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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Borderline hypertension attracts investigative interest since it is an early predictor of established hypertension and its sequelae. This condition offers the opportunity of studying arterial hypertension at its inception, before the development of secondary pressure-related changes. A number of abnormalities of the circulation have been described in borderline hypertension. The peripheral resistance is either elevated or inappropriately adjusted to the prevailing increased cardiac output and blood flow. Cardiac output, heart rate and stroke volume are elevated in a proportion of patients. Decreased plasma volume, enhanced pressor responsiveness and elevated plasma renin activity have also been noted. All these changes could hypothetically be explained by a neurogenic mechanism. Although the experimental evidence supporting a neurogenic origin of borderline hypertension is incomplete and often indirect, most findings point toward an abnormal autonomic control of the circulation in this disorder. It is postulated that in a subgroup of patients with borderline hypertension a neurogenic mechanism is in fact operative. There is a need for further characterization of this category of borderline hypertension and for description of its natural history, particularly in relation to the possible subsequent development of essential hypertension.
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PMID:Autonomic nervous cardiovascular regulation in borderline hypertension. 17 39

The systemic hemodynamic was investigated in 145 young male patients with borderline hypertension and 85 control subjects. Response of the cardiac output, stroke volume and the heart rate to sequential parasympathetic, beta-adrenergic and alpha-adrenergic blockade was used for assessment of the autonomic nervous tone. These investigations suggest that the apparently "innocent" minimal blood pressure elevation in borderline hypertension is associated with a number of physiologic abnormalities: The cardiac output, heart rate and stroke volume can be elevated. In all patients the peripheral resistance is abnormal. An abnormal distribution of plasma renin values is detectable. The plasma volume is decreased in a proportion of patients. A number of these abnormalities can be explained by a neurogenic mechanism. The elevation of the cardiac output is entirely neurogenic. In a substantial minority of patients, the elevation of peripheral resistance is attributable to increased sympathetic drive. Indirect evidence indicates that the plasma renin elevation in borderline hypertension may also be neurogenic. Hypothetically the decreased plasma volume may stem from sympathetic effects on postcapillary vessels, but at the present there is no experimental evidence of support this view. The change in autonomic function in borderline hypertension involves both the sympathetic and parasympathetic efferents. Increased sympathetic stimulation is coupled with decrease parasympathetic inhibition. This points toward abnormal integration of the autonomic control, presumably in the medulla oblongata. The mechanism of the autonomic abnormality is not fully elucidated. The role of baroreceptors requires further investigation. In some patients the altered autonomic integration appears to be related to psychosomatic mechanisms.
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PMID:Abnormalities of autonomic nervous control in borderline hypertension. 101 92

Hemodynamic changes in supine and upright position and during exercise were studied in 144 men including 37 normal subjects and 107 patients with borderline hypertension. Borderline hypertensives were classified in 4 groups, according to the basal level of heart rate and stroke index. In the first two groups, stroke index was normal, but heart rate was either decreased (Group I) or elevated (Group II): supine total peripheral resistance was superior (Group I; p less than 0.02) or equal (Group II) to normal values; plasma volume was normal or slightly decreased; hemodynamic response to tilt test closely approximated the normal; impaired adaptation of cardiac index and stroke index to exercise was observed in Group II (p less than 0.001). In the other two groups, stroke index was significantly elevated (p less than 0.0001) but heart rate was either decreased (Group III) or increased (Group IV); supine total peripheral resistance values were decreased (p less than 0.001); plasma volume was equally reduced (p less than 0.001); abnormal percentile increase in diastolic arterial pressure (p less than 0.02; p less than 0.001) and total peripheral resistance during tilt test were observed; during exercise, only the patients of Group IV had an impaired adaptation of cardiac index (p less than 0.001) and total peripheral resistance (p less than 0.02). The study provide evidence that in boderline hypertension i) a high basal level of stroke volume is associated with a reduced plasma volume and an imparied adaptation of total peripheral resistance during tilt, ii) a high basal level of heart rate is associated with an impaired adapatation of cardiac output during exercise, and iii) only patients having an increase in both heart rate and stroke volume exhibited a specific hemodynamic pattern including: reduction of plasma volume, impaired adaptation of cardiac output during exercise, impaired adaptation of total peripheral resistance during tilt and exercise.
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PMID:The stroke volume in juvenile borderline hypertension. 112 Oct 55

Of 145 patients with borderline hypertension, 30% had increased resting cardiac index (QI), whereas the remainder had normal values. The specific aim of this study was to investigate cardiac regulation in patients who had normal resting QI. Eighty-five control subjects were used for comparison. At rest, patients with normal QI showed evidence of decreased parasympathetic inhibition; the QI after injection of atropine increased less than in control subjects. After complete cardiac autonomic blockade with propranolol and atropine, QI and stroke volume were significantly lower in patients than in control subjects. The mechanism of this low QI was further analyzed. Central blood volume, which strongly correlates with stroke volume, was used as an estimate of the cardiac venous filling. After blockade, stroke volume was decreased in patients, but central blood volume was normal. Patients also showed a decreased heart rate and QI response to infusion of isoproterenol. It is therefore postulated that two components may be responsible for the low QI in the "denervated" heart: patients exhibit a decreased responsiveness to sympathetic stimulation, and they may also be less responsive to venous filling. Behind the facade of cardiac normality in these borderline hypertensive patients with normal cardiac output, there is evidence of altered autonomic control of the heart (decreased vagal inhibition) and of changed cardiac response to sympathetic stimulation and possibly to venous filling.
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PMID:Altered cardiac responsiveness and regulation in the normal cardiac output type of borderlind hlpertension. 113 80

Left ventricular hypertrophy is more common in hypertensive individuals than in normotensive persons. Its presence in hypertensive patients is associated with an increased incidence of ventricular arrhythmias, myocardial infarction, congestive heart failure, stroke and cardiovascular mortality. Echocardiography is more sensitive than electrocardiography in detecting left ventricular hypertrophy. Echocardiographic evidence of this condition in patients with borderline hypertension may identify those who need treatment. Weight reduction and drug therapy can prevent or reverse ventricular hypertrophy in hypertensive patients. Recent studies suggest that some antihypertensive drugs are more effective than others in reducing left ventricular hypertrophy. These agents include beta-adrenergic blockers, angiotensin converting enzyme inhibitors, calcium channel blockers and sympatholytic agents. Although little evidence exists to show that reduction of left ventricular mass decreases cardiovascular morbidity and mortality, avoidance of antihypertensive agents that may aggravate hypertrophy would seem prudent.
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PMID:Left ventricular hypertrophy and antihypertensive therapy. 138 79

A health risk appraisal function has been developed for the prediction of stroke using the Framingham Study cohort. The stroke risk factors included in the profile are age, systolic blood pressure, the use of antihypertensive therapy, diabetes mellitus, cigarette smoking, prior cardiovascular disease (coronary heart disease, cardiac failure, or intermittent claudication), atrial fibrillation, and left ventricular hypertrophy by electrocardiogram. Based on 472 stroke events occurring during 10 years' follow-up from biennial examinations 9 and 14, stroke probabilities were computed using the Cox proportional hazards model for each sex based on a point system. On the basis of the risk factors in the profile, which can be readily determined on routine physical examination in a physician's office, stroke risk can be estimated. An individual's risk can be related to the average risk of stroke for persons of the same age and sex. The information that one's risk of stroke is several times higher than average may provide the impetus for risk factor modification. It may also help to identify persons at substantially increased stroke risk resulting from borderline levels of multiple risk factors such as those with mild or borderline hypertension and facilitate multifactorial risk factor modification.
Stroke 1991 Mar
PMID:Probability of stroke: a risk profile from the Framingham Study. 200 1

An increased sympathetic drive combined with decreased parasympathetic inhibition is found in patients with borderline hypertension, who characteristically have rapid heart rates, high cardiac output and relatively normal vascular resistance (hyperkinetic state). In established hypertension, cardiac output is normal, vascular resistance is elevated and signs of increased sympathetic drive are absent. Apparently hemodynamics and sympathetic drive change during hypertension. The mechanism of the hemodynamic transition in the course of hypertension is well understood. Cardiac output returns from elevated to normal values as beta-adrenergic receptors down-regulate and stroke volume decreases (due to decreased cardiac compliance). The high blood pressure induces vascular hypertrophy, which in turn leads to increased vascular resistance. The mechanism of the change of sympathetic tone from elevated in borderline hypertension to apparently normal in established hypertension can best be explained within the conceptual framework of the "blood-pressure-seeking" properties of the brain. In hypertension, the central nervous system seeks to maintain systemic blood pressure at the higher level. As hypertension advances and vascular hypertrophy develops, arterioles become hyperresponsive to vasoconstriction. At this point, less sympathetic drive is needed to maintain pressure-elevating vasoconstriction, and the central sympathetic drive is down-regulated. The etiology of increased sympathetic drive in hypertension remains unresolved. Subjects with increased sympathetic drive are also usually overweight and have elevated levels of insulin, cholesterol and triglycerides, as well as decreased high-density lipoproteins. Future research must focus on the link between coronary risk factors and sympathetic overactivity in hypertension.
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PMID:Autonomic nervous system dysregulation in human hypertension. 202 Nov 14

Using a pulsed Doppler velocimeter with spectral analysis, it is possible to measure instantaneous ascending aortic blood velocity by the suprasternal approach. Cardiac output, stroke volume and maximal acceleration are evaluated from the aortic velocity curve. Maximal aortic acceleration is increased in patients with borderline hypertension by comparison with normal subjects and patients with sustained essential hypertension of the same age. Stroke distance is calculated as the ratio between stroke volume and the cross-sectional area of aortic valve measured by echocardiography. Stroke distance is significantly decreased in patients with sustained hypertension, suggesting that the distance covered by a column of blood passing through the aortic root during one cardiac cycle is smaller in patients with hypertension than in normal subjects.
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PMID:Non-invasive study of cardiac performance using Doppler ultrasound in patients with hypertension. 209 92

Renal transplantations were performed, using microsurgical techniques, with adult male two-kidney, one clip hypertensive rats (n = 9) and sham-operated normotensive Wistar-Kyoto rats (n = 8) as kidney donors and with F1 hybrids, bred from Wistar-Kyoto and stroke-prone spontaneously hypertensive rat parents, as recipients. Systolic blood pressure before surgery was 200 +/- 2.7 mm Hg in hypertensive and 115 +/- 1.7 mm Hg in normotensive donors and 144 +/- 7.1 and 138 +/- 3.5 mm Hg in the two groups of recipients. Renal hypertension in donors was maintained for 14 weeks before surgery was performed and the nonischemic kidneys were transplanted. Bilaterally nephrectomized recipients of renal grafts from hypertensive donors developed sustained hypertension (185 +/- 3.9 mm Hg). In contrast, in recipients of renal grafts from normotensive donors, blood pressure decreased significantly to the level of the donors (111 +/- 3.7 mm Hg). Posttransplantation hypertension in recipients of renal grafts from hypertensive donors was associated with intrarenal vascular hypertrophy, smaller kidneys, a decreased glomerular filtration rate, an increased plasma urea concentration, and polydipsia as compared with normotensive transplanted controls. Renal pyelograms revealed no gross anatomic alterations of transplanted kidneys. Our data indicate that secondary damage to the renal grafts caused by high perfusion pressure before transplantation can induce hypertension in recipients of these kidneys. Furthermore, our data suggest that renal mechanisms may be necessary to maintain borderline hypertension in F1 hybrids.
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PMID:Hypertension in rats induced by renal grafts from renovascular hypertensive donors. 231 24

The Tecumseh project investigates the evolution of hypertension in a healthy population. Of 946 subjects aged 18 through 38 years, 124 had clinic blood pressure readings higher than 140/90 mm Hg (the mean for borderline hypertensive subjects was 130/94 mm Hg). Compared with normotensive subjects, borderline hypertensive subjects had higher home blood pressures (mean, 12/7 mm Hg higher). Their childhood and postpubertal blood pressures were elevated (6/4 mm Hg higher than normal at age 6 years and 12/7 mm Hg higher than normal at age 21 years), and hypertensive target organ changes were detected. Borderline hypertensive subjects also had elevated minimal forearm resistance (0.22 U higher than normal), decreased stroke index (1.8 mL/m2 lower than normal), and impaired ventricular diastolic relaxation (mitral Doppler peak early diastolic blood flow [E] to peak late diastolic blood flow [A] ratio 0.13 lower than normal). Borderline hypertensive subjects had significant abnormalities in other coronary risk factors (cholesterol levels were 0.39 mmol/L higher, triglyceride levels were 0.45 mmol/L higher, high-density lipoprotein levels were 0.08 mmol/L lower, insulin levels were 38 pmol/L higher, and 16.5% more of them were overweight). Borderline hypertension is neither transient nor innocuous. Its association with other predictors of atherosclerosis calls for clinical attention.
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PMID:The association of borderline hypertension with target organ changes and higher coronary risk. Tecumseh Blood Pressure study. 236 31


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