Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of the types of hyperlipoproteinaemias revealed 2 peaks of frequency, i. e. in the types IIa and IIb corresponding 41% and in the types IV and V corresponding 55%. Weight indices and disturbed glucose tolerance are in the types III-V significantly higher than in the types IIa and IIb. The risk factor hypertension was registered in 34% in the investigation material. The highest prevalence rates for myocardial infarctions were in the patients of the types IIb and III, for PAD in the type III. The addition of hypertension and diabetes mellitus to hyperlipoproteinaemia reveals an exacerbation of the vascular risk. Changes of the fundus oculi, which correspond to the picture of a fundus hypertonicus cause to think of the presence of a hyperlipoproteinaemia in all patients with normotension.
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PMID:[Vascular complications in primary hyperlipoproteinemias (HLP) with special reference to changes in the eye fundus]. 48 17

Patients with hypertension due to the release of large amounts of NE from a pheochromocytoma and patients with PAD and postural hypotension due to diminished NE release from adrenergic axon terminals represent the extremes of the spectrum of adrenergic pathophysiolgic findings. It is reasonable to suspect that some more common disorders lie between these extremes and to anticipate that potential roles of the adrenergic nervous system in the pathogenesis of these disorders will be extensively studied with the availability of sensitive isotope-derivative methods for the measurement of catecholamine levels in plasma and in tissue.
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PMID:Pheochromocytoma and autonomic dysfunction. 86 50

Experience with 1000 cases of aorto-(bi)femoral bypass is presented evaluating factors influencing the overall patency rate and late survival, over a period of 25 years. There were 820 cases with bilateral and 180 with a unilateral bypass. Mortality was 3.3% and death rate 39.4%. Re-do procedures have been excluded. Operative indications were for stage I disease (moderate claudication) (17.6%), stage II (advanced claudication) (53.2%), stage III (rest pain and/or pregangrenous changes) (22.7%) and stage IV (gangrenous tissue loss (6.5%). Myocardial infarction was the predominant cause of late death in 192 cases (48.7%), followed by cancer in 48 (13%), cerebrovascular disease in 43 (11%), chronic lung disease with cor pulmonale in 15 (3.8%) and miscellaneous causes in 52 (13.2%) of patients. The cause of death was unknown in 31 (7.8%) cases. Co-existent peripheral arteriopathy (PAD) noted in 377 (37.7%) patients, was found to be a major determinant of late graft patency. Carotid artery disease and renovascular hypertension were corrected surgically, prior to aorto-femoral bypass in the 5.6% and concomitantly in 4.2%. Coronary artery disease in 273 (27.3%) patients and hypertension in 269 (26.9%), had a great influence on late survival as did age and smoking habits. Endarterectomy together with profundaplasty was carried out in 162 (16.2%) instances. It was our policy to extend the graft limb over the profunda femoris and in cases with co-existent superficial femoral artery disease 208 (20.8%). In 630 (63%) instances, the distal anastomosis was performed at the level of common femoral artery. Immediate graft patency was obtained in 99.3% of the cases. Late patency rate for stages I and II at 5, 10 and 15 years was 82%, 76% and 72% respectively. Following secondary operation for graft occlusion, the 15 year patency was increased to 71%. Co-existent superficial femoral disease can be alleviated by appropriate concomitant profundaplasty. Amputation rates were 0.8% for stage II, 1.5% for stage III and 2.4% for stage IV disease. Twenty year life table analysis showed a reduced survival (54%), in comparison with normal population (77%).
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PMID:Aorto-femoral bypass and determinants of early success and late favourable outcome. Experience with 1000 consecutive cases. 128 3

The prevalence of arterial hypertension (AH) was studied in 1423 individuals (702 males and 721 females) aged 21 years (Fig. 1, Table 1). Systolic (SBP) and diastolic (DBP) blood pressures and heart rate (HR) were measured three times on two different occasions separated by at least one week. Three different criteria were used to define AH (Table 3): 1) World Health Organization (WHO) [PAD > or = 95 mmHg in one casual determination]; Joint National Committee IV (JNC-4) [PAD > or = 90 mmHg on two different occasions]; and 3) Statistical [PAD > percentile 95 of the respective distribution]. BP was distributed normally in both males and females (Fig. 4). DBP decreased progressively along the six measurements (Fig. 2, Table 2), with the average of DBP determinations 4-6 being significantly lower than the average of determinations 1-3 (p < 0.05). SBP behaved in the same way (Fig. 2, Table 2), but in this case the 2nd and 3rd determinations within each occasion (2-3 and 5-6) were significantly lower than determinations 1 and 4, respectively (p < 0.05). As a result, the percentage of individuals of either sex with DBP > 90 mmHg was 14.7% based on the 1st determination (Fig. 5), but if the averages of determinations 1 to 3 or 1 to 6 were considered, these percentages decreased to 8.7% and 4% respectively (Fig. 5). With the WHO criterion (PAD > or = 160/95 mmHg based on the first determination) there were 3.3% of individuals with AH. With the statistical criterion the prevalence of AH was always 5%, but the actual value of percentile 95 was progressively lower as we took into account the 1st. determination, the average of 1-3 or the average of 1-6: 100, 95 and 90 mmHg in males and 90, 88 and 84 mmHg in females, respectively (Fig. 6). With the JNC-4 criterion there were 1.6% of individuals with AH (Fig. 5). These low figures were caused by the lack of repeatability of DBP readings in the second determination, since 79% of the individuals with DBP > or = 90 mmHg on the first occasion were normotensive on the second one, whereas more than 95% of those being initially normotensive remained in that category on the second visit (Fig. 7). The FC did not show important changes (Fig. 8), and the percentage of individuals with systolic AH was low (Table 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Definition of hypertension based on a prevalence study of 1,423 young adults]. 130 3

In 2208 boys aged 15 to 22 years the incidence of risk factors of atherosclerosis were determined. The risk factors were found in 33.7% of boys. The level of risk factors in youth has increased with age (p = 0.001), especially hypertension (p = 0.001) and smoking (p = 0.001). The authors concluded that the most important methods of prevention of atherosclerosis in youth should be: identification of high-risk individuals (overweight, hypertension, hyperlipidemia, family history of CHD and PAD, ischemic postexercise ST segment depression), health education and motivation for change, modification nutritional habits in cases of hyperlipidemia and overweight (prevention of early atherosclerotic lesions in childhood), early diagnosis and control of hypertension, practice of low salt intake, avoidance of smoking, sufficient physical activity (prevention of atherosclerotic disease mainly in adulthood).
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PMID:Epidemiology of risk factors of atherosclerosis and preventive program for youth. 221 95

The efficacy of captopril 25 mg/day as monotherapy or when necessary, in association with hydrochlorothiazide 25 mg/day, was studied during three months in 472 patients, average age 45 (17-59) years, 51% males with mild (73%) 95 less than PAD less than 104 mmHg, and moderate (27%) arterial hypertension 104 less than PAD less than 114 mmHg. Were included in the study hypertensive patients with previous antihypertensive therapy or when in the course of any previous antihypertensive treatment (52.4%) blood pressure control were not observed and side effects compromised patient's compliance. Captopril 25 mg/day was used once a day as single dose or subdivided in two daily doses (12.5 mg b.i.d.), during 30 days. If blood pressure was not normalized or dyastolic blood pressure drop was not equal or bigger than 10% after this period, it was added hydrochlorothiazide 25 mg/day. After three months under treatment, 411 (87%) patients normalized their dyastolic blood pressure DBP (less than 90 mmHg), from them, 273 (57.6%) had received only captopril and the others 138 (29.4%) with the addition of hydrochlorothiazide. The drop of mean arterial pressure, MAP = 2 DBP + 1 SBP was in average, 17.3 mmHg, in the 3 patients whose blood pressure normalized with captopril alone, and in average of 18.5 mmHg in those patients requiring addition of hydrochlorothiazide (difference without statistical significance). A small decrease of body weight, but with statistical significance (p less than 0.001) were observed during the use of captopril as monotherapy. Expressive reduction of side effects were observed during the period under captopril related to the period with previous antihypertensive therapy.
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PMID:[Treatment of mild and moderate hypertension with the use of captopril alone or combined with hydrochlorothiazide. A multicenter study]. 269 33

The reproducibility of a novel ambulatory blood pressure (B.P.) monitoring was tested, for clinical trial in hypertension. The spacelabs apparatus is based on standard auscultatory and oscillometric blood pressure measurements. Ten normotensive patients and 15 hypertensive patients were investigated as follows: their blood pressure was monitored twice over a 24 hr period at an interval of 30 and 15 days respectively. The monitoring data were expressed as the mean of the average blood pressure over day-time (7 hr-22 hr) and 24 hr as well as 24 hr. B.P. profiles (means of 4 measurements per hour). The statistical analysis of the two subpopulations of patients showed a satisfaction reproducibility of both the 24 hr B.P. curves (normotensive patients: PAS: r = 0.94; PAD: r = 0.92; Hypertensive patients PAS: r = 0.82; PAD: r = 0.64 p less than 0.001). and blood pressure levels (normotensive patients: J1: 113 +/- 10/70 +/- 6 mmHg; J30: 110 +/- 10/68 +/- 6 mmHg. Hypertensive patients: J1: 150 +/- 10/98 +/- 9 mmHg; J15: 155 +/- 15/96 +/- 8 mmHg). In contrast, analyzing each patient individually exhibited a correct reproducibility of the B.P. levels but the 24 hr--profiles of either the diastolic or systolic blood pressure could not be correlated with sufficient reliability (normotensive patients: 7 times out of 10 for PAS, and 4 times out of 10 for PAD; hypertensive patients: 5 times out of 15 for PAS, and 3 times out of 15 for PAD). In addition, the patient activity, should be carefully controlled during ambulatory blood pressure measurements.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ambulatory recording of blood pressure. Study of the reproducibility of findings in 25 subjects]. 309 10

Hypotension, bradycardia, pulmonary artery hypertension, neutropenia, and thrombocytopenia have been suspected to be due to complement activation following protamine reversal of heparin. This investigation examined these phenomena in complement-depleted animals. Eight dogs received intraperitoneal naja n. naja cobra venom factor (CVF), 20 U/kg, 48 and 24 hr prior to anticoagulation with sodium heparin, 150 IU/kg, and reversal 30 min later with protamine sulfate, 1.5 mg/kg. Decomplementation was confirmed in all dogs. Systemic blood pressure (BP), pulse (HR), pulmonary artery systolic and diastolic pressures, (PAS, PAD), cardiac output (CO), platelet count (PTC), and white blood count (WBC) with differential were monitored. The maximal mean changes for the entire group were BP, -43 mm Hg; HR, -16; PAS, +6 mm Hg; PAD, +3 mm Hg; CO, -27%; PTC, -49%; and WBC, -48%. These hemodynamic and hematologic responses, occurring in the face of CVF-induced decomplementation, support the conclusion that complement components C3 and C5-C9 are not influential factors contributing to these protamine-heparin-induced events.
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PMID:Complement depletion and persistent hemodynamic-hematologic responses in protamine-heparin reactions. 341 56

We studied (via acute vasodilator testing with nifedipine) 27 patients with pulmonary arterial hypertension (PAH) (11 primary, 16 secondary PAH, [including six patients with Raynaud's phenomenon]) in order to identify predictors of hemodynamic response and specifically to assess whether patients with Raynaud's phenomenon and pulmonary hypertension were more likely to respond to nifedipine. Nifedipine decreased resting mean pulmonary artery (PA) pressure and pulmonary vascular resistance (PVR) in patients with Raynaud's phenomenon (delta PA - 6.8 +/- 10.5 mm Hg; delta PAD - PCW gradient - 9.3 +/- 4.7 mm Hg; delta PVR - 255 +/- 201 dynes.s.cm-5, all p less than .05) versus (delta PA 0.3 +/- 4.0 mm Hg; delta PAD - PCW gradient 0.4 +/- 5.0 mm Hg; delta PVR - 58 +/- 132 dynes.sec.cm-5, all NS), in the patients without Raynaud syndrome. These data suggest that patients with both primary and secondary PAH may benefit from nifedipine therapy, but that patients with Raynaud's phenomenon may respond particularly well, perhaps because of vasodilator-reversible pulmonary vasoconstriction. An alternative hypothesis is that prior chronic vasodilator therapy in the majority of our patients with Raynaud's phenomenon preserved pulmonary vasoreactivity.
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PMID:Nifedipine in pulmonary arterial hypertension. Importance of Raynaud's phenomenon. 362 18

25 patients with essential arterial hypertension were treated with single daily doses of 400 g acebutolol administered for EIGHT weeks in outpatients' departments. The drug proved to be extremely effective in reducing PAS and PAD values in both lying and standing positions. No undesirable side effects were observed except in one case where cardiac insufficiency was controlled by digitalis. It can therefore be concluded that acebutolol is a beta-adrenolytic drug which is reliably effective in the treatment of essential arterial hypertension, well tolerated and easily administered.
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PMID:[Treatment of essential arterial hypertension with a single daily dose of acebutolol]. 664 73


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