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      The Effect of Blood Pressure Variability on Coronary Atherosclerosis Plaques

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          Abstract

          Hypertension is one of the most important risk factors for coronary heart disease (CHD). The regulation of blood pressure plays a significant role in the development and prognosis of CHD. Blood pressure variability (BPV) refers to the degree of fluctuation of blood pressure over a period of time and is an important indicator of blood pressure stability. Blood pressure fluctuations are complex physiological phenomena, being affected by physiological and pharmacological effects and regulated by behavioral, environmental, hydrodynamic, and neural factors. According to the different time periods for measuring BPV, it can be divided into very short-term, short-term, mid-term, and long-term. Multiple cardiovascular disease animal models and clinical experiments have consistently indicated that abnormal BPV is closely related to coronary events and is a risk factor for CHD independently of average blood pressure. Thrombosis secondary to plaque rupture (PR) or plaque erosion can cause varying blood flow impairment, which is the main pathological basis of CHD. Plaque morphology and composition can influence the clinical outcome, treatment, and prognosis of patients with CHD. Research has shown that PR is more easily induced by hypertension. After adjusting for the traditional factors associated with plaque development, in recent years, some new discoveries have been made on the influence of abnormal BPV on the morphology and composition of coronary plaques and related mechanisms, including inflammation and hemodynamics. This article reviews the impact of BPV on coronary plaques and their related mechanisms, with a view to prevent the occurrence and development of CHD by controlling BPV and to provide new prevention and treatment strategies for the clinical treatment of abnormal blood pressure.

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          Global, Regional, and National Burden of Cardiovascular Diseases for 10 Causes, 1990 to 2015

          Background The burden of cardiovascular diseases (CVDs) remains unclear in many regions of the world. Objectives The GBD (Global Burden of Disease) 2015 study integrated data on disease incidence, prevalence, and mortality to produce consistent, up-to-date estimates for cardiovascular burden. Methods CVD mortality was estimated from vital registration and verbal autopsy data. CVD prevalence was estimated using modeling software and data from health surveys, prospective cohorts, health system administrative data, and registries. Years lived with disability (YLD) were estimated by multiplying prevalence by disability weights. Years of life lost (YLL) were estimated by multiplying age-specific CVD deaths by a reference life expectancy. A sociodemographic index (SDI) was created for each location based on income per capita, educational attainment, and fertility. Results In 2015, there were an estimated 422.7 million cases of CVD (95% uncertainty interval: 415.53 to 427.87 million cases) and 17.92 million CVD deaths (95% uncertainty interval: 17.59 to 18.28 million CVD deaths). Declines in the age-standardized CVD death rate occurred between 1990 and 2015 in all high-income and some middle-income countries. Ischemic heart disease was the leading cause of CVD health lost globally, as well as in each world region, followed by stroke. As SDI increased beyond 0.25, the highest CVD mortality shifted from women to men. CVD mortality decreased sharply for both sexes in countries with an SDI >0.75. Conclusions CVDs remain a major cause of health loss for all regions of the world. Sociodemographic change over the past 25 years has been associated with dramatic declines in CVD in regions with very high SDI, but only a gradual decrease or no change in most regions. Future updates of the GBD study can be used to guide policymakers who are focused on reducing the overall burden of noncommunicable disease and achieving specific global health targets for CVD.
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            Lessons From Sudden Coronary Death

            Arteriosclerosis, Thrombosis, and Vascular Biology, 20(5), 1262-1275
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              The changing landscape of atherosclerosis

              Emerging evidence has spurred a considerable evolution of concepts relating to atherosclerosis, and has called into question many previous notions. Here I review this evidence, and discuss its implications for understanding of atherosclerosis. The risk of developing atherosclerosis is no longer concentrated in Western countries, and it is instead involved in the majority of deaths worldwide. Atherosclerosis now affects younger people, and more women and individuals from a diverse range of ethnic backgrounds, than was formerly the case. The risk factor profile has shifted as levels of low-density lipoprotein (LDL) cholesterol, blood pressure and smoking have decreased. Recent research has challenged the protective effects of high-density lipoprotein, and now focuses on triglyceride-rich lipoproteins in addition to low-density lipoprotein as causal in atherosclerosis. Non-traditional drivers of atherosclerosis-such as disturbed sleep, physical inactivity, the microbiome, air pollution and environmental stress-have also gained attention. Inflammatory pathways and leukocytes link traditional and emerging risk factors alike to the altered behaviour of arterial wall cells. Probing the pathogenesis of atherosclerosis has highlighted the role of the bone marrow: somatic mutations in stem cells can cause clonal haematopoiesis, which represents a previously unrecognized but common and potent age-related contributor to the risk of developing cardiovascular disease. Characterizations of the mechanisms that underpin thrombotic complications of atherosclerosis have evolved beyond the 'vulnerable plaque' concept. These advances in our understanding of the biology of atherosclerosis have opened avenues to therapeutic interventions that promise to improve the prevention and treatment of now-ubiquitous atherosclerotic diseases.
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                Author and article information

                Contributors
                Journal
                Front Cardiovasc Med
                Front Cardiovasc Med
                Front. Cardiovasc. Med.
                Frontiers in Cardiovascular Medicine
                Frontiers Media S.A.
                2297-055X
                15 March 2022
                2022
                : 9
                : 803810
                Affiliations
                [1] 1Department of Cardiology, 2nd Affiliated Hospital of Harbin Medical University , Harbin, China
                [2] 2Key Laboratory of Myocardial Ischemia, Ministry of Education, Harbin Medical University , Harbin, China
                Author notes

                Edited by: Guido Iaccarino, University of Naples Federico II, Italy

                Reviewed by: Bertram Pitt, University of Michigan, United States; Alex Bobik, Baker Heart and Diabetes Institute, Australia

                *Correspondence: Haibo Jia jhb101180@ 123456163.com

                This article was submitted to Hypertension, a section of the journal Frontiers in Cardiovascular Medicine

                †These authors have contributed equally to this work and share first authorship

                Article
                10.3389/fcvm.2022.803810
                8965230
                35369353
                1a27eadc-030e-436d-9535-4b7103c8b8bd
                Copyright © 2022 Liu, Luo, Jia and Yu.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 28 October 2021
                : 18 February 2022
                Page count
                Figures: 1, Tables: 1, Equations: 0, References: 95, Pages: 10, Words: 8857
                Categories
                Cardiovascular Medicine
                Review

                blood pressure variability,coronary heart disease,plaque rupture,plaque erosion,inflammation,hemodynamics,smooth muscle cell,endothelial cell

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