essential hypertension
Introduction
Introduction to essential hypertension In the vast majority of patients, the cause of hypertension is unknown, called primary hypertension, accounting for more than 95% of total hypertension; in less than 5% of patients, elevated blood pressure is a clinical condition of certain diseases. Performance, which has a clear and independent cause, is called secondary hypertension. Essential hypertension, also known as hypertension, in addition to the symptoms associated with high blood pressure itself, long-term hypertension can also become an important risk factor for a variety of cardiovascular and cerebrovascular diseases, and affect important organs such as the heart and brain The function of the kidneys can eventually lead to the failure of these organs. basic knowledge Probability ratio: Essential hypertension is related to heredity, the patient population is generally around 10%, and the patients over 50 years old are around 15%. Susceptible people: no special people Mode of infection: non-infectious Complications: coronary heart disease, heart failure, arrhythmia, transient ischemic attack, hypertensive encephalopathy, aortic dissection
Cause
Cause of primary hypertension
Gender and age (15%):
In most parts of the world, the prevalence of hypertension is higher in men than in women, especially before the age of 35. After 35 years of age, the prevalence of hypertension and blood pressure in women may exceed that of men, possibly with pregnancy, pregnancy and postpartum eating habits. Associated with endocrine changes, the average blood pressure increases with age for both men and women, with increased systolic blood pressure more pronounced than diastolic blood pressure.
Occupation (12%):
The prevalence of hypertension in people with mental work and intense work is higher than that of manual workers. The prevalence of urban residents is higher than that of rural residents, and the age of onset is early. The possible causes and life stress, mental factors, psychological factors and social occupations related.
Diet and blood pressure (13%):
It has been confirmed that excessive intake of sodium salt, heavy drinking, long-term consumption of espresso, lack of calcium in the diet, excessive consumption of saturated fatty acids in the diet, and a decrease in the ratio of unsaturated fatty acids to saturated fatty acids can promote blood pressure. On the contrary, there are Adequate potassium, calcium, magnesium and high-quality protein can prevent blood pressure from increasing. The blood pressure of vegetarians is often lower than that of meat-based ones, and the blood pressure level of frequent fish eating areas is often low. It can be seen that dietary and nutritional factors are Blood pressure regulation plays an important role.
Smoking factor (20%):
Smoking not only has adverse effects on the respiratory system, but also a risk factor for coronary heart disease, and can increase blood pressure. Nicotine and trace elements in tobacco contain high levels of cadmium, and excessive intake of nicotine and cadmium can lead to elevated blood pressure.
Obesity and overweight (10%):
The prevalence of hypertension in obese people is 2 to 6 times that of normal weight. Hypertension, obesity, insulin resistance, hyperinsulinemia, hypertriglyceridemia and low HDL cholesterol often coexist. Hypertension and diabetes often induce atherosclerotic cardiovascular disease, so losing weight can not only lower blood pressure, but also benefit diabetes and coronary heart disease.
Genetic factors (15%):
Hypertension has a certain relationship with heredity. Most scholars believe that hypertension is a multi-gene inheritance. Epidemiological investigations have found that the prevalence of hypertension in hypertensive patients is significantly higher, especially in monozygotic twins; parents have high blood pressure. The probability of high blood pressure in their children is as high as 45%. On the contrary, if the blood pressure of both parents is normal, the probability of their children suffering from hypertension is only 3%. It is currently considered that essential hypertension is a certain congenital genetic gene and many A multifactorial disease caused by the interaction of pathogenic pressurization factors and physiological decompression factors.
Regional differences (10%):
The blood pressure levels of different populations are different. The average systolic blood pressure in the northern part of China is higher than that in the south, and the prevalence of hypertension is also increased. The possible causes are related to climatic conditions, eating habits, lifestyle, etc. Differences in blood pressure levels between people may be related to genetic factors in addition to the above factors.
Mental and psychological factors (8%):
Mental stress, poor mental stimulation, cultural quality, economic conditions, noise, personality, etc. may affect blood pressure levels.
Pathogenesis
The pathogenesis of essential hypertension is complex and has not yet been fully elucidated. It is currently believed that the following factors play an important role in the pathogenesis of hypertension.
Pathogenesis
(1) Heart output changes:
Early hypertensive patients often have increased cardiac output, indicating that increased cardiac output plays a role in the initiation mechanism of essential hypertension, which may be related to sympathetic excitation and increased secretion of catecholamines.
(2) Kidney factors:
The kidney is the main organ that regulates water, electrolytes, blood volume and excretion of metabolites in the body. Abnormal renal function can lead to water, sodium retention and increased blood volume, causing blood pressure to rise, and the kidneys can also secrete pressurized and antihypertensive substances. The kidney plays an important role in maintaining the balance of blood pressure in the body.
Renal cells can synthesize and excrete renin. Renin has a significant regulation of blood pressure. The renin-angiotensin-aldosterone system regulates blood pressure. The kidney also secretes antihypertensive substances, such as renal medullary stromal cells. Prostaglandins PGA, PGE, etc., they have the effect of regulating renal blood flow distribution, inhibiting sodium reabsorption and dilating blood vessels, and any cause of increased excretion of blood pressure or decreased blood pressure, and the imbalance between the two. Can affect blood pressure levels.
(3) Renin-angiotensin-aldosterone system (RAAS):
The system consists of a series of hormones and corresponding enzymes. RAAS plays an important role in regulating water, electrolyte balance and blood volume, vascular tone and blood pressure. Renin is mainly synthesized and excreted by renal mesangial cells, which can promote the main Angiotensinogen (AN) synthesized by the liver is converted to angiotensin I (AngI). AngI has little biological activity and must be converted to angiotensin II (Ang II) by angiotensin converting enzyme to vascular smooth muscle and adrenal gland. Cortex and brain play a role, AngII can be converted to angiotensin III (AngIII) under the action of aminopeptidase, but AngIII vasoconstriction is only 30% to 50% of AngII, and its pressurization is only 20% of AngII. AngII is a powerfully pressurized substance that can directly contract the smooth muscle of small arteries. It can also be indirectly pressurized by the brain and autonomic nervous system, and can promote the excretion of aldosterone in the adrenal cortical globular zone. The latter has the retention of sodium water and increase blood volume. Under normal circumstances, renin, angiotensin and aldosterone are in dynamic equilibrium, mutual feedback and constraints, under pathological conditions, RAAS can become hypertensive Important mechanisms, recent studies have confirmed that different tissues (heart, blood vessel wall, kidney, brain, etc.) can autocrine and paracrine RAAS, RAAS excretion abnormalities in these tissues, leading to vascular smooth muscle cell proliferation, vasoconstriction, myocardial Cellular hypertrophy and fibrosis of cardiomyocytes have a more important role in thickening of the vessel wall, increased vascular resistance, decreased left ventricular hypertrophy and compliance, and a sustained increase in blood pressure.
(4) abnormal cell membrane ion transport:
Through the study of sodium and potassium ion concentration and gradient on both sides of the cell membrane, it has been confirmed that patients with essential hypertension have introverted sodium, potassium synergistic function and sodium pump inhibition, which increases intracellular sodium ions, which not only promotes arteries. The wall has increased sensitivity to certain vasoactive substances in the blood, and increases the permeability of vascular smooth muscle cell membrane to calcium ions, which increases intracellular calcium ions, strengthens vascular smooth muscle excitation-contraction coupling, and causes vasoconstriction or, leading to increased peripheral vascular resistance and elevated blood pressure, the basic cause of abnormal ion transport of cell membrane is congenital genetic defects, and endocrine factors may aggravate this defect.
(5) Increased sympathetic activity:
Sympathetic nerves are widely distributed in the cardiovascular system, and sympathetic nerve excitability increases in the heart, which can lead to increased heart rate, increased myocardial contractility and increased cardiac output; acting on vascular alpha receptors can cause small arteries to contract, peripheral vascular resistance Increased and elevated blood pressure, norepinephrine as a sympathetic neurotransmitter has a strong vasoconstriction and a boosting effect, indicating that sympathetic dysfunction and increased activity play a role in the pathogenesis of hypertension.
(6) Increased vascular tone and thickened wall:
The imbalance of blood circulation itself, leading to increased tension of small arteries and venules, is an important cause of hypertension. Hypertensive patients have increased sensitivity and reactivity to vasoactive substances (especially boosting substances) due to vascular smooth muscle, leading to vascular tone. Increased, peripheral vascular resistance increased and blood pressure increased, the main cause of increased vascular smooth muscle sensitivity in hypertensive patients is cell membrane properties and ion transport abnormalities, especially membrane permeability to calcium ions increased, membrane potential and membrane stability decreased, And the membrane is associated with increased sodium ion permeability.
(7) vasodilators:
In addition to blood pressure substances and systems in the body, there are many endogenous decompression (vasodilator) substances and systems to antagonize to maintain relatively stable blood pressure, lack of decompression substances or decreased function in the body may also lead to increased blood pressure. Another reason is that the kinin-prostaglandin system is deficient in function, the release of bradykinin is reduced, and prostaglandin (PG) substances (such as PG12, PGF2, and PGA2) with strong vasodilator effects are reduced, which can increase peripheral vascular resistance. Increase blood pressure, in addition, there are many vasodilators and antihypertensive substances in the body, such as atrial peptide (atrial natriuretic peptide), calcitonin gene-related peptide, urinary sodium hormone, antihypertensive peptide and renal medullary blood pressure reduction A decrease in the substance can lead to an increase in blood pressure. The endothelial cell excretion of endothelial cells (mainly nitric oxide) and prostacyclin also have a strong vasodilator effect. Once the release is reduced, the thromboxane produced by the endothelial cells is reversed. The increase in endothelin-like vasoconstrictors is also one of the causes of elevated blood pressure.
(8) Genetics:
The establishment of experimental spontaneously hypertensive rat strains has opened up new avenues for the study of hypertension and genetics. It is currently believed that human essential hypertension is a polygenic hereditary disease, and gene expression is largely Due to environmental factors, the cause of genetic deviation is unknown.
(9) Neurological and spiritual factors:
The role of central nervous system dysfunction in the pathogenesis of hypertension has long been recognized, mental stress can promote the release of adrenaline, cerebral cortex excitation and inhibition disorders, causing subcortical vasomotor dysfunction, sympathetic excitation and peripheral vascular persistence Sexual contraction, leading to elevated blood pressure, there are many blood pressure regulating substances in the central nervous system, such as angiotensin, vasopressin, endorphin, substance P, enkephalin, and neuropathic Peptides and neuropeptide Y, etc., which play a role in the regulation of cardiovascular system function and blood pressure levels.
(10) Abnormal ratio of receptors:
It has been reported that the total number of -receptors in normal blood pressure rats and salt-sensitive hypertensive rats is the same, but the ratio of 1 to 2 receptors is quite different, and the number of 1 receptors in salt-sensitive rats is down-regulated, while the number of 2 receptors is down-regulated. The increase indicates that the cardiac -type receptors (2 and 1) are differently adjusted during the occurrence of hypertension in this type of hypertensive rats. Some patients have myocardial fibrils in 15 middle-aged salt-sensitive hypertensive patients and 15 normal blood-pressure patients. Cell culture, determination of the total number of 2, 2 receptors, the number of receptors did not increase, the number of 2 receptors in the hypertension group was reduced by half compared with normal people. From the above data, the number of and receptors in the heart and blood vessels of hypertensive patients and The proportion is different from normal, and these differences may also be one of the causes of high blood pressure.
(11) Hyperinsulinemia:
In recent years, studies have confirmed that hypertensive patients are often accompanied by hyperinsulinemia and insulin resistance. The mechanisms of hyperinsulinemia-induced hypertension include:
1 Insulin causes renal tubular reabsorption of sodium, which increases total sodium in the body, leading to an increase in extracellular fluid volume. The body maintains sodium balance and promotes urinary excretion by increasing glomerular perfusion pressure, thereby increasing blood pressure.
2 Insulin enhances sympathetic nerve activity, and increased sympathetic nerve activity can increase renal tubular sodium reabsorption, increase cardiac output and peripheral vascular resistance, leading to elevated blood pressure.
3 insulin stimulates H-Na exchange activity, which is related to Ca2 ion exchange, which increases intracellular Na ion and Ca2 ion, thereby enhancing vascular smooth muscle to vasopressor substances (such as norepinephrine, angiotensin II) and The sensitivity of blood volume expansion promotes blood pressure.
4 insulin can stimulate the thickening of the blood vessel wall, the narrowing of the blood vessel cavity, and increase the peripheral vascular resistance and lead to an increase in blood pressure.
In summary, the pathogenesis of hypertension is extremely complicated, and its occurrence and development are often the result of a combination of various factors. For specific patients, the situation varies from person to person, and the effects of these factors may be different. A comprehensive consideration and comprehensive analysis must be made.
2. Pathology
Early hypertension can only manifest as increased cardiac output and/or increased systemic small arterial tone, contraction or spasm. As hypertension persists and progression, it can cause pathological changes in systemic arterioles and target organs. The degree of damage is not only related to blood pressure, but also related to the fluctuation of blood pressure. It is also related to the presence or absence of other risk factors (such as diabetes, coronary heart disease, hyperlipidemia, etc.). Hypertension can not only cause arterial wall hypertrophy, lumen Narrowing and hardening, and can promote the deposition of platelets and lipids on the blood vessel wall, leading to vascular occlusion. The heart is the main target organ of hypertension. Long-term high blood pressure can cause left ventricular hypertrophy. Early heart chamber may not expand, mainly causing diastolic function. Incomplete, followed by elevated blood pressure, endothelium-derived endothelial cells (mainly nitric oxide) and prostacyclin also have strong vasodilator effects. Once released, thrombin and endothelium are produced by endothelial cells. The increase in vasoconstrictor substances is also one of the causes of elevated blood pressure.
(1) Arteries: Early arteriolar arteries in the early stage of hypertension mainly show contraction and increased tension. Over time, hypertension affects the vascular endothelium and smooth muscle cells, and the endometrial permeability changes the arterial wall. The surface is not smooth, uneven, followed by increased permeability of the arterial wall, red blood cells in the circulation, platelets can enter the endometrium and adhere to it, smooth muscle cells migrate from the middle layer to the endometrial deposition and hyperplasia, the intima thickens, connective tissue Increase, so the wall thickens, hardens, narrowed, even occluded, can lead to small arteriosclerosis, in addition, increased eddy currents in blood flow during hypertension, can increase endovascular damage, is conducive to platelet and lipid adhesion And deposit on the blood vessel wall, and can cause vascular expansion, stimulate the increase of lysosomes in smooth muscle cells, clear the cholesterol in the arterial wall, reduce the capacity of low-density lipoprotein, easily lead to the formation of atherosclerosis, so hypertension is coronary heart disease Important risk factors.
(2) Heart: The heart is one of the main target organs of hypertension. This disease can lead to changes in heart function and structure. Long-term high blood pressure keeps the heart in a state of heavy load, which can cause left ventricular hypertrophy, mainly as left. Room centripetal hypertrophy, that is, the wall of the chamber, the ventricular septum is symmetric hypertrophy, the ventricular cavity is not enlarged, more common in hypertensive patients with significantly increased peripheral resistance and relatively low cardiac output and no heart failure; cardiac output is relatively high or repeated In patients with heart failure, it can be characterized by eccentric hypertrophy, that is, the ventricular cavity is enlarged, but the ratio of the wall to the chamber does not increase.
Hypertension caused by left ventricular hypertrophy is not only related to blood pressure levels, but also related to various neurohormones and certain active substances. In the past, norepinephrine and angiotensin II were suspected to be irritants of left ventricular hypertrophy. Endothelin-1, insulin and platelet growth factor (PDGF), growth response gene-1 (EGr-1) are both myocardial growth inducers, while EGr-1 product may be the third messenger. In addition, the capacity factor is left. Ventricular hypertrophy also plays an important role. Left ventricular hypertrophy and hypertension cause coronary atherosclerosis and/or atherosclerotic lesions are the pathological basis of hypertension heart damage.
Left ventricular hypertrophy (LVH) and remodeling are independent risk factors for cardiovascular disease. It is one of the determinants of heart failure and fatal arrhythmia. Ventricular remodeling refers to changes in ventricular structure and causes ventricles. Abnormal sarcoplasm and volume, increased ventricular volume, changes in ventricular morphology and geometric configuration, remodeling is often a self-perpetuating process, the nature and mechanism of left ventricular hypertrophy and remodeling and the following factors related:
1 Cardiomyocyte hypertrophy: long-term mechanical traction with hypertension and activation of angiotensin II in the myocardium, and increased catecholamine activity, which stimulates the synthesis of fetal isoform contractile protein. The life span of this protein is 4 to 5 years, and normal. Cardiomyocytes can survive for 90 to 100 years. Therefore, the increase of this type of fetal protein not only increases myocardial oxygen consumption and energy consumption, but also increases myocardial contractility, which may lead to heart failure and shortened myocardial life.
2 myocardial interstitial fibrosis: interstitial fibroblast hypertrophy, interstitial collagen content increased, angiotensin II and aldosterone can activate and promote fibroblast proliferation, hypertrophy, myocardial interstitial fibrosis to myocardial compliance Decreased, ventricular diastolic dysfunction, myocardial fibrosis is divided into reactive fibrosis and repair fibrosis, the former is characterized by accumulation along the blood vessels and radiating around, more common in hypertension, etc.; the latter is myocardial necrosis repair fiber Collagen hyperplasia, it is currently believed that myocardial fibrosis is mainly related to the activity of circulating renin-angiotensin-aldosterone system, and left ventricular hypertrophy is related to myocardial local renin-angiotensin-aldosterone activity. Hypertensive patients often have circulation and myocardial Local renin-angiotensin-aldosterone system activation.
3 coronary artery changes: hypertension can cause extravascular membrane fibrosis, middle layer thickening (smooth muscle cell proliferation), intimal hyalinization and endothelial cell damage, hyperplasia, coronary stenosis and increased blood flow resistance, and can promote porridge The formation of sclerosing plaques, therefore, hypertension can not only lead to coronary heart disease, but also can cause small coronary lesions, eventually leading to left ventricular hypertrophy and cardiac insufficiency.
(3) Kidney: The damage of primary benign hypertension to the kidney is mainly manifested as benign renal arteriosclerosis. Due to the slow progress of the disease, the prevalence of elderly patients is high. It is the pathological basis of hypertensive kidney disease. Arteriosclerosis is mainly involved in arterioles and interlobular arteries, which can cause renal parenchymal ischemia, atrophy, fibrosis and necrosis, leading to chronic renal insufficiency, which can aggravate hypertension and form a vicious circle.
The kidney volume of patients with early and mild hypertension is normal, and the kidneys of moderate to severe and advanced patients can be lightly and moderately reduced. The surface of the subcortical cortex can be fine-grained and uneven. Light microscopic examination of the intima of the small arterioles and interlobular arteries Sexual thickening, narrowing of the lumen, hyaline degeneration of the small arteries, immunofluorescence, immunoglobulin IgM, complement C3 and 2 microglobulin deposition in the lesion, in addition, renal tubules, renal interstitial and kidney The pellet can be secondary to ischemic changes.
Malignant hypertension can cause extensive acute arteriolar damage, and the kidney often suffers serious damage. It is mainly characterized by proliferative endometritis of the small arteries and interlobular arteries. The lumen is significantly narrowed or even completely occluded. Thinning or rupture of the endothelium, small arteries may be mucoid degeneration or fibrin degeneration, but no acute inflammatory cell infiltration and cell necrosis, due to severe damage to the renal vascular network, can cause ischemic necrosis, degeneration and fibrosis of the renal parenchyma Can cause kidney failure.
(4) Brain: The brain is the main target organ of hypertension, and it is also the cause of death or disability of hypertension in Chinese patients. The occurrence of hypertensive cerebrovascular accidents in China (including cerebral hemorrhage and/or cerebral infarction) The rate is 5 times higher than that of myocardial infarction. Hypertensive patients have a 6-fold higher cerebrovascular accident than normal blood pressure. The main complication of hypertension in Western countries is the involvement of the heart, which can cause heart failure and complicated coronary heart disease, myocardial infarction, and cerebrovascular disease. The accident rate is low and there is a big difference between the two.
Hypertensive brain lesions are mainly secondary to cerebrovascular disease. Because hypertension can cause aneurysms in some weak parts of the blood vessels of the brain, and it is more common in small arteries with an inner diameter of 100 ~ 300m. This microaneurysm is firstly performed by Charcot and Bouchard was discovered in 1872, so it is also called Charcot-Bouchard microaneurysm, which is distributed in the perforating artery supply area and nucleus of the basal ganglia, globus pallidus, outer capsule, thalamus and pons, and a few are distributed in the cerebral cortex. And the cerebellum, micro-aneurysm tube wall is thin, the middle layer and elastic layer are often replaced by connective tissue, the endometrium is often damaged by high-pressure blood flow impact, once the micro-aneurysm rupture can produce the corresponding part of bleeding symptoms, is hypertensive cerebral hemorrhage The main reason, in addition, high blood pressure is beneficial to the low-density lipoprotein from the endothelium into the wall of the blood vessels, resulting in cell wall fat degeneration or cellulose-like necrosis, the latter more common in patients with malignant hypertension or more severe hypertension The above vascular lesions can reduce vascular compliance, increase stiffness and brittleness of the wall, and easily cause rupture and bleeding.
Hypertension is also an important cause of cerebral infarction. It is more common in the elderly and hypertensive patients with increased systolic blood pressure or increased systolic blood pressure. Hypertension can lead to cerebral arteriosclerosis, narrowing or occlusion of the lumen, which is more common in clinical practice. The anterior, middle, posterior and basilar artery penetrating branches, due to occlusion or stenosis of the cerebral tissue, cause ischemia, necrosis and softening of the brain tissue, which can form a lacunar-like cerebral infarction, and corresponding clinical signs appear.
(5) Others: Hypertension can affect all organs of the body. Eye lesions are also a common complication of hypertension. It is most important for fundus arteriosclerosis and retinopathy. It can manifest as fundus vasospasm, contraction, exudation, hemorrhage and optic disc edema. It can lead to decreased vision and eye symptoms in patients. In addition, hypertension is also an important cause of aortic dissection.
Prevention
Prevention of essential hypertension
Prevention of hypertension not only reduces the prevalence of hypertension, but more importantly reduces or delays the onset of heart and cerebrovascular complications. Prevention of hypertension is divided into three levels: primary prevention is aimed at high-risk groups of hypertension. For the general population, preventive measures are taken when there are risk factors and no hypertension has occurred. Secondary prevention is a systematic and planned comprehensive treatment for patients with diagnosed hypertension to prevent aggravation or complications. In essence, it is primary prevention of arteriosclerosis, stroke, coronary heart disease, etc., tertiary prevention refers to the rescue of critically ill patients with hypertension, prevention of complications, reduction of death, and rehabilitation treatment after successful rescue. The prevention of hypertension is focused on primary prevention and secondary prevention.
1. Primary prevention measures
(1) Weight loss: Overweight and obesity are the main risk factors for hypertension. According to China's recently established standards, when the body mass index is >23, it is called overweight. The main measure of weight loss is to limit excessive intake and increase exercise.
(2) Reasonable diet: including reducing sodium intake, appropriately increasing potassium, calcium, and magnesium intake, and reducing dietary fat.
(3) Restricted drinking: Some studies have suggested that drinking and blood pressure have u-shaped curve relationship, and there is a threshold reaction (40g alcohol is the threshold). In order to prevent high blood pressure, it is best not to drink alcohol; if you have drinking habits, you should abstain from alcohol or try to Drink less alcohol (<50m1/d).
(4) Increase physical activity: The risk of high blood pressure is 1.52 times higher than that of physical activity. Therefore, it is recommended to adhere to regular physical activity, especially aerobic exercise.
(5) Psychological balance: The psychological pressure caused by personal factors and environmental factors often causes patients to adopt unhealthy lifestyles. The latter is related to the increased risk of hypertension and cardiovascular disease. Therefore, it should be treated correctly and try to alleviate various psychological pressures. .
2. Secondary preventive measures
Reasonable treatment for high blood pressure includes:
(1) The application of simple, effective, safe and inexpensive antihypertensive drugs reduces blood pressure to normal.
(2) Protect the target organ.
(3) Treatment with consideration of other risk factors.
(4) Improve the quality of life.
In short, comprehensive measures should be taken to individualize treatments that vary from person to person in order to achieve optimal results.
3. Carrying out comprehensive prevention and treatment of hypertension community is the fundamental way
(1) Hospital health education: All types of medical care institutions and their staff, at the same time implementing health care in clinical practice, implement health education, and achieve tertiary prevention through health education.
(2) Integrated community prevention and treatment: establish a prevention and treatment network, conduct personnel training, conduct epidemiological investigations, including baseline surveys and prospective heart, cerebrovascular disease surveys, grouping of people and implementation of interventions, and randomize the participants in the prevention and treatment Implement three levels of preventive measures for the intervention group.
4. Joint intervention of multiple cardiovascular risk factors
Several population studies have shown that although randomized clinical trials have confirmed the benefits of lowering blood pressure, the incidence of coronary heart disease, stroke, and overall mortality are still significantly higher in treated hypertensive patients than in non-hypertensive patients. Compared with non-hypertensive patients, the treated patients with hypertension have more severe arteriosclerosis and more obvious LVN. Therefore, it is suggested that there are many risk factors involved in the process of producing hypertension complications, and the prevention and treatment are high. At the same time of blood pressure, joint intervention of various cardiovascular risk factors should be performed.
(1) Smoking cessation: Smoking cessation can reduce the risk of various diseases including stroke, especially for young and middle-aged people. There is no difference in life expectancy between quitters and non-smokers before the age of 35.
(2) Lowering cholesterol: The risk of coronary heart disease is proportional to the decrease in cholesterol. When HMG coenzyme A reductase inhibitor is used to lower cholesterol by 1 to 1.5 mmol/L (40 to 60 mg/d), it can cause major coronary heart disease. The risk is reduced by 1/5 to 1/3. In addition, lowering cholesterol also reduces the risk of stroke.
(3) Treatment of diabetes: The results of the UKPDS trial for 10 years showed that insulin and sulfonylurea hypoglycemic agents can reduce the incidence of diabetic microangiopathy by 1/4, although coronary heart disease has a significant downward trend, but for large blood vessels. The impact of the incident is not yet clear.
(4) Antiplatelet therapy: For patients with coronary heart disease, the use of antiplatelet drugs such as aspirin can reduce the mortality rate of stroke. For those without a history of cardiovascular disease, antiplatelet therapy can reduce the risk of coronary heart disease, but whether to reduce stroke or total cardiovascular disease The risk of death is unclear. The HOT study confirmed that taking 75 mg of aspirin every day reduced the incidence of coronary heart disease by 1/3, but there was no significant decrease in ischemic stroke or cardiovascular mortality.
(5) Interventions of other risk factors: There is evidence that weight loss, exercise, and reduction of fibrinogen may improve the risk of cardiovascular disease, but it has not been confirmed by large clinical trials to supplement antioxidant vitamins such as vitamin C and vitamin E. And the reduction of cysteine-like vitamins such as folic acid, vitamin B12, and lowering uric acid levels may be beneficial, but it needs to be confirmed by large clinical trials.
Complication
Essential hypertension complications Complications coronary heart disease heart failure arrhythmia transient ischemic attack hypertensive encephalopathy aortic dissection
Complications of hypertension are divided into the heart, cerebral blood vessels, kidneys, fundus, aorta and peripheral arteries.
Left ventricular hypertrophy
It has been thought that hypertensive patients with left ventricular hypertrophy is a physiological, benign, and adaptive compensatory process of the heart. However, in recent years, studies have found that left ventricular hypertrophy is independent of cardiovascular disease incidence and mortality. The predictive factor has become a new target for the treatment and prevention of hypertension.
The exact incidence of left ventricular hypertrophy in patients with hypertension is unknown. The Framingham Heart Study investigated the prevalence of hypertension and left ventricular hypertrophy in the Framingham area of the United States from 1950 to 1989. It was found that with the widespread use of antihypertensive drugs, the ECG was detected left. The ventricular hypertrophy was significantly reduced. The male population decreased from 4.5% to 2.5% in the general population; the female decreased from 3.6% to 1.1%, and the incidence of left ventricular hypertrophy in patients with mild to moderate hypertension was 20% to 50%. Severe hypertension The incidence of left ventricular hypertrophy in patients is as high as 90%. It is presumed that the incidence of left ventricular hypertrophy in male hypertensive patients is 25%, and the incidence of left ventricular hypertrophy in female hypertensive patients is 26%.
2. Coronary heart disease
In addition to type 2 diabetes and smoking, hypertension is the strongest risk factor for coronary heart disease. Hypertensive patients with coronary heart disease are about twice as high as those with normal blood pressure. 50% of male coronary heart disease and 75% of female coronary heart disease have hypertension. In Western countries, the risk of coronary heart disease caused by hypertension is 2 to 3 times that of cerebrovascular disease. Most hypertensive patients die of coronary heart disease. In comparison, systolic blood pressure has a greater impact on coronary heart disease than diastolic blood pressure. For example, male systolic blood pressure 19.7 to 21.3 kPa (148 to 160 mmHg) is twice as dangerous as coronary heart disease compared with systolic blood pressure <19.7 kPa (148 mmHg).
3. Heart failure
In the Framingham Heart Study, coronary heart disease and hypertension are the most common causes of congestive heart failure, accounting for approximately 90%. Multivariate analysis of the general population indicates that in men, hypertension accounts for 39% of the causes of heart failure in women. Hypertension accounts for 59% of the causes of heart failure, and the risk of heart failure in hypertensive patients is 2 to 3 times higher than that of patients without hypertension. The long-term (36-year) study of hypertension shows that men aged 35-64 are high. Blood pressure, relative risk of heart failure 4.0, 65-94 year old male hypertension, relative risk of heart failure 1.9; 35-64 year old female hypertension, relative risk of heart failure 3.0, 65-94 years old female hypertension, heart failure Relative risk 1.9, due to the widespread use of antihypertensive drugs, the proportion of high blood pressure complicated with heart failure has dropped significantly, currently accounting for 10% to 20% of the cause of heart failure.
4. Arrhythmia
Hypertension can be complicated by a variety of arrhythmias, including atrial arrhythmia, ventricular arrhythmia, atrioventricular block and indoor conduction block. The incidence of arrhythmia reported in the literature is 20% to 90%. The reason is that the method of recording arrhythmia is different. The common electrocardiogram is applied early, and Hoher monitoring is used in recent years. When evaluating Hoher results, the diagnostic criteria used are not consistent.
5. Sudden cardiac death
Sudden death refers to natural occurrence, unexpected sudden death. Sudden cardiac death refers to sudden death due to cardiac causes. Cardiac sudden death accounts for about 50% of cardiovascular deaths, mainly caused by acute coronary events. Caused by ventricular arrhythmia, accounting for about 80% of the cause of sudden cardiac death, high blood pressure complicated with sudden cardiac death is not uncommon. It is estimated that at least one third of the deaths of hypertensive patients are sudden cardiac death.
6. Transient ischemic attack
Transient cerebral ischemic attack (TIA) refers to transient neurological dysfunction caused by focal cerebral ischemia or retinal ischemia. The onset is sudden, lasting for a few minutes or hours, and fully recovered within 24 hours. There are no sequelae, but it can be repeated. It is estimated that there are 200,000 to 500,000 TIAs in the United States every year. About 5 million Americans have been diagnosed with TIA because many TIAs have not caused medical attention. The incidence of TIA is often Underestimated, among the many risk factors of TIA, hypertension ranked first, according to statistics, 40% of TIA with hypertension.
7. Ischemic stroke
In Western countries, among the causes of hypertension, heart failure is the first, and stroke is the second. In China, stroke is the first, heart failure is the second, and stroke is increasing with age. More common in the West, due to the effective control of smoking and other risk factors, as well as the widespread use of antihypertensive drugs, the incidence of stroke is decreasing year by year, but due to the aging population, the absolute number of strokes is still rising, is expected in 2015 At the peak, at present, there are about 700,000 strokes per year in the United States. According to statistics, the mortality rate of stroke in China is 228/100,000 for men and 156/100,000 for women. 80% to 85% of strokes are ischemic strokes, and about 15% are Hemorrhagic stroke.
8. Hemorrhagic stroke
Primary hemorrhagic stroke includes primary cerebral hemorrhage and primary subarachnoid hemorrhage. According to statistics, 94% of patients with cerebral hemorrhage have a history of hypertension, and hypertension is the most important risk factor for cerebral hemorrhage. In every 100,000 ordinary people in the world, 10 to 20 people have cerebral hemorrhage. The incidence rate increases with age. Men are more common in women. In China, cerebral hemorrhage accounts for the first cause of death in patients with hypertension.
9. Hypertensive encephalopathy
Refers to the acute cerebral circulatory disorder syndrome caused by rapid and persistently elevated blood pressure. Although the exact incidence of hypertensive encephalopathy in hypertensive patients is unclear, the incidence of critically ill hypertension including hypertensive encephalopathy is below 1%.
10. Hypertensive kidney disease
The kidney is closely related to high blood pressure. The kidney is an important organ regulating blood pressure, and it is also one of the main target organs of hypertension damage. The two affect each other and even constitute a vicious circle. It is reported that untreated hypertensive patients The incidence of urinary protein is 42%, about 18% of hypertension eventually develops renal insufficiency, 10% to 18% die of renal failure, and end-stage renal disease (ESRD) is attributed to hypertension, 49%, due to hypertension Kidney transplantation for renal cirrhosis accounts for 25% of all kidney transplant patients. Hypertensive renal damage is more common in elderly people over 65 years old, and males are more likely to occur.
11. Hypertensive retinopathy
The fundus is the only part of the whole body that can be seen visually and its related changes, and reflects the other important organs in the body to a certain extent. In the early stage of hypertension, the fundus is often normal and can be maintained for a long time. When it continues to rise, it can cause systemic small arteriosclerosis, which occurs in the retina, called hypertensive retinal arteriosclerosis, or hypertensive retinopathy. It is estimated that about 70% of hypertensive patients have hypertension retinopathy. The longer the course of hypertension, the higher the incidence.
12. Aortic aneurysm
Aneurysm refers to abnormal expansion of the arterial wall. After expansion, the diameter of the lumen is more than 1.5 times of the normal diameter, often involving the aorta, radial artery, followed by the radial artery, femoral artery and carotid artery. Among them, aortic aneurysm can occur in the abdomen. Aorta, thoracic aorta ( descending aorta), ascending aorta and aortic arch, the presence of aortic aneurysm is often a hallmark of diffuse aortic lesions: 25% to 28% of patients with thoracic aortic aneurysms also have abdominal aortic aneurysms. 13% of patients with aortic aneurysm have multiple aneurysms. In aortic aneurysms, abdominal aortic aneurysms are the most common, accounting for about 3/4 of aortic aneurysms. The most common abdominal aorta under the renal artery, abdominal aorta Tumors are more common in men, with a male to female ratio of about 4:1. In the West, the incidence of abdominal aortic aneurysms (diameter 3 cm) in men aged 65 years is about 6%. For every 10 years of age, the incidence increases by 6%, under 55 years old. The female is rare.
13. Aortic dissection
Aortic dissection refers to the infiltration of blood in the aortic lumen into the middle layer of the aortic wall. This disease is a rare and fatal disease, but the incidence is often underestimated. It is estimated that about 100 people die in the aortic dissection in 100,000 men each year in the United States. About 0.8 of the 100,000 women, in the large series of autopsy, the detection rate of aortic dissection is 0.2% to 0.8%, and the number of diagnosed patients before birth is 40.4% to 84%. Men are more common than women, the ratio of men to women. About 2:1 to 5:1, 75% occur in 40 to 70 years old, mostly concentrated in 50 to 65 years old.
14. Occlusive peripheral atherosclerosis
Occlusive peripheral atherosclerosis, also known as peripheral arterial disease, refers to atherosclerosis involving the peripheral arteries, causing stenosis of the limb arteries to cause occlusion, resulting in limb ischemia and other symptoms, symptomatic occlusive peripheral atherosclerosis in men over 60 years old The incidence of sclerosing is 2% to 3%, and females are 1% to 2%. The incidence of asymptomatic occlusive peripheral atherosclerosis is about 3-4 times that of symptoms. After age adjustment, occlusive peripheral atherosclerosis The incidence of hardening is about 12%.
Symptom
Symptoms of essential hypertension Common symptoms Intracranial hypertension, multiple dreams, dizziness, headache, dizziness, tinnitus, neurological headache, cardiac hypertrophy, autonomic nerve reflex, forgetfulness
General symptoms
According to the clinical manifestations and the progress of the disease, hypertension can be roughly divided into slow-moving (slow) hypertension and rapid-entry (malignant) hypertension.
The vast majority of essential hypertension (95% to 99% of essential hypertension) is a slow-moving type of hypertension, more common in middle and old age, characterized by insidious onset, slow progress, and a course of disease for more than 10 years. For decades, there are few symptoms in the early stage. About half of the patients have accidentally discovered an increase in blood pressure after taking blood tests because of physical examination or other medical treatment. Many patients will have various nerves once they know that they have high blood pressure. Symptomatic symptoms, such as dizziness, head swelling, insomnia, forgetfulness, tinnitus, fatigue, dreams, irritability, etc., 1/3 to 1/2 hypertensive patients seek medical treatment for headache, head swelling or palpitations, and many patients Seek medical attention until the occurrence of serious complications of hypertension and functional or organic damage to the target organ and corresponding clinical manifestations.
2. Target organ damage symptoms
(1) Heart:
The symptoms of heart damage in hypertension are mainly related to the continuous increase of blood pressure. The latter can aggravate the left ventricular afterload, leading to cardiac hypertrophy, which in turn causes heart chamber enlargement and repeated heart failure. In addition, hypertension is the main risk factor for coronary heart disease. Often combined with coronary heart disease can have angina pectoris, myocardial infarction and other symptoms, early left ventricle without hypertrophy, and normal systolic function, left ventricular centripetal hypertrophy with the progress of the disease, at this time its systolic function is still normal, with Hypertensive heart disease and worsening of the condition, symptoms of cardiac insufficiency, such as palpitations, labor dyspnea, if the blood pressure and condition are not controlled in time, may occur at night with paroxysmal dyspnea, sitting breathing, coughing pink Color foamy sputum, signs of acute left heart failure and pulmonary edema such as blisters at the bottom of the lungs, recurrent heart failure, left ventricular can produce eccentric hypertrophy, enlarged heart chamber, at this time, left ventricular systolic and diastolic function is significantly damaged, Even heart failure can occur.
Cardiac examination of hypertensive heart disease can be manifested as apical beat, enhanced and lifted to the left, the heart sounds to the left to enlarge, the apex can have systolic murmur (1/6 ~ 2 / 6), if concurrent Left ventricular enlargement or papillary muscle ischemia and dysfunction, there may be signs of mitral regurgitation, systolic murmur can be enhanced to 3 / 6 ~ 4 / 6 level, when the heart is insufficiency, the apex often has the third The heart sounds gallop or the pathological fourth heart sounds, the second heart sound in the aortic valve area is hyperthyroidism, and the aortic sclerosis can be metallic, the systolic murmur can occur due to aortic dilation, and even the aortic valve is relatively closed. Diastolic murmurs that produce mild aortic regurgitation, and hypertensive heart disease can also produce a variety of arrhythmias, such as premature contractions, paroxysmal supraventricular or ventricular tachycardia, atrial fibrillation Etc., the corresponding clinical manifestations can occur.
(2) Kidney:
()1.0102
1.5%5%
(3)
CT
60(TIA)CT
(4)
Examine
1.
2.
3.,,
4.X
5.
6.
7.()
8.10
Diagnosis
diagnosis
1.
2.
3.
(1)(SBP)18.7kPa(140mmHg)()(DBP)12.0kPa(90mmHg)1999WHO18
(2)
4
<55<651
;
3123
3()11
4.
Differential diagnosis
;()()
1.2060
2.>180/110mmHg(24.0/14.7kPa)
3.SBP/SBPDBP/DBP>90%
4.
5.
