Hypertension – the Silent Killer

Hypertension – the Silent Killer

Journal of Pre-Clinical and Clinical Research, 2011, Vol 5, No 2, 43-46 REVIEW www.jpccr.eu Hypertension – The Silent Killer Katarzyna Sawicka1,2, Michał Szczyrek1, Iwona Jastrzębska1, Marek Prasał2, Agnieszka Zwolak1, Jadwiga Daniluk1 1 Chair of Internal Medicine and Department of Internal Medicine in Nursing, Medical University, Lublin, Poland 2 Department of Cardiology, Medical University, Lublin, Poland Abstract Hypertension is often called ‘the silent killer’ because it shows no early symptoms and, simultaneously, is the single most signifi cant risk factor for atherosclerosis and all clinical manifestations of atherosclerosis. It is an independent predisposing factor for heart failure, coronary artery disease, stroke, renal disease, and peripheral arterial disease. It is the most important risk factor for cardiovascular morbidity and mortality in industrialized countries. Key words hypertension, complications of hypertension INTRODUCTION diastolic blood pressure fall into diff erent categories, the highest category is used in assessing total cardiovascular Th e leading cause of mortality, responsible for roughly risk [1, 3]. one-third of all deaths globally, is cardiovascular disease. Th ere are 2 types of hypertension depending on etiology Th e majority of these events are caused not by one single – ‘primary’ (also called ‘essential’) hypertension and cardiovascular risk factor, but rather a mixture of several ‘secondary’ hypertension. Essential hypertension is the most factors. Th e most important of these in industrialized prevalent type, aff ecting 90-95% of hypertensive patients [4]. countries is not only hypertension, but also high levels of Th e pathogenesis of primary hypertension is multifactorial blood lipids, obesity, physical inactivity, smoking, glucose and complicated. Genetic factors play an important role. intolerance/diabetes and age. High blood pressure certainly Environmental factors, such as sedentary lifestyle, stress, represents a modifi able risk factor [1]. In the year 2000 it smoking, obesity [5], salt (sodium) sensitivity [6] and alcohol is estimated that nearly one billion people (~26% of the intake, also are signifi cant. Th e aforementioned factors, adult population worldwide) had hypertension. Th e number for example increased salt intake and obesity, have long patients with hypertension increases every year, and by 2025 been known culprits. Th ese factors alone are probably not is expected to rise to 29% of the population [2]. suffi cient to raise blood pressure to abnormal levels, but are synergistic with a genetic predisposition. Other factors that Defi nition and etiology. Hypertension, also known as may be involved in the pathogenesis of primary hypertension high blood pressure, is defi ned as systolic blood pressure are hyperactivity of the renin-angiotensin-aldosteron system of 140 mmHg or higher and/or diastolic blood pressure of and sympathetic nervous system, abnormal production 90 mmHg or higher. Th e classifi cation of blood pressure of natriuretic peptides, and defi ciency in endothelial used in the 2007 ESH/ESC Guidelines comprises categories vasodilatation substances [1, 3]. of optimal (systolic blood pressure less than 120 mmHg and Approximately 5-10% of patients with hypertension have diastolic blood pressure less than 80 mmHg), normal (systolic identifi able secondary hypertension. It is important to blood pressure 120-129 mmHg and/or diastolic blood pressure recognize this type hypertension since it is treated diff erently 80-84 mmHg), and high-normal (systolic blood pressure 130- to essential hypertension, by treating the underlying cause 139 mmHg and/or diastolic blood pressure 85-89 mmHg) of the elevated blood pressure. Th e history, examination, blood pressure, followed by 3 grades of hypertension, and and routine laboratory tests may identify such patients, in a separate category for isolated systolic hypertension. Th e particular, patients who suddenly develop severe hypertension 3 grades of hypertension correspond to: at an early age and which is treatment resistant. Th e causes 1) mild (systolic blood pressure 140-159 mmHg and/or dia- include renal disease (renal artery stenosis), obstructive stolic blood pressure 90-99 mmHg); sleep apnea, primary aldosteronism, Cushing’s syndrome, 2) moderate (systolic blood pressure 160-179 mmHg and/or pheochromocytoma, coarctation of the aorta (uncommon), diastolic blood pressure 100-109 mmHg); hypertension associated with pregnancy, estrogen use, as 3) severe hypertension (systolic blood pressure 180 or greater well as other causes (eg. medications) [1, 3]. and/or diastolic blood pressure 110 mmHg or greater). Isolated systolic hypertension (systolic blood pressure Complications of hypertension. Hypertension is oft en 140 mmHg or higher), is graded as 1, 2, or 3, according to called ‘the silent killer’ because it is a disease that shows no early the systolic blood pressure level, provided that the diastolic symptoms, and simultaneously, is the single most signifi cant blood pressure is less than 90 mmHg. When systolic and risk factor for heart disease: myocardial infarction, left ventricular hypertrophy, congestive heart failure, aneurysm, Corresponding author: Katarzyna Sawicka Chair of Internal Medicine and Depart- stroke, as well as chronic kidney disease (hypertensive ment of Internal Medicine in Nursing, Medical University, Lublin, Jaczewskiego 8, 20-954 Lublin, Poland. nephropathy) and hypertensive retinopathy [1, 3]. Th e E-mail: [email protected] complications of hypertension are related either to sustained Received: 15 July 2011; accepted: 24 September 2011 elevations of blood pressure, with consequent changes in the 44 Journal of Pre-Clinical and Clinical Research, 2011, Vol 5, No 2 Katarzyna Sawicka, Michał Szczyrek, Iwona Jastrzębska, Marek Prasał, Agnieszka Zwolak, Jadwiga Daniluk. Hypertension – The Silent Killer vasculature and heart, or to the accompanying atherosclerosis such as atherosclerotic coronary artery disease or valvular that is accelerated by long-standing hypertension. heart disease. In addition, patients with isolated systolic Mild to moderate primary hypertension is largely hypertension may encounter this complication a little earlier. asymptomatic for many years. Th e most frequent symptoms, In contrast, diastolic function in hypertension is impaired headache, fatigue, dizziness and facial fl ushing, are also very even at an early stage. Th e factors that aff ect diastolic non-specifi c. Suboccipital pulsating headaches, occurring function in hypertensive patients are multiple. One of these early in the morning and subsiding during the day, are factors is aging, which is associated with a decline in left said to be characteristic, but any type of headache may ventricular relaxation and increased diastolic stiff ness [13, occur [1, 7]. Accelerated hypertension is associated with 14]. Diastolic dysfunction is also signifi cantly related to somnolence, confusion, visual disturbances, nausea and myocardial ischemia and enhanced loading conditions on vomiting (hypertensive encephalopathy) [1]. the heart. In addition, neurohumoral factors and alterations Hypertension is a well-known risk factor that predisposes at the cellular level may be involved [15, 16]. It is generally to the development of left ventricular hypertrophy, coronary accepted that diastolic dysfunction can lead to congestive fl ow abnormalities, and systolic and diastolic dysfunction. heart failure even when systolic function is normal. Under Th is complex of abnormalities is known as hypertensive heart such circumstances the heart is not dilated, but fi lling disease and eventually leads to heart failure [8]. Already in conditions of the left ventricular are impaired because the Framingham Study in which 5,127 people were followed of its inability to relax appropriately. As a consequence, up for 14-18 years, 492 cases of coronary heart disease were stroke volume decreases, left ventricular fi lling pressure identifi ed, and 142 cases of congestive heart failure [9]. increases, and pulmonary congestion ensues [13, 14]. First Left ventricular hypertrophy in hypertension is associated apparent during exercise, the signs of left ventricular failure with an increase in the size of cardiac myocytes, an increase in become increasingly evident at rest. Although it is not size as well as number of non-myocyte cells (e.g., fi broblasts), entirely clear which structural abnormalities dictate the accumulation of collagens, and infi ltration by monocytes and transition from adaptive hypertrophy to congestive heart lymphocytes. Th erefore, whereas myocytes can hypertrophy failure, molecular changes in contractile proteins as well only because they are terminally diff erentiated, the interstitial as disturbances in collagen cross-linking are among the cells undergo both hypertrophy and hyperplasia. Th e excess mechanisms potentially involved. Ventricular dilatation collagen produced and deposited by the fi broblasts leads to is accompanied by wall thinning, augmented systolic wall interstitial and perivascular fi brosis. Th is entire process has stress, and a reduction in the ejection fraction, the latter been referred to as cardiac remodeling and signifi cantly being aggravated by the increased aft erload. Th erefore, as alters the physical properties of the myocardium [10]. the heart increases in size, pump function and contractility Th e intramyocardial vascular bed is also aff ected by the progressively deteriorate. Clinically, this situation

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