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Biomedical subjects

T Thien

Publications and source records attributed to T Thien.

At least 73 records · Page 4Linked to original sources
PubMed1997

Magnetic resonance angiography has a high reliability in the detection of renal artery stenosis.

In this prospective study we examined the value of magnetic resonance angiography (MRA) in the imaging of the proximal renal arteries, with the main aim of detecting renal arterial stenosis, as compared with intraarterial digital subtraction angiography. The study was done among a group of 38 hypertensive patients seen in the outpatient department of the department of medicine of our university hospital. In all patients a magnetic resonance angiography and an intraarterial subtraction angiography of the renal arteries was made, and the outcomes of the investigations were compared. Clinical and biochemical data of the patients also were analyzed in relation to the presence or absence of a stenosis. In one patient, MRA resulted in technical failure because of unsuspected claustrophobia. Of the remaining 37 patients, 14 had renal artery stenosis. Of 12 patients in whom the stenoses were >50% of luminal surface on intraarterial digital subtraction angiography, eight were unilateral and four bilateral. All these stenoses were recognized by magnetic resonance angiography. There was also one false positive result by magnetic resonance. Thus, for the identification of stenoses >50%, magnetic resonance has a sensitivity of 100% and a specificity of 96%. Of the 12 accessory renal arteries seen on digital subtraction angiography, only three were identified by magnetic resonance angiography. We conclude that magnetic resonance angiography has great accuracy in depicting the main renal arteries and detecting clinically significant renal artery stenosis; however, the identification of accessory renal arteries is suboptimal and should be improved.

Adult↗
PubMed1997

The influence of cuff size on blood pressure measurement.

The objective of the study was to determine the effect of the use of cuffs with different bladder sizes on the outcome of blood pressure (BP) measurements. Two sizes of bladders previously in common use in the study location (13 x 23 cm and 16 x 23 cm) were compared with the current size (13 x 36 cm). A fully randomised, experimental study was carried out on a study population comprising 130 subjects (61 men, 69 women, aged between 22 and 70, mean 49) who were not undergoing special treatment for cardiovascular disease or hypertension at that time. The mean arm circumference was 32.9 cm (range 25-40 cm). BP measurements were carried out by one person, using a Hawksley random zero sphygmomanometer under standardised conditions. With the smallest bladder (13 x 23 cm) the highest systolic and diastolic BP was measured (mean SBP 127.2 mean DBP 77.0 mm Hg), followed by the bladder of 13 x 36 cm (125.1 resp. 75.4 mm Hg). The lowest BP was measured with the bladder of 16 x 23 cm (123.7 resp. 74.4 mm Hg). Differences between bladders were significant for all arm circumferences. Over the entire range of arm circumferences in the present study there is a small systematic difference in the BP measurements taken by the various bladder sizes. For individual readings the difference is less marked, in comparison to other factors that can affect BP measurements. However, in longitudinal studies a systematic error in BP can occur when measurements are made with different bladders during the study.

Adult↗
PubMed1997

Cardiovascular pharmacology of purines.

1. This review focuses on the extracellular actions of ATP and adenosine, and in particular their role in cardiovascular regulation. 2. ATP serves as a co-transmitter within the sympathetic nervous system, and is also released from endothelium and aggregating thrombocytes. ATP acts on P2x purinoceptors on vascular smooth muscle cells to induce vasoconstriction. Stimulation of P2y purinoceptors on endothelial cells releases endothelium-derived relaxing factors and causes vasodilatation. This dual action of ATP may have pathophysiological importance by inducing vasospasm at sites of impaired endothelial function and thrombus formation. 3. Adenosine is generated by enzymic degradation of ATP. Its formation is enhanced during ischaemia. Adenosine inhibits noradrenaline release from sympathetic nerve endings, causes vasodilatation via endothelium-dependent and endothelium-independent actions, has important anti-arrhythmic properties and prevents deleterious sequelae of ischaemia. In humans, adenosine evokes a sympatho-excitatory reflex mediated by chemically sensitive receptors and afferent nerves in the kidney, heart and forearm. This reflex may be active during exercise and ischaemia and, because of its potential adverse consequences, it should be considered when developing new therapies to potentiate the anti-ischaemic actions of endogenous adenosine in humans. Adenosine appears to mediate ischaemia-induced pain; a reduced sensitivity to adenosine may underlie silent ischaemia. 4. New drugs that interact with adenosine formation or degradation or with adenosine receptors are under development. These have potential therapeutic application in the treatment of ischaemia and other circulatory disorders.

Adenosine↗
PubMed1997

Clinical and haemodynamic sequelae of deep venous thrombosis: retrospective evaluation after 7-13 years.

1. In contrast to the extensive documentation on diagnosis and treatment of deep venous thrombosis (DVT), information about long-term complications, like the post-thrombotic syndrome (PTS), is scarce. Most studies report on clinical examination only, whereas adequate haemodynamic investigation is lacking. Therefore 81 patients with venographically confirmed lower extremity DVT were clinically and haemodynamically reexamined 7-13 years after DVT (mean 10 years) to assess PTS. Interest was focused on the relation between clinical and haemodynamic PTS and the relation between location of the initial DVT and incidence of PTS. 2. Clinical signs and symptoms of PTS were classified according to the latest consensus of the international consensus committee on chronic venous disease. Non-invasive venous vascular laboratory tests were performed to assess the venous outflow resistance and calf muscle pump function (CMP). CMP was determined by the supine venous pump function test (SVPT). 3. Clinically only 20 of 81 patients (25%) were asymptomatic, 34 (42%) had mild PTS (class 1-3), 25 (31%) moderate PTS (class 4) and 2 (2%) severe PTS (class 5-6); 57% had an abnormal CMP. Both the severity of clinical symptoms and the haemodynamic abnormalities were related to the location of the initial thrombus. Of the patients with distal DVT 11% developed moderate clinical PTS and 39% developed an abnormal CMP. CMP and difference in CMP between post-thrombotic and non-thrombotic leg were significantly related to the different classes of PTS. 4. This study indicates that 7-13 years after DVT 31% of the patients had moderate and 2% had severe clinical PTS, while 57% of the patients had abnormal haemodynamic findings (both related to the initial site of the thrombosis). Secondly, it reveals that the risk of PTS after distal DVT is not negligible, which causes concern about not diagnosing and treating patients with distal DVT. Thirdly, we have demonstrated that a functional test, such as the SVPT, is a sensitive test to assess post-thrombotic damage. Therefore its use as a screening tool after a period of DVT should be investigated to select patients at risk of PTS.

Adult↗
PubMed1997

Endothelin and active renin levels in essential hypertension and hypertension with renal artery stenosis before and after percutaneous transluminal renal angioplasty.

OBJECTIVE: To determine whether active renin and endothelin levels in venous plasma differ between patients with renal artery stenosis and patients with primary hypertension. Among the patients with renal artery stenosis we also compared active renin and endothelin levels between subjects who had been cured or whose blood pressure had improved after treatment of the stenosis and those without a beneficial reaction after such treatment. METHODS: We measured immunoreactive endothelin and active renin levels in peripheral venous plasma before and 1 h after angiotensin converting enzyme inhibition in 25 patients with primary hypertension and in 27 patients with hypertension and renal artery stenosis. Percutaneous transluminal angioplasty was performed in 21 patients of the latter group. For 11 patients of this group, hypertension was cured or there was an improvement, whereas 10 other patients did not respond to this treatment. Baseline active renin and endothelin levels were compared between these groups, as were the clinical characteristics of the patients. RESULTS: Baseline endothelin levels were similar in members of the renal artery stenosis [median 3.6 pg/ml (range 1.4-11.7)] and in members of the no stenosis group [5.0 pg/ml (1.5-8.0)]. Also baseline endothelin levels did not differ between members of the successfully treated [3.6 pg/ml (1.8-8.9)] and unsuccessfully treated groups [3.75 pg/ml (1.4-8.3)]. Angiotensin converting enzyme (ACE) inhibition failed to cause a significant change in endothelin level in members of any of the patient groups. Although baseline renin levels differed significantly between members of the renal artery stenosis and no stenosis groups [40.2 microu/ml (0.9-543) versus 13.4 microu/ml (2.5-931), (P< 0.05)], there was no difference in baseline renin levels between the members of successful and unsuccessful groups [25.7 microu/ml (9.2-475.6) versus 65.3 microu/ml (12.3-542.6)]. ACE inhibition caused a significant increase in renin level in members of all groups except the unsuccessfully treated group. CONCLUSIONS: Circulating endothelin levels did not differ significantly among patients with essential hypertension, hypertension with renal artery stenosis and proven renovascular hypertension and, although the renin-angiotensin system was clearly activated in members of the renovascular hypertension group, ACE inhibition did not affect their endothelin levels. These results suggest that endothelin does not play a direct role in the pathophysiology of renovascular hypertension.

Adult↗
PubMed1997

Long-term beta 1-adrenergic blockade restores adrenomedullary activity in primary hypertension.

In this study we examined the effects of long-term treatment of 19 patients with primary hypertension with the beta 1-adrenoceptor antagonist atenolol on norepinephrine and epinephrine kinetics, at rest and during sympathoadrenal stimulation by lower body negative pressure. Norepinephrine and epinephrine kinetics were measured by using the radioisotope-dilution technique by steady-state infusion of tritiated norepinephrine and epinephrine. The patients were studied before and at the end of 3 months of treatment with atenolol (50 or 100 mg daily). A control group of four normotensive subjects was studied before and after 3 months without any drug treatment. In this group, only arterial blood samples were collected without infusion of the tritiated catecholamines. Atenolol decreased blood pressure and heart rate, but forearm vascular resistance was not affected by atenolol. During atenolol, baseline arterial plasma epinephrine decreased from 0.23 +/- 0.02 to 0.17 +/- 0.01 nM (p < 0.05), and this was accompanied by a decrease in total body epinephrine spillover from 0.50 +/- 0.05 to 0.35 +/- 0.04 nmol/min (p < 0.05). In the control group, arterial plasma epinephrine had not decreased after 3 months. In addition, the increment of arterial plasma epinephrine during lower body negative pressure at -40 mm Hg was attenuated during atenolol. Atenolol had no effect on total body and forearm norepinephrine spillover rates, either at rest or during lower body negative pressure. Clearance rates of epinephrine and norepinephrine were not significantly affected by atenolol. These results suggest that treatment of patients with primary hypertension with the beta 1-adrenoceptor blocker atenolol inhibits the adrenomedullary secretion of epinephrine, but it does not affect the biochemical indices of sympathoneural activity. It remains speculative whether this selective effect of atenolol on epinephrine secretion contributes to its hypotensive action and to its cardioprotective effects in the long term.

Adrenergic beta-Antagonists↗
PubMed1997

Adrenomedullary secretion of epinephrine is increased in mild essential hypertension.

To assess whether patients with mild essential hypertension have excessive activities of the sympathoneuronal and adrenomedullary systems, we examined total body and forearm spillovers and norepinephrine and epinephrine clearances in 47 subjects with mild essential hypertension (25 men, 22 women, aged 38.1 +/- 6.7 years) and 43 normotensive subjects (19 men, 24 women, aged 36.5 +/- 5.9 years). The isotope dilution method with infusions of tritiated norepinephrine and epinephrine was used at rest and during sympathetic stimulation by lower body negative pressure at -15 and -40 mm Hg. Hypertensive subjects had a higher arterial plasma epinephrine concentration (0.20 +/- 0.01 nmol.L-1: mean +/- SE) than normotensive subjects (0.15 +/- 0.01) (P < .01). The increased arterial plasma epinephrine levels appeared to be due to a higher total body epinephrine spillover rate in the hypertensive subjects (0.23 +/- 0.02 nmol.min-1.m-2) than the normotensive subjects (0.18 +/- 0.01) (P < .05) and not to a decreased plasma clearance of epinephrine. The arterial plasma norepinephrine level, total body and forearm norepinephrine spillover rates, and plasma norepinephrine clearance were not altered in the hypertensive subjects. The responses of the catecholamine kinetic variables to lower body negative pressure were not consistently different between normotensive and hypertensive individuals. These data indicate that individuals with mild essential hypertension (1) have elevated arterial plasma epinephrine concentrations that are due to an increased total body epinephrine spillover rate, indicating an increased adrenomedullary secretion of epinephrine; (2) have no increased generalized sympathoneuronal activity and no increased forearm norepinephrine spillover; and (3) have similar responses of both the sympathoneuronal and adrenomedullary systems to sympathetic stimulation by lower body negative pressure.

Adrenal Medulla↗
PubMed1996

Quantitative gait analysis in patients with vascular parkinsonism.

Until now the clinical criteria for the diagnosis of vascular parkinsonism (VP) have been disputed. The purpose of the present study is to investigate whether quantitative gait analysis can differentiate between the gait pattern of patients with VP and the gait pattern of patients with idiopathic Parkinson's disease (PD). Twelve patients with VP, 12 patients with PD, and 10 neurologically nondiseased controls were examined by quantitative gait analysis. Patients with VP, having a similar gait velocity and stride length, showed relatively preserved arm swing with markedly more anteflexion in the shoulder on the forward sway of the arm swing than patients with PD. Patients with VP also showed less flexion dystonic posture of the elbow, hip, knee, and trunk than did patients with PD. There was no significant difference in the excursions and coordination of arm swing in the patients with VP compared with the control group. Both patient groups showed reduced leg movements, reduced hip extension, and reduced knee flexion and extension as compared with the controls.

Aged↗
PubMed1996

Interaction of sulphonylurea derivatives with vascular ATP-sensitive potassium channels in humans.

Cardiovascular adenosine-5'-triphosphate-sensitive potassium (KATP) channels have been reported to play an important role in endogenous cardioprotective mechanisms. Sulphonylurea derivatives can inhibit these cardioprotective mechanisms in animal models. We investigated whether therapeutic concentrations of sulphonylurea derivatives can block vascular KATP channels in humans. The forearm vasodilator responses to administration of the specific KATP channel opener diazoxide into the brachial artery of healthy male volunteers were recorded by venous occlusion plethysmography. This procedure was repeated with concomitant intraarterial infusion of:1) the sulphonylurea derivative glibenclamide (0.33 or 3.3 micrograms. min-1. dl-1, both n = 12), 2) the new sulphonylurea derivative glimepiride (2.5 micrograms.min-1. dl-1, n = 12) or 3) placebo (n = 12). The effects of glibenclamide on the vasodilator responses to sodium nitroprusside were also studied (n = 12). Glibenclamide significantly inhibited the diazoxide-induced increase in forearm blood flow ratio (ANOVA with repeated measures: p < 0.01). During the highest diazoxide dose this ratio (mean +/- SEM) was lowered from 892 +/- 165 to 449 +/- 105%, and from 1044 +/- 248 to 663 +/- 114% by low- and high-dose glibenclamide, respectively. In contrast, neither glimepiride nor placebo attenuate diazoxide-induced vasodilation. Furthermore, glibenclamide did not affect nitroprusside-induced vasodilation. We conclude that therapeutic concentrations of the classical sulphonylurea derivative glibenclamide result in significant blockade of vascular KATP channels in humans. The newly developed glimepiride seems to be devoid of these properties.

Adult↗
PubMed1996

Skin blood flow and autonomic reactivity in human poikilothermia.

Autonomic reactivity is pivotal in maintaining a constant body core temperature. Skin vasomotor reflexes and cardiovascular reactivity were investigated in four women (aged 28-37 years) with acquired poikilothermia, during steady-state spontaneous hypothermia (rectal temperature (Tr) = 33.7 +/- 1.0 degrees C [mean +/- SD]) and steady-state normothermia (Tr = 36.7 +/- 0.3 degrees C), as well as in 12 normothermic control subjects. Baseline finger temperature (Tf) during hypothermia was significantly lower than during normothermia (Tf = 32.4 +/- 1.2 compared with 36.2 +/- 0.3 degrees C, respectively), and than in the controls (Tf = 34.8 +/- 0.8 degrees C). No significant differences in baseline skin blood flow and forearm blood flow were found between subjects during hypothermia or normothermia and controls, suggesting a failure of sympathetic drive to counter-regulate hypothermia in the subjects. Skin vasoconstrictor responses to the contralateral cooling test and neck cooling test were markedly attenuated in three subjects, and to the finger cooling test in two subjects, during normothermia compared with hypothermia. Blood pressure responses to the Valsalva manoeuvre and head-up tilting were normal in all subjects, whereas the heart rate response to head-up tilting was blunted in three subjects during hypothermia. The responses of blood pressure and forearm blood flow to the cold pressor test in the subjects during both thermal conditions were comparable with the controls. We conclude that in our subjects, without generalized autonomic failure, poikilothermia has to be attributed predominantly to disorders of the central thermoregulatory pathways. Our findings during hypothermia and normothermia indicate that variations in core and skin temperature significantly affect skin vasomotor reactivity.

Adult↗
PubMed1996

Blockade of vascular ATP-sensitive potassium channels reduces the vasodilator response to ischaemia in humans.

Experimental data show that ATP-sensitive potassium (KATP) channels not only occur in pancreatic beta cells, but also in the cardiovascular system, where they mediate important cardioprotective mechanisms. Sulphonylurea derivatives can block the cardiovascular KATP channels and may therefore interfere with these cardioprotective mechanisms. Therefore, it is of clinical importance to investigate whether sulphonylurea derivatives interact with vascular KATP channels in humans. Using venous-occlusion strain-gauge plethysmography, we investigated whether ischaemia-induced reactive hyperaemia is reduced by the sulphonylurea derivative glibenclamide in 12 healthy male non-smoking volunteers. Forearm vasodilator responses to three periods of arterial occlusion (2, 5 and 13 min) during concomitant infusion of placebo into the brachial artery were compared with responses during concomitant intra-arterial infusion of glibenclamide (0.33 microgram.min-1.dl-1). A control study (n = 6) showed that time itself did not change the vasodilator response to ischaemia. Glibenclamide significantly increased minimal vascular resistance (from 2.1 +/- 0.1 to 2.3 +/- 0.2 arbitrary units, Student's t-test: p = 0.01), and reduced mean forearm blood flow (from 37.5 +/- 2.0 to 35.4 +/- 2.0 ml min-1.dl-1 after 13 min occlusion, ANOVA with repeated measures: p = 0.006) and flow debt repayment during the first reperfusion minute (ANOVA with repeated measures: p = 0.04). In contrast, total flow debt repayment was not affected. Infusion of glibenclamide into the brachial artery resulted in local concentrations in the clinically relevant range, whereas the systemic concentration remained too low to elicit hypoglycaemic effects. Our results suggest that therapeutic concentrations of glibenclamide induce a slight but significant reduction in the early and peak vasodilation during reactive hyperaemia.

Adenosine Triphosphate↗
PubMed1996

Cardiovascular effects of sulphonylurea derivatives.

The classical sulphonylurea derivatives like glibenclamide and tolbutamide are widely prescribed in non-insulin dependent diabetes mellitus in order to stimulate insulin secretion. The insulinotropic effect of these agents is based on the closure of adenosine-5'-triphosphate (ATP)-sensitive potassium channels (KATP-channels) in the beta-cells of the pancreas. Interestingly, the cardiovascular system also shares these KATP-channels. The open state probability of these channels is regulated by the intracellular concentration of ATP. During ischaemia, the KATP-channels are thought to open by a fall in the cytosolic ATP concentration. The increase in the extracellular adenosine concentration, and the release of endothelium-derived hyperpolarizing factor (EDHF) during ischaemia may further contribute to the opening of cardiovascular KATP-channels. Sulphonylurea derivatives like glibenclamide and tolbutamide have been reported to block the opening of KATP-channels in several types of tissues including myocardial and vascular smooth muscle cells. Since the opening of KATP-channels is regarded as an endogenous cardioprotective mechanism, the blocking effect of sulphonylurea derivatives in the cardiovascular system may have deleterious effects. Human studies on this issue have just been initiated, and preliminary results point towards a significant interaction between glibenclamide and cardiovascular KATP-channels at clinically relevant concentrations. In this regard, the introduction of more pancreas specific sulphonylurea derivatives like glimepiride, which do not interact with cardiovascular KATP-channels, is a promising development.

Adenosine Triphosphate↗
PubMed1996

Diagnosis of deep vein thrombosis, an overview.

Because clinical signs and symptoms are unreliable the diagnosis of deep vein thrombosis (DVT) should be objectified. Advantages and disadvantages of contrast venography, plethysmography, ultrasound techniques, fibrinogen leg scanning, computer-assisted tomography, magnetic resonance imaging and blood tests are discussed. In patients with a first event of suspected DVT non-invasive methods like serial plethysmography or ultrasound testing are sensitive and specific enough to make a treatment decision. It is safe to withhold anticoagulants if the test remains normal within 1 week. In patients with suspected recurrent DVT new non-invasive techniques are being tested, but up to now the definitive objective diagnostic test continues to be contrast venography. In first period as well as in recurrent DVT D-Dimer testing could be an additional test to exclude active thromboembolism.

Diagnostic Imaging↗
PubMed1996

Differential effects of low- and high-intensity lower body negative pressure on noradrenaline and adrenaline kinetics in humans.

1. Lower body negative pressure provides a means to examine neurocirculatory reflexive responses to decreases in venous return to the heart. We assessed whether the pattern of catecholaminergic responses to lower body negative pressure depends on the intensity of the stimulus (-15 versus -40 mmHg). 2. In 14 healthy subjects, responses of forearm blood flow and noradrenaline spillover and of total body noradrenaline and adrenaline spillover were assessed during infusion of [3H]noradrenaline and [3H]adrenaline during -15 and -40 mmHg of lower body negative pressure. 3. During lower body negative pressure at -15 mmHg, heart rate and pulse pressure did not change, but forearm vascular resistance increased by 25-50%. Forearm noradrenaline spillover increased by about 50%, from 0.63 +/- 0.16 to 0.94 +/- 0.23 pmol min-1 100 ml-1 (P < 0.05). Total body noradrenaline spillover did not change, and total body adrenaline spillover increased significantly by about 30%. Clearances of noradrenaline and adrenaline were unchanged. 4. During lower body negative pressure at -40 mmHg, heart rate increased and pulse pressure decreased. Forearm vascular resistance increased by about 100%, and forearm noradrenaline spillover increased by 80%, from 0.73 +/- 0.19 to 1.32 +/- 0.36 pmol min-1 100 ml-1 (P < 0.05). Total body noradrenaline spillover increased by 30%, and total body adrenaline spillover increased by about 50%. Clearances of both noradrenaline and adrenaline decreased. 5. The results are consistent with the view that selective deactivation of cardiopulmonary baroreceptors during low-intensity lower body negative pressure increases sympathoneural traffic to forearm skeletal muscle and increases adrenomedullary secretion without a concomitant generalized increase in sympathoneural outflows. Concurrent deactivation of cardiopulmonary and arterial baroreceptors during high-intensity lower body negative pressure evokes a more generalized increase in sympathoneural activity, accompanied by further increased adrenomedullary secretion and decreased plasma clearances of noradrenaline and adrenaline. The findings support differential increases in skeletal sympathoneural and adrenomedullary outflows during orthostasis, with more generalized sympathoneural responses to systemic hypotension.

Adult↗