding the trend in IHD may inform policymakers and healthcare professionals in effectively allocating resources to reduce the burden of IHD and improve national health outcomes.
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Bosentan and Pulmonary Hypertension Caused by COVID-19: A Pilot Randomized Double-blind Clinical Study
Authors: Fahime Shokrollahi, Ali Pazoki, Abbas Allami, Shahin Aliakbari and Kimia Rahimi ArdaliIntroduction/ObjectiveCoronavirus disease 2019 (COVID-19) has been the biggest pandemic in history, with severe complications, such as acute respiratory distress syndrome and pulmonary hypertension (PH). An endothelin-1 (ET-1) receptor antagonist, such as bosentan, may be beneficial in treating elevated ET-1 levels. Hence, our study aimed to evaluate the therapeutic effects of bosentan in patients with COVID-19-induced PH.
MethodsA single-centre, randomized, double-blind study involving 72 participants was carried out; 36 received bosentan and the other 36 received a placebo. Pulmonary arterial pressure, tricuspid valve pressure gradient, and right atrial pressure were measured using echocardiography. The Cox proportional hazards regression model was used to investigate the impact of bosentan and patients' age on mortality during a 6-month follow-up period.
ResultsIn-hospital mortality was significantly lower in the case group (13%) compared with the control group (33.3%) (P=0.003). Additionally, bosentan improved echocardiographic parameters, such as systolic pulmonary artery pressure and tricuspid regurgitation gradient (P=0.011 and P=0.003, respectively). Bosentan use was a significant predictor of long-term mortality rates for 600 days [age-adjusted hazard ratio of 5.24 (95% CI 1.34 to 20.46)].
ConclusionThis study provided a mixed perspective on the use of bosentan therapy in patients with COVID-19-related PH. Bosentan effectively reduced in-hospital mortality and improved echocardiographic measures. However, the treatment group showed an increased requirement for supplemental oxygen therapy and long-term mortality. Further studies with larger sample sizes are necessary to elucidate the effects of bosentan in PH following COVID-19.
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Volumes & issues
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Volume 22 (2024)
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Volume 21 (2023)
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Volume 20 (2022)
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Volume 19 (2021)
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Volume 18 (2020)
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Volume 17 (2019)
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Volume 16 (2018)
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Volume 15 (2017)
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Volume 14 (2016)
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Volume 13 (2015)
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Volume 12 (2014)
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Volume 11 (2013)
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Volume 10 (2012)
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Volume 9 (2011)
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Volume 8 (2010)
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Volume 7 (2009)
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Volume 6 (2008)
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Volume 5 (2007)
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Volume 4 (2006)
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Volume 3 (2005)
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Volume 2 (2004)
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Volume 1 (2003)