Systolic hypertension in the elderly. Pathophysiology and management.

Isolated systolic hypertension occurs with increased prevalence in the elderly population. It is characterized by reduced vascular compliance, often combined with increased peripheral resistance. These changes are not specific to patients with systolic hypertension, occurring, perhaps to a lesser extent, in the normotensive aging population as well. Systolic hypertension is associated with a risk of cardiovascular morbidity and mortality that possibly exceeds that associated with systolic-diastolic hypertension. However, until the recent report of the Systolic Hypertension in the Elderly Program, the benefit of treatment of this population was undocumented. The Systolic Hypertension in the Elderly Program demonstrated that lowering of blood pressure with a diuretic, combined, when necessary, with a beta blocker, reduced the rate of myocardial infarction and stroke. Other agents may also be effective in lowering blood pressure, although their ability to reduce cardiovascular morbidity and mortality in this population remains to be documented. The results suggest that pharmacologic treatment be considered for patients older than 60 years whose systolic blood pressure remains above 160 mm Hg (with a diastolic pressure below 90 mm Hg). Whether treatment should be recommended for all patients with systolic hypertension, or, alternatively, for only those at higher risk for cardiovascular events, remains controversial.     

Pathophysiology of isolated systolic hypertension in elderly patients: Doppler echocardiographic insights

Systemic hemodynamics were evaluated with aortic pulsed wave Doppler echocardiography in 79 elderly subjects with isolated systolic hypertension participating in the Systolic Hypertension in the Elderly Program (SHEP) and were compared with the values in 39 normal age-matched subjects. Cardiac output was elevated (4.50 +/- 1.13 L/min versus 3.94 +/- 1.12 L/min, p less than 0.05) in patients with isolated systolic hypertension in comparison with values in normal elderly subjects. Systemic vascular resistance did not differ between both groups (2140 +/- 536 dyn.sec/cm-5 versus 2011 +/- 553 dyn.sec/cm-5, p = NS). The mean acceleration of blood during left ventricular ejection was similar in patients with isolated systolic hypertension in comparison with normals (12.6 +/- 5.6 m/sec2 versus 11.5 +/- 3.5 m/sec2, p = NS). Patients with isolated systolic hypertension had significantly decreased arterial compliance, as measured by the stroke volume-to-pulse pressure ratio (0.77 +/- 0.26 cm3/mm Hg versus 1.11 +/- 0.30 cm3/mm Hg, p less than 0.0001). The prevalence of aortic and mitral regurgitation as well as valvular and annular calcification did not differ between analyzed groups. Isolated systolic hypertension in elderly patients appears to be multifactorial, with reduced arterial compliance and increased cardiac output both playing a role.     

Pathophysiology of hypertension

Environmental factors such as excessive sodium ingestion and increasing adiposity are suspected to play a major role in the development of hypertension in elderly persons. Both aging and hypertension are associated with similar vascular structural changes including atherosclerosis. Despite the observed age-related changes in vascular structure, other factors must be important in contributing to the elevated pressure in isolated systolic hypertension. Alterations in sympathetic nervous system function may play a major role in the age-related increases in blood pressure and hypertension, especially isolated systolic hypertension.     

Pathophysiology of renovascular hypertension

Renovascular hypertension has its experimental counterpart in the two-kidney, one clip model (Goldblatt hypertension). From the study of this model, a general pathophysiological scheme has evolved suggesting that temporal stages in the development and maintenance of hypertension are regulated by complicated hormonal and neural interrelations. The central roles played by the renin-angiotensin system and the renal nerves is discussed as they relate to other hormones. In addition, the possible contribution of converting enzyme inhibitors to understanding the pathophysiology of this condition is discussed.     

Pathophysiology of portal hypertension

Portal hypertension is a common clinical syndrome associated with chronic liver diseases, and is characterized by a pathological increase in portal pressure that leads to the formation of portosystemic collaterals resulting in shunting of portal blood into the systemic circulation. The increase in portal pressure is due to an increase in vascular resistance and an elevated portal blood flow. The site of increased resistance is variable, and dependent upon the disease process. The site of relative obstruction may be prehepatic, hepatic, or posthepatic. There are several intrahepatic lesions that lead to increased resistance. Some of these lesions are irreversible, like fibrosis, regenerating nodules, and capillarization of the space of Disse; however, there is a functional component, increased vascular tone, which contributes to increased intrahepatic resistance and is potentially reversible. Another important factor contributing to the increased portal pressure is elevated portal blood flow. Peripheral vasodilatation initiates the classical profile of decreased systemic resistance, expanded plasma volume, elevated splanchnic blood flow, and elevated cardiac index, which characterize the hyperdynamic circulatory state. This hyperdynamic circulation is responsible for various complications of portal hypertension.     

Pathophysiology of obesity hypertension

Excess weight gain is a major cause of essential hypertension, and abnormal kidney function appears to be a cause as well as a consequence of obesity hypertension. Excess renal sodium reabsorption and a hypertensive shift of pressure natriuresis play a major role in mediating increased blood pressure associated with weight gain. Activation of the renin-angiotensin and sympathetic nervous systems and physical compression of the kidneys appear to contribute to obesity-induced increases in sodium reabsorption and hypertension.     

Pathophysiology of exercise hypertension

The blood pressure is not a fixed entity but rather a parameter subject to substantial situational fluctuations. Studies based on ambulatory blood pressure measurement as well as exercise testing have shown that the highest blood pressure values in an individual can be recorded during physical exercise. During exercise in healthy subjects, in association with an increase in cardiac output and decrease in peripheral resistance, there is an increase in systolic arterial pressure with nearly constant diastolic pressure. In contrast to normotensive individuals, during dynamic exercise hypertensive patients demonstrate excessive pressure increases due to impaired vasodilatation. The mechanism responsible may be structural changes in the arteriolar walls but age is also an important determinant. The extent of blood pressure increase is more dependent on the mass of contracting muscle than on the mode of contraction. During isometric exercise, there is an increase in both systolic and diastolic blood pressure, predominantly reflex-induced, which is more marked in patients with manifest hypertension at rest than in those with borderline hypertension or in normotensive subjects. During dynamic exercise in a subgroup of patients with coronary artery disease, in contrast to normal subjects in whom the diastolic pressure remains constant, an increase in up to 15 mm Hg in this parameter may be found as a result of ischemia induction with left ventricular dysfunction, inadequately increased cardiac output and reflex vasoconstriction. During dynamic exercise, there is an increase in norepinephrine, more marked in hypertensive than normotensive subjects together with an increase in plasma renin activity; plasma aldosterone changes are in parallel with those of renin activity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pathophysiology of systemic hypertension

Systemic hypertension can be regarded as a quantitative disorder of blood pressure regulation. No single cause of hypertension has been identified, and it is likely that different mechanisms may be dominant in different individuals. In patients with sustained hypertension, there is usually increased peripheral resistance and normal cardiac output. The hemodynamic pattern of hypertension appears to vary according to the subject's age. Factors that may increase peripheral resistance are a decrease in the number of arterioles, changes in the caliber of the arterioles and increase in blood viscosity. Possible components of increased vascular tone in hypertensive patients include elevation of levels of circulating catecholamines and angiotensin II, increased number/affinity of receptors, changes in membrane permeability and increased excitation-contraction coupling. The major hormonal component that mediates vasoconstriction is the renin-angiotensin-aldosterone system. Genetic, environmental and psychologic factors may also play a role in hypertension.     

Pathophysiology of valvular aortic stenosis in the elderly

Aortic stenosis in the elderly is related to calcification of either a bicuspid valve or a morphologically normal tricuspid valve. There is increasing evidence that factors relating to atherosclerosis are involved in valvular calcification and that it is an actively regulated process rather than a degenerative one. With severe aortic stenosis left ventricular hypertrophy occurs, decreasing wall stress and supporting the left ventricular ejection fraction. However, with pathologic hypertrophy there is a dropout of myocardial cells, subendocardial ischemia, and fibrosis. Eventually, symptoms of angina, non-Q wave myocardial infarction, exertional syncope, and heart failure occur. Once symptoms begin, the prognosis is poor, with sudden death occurring in about one third of patients who die. In the elderly, symptoms can be recognized very late in the course of the disease since they can be attributed to other problems and since the elderly patient may have reduced physical activity to a minimum. The more comorbidities that exist, the greater the risk of valve replacement. Symptomatic patients with severe aortic stenosis even over age 80 can be operated upon with a relatively low mortality and morbidity. In patients over age 80, prolongation of life for any meaningful length of time is not as important as relief of symptoms and improvement in the quality of life. Thus, it is unlikely that any truly asymptomatic patient over age 80, even with severe aortic stenosis, should be sent to surgery.     

Pathophysiology of blood pressure in the elderly.

Several of the factors responsible for circulatory control are modified in the elderly. Loss of elasticity of the aortic wall produces a widened pulse pressure and a high incidence of systolic hypertension. Attempts to normalize this may be associated with disabling diastolic hypotension. Arterial baroreceptor sensitivity and responsiveness of the renin-angiotensin system is reduced. Further, the renal capacity to conserve sodium and water is impaired. All these increase the risks associated with antihypertensive treatment, but do not contra-indicate such treatment.     

Pathophysiology of portal hypertension.

Portal hypertension is characterized by a pathologic increase in portal venous pressure that leads to the formation of an extensive network of portosystemic collaterals that divert a large fraction of portal blood to the systemic circulation, bypassing the liver. Experimental models have improved understanding of the pathophysiology of portal hypertension. It is now clear that an increased vascular resistance to portal blood flow is the initial factor responsible for the increase in portal pressure. This resistance is exerted along the hepatic and portal-collateral circulation and is in part modifiable by pharmacologic agents. In a latter stage, an increased portal venous blood inflow, promoted by splanchnic vasodilation, contributes to maintenance and aggravation of portal hypertension. Humoral vasodilatory agents play an important role in the splanchnic vasodilation. Several vasodilators are likely to be involved, including glucagon, prostacyclin, endotoxins, and nitric oxide. The splanchnic vasodilation is associated with a hyperkinetic systemic circulation, with reduced arterial pressure and peripheral resistance and increased cardiac output. The splanchnic circulation is probably the vascular territory in which the vasodilation is more pronounced. Therefore, splanchnic and systemic vasodilation probably share some pathophysiologic events. An expanded plasma volume is observed in all forms of portal hypertension. Expansion of plasma volume is due to renal sodium retention, which has been shown to precede the increase in cardiac output and can be prevented or reversed by sodium restriction and spironolactone. The expanded blood volume represents another mechanism that contributes to further increases in portal pressure.     

Pathophysiology of type 2 diabetes in the elderly.

Diabetes is common in the elderly. Recently, investigators have begun to systematically study the pathogenesis of this illness in the aged. These studies suggest that although there are many similarities between diabetes in middle-aged and elderly subjects, there are several ways in which diabetes in the elderly is unique. These differences may have important therapeutic relevance to this patient population.     

Pathophysiology and classification of pulmonary hypertension

Pulmonary hypertension is present when the mean pulmonary pressure is increased above 25 mm Hg in a rest or above 30 mm Hg during exercise. It is possible to divide it from different point of view. Well known is pathophysiologic classification and Venice classification suggested by WHO symposium 2003. The rise of arterial pulmonary pressure is caused by three essential abnormalities, these are elevated pulmonary vascular resistance, blood flow and pulmonary artery wedge pressure. Vasoconstriction, remodeling of vessels and in situ trombosis are pathogenetic mechanism which contribute to rise of pulmonary hypertension.     

Pathophysiology of exercise intolerance in pulmonary arterial hypertension

Pulmonary arterial hypertension (PAH) is a chronic disease with poor prognosis and important exercise limitation despite the proliferation of treatment options in the last decade. Chronically increased right ventricular (RV) afterload results in right heart failure and without treatment, rapid clinical deterioration is common. Exercise intolerance is the cardinal feature of the disease impacting upon quality of life and clinical outcome. The pathophysiological mechanisms that lead to reduced exercise capacity in this population are complex with ventriculoarterial uncoupling likely to be the predominant feature. The relative contributions of additional factors that contribute to exercise limitation beyond ventriculoarterial uncoupling have not been characterized. This review addresses these factors with a focus on recent developments and uncertainties. RV maladaptation and the intricate interplay between the heart, abnormal pulmonary vascular bed and peripheral factors such as dysfunction of the respiratory and peripheral muscles are discussed in detail.     

老年难治性高血压

老年高血压的诊断也以收缩压(SBP)≥140mmHg和／或舒张压(DBP)≥90mmHg作为标准，单纯收缩期高血压(ISH)多见。随着增龄，老年人心脏收缩力下降，心排血量降低；主动脉及其主要分支的弹性降低，顺应性下降外周血管阻力逐渐升高；主动脉壁的可膨胀性在心脏收缩时也下降，脉压增大，收缩压较舒张压增高更明显。     

Treating hypertension in the elderly

This article discusses various topics related to treating hypertension in the elderly, including pseudohypertension, systolic hypertension, characteristics of young and elderly hypertensive patients, diagnostic considerations in evaluating elderly hypertensive patients, and general therapeutic considerations.