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Pathophysiological effects of the autonomic nervous system are clearly seen in young patients with a high cardiac output and borderline hypertension. As the hypertension progresses, there is a change from the hyperkinetic circulation in borderline hypertension to the increased vascular resistance seen in established hypertension. This hemodynamic transition is caused by decreased beta-adrenergic responsiveness and decreased end-diastolic distension of the heart combined with an increased alpha-adrenergic responsiveness of the resistance vessels. In parallel, the sympathetic tone decreases in the course of hypertension. This transition in sympathetic tone can be explained by the hypothesis of the 'blood pressure seeking properties of the brain'. The central nervous system 'seeks' to maintain a higher pressure. When vascular overresponsiveness sets in, less sympathetic drive is needed to maintain a neurogenic hypertension. Sympathetic overactivity in borderline hypertension is associated with overweight subjects, insulin resistance and dyslipidemia. This suggests a new area of research to investigate the basis of metabolic abnormalities in hypertension.
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PMID:Changing role of the autonomic nervous system in human hypertension. 209 97

The pathophysiology of various stages of hypertension is different. In early hyperkinetic borderline hypertension, the sympathetic drive to the heart and blood vessels is increased while the parasympathetic cardiac inhibition is decreased. The elevated cardiac output, vascular resistance, and blood pressure at that stage can be fully normalized by autonomic blockade. As hypertension advances, a hyperkinetic circulation is less evident, since beta-adrenergic responsiveness and cardiac compliance tend to decrease. Simultaneously hypertrophy of the resistance vessels increases the baseline vascular resistance and the vessels' responsiveness to constrictive stimuli. Eventually a picture of a normal cardiac output/high vascular resistance typical for established essential hypertension emerges. As the blood vessels become hyperreactive, the same degree of vasoconstriction/blood pressure elevation can be achieved with less sympathetic tone. In that phase the sympathetic overactivity is less evident, as the brain resets itself to maintain the same blood pressure elevation with a small amount of sympathetic discharge. While sympathetic overactivity may be less evident in established hypertension, it remains an important pathophysiologic factor, not only for the maintenance of blood pressure, but also for a number of other abnormalities in hypertension. Hypertension is intimately associated with higher levels of pressure-unrelated risk for development of atherosclerosis: dyslipidemia, overweight, and hyperinsulinemia. Furthermore, a number of factors in hypertension favor a poorer outcome from coronary heart disease. These pressure-independent factors increase the risk of coronary thrombosis, arrhythmic deaths, and coronary spasms. Sympathetic overreactivity appears to be crucially implicated in the evolution of this added coronary risk in hypertension. Understanding the pathophysiology of coronary risk and its relationship to sympathetic overreactivity in hypertension is helpful in seeking further improvements in clinical practice. At present antihypertensive treatment is less efficacious in reducing coronary events in hypertension than would be expected. Judicious use of appropriate drugs promises to further improve the efficacy of antihypertensive treatment in those patients who, in addition to high blood pressure, also have other associated risk factors.
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PMID:Abnormalities of autonomic nervous control in human hypertension. 806 76

Plasma lipoprotein levels and carotid-femoral pulse wave velocity, used as a marker of aortic rigidity, were evaluated in 53 young subjects with borderline hypertension by comparison with normotensive controls of the same age and body surface area. Subjects with body weight excess, exaggerated alcohol intake, and/or tobacco consumption were excluded from the study. Borderline hypertensive patients were characterized by significantly higher values of pulse wave velocity and plasma levels of glucose, total cholesterol, high density lipoprotein subfraction HDL3, apolipoprotein B, and lipoprotein (a). There were no group/sex interactions. A significant dyslipidemia was observed in 13 males of the 53 borderline hypertensive subjects. Only in this subgroup did subjects exhibit a strong positive relationship between pulse wave velocity and either plasma total cholesterol or apolipoprotein B. The correlation was observed even after adjustment for blood pressure. The study provides evidence that, in young males with borderline hypertension, some abnormalities of plasma lipoproteins requiring treatment may be present and are associated with an increased stiffness of the arterial wall.
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PMID:Abnormalities of lipid metabolism and arterial rigidity in young subjects with borderline hypertension. 817 14

Considerable progress has been made in our understanding of the role of the nervous system in human hypertension. The evidence for a widespread autonomic abnormality in the early phases of hypertension is overwhelming and excessive sympathetic activity is consistently present in such patients since their childhood. The enhanced sympathetic tone in hypertension is associated with the metabolic syndrome of insulin resistance and dyslipidemia. Multiple mechanisms by which sympathetic overactivity could cause both hypertension and the metabolic syndrome have been documented. Furthermore, the excessive sympathetic tone is conducive to coronary heart disease through its association with high hematocrit values and with excessive platelet aggregability. Surprisingly, the myth that patients with neurogenic hypertension have a benign prognosis continues to persist. Much of the misunderstanding stems from the idea that patients with neurogenic hypertension, commonly called "white coat" or borderline hypertension, do not develop established hypertension. There is no support for such an assessment; in fact, patients with neurogenic hypertension are at a high risk of future accelerated hypertension. Another misunderstanding relates to differences in hemodynamics between neurogenic and established hypertension. It is true that patients with neurogenic hypertension initially show an increase of cardiac output. However, this later evolves into a classic picture of established high resistance hypertension. The hemodynamic transition is secondary to a decrease in cardiac responsiveness and an increase in vascular responsiveness over the course of hypertension. With passage of time, vascular reactivity increases, yet sympathetic tone tends to decrease. This can be explained by the "blood pressure seeking behavior of the central nervous system." In hypertension, the central nervous system appears to seek a higher blood pressure level and, as the vasculature becomes hyperresponsive, less sympathetic tone is needed to maintain the elevated blood pressure. This decrease of sympathetic tone in later phases of hypertension should not be viewed as a normalization, since sympathetic tone in relationship to vascular hyperresponsiveness remains excessive and the central nervous system maintains a crucial role in sustaining high blood pressure in hypertension.
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PMID:Sympathetic overactivity in hypertension. A moving target. 893 44

We evaluated time-related blood pressure trends in the Tecumseh study participants, none of whom received antihypertensive treatment. At baseline the blood pressures were measured in the field clinic and by self measurement at home (twice daily for 7 days). After a mean of 3.2 +/- 0.42 years, the clinic and home pressure readings were repeated. Nine hundred forty-six subjects had clinic and home blood pressure readings at baseline. Of these 735 (380 men, 355 women; average age, 32 years) also completed the second examination. Blood pressure, morphometric data, and biochemical measures at the first examination were used as predictors of future clinic blood pressures. Five hundred ninety-six subjects were normotensive on both examinations (81%). Of 79 subjects (10.7%) with clinic hypertension (> 140 mg Hg systolic or 90 mm Hg diastolic) at baseline, 38 remained hypertensive ("sustained hypertension") and 41 became normotensive ("transient hypertension") after 3 years. Another 60 normotensives at baseline (10.4%) became hypertensive on second examination ("de novo hypertensives"; incidence; 8.1%). The home blood pressure readings on both examinations were reproducible. The three hypertensive groups had elevated home blood pressure, were overweight, had dyslipidemia, and higher insulin values. Only the home blood pressure proved predictive of subsequent blood pressure trends. A home blood pressure of 128 and 83 mm Hg or higher detected "sustained" hypertension with a 48% sensitivity and 93% specificity. Readings of 120 and 80 mm Hg or lower predicted future normotension with a 45% sensitivity and a 91% specificity. We conclude that self determination of the blood pressure at home is useful in the management of borderline hypertension. An algorithm for the management of these patients is proposed.
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PMID:Home blood pressure as a predictor of future blood pressure stability in borderline hypertension. The Tecumseh Study. 939 47

Heart rate and blood pressure are highly correlated and in large population studies, individuals with high blood pressure tend to have high heart rates. Fast heart rate precedes the development of high blood pressure and serves as an early indicator of coronary heart disease. Not only does the heart rate predict coronary mortality, but also the non-cardiovascular mortality and is, therefore, an overall predictor of longevity. In the Tecumseh Blood Pressure study, we have seen that 37% of all patients with borderline hypertension have the 'hyperkinetic hypertension state', which consists of elevated cardiac output, high heart rate, high sympathetic tone, and decreased parasympathetic tone. In this population, evidence of high heart rate exists in these individuals as children, and persists through early adulthood. This suggests that tachycardia is a reliable marker of high sympathetic tone. High sympathetic tone might be the mechanism whereby heart rate is associated with high insulin, insulin resistance, dyslipidemia, high hematocrit and excess weight. These mechanisms are discussed in details in this review. Tachycardia is a strong risk factor for sudden death and arrythmia. Heart rate, as one of the prime determinants of cardiac work, may contribute to greater cardiac strain. Animal studies have shown that a higher heart rate may be associated with a greater development of atherosclerotic plaque in coronary vasculature. Therefore, heart rate elevation is not merely a sign of underlying pathology, but it may also cause further damage that leads to increased mortality. In the treatment of hypertension, reducing heart rate by pharmacologic and non-pharmacologic measures may have a greater effect on coronary mortality than blood pressure reduction alone.
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PMID:Tachycardia: an important determinant of coronary risk in hypertension. 953 91

Borderline hypertension is a widespread condition and because of its large prevalence, it has a major impact on the cardiovascular mortality of the population. A modest elevation of blood pressure in borderline hypertension is closely associated with multiple rheologic, hemodynamic, humoral and metabolic abnormalities. Many of these abnormalities, independently of the blood pressure, increase the coronary risk in patients with borderline hypertension. There is no sufficient evidence in the literature to propose a well structured algorithm of management and treatment of borderline hypertension. Establishing a reliable baseline blood pressure (by ambulatory or home blood pressure monitoring) is the first step in the management of borderline hypertension. One year of intensive nonpharmacologic treatment is recommended as the first therapeutic modality. If this fails to decrease the blood pressure, pharmacologic treatment with small doses of antihypertensive medication is recommended in patients with dyslipidemia or in patients whose out of office blood pressure remains elevated.
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PMID:Borderline hypertension. 1042 97

Patients with hypertension (78 men, 113 women aged 20-73 years) were stratified according to risk of development of cardiovascular complications. In low and moderate risk patients (n=31) with borderline hypertension, dyslipidemia and pronounced obesity mainly non-drug measures were employed directed at lowering of excess body mass. Medium risk patients (n=25) with isolated hypertension group were treated with angiotensin converting enzyme inhibitors and phenylalkylamine calcium antagonists. High risk patients (n=55) with metabolic syndrome received same antihypertensive drugs as medium risk patients. In very high risk patients (n=79) with diabetes, excessive body mass, dyslipidemia and proteinuria complex therapy consisting of antihypertensive and hypoglycemic drugs and non-drug interventions was used. This risk stratification based management of patients with hypertension on turned out to be highly effective and resulted not only in normalization of blood pressure but also in improvement of carbohydrate and lipid metabolism, lowering of resistance to insulin and excessive body mass, and improvement of renal function.
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PMID:[Stratification of patients with hypertension and selection of antihypertensive therapy]. 1249 81

Most children who are normal weight for height and otherwise healthy have risk factor levels associated with the absence of heart disease (ie, they do not smoke, do not have diabetes, are physically active, have low-density lipoprotein levels < 110 mg/dL, and have blood pressure < 120/80 mm Hg). However, by adolescence, the earliest lesions in the atherosclerotic process, fatty streaks and raised lesions, are present in the coronary arteries and the abdominal aorta. The severity of early atherogenesis is related to the coexistence of the major cardiovascular risk factors. Most commonly, the associated risk disturbances are mild: borderline hypertension, mild dyslipidemia, insulin resistance, overweight, physical inactivity, and initiation of tobacco use. Rarely, more severe risk factors are present: familial hypercholesterolemia (a genetic disorder of lipid metabolism), diabetes mellitus, secondary hypertension of long standing, or risk factors associated with chronic conditions such as end-stage renal disease. Thus, cardiovascular risk management in this age group has two components: primordial prevention (the prevention of the development of cardiovascular risk in the first place) and primary prevention (more aggressive treatment of identified risk factors in high-risk individuals either through behavioral or pharmacologic means). Trials beginning in adolescence of the primary prevention of atherosclerosis-related diseases have not been undertaken; thus, the decision to initiate pharmacologic management in high-risk adolescents requires careful thought.
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PMID:Cardiovascular risk factors in adolescents. 1703 66