Mechanical Effects of Cardiovascular Drugs and Devices
Michel R. Labrosse in Cardiovascular Mechanics, 2018
One of the most prevalent diseases of the cardiovascular system is atherosclerosis, which has been reviewed in Chapter 7. Atherosclerosis is the buildup of cholesterol plaque in the walls of the arteries. The initial lesion usually occurs decades before clinically significant effects are observed; thus, treatment of lesions has evolved as the primary remedy for vessel narrowing due to atherosclerosis. The lesion is marked by intracellular lipid accumulation, forming a fatty streak in the vessel wall. Further lipid accumulation expands to an extracellular lipid pool, which provides a site for calcification. This is followed by increased proliferation of smooth muscle and collagen deposition. When the lesion is severe, it erupts through the vessel wall, attracting platelets and forming a thrombus at the site. Atherosclerosis occurs all over the body but is most problematic in the peripheral, coronary, and cerebral arteries, which feed important capillary beds.
Surgical pathology
Jonathan M. Fishman, Vivian A. Elwell, Rajat Chowdhury in OSCEs for the MRCS Part B, 2017
Complications of atherosclerosis include: Distal ischaemiaVessel occlusionPlaque ulceration, ruptureThrombosisHaemorrhage into a plaqueEmbolism – Lipid or thrombusCalcificationAneurysm formation
Atherosclerosis, Arteriolosclerosis and Vasculitis
Jeremy R. Jass in Understanding Pathology, 2020
Epidemiological studies have shown that the major risk factors of atherosclerosis are diet (i.e. one high in cholesterol), hyperlipidemia of genetic origin, hypertension, smoking and diabetes mellitus. Other risk factors include male gender, obesity, age and physical inactivity. In the past, two main theories were put forward to explain the growth of an atheromatous plaque. The first envisaged the insudation of cholesterol from the bloodstream into the intima, this in turn stimulating the proliferation of smooth muscle cells. The second theory focused on the progressive laying down and organisation of platelet thrombi. The contemporary view combines elements of both theories but views atherosclerosis as an inflammatory response to intimal injury (Ross & Fuster, 1996). The suggested steps are shown in Figure 25. Thrombosis is now viewed as a late complication of atheroma, rather than as a predisposing event. The sequence of events outlined in Figure 25 fits with the risk posed by hypercholesterolemia and the direct damaging influence of hypertension and cigarette smoke upon endothelial cells. Considerable research is under way to map the molecular steps involved in the above pathway, with the aim of developing therapeutic strategies to block the process of atherogenesis. However, a healthy diet, regular exercise and avoidance of tobacco would be a useful start to preventing this disease. Lifestyle improvements such as these are already having a beneficial effect in the West.
Canvassing the aetiology, prognosis and molecular signatures of obstructive sleep apnoea
Published in Biomarkers, 2019
Sartaj Khurana, Shivani Sharda, Biswajit Saha, Sachin Kumar, Randeep Guleria, Sudeep Bose
Atherosclerosis is a chronic inflammatory process involving the narrowing of the arteries due to the development of plaque around the arterial wall. It causes disruption in the flow of blood around the body resulting in fatal complications such as stroke and heart attack. It is evident that there is a positive correlation between the severity of OSA and the presence of increased coronary atherosclerotic plaque volume suggesting the onset of cardiovascular diseases in OSA subjects (Turmel et al. 2009). Recent studies have shown that OSA is associated with multiple factors that cause endothelial damage such as inflammation, escalated plasma levels of vascular endothelial growth factor (VEGF) and reactive oxygen species (ROS). The carotid intima-media thickness (CIMT), which is a measurement of the intima and media layers of the carotid artery is used as an early marker of atherosclerosis. It was found to be higher in OSA subjects compared with non-OSA (Minoguchi et al. 2005) and increased IMT predicts the occurrence of atherosclerotic plaques (Zureik et al. 2000) resulting in stroke (Kitamura et al. 2004). It has also been demonstrated that patients with AHI>15 have larger volumes of atherosclerotic plaques than those with AHI<15 (Turmel et al. 2009) and CPAP treatment has shown promising results by reversing the early signs of atherosclerosis (Drager et al. 2007).
Bidirectional role of reactive oxygen species during inflammasome activation in acrolein-induced human EAhy926 cells pyroptosis
Published in Toxicology Mechanisms and Methods, 2021
Liping Jiang, Songsong Luo, Tianming Qiu, Qiannan Li, Chunteng Jiang, Xiance Sun, Guang Yang, Cong Zhang, Xiaofang Liu, Lijie Jiang
Atherosclerosis, which is a chronic inflammatory disease, is the leading cause of mortality worldwide (Soehnlein and Libby 2021; Xu et al. 2021). Early stages of atherogenesis characteristics are endothelial cell dysfunction, persistent inflammatory response, and changed vascular homeostasis (Mehta and Malik 2006; Badimón et al. 2009). Arterial inflammation is triggered by endothelium, ultimately results in endothelial cell activation and recruited inflammatory cells to the blood vessels (Mudau et al. 2012). Genetic, lifestyle, and environmental factors would all contribute to the occurrence of arteriosclerotic vascular disease. Epidemiological studies have shown evidence of the link between cigarette smoke and atherosclerosis (Barnoya and Glantz 2005; Raghuveer et al. 2016; Arnett et al. 2019). However, the mechanism of tobacco smoke-induced atherosclerosis remains unclear.
Understanding the role of alternative macrophage phenotypes in human atherosclerosis
Published in Expert Review of Cardiovascular Therapy, 2022
Kenji Kawai, Aimee E. Vozenilek, Rika Kawakami, Yu Sato, Saikat Kumar B Ghosh, Renu Virmani, Aloke V. Finn
Atherosclerotic lesions develop over time and hamper blood flow to vital organs. Narrowing of coronary and peripheral vessels due to atherosclerosis causes clinical symptoms (i.e. chest pain/angina pectoris for coronary arterial disease and claudication for peripheral arterial disease). A sudden rupture of an otherwise non-flow limiting coronary atherosclerotic plaque can cause thrombosis, which itself can lead to ischemia [1]. Rupture of coronary plaque is the leading cause of myocardial infarction, a major cause of death [2]. In 2019, as reported by the World Health Organization (WHO), ischemic heart disease was the leading cause of death and accounted for 16% of all deaths. The incidence of ischemic heart disease is expected to continue increasing in coming years, due to increasing prevalence of co-morbidities such as obesity, diabetes, and metabolic syndrome [3].
Related Knowledge Centers
- Arteriosclerosis
- Coronary Artery Disease
- Atheroma
- Stroke
- Artery
- Dyslipidemia
- Lesion
- Peripheral Artery Disease
- Kidney Disease
- Acute-Phase Protein