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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Available data suggest that exercise capacity is limited in hypertension. The mechanism of this reduced maximal exercise capacity has not been fully elucidated. In this study 22 patients with mild essential hypertension (162 +/- 22 mmHg systolic and 95 +/- 8 mmHg diastolic) and 36 normotensive control subjects (128 +/- 13 mmHg systolic and 80 +/- 7 mmHg diastolic) (P less than 0.01) performed an ergometer test till exhaustion. Body mass index in the two groups did not differ. The maximal oxygen consumption VO2 was lower in the hypertensive group (18 +/- 7 versus 23 +/- 8 ml/kg/min; P less than 0.02) as was the maximal workload (141 +/- 52 vs. 185 +/- 70 Watt; P less than 0.01). Rate pressure product rose only 2.7 fold in hypertensive patients versus 3.5 fold in the control group (P less than 0.001). In hypertensive patients maximal workload decreased with increasing resting systolic blood pressure (P less than 0.05) while in the normotensive subjects maximal workload rose with increasing resting systolic blood pressure (P less than 0.05). In conclusion both high and low blood pressure was associated with a decreased maximal voluntary exercise capacity. Even mild hypertension was accompanied by lower maximal exercise capacity. Hypertensive patients also had a lower maximal VO2 and lower maximal rate pressure product than did normotensive subjects.
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PMID:Decreased exercise capacity in mild essential hypertension: non-invasive indicators of limiting factors. 159 48

To study whether exercise blood pressure is more closely related to the complications of hypertension than resting blood pressure, 169 patients with essential hypertension, aged 16-66 years, (WHO stages I and II), underwent a graded uninterrupted exercise test on the bicycle ergometer up to exhaustion. BP was measured in intra-arterially. Target organ damage was assessed by eye-fundus grade and by electrocardiographic voltage criteria and T-wave patterns. After adjustment for relevant covariates (age, gender, body height and weight), the manifestations of target organ damage were significantly related to systolic (r ranging from 0.19 to 0.39) and diastolic (r ranging from 0.11 to 0.30) intra-arterial pressure at supine rest. The complications of hypertension were not more closely related to BP during upright submaximal and peak exercise than to resting BP, and exercise BP did not contribute independently from BP at rest to their variance. In conclusion, exercise BP is not better related to target organ damage than BP at rest in patients with essential hypertension.
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PMID:Exercise blood pressure and target organ damage in essential hypertension. 207 69

The effects of long-term treatment with diltiazem on blood pressure, central haemodynamics and exercise endurance were studied in 16 men (mean age 52 years) with essential hypertension. Intra-arterial pressure and heart rate (HR) were monitored continuously. Cardiac output (CO) was measured by Cardiogreen at rest (supine and sitting) and during 50 W, 100 W and 150 W bicycle exercise. Haemodynamic measurements were repeated after continuous bicycling at 150 W for 20 min or until exhaustion. After 1 year on diltiazem (mean daily dose 278 mg) intra-arterial pressure was reduced (P less than 0.001) in all situations (at rest sitting from 183/108 mmHg to 157/92 mmHg (14%] due to reduction in total peripheral resistance. HR was reduced at rest (7%) and during exercise (10%). Stroke volume tended to increase while CO was unchanged. Exercise time at constant workload increased by 25%. After a peak level, intra-arterial pressure fell by 3% to 5% (P less than 0.05) due to a decrease in total peripheral resistance both before and during diltiazem treatment. Stroke volume and CO remained unchanged during endurance exercise while HR showed a small increase. Thus, there was no reduction in the overall cardiac pump function after long-term diltiazem treatment, and blood flow during exercise was maintained.
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PMID:Effect of long-term diltiazem treatment on central haemodynamics and exercise endurance in essential hypertension. 235 Nov 63

Ketanserin (120 mg/day) or placebo was given orally to 14 patients with mild to moderate essential hypertension according to a double-blind crossover protocol, each treatment period lasting 6 weeks. Resting intraarterial pressure in the recumbent position was reduced from 150/84 to 141/77 mm Hg; the hypotensive effect persisted throughout an uninterrupted graded exercise test to the point of exhaustion. The hemodynamic effects were similar at rest and during exercise. Overall, systemic vascular resistance decreased by 14%, heart rate fell by 5%, but stroke volume and cardiac output increased. The pressor responses to methoxamine and to phenylephrine were reduced by ketanserin.
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PMID:Hemodynamic response to chronic ketanserin treatment in essential hypertension. 241 34

A wide spectrum of cardiac hypertrophy has been observed in hypertensive patients. In this study, the responses of hemodynamics and sympathetic drives to exercise among hypertensive patients with various types of left ventricular hypertrophy were investigated. Twenty-five patients with untreated essential hypertension (WHO I and II) were classified as those with and without asymmetric hypertrophy (with AH, n = 7; without AH, n = 18) by their echocardiographic patterns. Ten normotensives served as controls. Exercise was performed on a braked bicycle ergometer; the initial work load was 50 watt. The work load increased progressively by 25 watt at three minute-intervals to the target heart rate, exhaustion, or positive ST.T changes. Blood pressure, heart rate, plasma norepinephrine and hemodynamic parameters by echocardiography were estimated at rest and during exercise. Systolic blood pressure and increased heart rate by exercise in all groups. In patients with AH, a rapid increase was observed, and the increase in systolic blood pressure at submaximum exercise was significantly greater than those in normotensives or patients without AH (p less than 0.05). During exercise, endsystolic dimension decreased in normotensives and in patients without AH (p less than 0.01), but the change was not significant in patients with AH. Percent fractional shortening and percent systolic wall thickening of the interventricular septum and left ventricular posterior wall increased significantly in normotensives and in patients without AH (p less than 0.05), but they were unaltered in patients with AH. Although plasma norepinephrine significantly increased in all groups by exercise, the increase in patients with ASH was greater than those in the other groups (p less than 0.05). These results suggest that hyperresponsiveness of systolic blood pressure and heart rate to exercise may play a role in the pathogenesis of AH, and that this type of hypertrophy could be associated with abnormalities of the sympathetic nervous system.
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PMID:[The pattern of left ventricular hypertrophy in hypertension and its relation to the hemodynamic and sympathetic responses to exercise]. 294 85

The effects of acute exercise on plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and plasma renin activity (PRA) were studied in 13 patients with previously untreated essential hypertension, and 8 matched normotensive control subjects. Resting levels of ANP and PRA were similar in the two groups, while resting AVP concentrations were 1.4 times higher in hypertensive subjects. Graded exercise was performed on a bicycle ergometer with workload increased each minute until exhaustion (Wmax). Wmax was higher in normal subjects than in hypertensive patients. Blood pressure and heart rate rose more steeply in hypertensive patients. Plasma ANP increased during acute exercise in both groups, but the average increase in hypertensives was substantially greater than in normal subjects (P less than 0.05). The increase in ANP during exercise was greater in hypertensives with left ventricular (LV) hypertrophy, and there was a positive correlation between LV mass and the percentage rise in ANP during exercise (r = 0.56, P less than 0.005). Plasma AVP did not alter during exercise. Plasma renin concentrations showed a small rise during exercise in both groups, which was 16% less in hypertensive subjects (P less than 0.05). The enhancement of ANP release during exercise in hypertensive subjects may reflect both cardiac structural changes and increased redistribution of blood to the cardiopulmonary compartment.
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PMID:Exaggerated atrial natriuretic peptide release during acute exercise in essential hypertension. 297 6

Biophysical assessment of circulation was performed in 135 patients with essential hypertension and 39 healthy subjects at rest and during exercise. An increase in arterial impedance was found to play a major part in the mechanisms of blood pressure elevation. In patients with eukinetic hemodynamics, the markedness of left ventricular hypertrophy was associated with adequate circulatory biophysical mode at rest and with the limitation of adaptive changes during exercise. In patients with hypokinetic hemodynamics, the hypertrophied myocardium adjusts itself to an increased after load at the expense of increments in the left ventricular oxygen demand (even at rest) and the exhaustion of myocardial functional reserve during muscular activity.
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PMID:[Several biophysical parameters of the cardiovascular system in patients with hypertensive disease]. 297 91

Ketanserin (120 mg/day) or placebo was given orally to 14 patients with mild to moderate essential hypertension according to a double blind crossover protocol, each treatment period lasting six weeks. Resting intra-arterial pressure in the recumbent position was reduced from 150/84 to 141/77 mm Hg; the hypotensive effect persisted throughout an uninterrupted graded exercise test to the point of exhaustion. The haemodynamic effects were similar at rest and during exercise. Overall, systemic vascular resistance decreased by 14%, heart rate fell by 5%, but stroke volume and cardiac output increased. Mean pulmonary arterial pressure and capillary wedge pressure were not significantly affected, but pulmonary vascular resistance decreased by 15%. The pressor response to methoxamine was significantly reduced by ketanserin. Both plasma noradrenaline and adrenaline concentrations increased, plasma renin activity and angiotensin II concentration decreased, and plasma aldosterone concentration was unchanged. The data indicate that ketanserin induces arteriolar dilatation, possibly related to an alpha-1-antagonistic action and to a reduced circulating angiotensin II concentration. The haemodynamic response is complex, and an increase in cardiac output limits the hypotensive effect. There is no firm evidence of an effect on venous tone as cardiac filling pressures do not change.
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PMID:Haemodynamic and humoral responses to chronic ketanserin treatment in essential hypertension. 636 88

Over the past few decades, recent developments in pacemaker technology from fixed-rate single-chamber pacemakers to dual chamber pacemakers with pacing algorithms have changed the therapeutic landscape resulting in better healthcare outcomes by improving rate response with minimal ventricular pacing. Here, we share our longest clinical experience with an elderly Chinese male patient who was diagnosed with third-degree atrioventricular (AV) block and was admitted in our hospital 33 years ago. An 85-year-old male patient from China was hospitalized due to dizziness and syncope, with an initial diagnosis revealing third-degree AV block with a heart rate of 35-40 beats per minute (bpm) along with Aase's syndrome and primary hypertension. A single-chamber pacemaker (VVI) was implanted immediately giving the patient symptomatic relief. However, 5-year post-surgery VVI was replaced due to battery exhaustion, while the primary electrode catheter was kept in use. Few years later, the patient again complained of dizziness and re-examination revealed VVI battery debilitation due to premature battery exhaustion. Single-chamber pacemaker was again implanted via the same position of right upper chest. However, after adjusting the frequency of stimulation of the pacemaker to 70 bpm, patient had a symptomatic relief. Considering the severity of patient's disease and knowing that cardiac dysfunction was reported previously, a tri-chamber pacemaker was chosen to take place of previous single-chamber pacemaker. For 33 years, the patient underwent 7 times replacement of pacemaker for battery exhaustion or inadequacy. We successfully performed overall seven pacemaker implantations and upgradation in an elderly Chinese patient diagnosed with third-degree AV block for 33 years. A long following up till now demonstrated no major complications with normal heart rate functioning.
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PMID:Seven times replacement of permanent cardiac pacemaker in 33 years to maintain adequate heart rate: a case report. 2673 49