Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The classical subclavian steal syndrome is a larcenous vertebrobasilar insufficiency, secondary to retrograde flow in the vertebral artery. The authors present their experience with an unusual variant of subclavian steal in which the ipsilateral vertebral artery was completely or partially occluded, or arose from the aortic arch. These patients had symptoms typical of vertebrobasilar insufficiency--dizziness or brain stem transient ischemic attacks--despite steal through relatively small cervical collaterals to the obstructed subclavian artery. Physical findings of diminished pulses and blood pressure in the involved upper extremity are similar to those in the common form of subclavian steal. The alternate collaterals found in these patients are documented by angiography and other potential collaterals are reviewed. All three symptomatic patients were treated successfully by carotid-subclavian bypass or anastomosis of the subclavian to the common carotid artery. They have remained asymptomatic for 1 1/2 to 3 years following operation. The potential for development of subclavian steal in the absence of a vertebral artery to provide collateral flow adds another reason for abandoning vertebral artery ligation as an alternative treatment for the subclavian steal syndrome.
J Cardiovasc Surg (Torino)
PMID:Subclavian steal with ipsilateral vertebral artery occlusive disease. 372 45

Fifty-five patients suffering from essential or renal hypertension who had been insufficiently treated previously with combination therapy using diuretics and beta-blockers as well as reserpine, clonidine, prazosin, captopril, or minoxidil have been included in this open study. In addition to receiving diuretics and beta-blockers alone or in combination with reserpine, clonidine, or methyldopa, the patients were given nitrendipine in a dose of 2 X 20 to 2 X 40 mg/day. A normalisation of blood pressure values was attained in 46 of the 55 patients; 18 of these patients have been treated for more than 1 year. Few side-effects were observed. Dizziness and ankle oedema each occurred once. A rash occurred in one patient, causing the withdrawal of nitrendipine. No complaints of headache and palpitations were made. It may be concluded that nitrendipine is well suited as a partner in the combination treatment of patients with essential or renal hypertension that is difficult to stabilise.
J Cardiovasc Pharmacol 1984
PMID:Nitrendipine in hypertension that is difficult to control. 608 67

More than 1,700 patients with essential or renal hypertension were treated with nitrendipine; data from 967 of these were included in a data pool, and safety data were evaluated. Treatment duration was between 7 days and 2 years. The most frequent side-effects were headache, flush, oedema, dizziness, and palpitations due to the pharmacodynamic effect of the drug. All other side-effects had an incidence below 2%. Eighty-two of the 967 patients stopped therapy before the end of the trial. In 33 of these patients, this was probably due to the side-effects of nitrendipine. Hematological and clinical chemistry data did not indicate any systemic or organ damage. When nitrendipine was combined with thiazides, a lowering of plasma potassium levels could be found, which, however, did not necessitate any therapy.
J Cardiovasc Pharmacol 1984
PMID:Safety aspects of long-term nitrendipine therapy. 608 68

Fifty-one patients with essential hypertension, 22 males and 29 females with a mean age of 51 (range, 28 to 65 years), were studied for more than 12 months in a controlled clinical trial with nitrendipine, a new calcium antagonist agent. No differences in age, severity of hypertension, and other risk factors between the two sexes were detected. Forty-four of 51 patients completed the study, and 38 (86.4%) achieved a normalization of blood pressure. Mean systolic blood pressure decreased from 196.0 +/- 12.9 mm Hg (means +/- SD) during placebo to 171.2 +/- 9.5 mm Hg (12.6%, p less than 0.001) after 12 months. Mean diastolic blood pressure at the same time decreased from 109.0 +/- 5.2 mm Hg to 88.5 +/- 3.6 mm Hg (18.8%, p less than 0.001). Heart rate also decreased slightly but significantly (p less than 0.01) after the fifth week. A significant change in weight was not observed throughout the trial. Plasma potassium remained unchanged during the year, and plasma sodium after a transient increase (p less than 0.001) in the fifth week returned very close to basal levels in the sixth month. Side-effects were observed in 17 patients, 5 of whom had to leave the trial, but in the rest they were usually mild and transient. These were mainly frontal and occipital headache, facial flushing, ankle and pretibial oedema, and dizziness. No relationship was detected between side-effects and body weight or plasma sodium disturbances. Preliminary data on a separate group of 27 elderly patients (66-83 years) showed a better and faster effect of nitrendipine given in low doses.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1984
PMID:Clinical experience with long-term nitrendipine treatment in essential hypertension. 608 73

Tolerability data recorded during long-term administration of methyldopa are presented here. Since diuretics and other antihypertensive agents were frequently coadministered with methyldopa, no attempt was made to assign possible drug relationships for any particular adverse effect. The most common clinical adverse effects among the entire study population were drowsiness and dizziness. Impotence was reported by 16% of 258 men.
J Cardiovasc Pharmacol 1981
PMID:Long-term treatment of hypertension with methyldopa. III. Tolerability. 617 72

Medroxalol, a new antihypertensive agent with alpha- and beta-adrenoreceptor blocking properties in both animals and humans, was administered in a single-blind study for 12 weeks to 29 patients with mild and moderate hypertension (standing blood pressure: 188-130/130-100 mm Hg). After 4 weeks of placebo administration, treatment with oral medroxalol was begun. Six weeks later, half the subjects added hydrochlorothiazide, 12.5 mg twice daily, to medroxalol for an additional 6 weeks, and the other half added placebo. During the final 4-week period medroxalol, but not hydrochlorothiazide, was discontinued and placebo substituted. Oral medroxalol doses of 100-400 mg twice daily reduced standing diastolic pressure to less than 100 mm Hg in 21 of the 26 subjects who completed the study. Compared to the last values on placebo, mean standing blood pressure was decreased by 15.6/12.0 mm Hg during the first 6 weeks of medroxalol at mean daily doses of 388-407 mg. Addition of hydrochlorothiazide permitted some decrease in medroxalol dosage. Upon medroxalol withdrawal, blood pressure and heart rate returned toward pretreatment values, with subjects continuing on diuretic showing lower blood pressures than the untreated individuals. Tolerance to medroxalol, with or without hydrochlorothiazide, was good. Mild orthostatic dizziness was the most frequent complaint associated with therapy, but postural hypotension was not found on physical examination. Medroxalol appears to be effective and well tolerated for reducing the blood pressure of most patients with mild to moderate hypertension and may be useful for chronic oral therapy of this disease.
J Cardiovasc Pharmacol
PMID:Treatment of mild and moderate hypertension with medroxalol, an alpha- and beta-adrenergic antagonist. 618 88

Thirteen of 308 patients (4.2%), who had received right-sided valved extracardiac conduits at the Mayo Clinic from November, 1972, to April, 1977, have required conduit replacement because of obstruction. Patients were 5 to 16 years old at initial operation and 8 to 20 years old at reoperation; the duration of conduit implantation was 27 to 79 months (mean 50). Four patients (31%) were asymptomatic; exertional dyspnea was present in eight (62%) and dizziness was reported in one (8%). Signs of conduit obstruction included increasing intensity of murmurs in 11 (85%), cyanosis in two (15%), and heart failure in one (8%). Peak pressure gradients from the right ventricle to the pulmonary arteries ranged from 50 to 140 mm Hg (mean 87) and correlated well with the degree of conduit obstruction. Catheter pullback allowed accurate localization of stenosis within the conduit, whereas angiography alone did not. The site of major obstruction was in the proximal conduit in five (38%), at the valve in nine (69%), and in the distal conduit or side branches in six (46%); stated differently, major stenosis affected the valve alone in five (38%), the graft alone in four (31%), and both the valve and the graft in four (31%). Valvular changes leading to stenosis included thrombosis, commissural fusion, and calcification, and changes consistent with insufficiency included tears, fusion of cusps to the conduit wall, and, in one case, infective endocarditis. Within the conduit, nonvalvular obstruction was due to formation of a thick fibrous peel (or neointima). Progressive thickening of the peel appeared to be due to organization of thrombus between the peel and conduit and not due to luminal mural thrombus. In one case, the peel formed a flap-valve, causing even further obstruction. Since many patients are asymptomatic, and since late conduit stenosis may develop unpredictably by several mechanisms, long-term follow-up is necessary.
J Thorac Cardiovasc Surg 1981 Apr
PMID:Clinicopathological correlates of obstructed right-sided porcine-valved extracardiac conduits. 720 68

A study of 97 persons (mean age = 66 yrs, 79% male) with an ICD for an average of 2.2 years was conducted to determine whether patients resume driving (N = 72) post-ICD insertion despite instructions not to do so. Those who had resumed were queried about their driving habits, the presence of symptoms associated with arrhythmias, the occurrence of shocks in the previous year, and the importance of driving to maintenance of lifestyle. Our assumption was that patients return to driving to maintain their pre-ICD lifestyle of functional independence, and to resume social roles such as provider for the family. Seventy-four percent of subjects reported driving an average of 60 mi/week despite being instructed not to drive by their physician or other health care provider. Of those who resumed driving, > 4% had received a shock while driving. Over 86% of subjects believe driving was an important part of maintaining one's lifestyle. Reasons for driving included necessity (62%), such as to work or a physician appointment, or social (58%), such as driving to the store or church. Symptoms such as dizziness, palpitations and lightheadedness were experienced by 80% of subjects, with 43% receiving a shock from their ICD within the previous year. There were significant correlations between driving and the importance of driving to maintaining one's lifestyle (p < .05), driving for necessity (p < .01), for social reasons (p < .01) and being the primary driver in the family (p < .05).
Prog Cardiovasc Nurs 1995
PMID:Factors related to driving in persons with an implantable cardioverter defibrillator. 747 57

In 26 patients with mild-to-moderate hypertension, 80.8% of whom had a history of concomitant diseases, the effect of moxonidine (0.2 mg b.i.d.) on the 24-h ambulatory blood pressure profile (ABPM) was compared with captopril (25 mg b.i.d.) in a double-blind, parallel-group study. After 4 weeks of treatment with placebo, ABPM was performed and the patients were treated with moxonidine (n = 14) or captopril (n = 12) for a further 4 weeks. ABPM was then repeated. Both moxonidine and captopril reduced systolic and diastolic blood pressure sufficiently and to the same extent. Mean 24-h pulse rate and standard laboratory parameters were not changed by active treatment. After drug withdrawal for 5 days, sitting blood pressure did not differ from baseline values in both groups. Serious adverse events did not occur, the most frequent complaints were nausea (2 of 14 patients receiving moxonidine) and dizziness (3 of 12 patients receiving captopril). We concluded that the blood pressure-lowering effects of moxonidine (0.2 mg b.i.d.) and captopril (25 mg b.i.d.) are comparable in patients with mild-to-moderate hypertension.
J Cardiovasc Pharmacol 1994
PMID:Twenty-four-hour blood pressure profiles in patients with mild-to-moderate hypertension: moxonidine versus captopril. 753 24

We compared the response of the oral angiotensin II (Ang II) receptor antagonist (ARA) UP 269-6 with an angiotensin converting enzyme inhibitor (ACEI) enalapril 20 mg or placebo, during salt depletion in normal men. We also evaluated safety and tolerability. Sixteen healthy, normotensive male volunteers followed a standardised salt-depletion regimen for 3 days before each study day. Seven different doses of UP 269-6 (5, 10, 20, 40, 80, 120 and 180 mg) were administered double blind in a four-panel dose escalation, with enalapril and placebo randomised within each panel. Supine and erect blood pressure (BP) and heart rate (HR); serum and urinary electrolytes; plasma active renin (PAR), aldosterone, and Ang II were measured at intervals. Urinary electrolytes and aldosterone were measured for the 24 h before dosing and for 24 h after dosing. Dizziness and light-headedness on standing were reported after UP 269-6 at higher doses. Enalapril caused one episode of symptomatic postural hypotension. No other drug-related adverse events (AE) were noted. There was a dose-related decrease in supine and erect systolic and diastolic BP (SBP, DBP) with UP 269-6 at > or = 40 mg, with no change in HR. Based on the maximal decrease in mean arterial pressure (MAP), UP 269-6 at 180 mg had an effect largely comparable to that of enalapril 20 mg. There was a dose-related increase in PAR with UP 269-6. Although this was greater with UP 269-6 180 mg than with enalapril, serum and 24-h urinary aldosterone suppression was greater with enalapril than with any dose of UP 269-6.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1995 Jun
PMID:Comparison of the oral angiotensin II receptor antagonist UP 269-6 or enalapril 20 mg on blood pressure and neurohormonal effects in salt-deplete man. 756 47


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