Copyright EMAP Publishing 2018 This article is not for distribution Clinical Practice Keywords Atherosclerosis/Cholesterol/ Ischaemia/Angina/Stenosis/Vasculitis Systems of life This article has been Vascular system double-blind peer reviewed In this article... ● Pathogenesis, types of and risk factors for arterial diseases ● Cellular mechanism of atherosclerosis ● Vasculitides, a rarer type of vascular disease Vascular system 2: diseases affecting the arterial system Key points Author Selina Jarvis is a research nurse and former Mary Seacole development In atherosclerosis, scholar at Kingston and St George’s University of London and King’s Health Partners a lipid-rich plaque (Guy’s and St Thomas’s Foundation Trust). forms on the innermost layer Abstract With its arteries and veins, the vascular system connects the heart with of the artery wall all other organs and tissues and circulates blood around the body. It can be affected by diseases with different pathogenic mechanisms. Many arterial diseases are Atherosclerosis underpinned by atherosclerosis, while some have genetic origins or are immune- plays a role in many mediated. This article, the second in a three-part series, describes the diseases where pathophysiology of the main arterial diseases. The first article in the series covered there is narrowing the anatomy and physiology of the vascular system, and the third will discuss or blockage of the diseases of the venous system. arteries Citation Jarvis S (2018) Vascular system 2: diseases affecting the arterial system. Modifiable risk Nursing Times [online]; 114: 5, 58-62. factors for arterial disease include hyperlipidaemia, he vascular system is a complex larger and medium arteries, such as the diabetes, network of blood vessels con- aorta and the coronary, cerebral and hypertension necting the heart with all other peripheral arteries (Zhao, 2018). These and smoking Torgans and tissues in the body become hardened and lined with athero- via the arteries (which bring oxygenated sclerotic ‘plaque’ – also known as ath- In the coronary blood to the organs and tissues) and veins eroma, which restricts the supply of oxy- arteries ischaemia (which return to the heart with deoxygen- genated blood to the organs and tissues. causes chest pain, ated blood). Its structure, physiology and The progressive formation of atheroma while in the arteries function are described in the first article of in the arterial vessels can begin in child- of the lower limbs it this three-part series. hood. It is the result of endothelial cell dys- causes claudication This article, the second in the series, function, lipid deposition and complex reviews the common diseases affecting the inflammatory processes. Vasculitides are arteries. In many of them, the underlying The squamous epithelial cells that form diseases of blood pathogenic process is atherosclerosis. the endothelium (innermost layer of the vessels caused by vessel wall) are delicate and vulnerable to immune-mediated Atherosclerosis hyperlipidaemia, hyperglycaemia (from processes The general term for the hardening of the diabetes), hypertension and toxins such as arteries is arteriosclerosis – from the Greek cigarette smoke, which culminates in low- arterio (artery) and skleros (hard). Arterio- grade inflammation. Once injured, the sclerosis can have different causes, endothelial cells change shape and their including blood vessel calcification (more properties are altered; they become common in older people), but is most com- increasingly permeable to fluids, lipids monly due to atherosclerosis. and immune cells. The disease is particularly prevalent in Monocytes are immune cells that survey CREDIT XXXXX the Western world and is the single largest the integrity of the endothelium. If they cause of arterial disease. It affects the detect damage, they go to the damaged Nursing Times [online] May 2018 / Vol 114 Issue 5 58 www.nursingtimes.net Copyright EMAP Publishing 2018 This article is not for distribution Clinical Practice Systems of life Fig 1. Mechanism of atherosclerosis Monocyte adherence and transendothelial migration External elastic membrane Monocyte Transendothelial Smooth muscle migration cell layer Rolling Adhesion Matrix Endothelium Activated resident Secretion of Foam cell macrophage inflammatory differentiation; fatty molecules streak formation Monocyte adherence Monocyte differentiation into macrophage and T-lymphocyte lipid-laden foam cell activation Monocyte Macrophage Foam cell Smooth muscle cell migration Circulating cell Activated phagocyte; Lipid-laden; recruited to secretes inflammatory plays active role inflammatory site molecules, free in cholesterol radicals and metabolism and proteases, and secretes scavenges lipoprotein macrophage particles products area, insert themselves beneath the layer of or due to atherosclerotic plaque rupture atherosclerotic narrowing, and atheroscle- cells and mature into macrophages. These and formation of new thrombus, which rosis is the most common cause of coro- trap cholesterol carriers circulating in the migrates and affects cerebral blood flow. nary artery disease (CAD) (Jarvis and vessels – particularly oxidised low-density Blockage of the arteries supplying the Saman, 2017). lipoproteins (LDLs) – and become lipid- lower limbs has similar effects, causing Narrowing or blockage of the coronary laden foam cells (Fig 1), which in turn peripheral arterial disease (PAD). arteries causes ischaemia, which often man- release a plethora of inflammatory sub- The atheroma tends to form at sites ifests as chest pain. In stable angina, there is stances and growth factors. This further where arteries bend, branch off or bifur- a fixed flow defect caused by a stable ath- encourages atheroma formation. cate (for example, where the two common eroma restricting blood supply to the myo- Cholesterol accumulates not only in carotid arteries divide into the two internal cardium. When a patient with stable angina foam cells, but also in the atheroma itself, and external carotid arteries). undertakes exercise or is under stress, there where it forms a lipid core. Lipid-rich Conversely, stretches of straight blood is a mismatch between blood supply to, and plaques contain inflammatory cells,vessel often remain atheroma free, com- blood demand of, the myocardium, which smooth muscle cells, cellular debris and a pared with areas where there is disturbed causes chest pain. Upon rest or stress reduc- fibrous capsule. The plaques are prone to blood flow. Such sites are characterised by tion, the symptoms resolve. rupture, which can ultimately block arte- alterations in blood flow and shear stresses In unstable angina (UA), which belongs rial blood flow, leading to a dramatic mis- (caused by frictional forces by the blood to a spectrum of conditions called acute match between supply to, and demand of, flow) on the endotheliumm, which plays a coronary syndrome, the atheroma pro- the affected organs or tissues. role in atherosclerosis (Zhao, 2018). gresses further and chest pain may also In the heart, aberrations in arterial occur at rest and become more frequent blood flow can lead to myocardial infarc- Coronary artery disease and/or more severe. However, in the case of tion (MI). In the arteries supplying the The coronary arteries provide oxygenated UA, there is no detectable myocardial cell brain, atherosclerosis can lead to a cere- blood to the heart (myocardium). The right necrosis when assessed using biochemical brovascular accident (stroke), either and left coronary arteries and their tests such as troponin levels (a myocardial because the arteries have become stenotic branches are easily affected by protein used as a marker of damage). Nursing Times [online] May 2018 / Vol 114 Issue 5 59 www.nursingtimes.net Copyright EMAP Publishing 2018 This article is not for distribution Clinical Practice Systems of life Complete abrogation of the coronary Fig 2. Circle of Willis blood supply can result in irreversible damage to the region of the myocardium Anterior communicating artery supplied by the affected artery. This often Frontal lobe occurs due to the rupture of an atheroma in the vessel wall, which triggers the for- Horizontal segment of Optic chiasm mation of a thrombus. anterior cerebral artery The thrombus causes acute ischaemia, which, if left untreated, can lead to myo- Temporal lobe Horizontal segment of cardial cell necrosis and MI involving middle cerebral artery either the whole thickness of the heart Right posterior muscle (ST elevation MI) or only part of the communicating cardiac wall (non-ST elevation MI). In case artery of ST elevation MI, without reperfusion within 6-12 hours, there will be irreversible Superior Left posterior cerebellar artery damage, cardiac remodeling, arrhythmias, communicating artery heart failure and a high risk of death (Jarvis Pontine branches and Saman, 2017). Right anterior Basilar artery Cerebrovascular disease inferior cerebellar The brain receives blood from two main artery paired arteries; the internal carotid and Right vertebral artery vertebral arteries, and where their branches terminate (at the base of the brain) form the anastomotic Circle of Willis supplying different regions of the brain (Fig 2). Table 1. Stroke types and risk factors Cerebrovascular disease (CVD) includes events, such as cerebrovascular accidents Haemorrhagic stroke Risk factors (strokes), in which brain tissue becomes Intracerebral haemorrhage Hypertension, trauma, vascular starved of oxygen and risks permanent malformations, bleeding