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Mitochondrial Dysfunction in Vascular Wall Cells and Its Role in Atherosclerosis.
Salnikova, D, Orekhova, V, Grechko, A, Starodubova, A, Bezsonov, E, Popkova, T, Orekhov, A
International journal of molecular sciences. 2021;(16)
Abstract
Altered mitochondrial function is currently recognized as an important factor in atherosclerosis initiation and progression. Mitochondrial dysfunction can be caused by mitochondrial DNA (mtDNA) mutations, which can be inherited or spontaneously acquired in various organs and tissues, having more or less profound effects depending on the tissue energy status. Arterial wall cells are among the most vulnerable to mitochondrial dysfunction due to their barrier and metabolic functions. In atherosclerosis, mitochondria cause alteration of cellular metabolism and respiration and are known to produce excessive amounts of reactive oxygen species (ROS) resulting in oxidative stress. These processes are involved in vascular disease and chronic inflammation associated with atherosclerosis. Currently, the list of known mtDNA mutations associated with human pathologies is growing, and many of the identified mtDNA variants are being tested as disease markers. Alleviation of oxidative stress and inflammation appears to be promising for atherosclerosis treatment. In this review, we discuss the role of mitochondrial dysfunction in atherosclerosis development, focusing on the key cell types of the arterial wall involved in the pathological processes. Accumulation of mtDNA mutations in isolated arterial wall cells, such as endothelial cells, may contribute to the development of local inflammatory process that helps explaining the focal distribution of atherosclerotic plaques on the arterial wall surface. We also discuss antioxidant and anti-inflammatory approaches that can potentially reduce the impact of mitochondrial dysfunction.
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Nutrition, atherosclerosis, arterial imaging, cardiovascular risk stratification, and manifestations in COVID-19 framework: a narrative review.
Munjral, S, Ahluwalia, P, Jamthikar, AD, Puvvula, A, Saba, L, Faa, G, Singh, IM, Chadha, PS, Turk, M, Johri, AM, et al
Frontiers in bioscience (Landmark edition). 2021;(11):1312-1339
Abstract
Background: Atherosclerosis is the primary cause of the cardiovascular disease (CVD). Several risk factors lead to atherosclerosis, and altered nutrition is one among those. Nutrition has been ignored quite often in the process of CVD risk assessment. Altered nutrition along with carotid ultrasound imaging-driven atherosclerotic plaque features can help in understanding and banishing the problems associated with the late diagnosis of CVD. Artificial intelligence (AI) is another promisingly adopted technology for CVD risk assessment and management. Therefore, we hypothesize that the risk of atherosclerotic CVD can be accurately monitored using carotid ultrasound imaging, predicted using AI-based algorithms, and reduced with the help of proper nutrition. Layout: The review presents a pathophysiological link between nutrition and atherosclerosis by gaining a deep insight into the processes involved at each stage of plaque development. After targeting the causes and finding out results by low-cost, user-friendly, ultrasound-based arterial imaging, it is important to (i) stratify the risks and (ii) monitor them by measuring plaque burden and computing risk score as part of the preventive framework. Artificial intelligence (AI)-based strategies are used to provide efficient CVD risk assessments. Finally, the review presents the role of AI for CVD risk assessment during COVID-19. Conclusions: By studying the mechanism of low-density lipoprotein formation, saturated and trans fat, and other dietary components that lead to plaque formation, we demonstrate the use of CVD risk assessment due to nutrition and atherosclerosis disease formation during normal and COVID times. Further, nutrition if included, as a part of the associated risk factors can benefit from atherosclerotic disease progression and its management using AI-based CVD risk assessment.
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Sympathetic neural modulation of arterial stiffness in humans.
Nardone, M, Floras, JS, Millar, PJ
American journal of physiology. Heart and circulatory physiology. 2020;(6):H1338-H1346
Abstract
Elevated large-artery stiffness is recognized as an independent predictor of cardiovascular and all-cause mortality. The mechanisms responsible for such stiffening are incompletely understood. Several recent cross-sectional and acute experimental studies have examined whether sympathetic outflow, quantified by microneurographic measures of muscle sympathetic nerve activity (MSNA), can modulate large-artery stiffness in humans. A major methodological challenge of this research has been the capacity to evaluate the independent neural contribution without influencing the dynamic blood pressure dependence of arterial stiffness. The focus of this review is to summarize the evidence examining 1) the relationship between resting MSNA and large-artery stiffness, as determined by carotid-femoral pulse wave velocity or pulse wave reflection characteristics (i.e., augmentation index) in men and women; 2) the effects of acute sympathoexcitatory or sympathoinhibitory maneuvers on carotid-femoral pulse wave velocity and augmentation index; and 3) the influence of sustained increases or decreases in sympathetic neurotransmitter release or circulating catecholamines on large-artery stiffness. The present results highlight the growing evidence that the sympathetic nervous system is capable of modulating arterial stiffness independent of prevailing hemodynamics and vasomotor tone.
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Intravascular lithotripsy for calcific coronary and peripheral artery stenoses.
Dini, CS, Tomberli, B, Mattesini, A, Ristalli, F, Valente, S, Stolcova, M, Meucci, F, Baldereschi, G, Fanelli, F, Shlofmitz, RA, et al
EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology. 2019;(8):714-721
Abstract
Heavily calcified lesions may be difficult to dilate adequately with conventional balloons and stents, which causes frequent periprocedural complications and higher rates of target lesion revascularisation (TLR). High-pressure non-compliant balloon angioplasty may be of insufficient force to modify calcium and, even when successful, may be limited in its ability to modify the entire calcified lesion. Scoring and cutting balloons hold theoretical value but data to support their efficacy are lacking and, because of their high lesion crossing profile, they often fail to reach the target lesion. Rotational and orbital atherectomy target superficial calcium; however, deep calcium, which may still impact on vessel expansion and luminal gain, is not affected. Intravascular lithotripsy (IVL), based on lithotripsy for renal calculi, is a new technology which uses sonic pressure waves to disrupt calcium with minimal impact to soft tissue. Energy is delivered via a balloon catheter, analogous to contemporary balloon catheters, with transmission through diluted ionic contrast in a semi-compliant balloon inflated at low pressure with sufficient diameter to achieve contact with the vessel wall. With coronary and peripheral balloons approved in Europe, peripheral balloons approved in the USA and multiple new trials beginning, we review the indications for these recently introduced devices, summarise the clinical outcomes of the available trials and describe the design of ongoing studies.
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5.
The Pressure of Aging.
AlGhatrif, M, Wang, M, Fedorova, OV, Bagrov, AY, Lakatta, EG
The Medical clinics of North America. 2017;(1):81-101
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Abstract
Significant hemodynamic changes ensue with aging, leading to an ever-growing epidemic of hypertension. Alterations in central arterial properties play a major role in these hemodynamic changes. These alterations are characterized by an initial decline in aortic distensibility and an increase of diastolic blood pressure, followed by a sharp increase in pulse wave velocity (PWV), and an increase in pulse pressure (PP) beyond the sixth decade. However, the trajectories of PWV and PP diverge with advancing age. There is an increased prevalence of salt-sensitive hypertension with advancing age that is, in part, mediated by marinobufagenin, an endogenous sodium pump ligand.
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Arterial ageing: Major nutritional and life-style effects.
Papaioannou, TG, Karatzi, K, Psaltopoulou, T, Tousoulis, D
Ageing research reviews. 2017;:162-163
Abstract
Arterial ageing is a key mechanism underling the development and progression of cardiovascular (CV) and other diseases. New technologies allow the non-invasive assessement of various biomechanical and biological aspects of arterial ageing. We discuss a few major factors in respect to arterial ageing pathophysiology, methods of assessment and some important nutritional and life-style parameters that substantially affect arterial ageing.
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7.
Nutrition and other lifestyle influences on arterial aging.
LaRocca, TJ, Martens, CR, Seals, DR
Ageing research reviews. 2017;:106-119
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Abstract
As our world's population ages, cardiovascular diseases (CVD) will become an increasingly urgent public health problem. A key antecedent to clinical CVD and many other chronic disorders of aging is age-related arterial dysfunction, characterized by increased arterial stiffness and impaired arterial endothelial function. Accumulating evidence demonstrates that diet and nutrition may favorably modulate these arterial functions with aging, but many important questions remain. In this review, we will summarize the available information on dietary patterns and nutritional factors that have been studied for their potential to reduce arterial stiffness and improve endothelial function with age, with an emphasis on: 1) underlying physiological mechanisms, and 2) emerging areas of research on nutrition and arterial aging that may hold promise for preventing age-related CVD.
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Comparison of cerebral blood flow measurement with [15O]-water positron emission tomography and arterial spin labeling magnetic resonance imaging: A systematic review.
Fan, AP, Jahanian, H, Holdsworth, SJ, Zaharchuk, G
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism. 2016;(5):842-61
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Abstract
Noninvasive imaging of cerebral blood flow provides critical information to understand normal brain physiology as well as to identify and manage patients with neurological disorders. To date, the reference standard for cerebral blood flow measurements is considered to be positron emission tomography using injection of the [(15)O]-water radiotracer. Although [(15)O]-water has been used to study brain perfusion under normal and pathological conditions, it is not widely used in clinical settings due to the need for an on-site cyclotron, the invasive nature of arterial blood sampling, and experimental complexity. As an alternative, arterial spin labeling is a promising magnetic resonance imaging technique that magnetically labels arterial blood as it flows into the brain to map cerebral blood flow. As arterial spin labeling becomes more widely adopted in research and clinical settings, efforts have sought to standardize the method and validate its cerebral blood flow values against positron emission tomography-based cerebral blood flow measurements. The purpose of this work is to critically review studies that performed both [(15)O]-water positron emission tomography and arterial spin labeling to measure brain perfusion, with the aim of better understanding the accuracy and reproducibility of arterial spin labeling relative to the positron emission tomography reference standard.
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Intra-Arterial Radionuclide Therapies for Liver Tumors.
Bozkurt, MF, Salanci, BV, Uğur, Ö
Seminars in nuclear medicine. 2016;(4):324-39
Abstract
Intra-arterial radionuclide therapies serve essentially as internal radiation treatment options for both primary and metastatic liver tumors, which imply delivering implantable radioactive microspheres into branches of hepatic arteries that feed liver tumors to provide a high dose of targeted radiation to tumor tissue, while sparing the healthy liver tissue from hazardous effects of radiation. The principle of this therapeutic option depends on the unique preferential arterial supply of malignant liver tumors in contrast with mostly portal venous supply of normal hepatocytes as well as excess amount of arterial neovascularization in the tumor bed. Therefore, intra-arterial radionuclide therapy can provide very high radiation exposure to tumor tissue, which is impossible to reach with external radiation therapy due to serious side effects and moreover, radiation can be targeted to tumor tissue selectively with less side effects. Yttrium-90 (Y-90), a high-energetic beta emitter is the most preferred radionuclide, which is used to label microspheres. Two types of Y-90 microspheres are commercially available that are made of resin and glass. Many studies in the literature have demonstrated that Y-90 microsphere therapy is an efficient and safe locoregional therapeutic option for unresectable primary and metastatic liver tumors such as hepatocellular carcinoma and liver metastases from colorectal cancer and breast cancer as well as neuroendocrine tumors. Furthermore, limited number of studies has reported its use in some relatively uncommon metastatic liver tumors from melanoma, pancreatic, renal, and lung cancer. Besides Y-90 microspheres, Iodine-131 lipiodol, Rhenium-188 lipiodol, Rhenium-188 microspheres, Holmium-166 chitosan, and Holmium-166 microspheres have been introduced as alternative radiopharmaceuticals for intra-arterial therapy for liver tumors.
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10.
Arterial tortuosity in genetic arteriopathies.
Morris, SA
Current opinion in cardiology. 2015;(6):587-93
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Abstract
PURPOSE OF REVIEW Arterial tortuosity is emerging as a common feature in genetically mediated thoracic aortic disease that may be prognostic. This review will summarize recent literature on arterial tortuosity in the setting of genetic arteriopathies. RECENT FINDINGS Although arterial tortuosity has been primarily described in Loeys-Dietz syndrome due to TGFBR1 and TGFBR2 mutations and in arterial tortuosity syndrome due to SLC210A mutations, recent studies that use quantitative measures of tortuosity suggest that tortuosity is present in many other genetic conditions associated with aortic dilation and dissection. The mechanisms of the development of tortuosity in these disorders are not fully understood, but are founded in the concept that there is abnormal, pathologic arterial lengthening in a fixed space, resulting in more tortuous vessels. Further studies suggest that patients with increased arterial tortuosity are at increased risk of adverse cardiovascular events, including aortic surgery, aortic dissection, and death. SUMMARY Arterial tortuosity is commonly present in genetically mediated aortic disease. Given the suboptimal performance of aortic dimension alone in predicting aortic dissection, quantification of tortuosity may augment the current algorithms for determining risk in patients with aortic disease.