1.
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.
2.
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.
3.
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.
4.
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.