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- Viitanen, Matti, 1950-
(author)
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Long-term effects of stroke
- 1987
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Doctoral thesis (other academic/artistic)abstract
- Stroke, which has an increasing incidence with age, causes an irreversible brain damage which may lead to impairment, disability and decreased life satisfaction or death.Risk factors for death, recurrent stroke and myocardial infarction, were analyzed in 409 stroke patients treated at the Stroke Unit, Department of Medicine, Umeå University Hospital, between Jan. 1, 1978 and Dec. 31, 1982. The causes of death were related with the time of survival. In fully co-operable (n=62) 4-6 year stroke survivors, the occurrence of motor and perceptual impairments, of self-care (ADL) disability and of self-reported decreased life satisfaction due to stroke was determined.The probability of survival was 77% three months after stroke, 69% after one year, and 37% after five years. Multivariate statistical analysis indicated that impairment of consciousness was the most important risk factor for death followed by age, previous cardiac failure, diabetes mellitus, intracerebral hemorrhage and male sex. During the first week, cerebrovascular disease (90%) was the most dominant primary cause of death, from the second to the fourth week pulmonary embolism (30%), bronchopneumonia during the second and third months and cardiac disease (37%) later than three months after stroke. The risk of recurrence was 14% during the first year after stroke and the accumulated risk of stroke recurrence after 5 years was 37% after stroke. The estimated probability of myocardial infarction was 7% at one year and 19% at 5 years. High age and a history of cardiac failure increased the risk of recurrent stroke. The risk of myocardial infarction was associated with high age, angina pectoris and diabetes mellitus. The highest risk of epilepsy was found between 6 and 12 months after stroke. Motor impairment prevailed in 36% of the long-term survivors, perceptual impairments in up to 57% and decreased ADL-capacity in 32%. As regards ecological perception, perceptual function variables were distinctly grouped into low and high level perception which together with motor function explained 71% of the variance of self-care ADL. While levels of global and of domain specific variables of life satisfaction appeared stable in clinically healthy reference populations aged 60 and 80 years, the stroke had produced a decrease in one or more aspects of life satisfaction for 61% of the long-term survivors. Although significantly associated with motor impairments and ADL disability, these changes could not only be attributed to physical problems.
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- Andrén, Lennart, 1946, et al.
(author)
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Ketanserin in hypertension. Early clinical evaluation and dose finding study of a new 5-HT2 receptor antagonist.
- 1983
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In: Acta medica Scandinavica. - 0001-6101. ; 214:2, s. 125-30
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Journal article (peer-reviewed)abstract
- Ketanserin, a new 5-hydroxy-tryptamine antagonist, was given at three different dosage levels (double-blind, randomized) in a dose finding study for 2 months to 31 patients with mild to moderately severe essential hypertension. Treatment with ketanserin was then continued until 9 months had been completed. A significant antihypertensive effect was demonstrated at daily dosages of 20 mg t.i.d. or 40 mg t.i.d. The antihypertensive effect was similar to that of previous multiple drug treatment with conventional drugs. However, 60 mg t.i.d. was not acceptable, at least not as initial dosage. At this dose level, 8 out of 10 patients had to be withdrawn from the study during the initial phase due to unwanted effects. It is conceivable that alpha 1-adrenoceptor blockade may have played a role at this dose level, since postural reactions were observed which was otherwise not the case during this study. Ketanserin is a new and interesting alternative in the treatment of hypertension. At the same time it offers a tool by which the role of 5-hydroxy-tryptamine in the regulation of arterial pressure can be investigated.
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- Eggertsen, Robert, 1948
(author)
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Beta-adrenoceptor blockade and vasodilatation in essential hypertension. Hemodynamic studies at rest and during exposure to stress.
- 1984
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In: Acta medica Scandinavica. Supplementum. - 0365-463X. ; 689, s. 1-46
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Journal article (peer-reviewed)abstract
- The purpose of this study was to evaluate the acute and long-term effects on blood pressure and hemodynamics both at rest and during acute exposure to loud noise of drugs with beta-adrenoceptor blocking and vasodilating properties. Prizidilol and carvedilol both act as nonselective beta-blocking and precapillary vasodilating compounds. Prizidilol (200 mg X 2) was compared to propranolol (80 mg X 2) plus hydralazine (25 mg X 2) and showed similar antihypertensive effect in a long-term double-blind randomized trial. Carvedilol was evaluated acutely with invasive (dye-dilution) and noninvasive (plethysmography) technique and showed an acute antihypertensive effect without causing a rise in TPR and with a decrease in regional resistance in the fore-arm. Acutely, carvedilol (25 mg and 50 mg) decreased blood pressure and regional resistance (50 mg) in contrast to propranolol (80 mg) which did not lower blood pressure acutely and caused an increase in regional resistance. In a long-term double-blind, randomized comparison, both propranolol (80 mg X 2) and carvedilol (25 mg X 2 and 50 mg X 2) showed a useful antihypertensive effect. After 29 days, however, it was still possible to demonstrate an acute decrease in resistance with carvedilol (50 mg) after tablet intake, indicating the vasodilating activity of this compound. When patients with essential hypertension were exposed to an even broad band noise (100 dBA), there was a rise in blood pressure due to an increase in TPR. Alpha 1-adrenoceptor blockade (prazosin 2 mg) prevented the rise in TPR but blood pressure increased in spite of this due to a rise in CO. Moreover, nonselective beta-adrenoceptor blockade and alpha 1-adrenoceptor blockade in combination (labetalol 200 mg) were unable to prevent the rise in blood pressure induced by noise. Finally, precapillary vasodilatation and beta-adrenoceptor blockade (prizidilol 400 mg) given as long-term treatment were also inefficient in preventing the noise-induced (105 dBA) rise in blood pressure. The absolute level of blood pressure obtained, however, was significantly lower than during placebo administration.
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- Eggertsen, Robert, 1948, et al.
(author)
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Haemodynamic effects of carvedilol, a new beta-adrenoceptor blocker and precapillary vasodilator in essential hypertension.
- 1984
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In: Journal of hypertension. - : Ovid Technologies (Wolters Kluwer Health). - 0263-6352. ; 2:5, s. 529-34
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Journal article (peer-reviewed)abstract
- Carvedilol (BM 14190) is a new antihypertensive compound which combines beta-adrenoceptor blocking and precapillary vasodilating properties but is devoid of intrinsic sympathomimetic activity. The acute and long-term effects on blood pressure and regional haemodynamics (forearm plethysmography) were studied with carvedilol 25 mg b.i.d. or 50 mg b.i.d. Comparisons were made with propranolol 80 mg b.i.d. in a randomized double-blind placebo controlled trial comprised of 30 patients with essential hypertension. After a four-week placebo period active therapy was given for four weeks. Carvedilol administered acutely reduced blood pressure at both doses, delta 13/6 mmHg (P less than 0.001/P less than 0.01) and 17/10 mmHg (P less than 0.001/P less than 0.01). Resistance in the forearm fell significantly with the higher dose. This was in contrast to propranolol which only reduced heart rate acutely, and as expected caused a rise in forearm resistance. After four weeks both compounds had reduced blood pressure significantly and to the same extent. Blood flow was still significantly reduced with propranolol in contrast to the findings with carvedilol. We conclude that carvedilol given orally has a useful antihypertensive effect both acutely and during prolonged treatment. It is well tolerated and its haemodynamic profile is attractive.
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- Eggertsen, Robert, 1948, et al.
(author)
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Hemodynamic effects of loud noise before and after central sympathetic nervous stimulation.
- 1987
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In: Acta medica Scandinavica. - : Wiley. - 0001-6101. ; 221:2, s. 159-64
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Journal article (peer-reviewed)abstract
- The hemodynamic effects of loud noise after central alpha 2-adrenoceptor stimulation were studied in 13 patients with mild (WHO 1) essential hypertension. The patients were randomized (double-blind) to treatment with either placebo or guanfacine 1-2 mg for four weeks and then crossed over and treated for another four weeks. All patients were exposed to a loud broad-band noise (105 dBA for 30 min) and all were studied both on placebo and guanfacine. Guanfacine significantly reduced the resting blood pressure from 141/92 to 134/88 mmHg (p less than 0.01) as well as heart rate at rest from 63 to 58 beats/min (p less than 0.05). Noise stimulation caused a significant increase in blood pressure and resistance in the placebo-treated group, while cardiac output decreased significantly. Pretreatment for one month with the central alpha 2-adrenoceptor stimulating agent guanfacine did not block the noise-induced pressor response nor the increase in peripheral resistance. A significant decrease in stroke volume was observed and cardiac output also tended to decrease in this group. It could be concluded that loud noise is a potent pressor stimulus which causes vasoconstriction and that the blood pressure response during noise could not be blocked by the centrally acting antihypertensive agent guanfacine. Since noise causes vasoconstriction it also induces an increased tone in the small arteries and, if the noise stimulus is sufficiently strong and repeated for a long time, it might cause structural changes in the resistance vessels and permanent arterial hypertension in humans.
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- Andrén, Lennart, 1946, et al.
(author)
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Circulatory effects of noise.
- 1983
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In: Acta medica Scandinavica. - : Wiley. - 0001-6101. ; 213:1, s. 31-5
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Journal article (peer-reviewed)abstract
- Thirteen patients with mild essential hypertension, mean age 44 years (range 21-59), were studied during "stress" before and after postsynaptic alpha-adrenoceptor blockade and combined postsynaptic alpha- and non-selective beta-adrenoceptor blockade. Loud broad band noise (100 dBA for 10 min) was used as the stress stimulus. Exposure to noise caused a significant increase in systolic (7%, p less than 0.05), diastolic (9%, p less than 0.01) and mean arterial pressure (6%, p less than 0.01). The blood pressure elevation was caused by an increase in total peripheral resistance (12%, p less than 0.05). There was no significant change in heart rate, stroke volume or cardiac output. The blood pressure response during noise stimulation was not affected by postsynaptic alpha-adrenoceptor blockade (prazosin, 2 mg orally). The hemodynamic reaction pattern, however, was totally reversed. Thus, the cardiac output increased significantly (9%, p less than 0.05), while the total peripheral resistance tended to decrease. Combined postsynaptic alpha- and non-selective beta-adrenoceptor blockade (labetalol, 200 mg orally) inhibited the increase in systolic blood pressure caused by noise, while the diastolic and mean arterial pressures still increased significantly (5%, p less than 0.01). Labetalol effectively blocked the stress-induced increase in total peripheral resistance and there was no significant increase in cardiac output after combined alpha- and beta-adrenoceptor blockade. Exposure to noise caused a significant increase in circulating noradrenaline (20%, p less than 0.05). Plasma adrenaline and plasma renin activity were not affected by noise stimulation. These results suggest that blood pressure elevation is essential during "stress" but that the hemodynamic pattern causing blood pressure elevation may vary and may be affected by pharmacological blockade of various parts of the sympathetic nervous system.
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- Andrén, Lennart, 1946, et al.
(author)
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Diltiazem in hypertensive patients with type II diabetes mellitus.
- 1988
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In: The American journal of cardiology. - : Elsevier BV. - 0002-9149. ; 62:11, s. 114G-120G
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Journal article (peer-reviewed)abstract
- Twenty-three patients with essential hypertension and diabetes mellitus type II were treated with the calcium antagonist diltiazem (120 to 180 mg twice daily). The mean dose was 307 mg/day. The study was a double-blind, placebo-controlled, crossover design. All measurements were performed 12 to 14 hours after drug intake. Blood pressure, heart rate and forearm blood flow were measured noninvasively. Platelet function was studied by measuring adenosine diphosphate-induced platelet aggregation and the platelet specific proteins, beta thromboglobulin and platelet factor 4. Thromboxane B2 formation in serum and the plasma concentration of diltiazem and its metabolites N-demethyldiltiazem, deacetyldiltiazem and N-demethyldeacetyldiltiazem were measured both during placebo and diltiazem treatment. Diabetic control was evaluated by following HbA1C, fasting blood glucose and urinary glucose. Diltiazem reduced both systolic and diastolic (supine and standing) blood pressure significantly. Forearm blood flow was significantly increased by 32%, p less than 0.05. Supine heart rate decreased significantly, while no such change was seen in the standing position. No significant changes were observed in platelet function during diltiazem treatment. There was no relation between the observed blood pressure reduction and the plasma concentration of diltiazem or its metabolites. A positive correlation between the change in heart rate and the metabolite N-demethyldeacetyldiltiazem was observed (r = 0.647, p = 0.005). Three patients were excluded during diltiazem treatment (skin exanthema, headache and atrial fibrillation) and 1 during placebo treatment (angina pectoris). No negative effect on diabetes control was observed. Thus, diltiazem could be used for treatment of hypertension in diabetic patients.
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