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)

Incidence, clinical picture, ECG features, as well as chosen diagnostic and therapeutic measures were investigated in patients attending the Basel University Medical Outpatients Department with the diagnosis of sick sinus syndrome. A retrospective study was conducted by selecting patients' charts with this diagnosis during the period 1979-1983. Forty-four patients (17 women, 27 men, mean age 64.5 +/- 14.5 years) were "discovered" and divided into three groups: Group 1: asymptomatic patients with pathological ECG (n = 7), Group 2: symptomatic patients with pathological ECG (n = 22), Group 3: main symptom syncope (n = 15). All patients had had an ECG and 15 a 24-hour-ECG. Carotid sinus massage was performed in three patients and sinus node recovery time was measured in another three. Seventeen patients remained without treatment, 13 received a permanent pacemaker, 9 of whom had additional medication, while 12 were anticoagulated. Three patients who were not anticoagulated suffered a stroke. More invasive electrophysiological investigations should be undertaken only with caution. In group 1, further diagnostic or therapeutic consequences need to be drawn. In the symptomatic patients from group 2, 24-hour-ECG is indicated when there is a history of palpitations, dizziness or severe heart failure. The immediate implantation of a pacemaker is justifiable in group 3 patients. Drugs with antiarrhythmic activity should be avoided in these patients before pacemaker implantation.
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PMID:[Sick sinus syndrome--clinical presentation, diagnostic and therapeutic measures in an ambulatory patient sample]. 398 2

The efficacy of muzolimine (BAY g 2821) in doses of 30 or 60 mg/day was studied over an observation period of 4 weeks in 48 patients with mild to moderate heart failure (NYHA stage 2 or 3) in a biometrically planned, multicentre study. Eleven of these patients were excluded from the evaluation of efficacy for various reasons. All 37 patients who remained (23 men and 14 women; mean age 59.6 years, mean body weight 73.8 kg) were treated throughout with one tablet per day (30 mg). A marked improvement of the symptoms of cardiac insufficiency was observed in these 37 evaluated cases in the course of the treatment period. At the end of the study body weight was reduced by 1.8 kg, heart rate fell from 84 to 75 beats/min and blood pressure decreased from 154/88 to 145/85 mm Hg on average. The laboratory parameters tested failed to show any clinically abnormal alterations. Twelve of 48 patients complained of side effects (dizziness, headaches, vomiting, nausea), these developing largely in the first 2 weeks and being transient in character. To summarize, it can be stated that patients with chronic heart failure (NYHA 2 and 3) can be effectively treated by muzolimine monotherapy.
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PMID:Muzolimine as monotherapy in the treatment of patients with congestive cardiac failure. 400

Calcium channel blockers are assuming increasingly important roles in the practice of emergency medicine. Two cases and a review of the literature relating to treatment of hypertensive emergencies with nifedipine are presented. Nifedipine has a rapid onset of action (buccal, 10-15 minutes; oral, 30-45 minutes) and peak effect (buccal, 30 minutes, oral, 60 minutes). The duration of effects is four to six hours regardless of the route of administration, with a mean arterial pressure reduction of 21.6% (248/134 mm Hg to 165/87 mm Hg). In patients with severe hypertension and left ventricular failure, a consistent reduction in systemic vascular resistance (2,088 dynes/sec/cm-5 to 1242 dynes/sec/cm-5) and cardiac index (2.76 l/min/m2 to 3.77 l/min/m2) has been reported. The patients in this study had severe hypertension (systolic blood pressure greater than 180 mm Hg, diastolic blood pressure greater than 120 mm Hg) and end organ involvement (including heart failure, left ventricular strain, headache, confusion, dizziness, and shortness of breath). Nifedipine (10 mg) was administered buccally with prompt reduction of blood pressure and resolution of the patients' symptoms. Nifedipine appears to be a safe, effective agent for the management of hypertensive emergencies. Its pharmacokinetic profile and routes of administration make it particularly valuable in the practice of emergency medicine.
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PMID:Nifedipine in the management of hypertensive emergencies: report of two cases and review of the literature. 406 18

34 patients have been controlled after beta-blocking therapy, for a mean period of 5 years. Symptoms and evolution: syncope disappeared, angoy passed from 47% to 23%, dyspnea from 65% to 47%, dizziness from 70% to 54%, weakness from 30% to 37%. A systolic murmur was present in 75% of the cases. Two patients died by heart failure. Phonocardiogram: the systolic murmur was unchanged, like the carotid pulse. Paradoxical splitting of the 2 degrees sound was more frequent, atrial sound unimodified, isometric contraction shortened (60%) and the Q-1 degree sound interval prolonged (90%). Electrocardiogram: 1 degree A/V block appeared in 24% of the cases, complete A/V block in 9%, atrial fibrillation in 3%. Left atrial enlargement was more frequent; left ventricular hypertrophy unchanged. Heart catheterization (10 cases, after a mean period of 5.5 years): left ventricular pressure gradient passed from 80% to 90%; a low cardiac index from 20% to 30%; telediastolic pressure of left ventricle was unmmodified in 10% of cases, more elevated in 50%, less elevated in 40%. Chest X ray: cardiac size was unchanged in 65% of cases, enlarged in 32%; smaller in 3%. In conclusion, symptoms improved in most of the patients; no case of sudden death was observed. Some data however show that the evolution of the myocardiopathy goes on to congestive heart failure and arise doubts on the real usefullness of beta-blocking drugs in the disease.
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PMID:[beta-Blocking therapy in obstructive hypertrophic cardiomyopathy. Long term results (author's transl)]. 610 83

After implantation of a ventricular demand pacemaker (VVI), occasional patients continue to have dizziness, syncope, or near syncope ("pacemaker syndrome"). To identify patients in whom VVI pacing may have deleterious effects, we compared cuff blood pressure responses to VVI pacing with blood pressure responses to atrioventricular sequential pacing (DVI) or sinus rhythm in 50 consecutive patients. Patients with intact ventriculoatrial conduction had a much greater decrease in systolic blood pressure with VVI pacing (24 +/- 11 mm Hg) than those with ventriculoatrial dissociation (-4 +/- 15 mm Hg) (P less than 0.005). Patients who were in heart failure had a lesser decrease in blood pressure with VVI pacing than did those without failure (P less than 0.05); 13 of the 14 heart failure patients lacked ventriculoatrial conduction. Ten patients had symptomatic dizziness after VVI pacing; the incidence of symptoms was higher in patients with ventriculoatrial conduction (9 of 23) than in those without ventriculoatrial conduction (1 of 27) (P less than 0.003). We conclude that the presence of intact ventriculoatrial conduction appears to be a crucial determinant of the hemodynamic response to VVI pacing, and its presence may identify patients who are at risk for "pacemaker syndrome."
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PMID:Hemodynamic and symptomatic consequences of ventricular pacing. 618 93

Labetalol is a combined alpha- and beta-adrenoceptor blocking agent for oral and intravenous use in the treatment of hypertension. It is a nonselective antagonist at beta-adrenoceptors and a competitive antagonist of postsynaptic alpha 1-adrenoceptors. Labetalol is more potent at beta that at alpha 1 adrenoceptors in man; the ratio of beta-alpha antagonism is 3:1 after oral and 6.9:1 after intravenous administration. Labetalol is readily absorbed in man after oral administration, but the drug, which is lipid soluble, undergoes considerable hepatic first-pass metabolism and has an absolute bioavailability of approximately 25%. There are no active metabolites, and the elimination half-life of the drug is approximately 6 hours. Unlike conventional beta-adrenoceptor blocking drugs without intrinsic sympathomimetic activity, labetalol, when given acutely, produces a decrease in peripheral vascular resistance and blood pressure with little alteration in heart rate or cardiac output. However, like conventional beta-blockers, labetalol may influence the renin-angiotensin-aldosterone system and respiratory function. Clinical studies have shown that the antihypertensive efficacy of labetalol is superior to placebo and to diuretic therapy and is at least comparable to that of conventional beta-blockers, methyldopa, clonidine and various adrenergic neuronal blockers. Labetalol administered alone or with a diuretic is often effective when other antihypertensive regimens have failed. Studies have shown that labetalol is effective in the treatment of essential hypertension, renal hypertension, pheochromocytoma, pregnancy hypertension and hypertensive emergencies. In addition, preliminary studies indicate that labetalol may be of value in the management of ischemic heart disease. The most troublesome side effect of labetalol therapy is posture-related dizziness. Other reported side effects of the drug include gastrointestinal disturbances, tiredness, headache, scalp tingling, skin rashes, urinary retention and impotence. Side effects related to the beta-adrenoceptor blocking effect of labetalol, including asthma, heart failure and Raynaud's phenomenon, have been reported in rare instances.
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PMID:Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. 631 May 29

The hemodynamic benefits and safety of combined therapy with captopril and hydralazine were studied during invasive hemodynamic monitoring in 14 patients with severe heart failure. In eight patients, the individual effects of both drugs were evaluated before the administration of combined therapy, whereas hydralazine was added to maintenance captopril therapy in the other six patients. In the first group, captopril alone produced a marked decrease in pulmonary wedge pressure (28 +/- 4 to 18 +/- 5 mm Hg) and mean arterial pressure (85 +/- 20 to 69 +/- 13 mm Hg) (both p less than 0.001) without a significant increase in cardiac index. Hydralazine alone produced a marked increase in cardiac index (1.6 +/- 0.4 to 2.7 +/- 0.5 liters/min per m2) (p less than 0.001), but with a minimal decrease in pulmonary wedge pressure (28 +/- 4 to 23 +/- 4 mm Hg) (p less than 0.05) and without a significant change in mean arterial pressure. The combination of captopril and hydralazine produced an increase in cardiac index similar to that of hydralazine alone and decreases in pulmonary wedge pressure and mean arterial pressure similar to those with captopril alone. Most important, when hydralazine was added to captopril in the entire group of 14 patients, cardiac index increased markedly with little additional decrease in mean arterial pressure and no significant increase in heart rate. The one patient who experienced symptomatic hypotension with combination therapy also had dizziness with captopril alone. Seven of the nine patients maintained on long-term treatment experienced symptomatic improvement. Thus, in patients with severe chronic heart failure, the combined use of captopril and hydralazine is feasible and produces acute hemodynamic improvement superior to that from either drug alone.
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PMID:Hemodynamic responses to combined therapy with captopril and hydralazine in patients with severe heart failure. 634 33

The effect of the converting enzyme inhibitor captopril as long term treatment was investigated in 14 patients with severe congestive heart failure in a double blind trial. Captopril reduced plasma concentrations of angiotensin II and noradrenaline, with a converse increase in active renin concentration. Effective renal plasma flow increased and renal vascular resistance fell; glomerular filtration rate did not change. Serum urea and creatinine concentrations rose. Both serum and total body potassium contents increased; there were no long term changes in serum concentration or total body content of sodium. Exercise tolerance was appreciably improved, and dyspnoea and fatigue lessened. Left ventricular end systolic and end diastolic dimensions were reduced. There was an appreciable reduction in complex ventricular ectopic rhythms. Adverse effects were few: weight gain and fluid retention were evident in five patients when captopril was introduced and two patients initially experienced mild postural dizziness; rashes in two patients did not recur when the drug was reintroduced at a lower dose; there was a significant reduction in white cell count overall, but the lowest individual white cell count was 4000 X 10(6)/l. Captopril thus seemed to be of considerable value in the long term treatment of severe cardiac failure.
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PMID:Captopril in heart failure. A double blind controlled trial. 638 12

Tocainide is an antiarrhythmic drug structurally related to lignocaine with similar electrophysiological, haemodynamic and antiarrhythmic effects. In contrast to lignocaine (lidocaine) it is well absorbed after oral administration and has a plasma half-life of about 15 hours. In several open and controlled therapeutic trials in patients with ventricular arrhythmias, often following a myocardial infarction, tocainide has been relatively effective and usually well tolerated. In treating ventricular ectopic beats and/or ventricular tachycardia tocainide has demonstrated effective suppression in 60 to 70% of patients in both open and controlled studies. It has an acute effect when infused in patients with ventricular arrhythmias complicating myocardial infarction, as well as a prophylactic effect when given orally. The majority of these studies have demonstrated tocainide to be more effective than placebo, but trials against other antiarrhythmic agents are few in number and vary in design. One study combining an infusion of tocainide with oral therapy compared to a bolus injection of lignocaine followed by a constant infusion in patients after myocardial infarction, found the two agents to be of similar efficacy. The most common adverse effects are neurological and gastrointestinal in nature, nausea and dizziness occurring most frequently. Adverse effects resulting in termination of therapy have been reported in about 16% of patients. Aggravation of pre-existing heart failure, increased ventricular arrhythmia, deterioration of conduction disturbances, convulsions, and cases of lupus erythematosus syndrome have occasionally been reported. Thus, tocainide appears to offer a worthwhile addition to the other antiarrhythmic agents available for ventricular arrhythmias. However, its relative place in therapy compared with other antiarrhythmic drugs is not yet clearly established.
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PMID:Tocainide. A review of its pharmacological properties and therapeutic efficacy. 641 45

Verapamil hydrochloride, a prototype calcium antagonist, is now marketed in the United States for the acute treatment of supraventricular tachyarrhythmias and for chronic management of vasospastic and chronic stable angina. It inhibits the slow inward channel in in the heart and blocks calcium influx in smooth muscle. Its intrinsic negative inotropic action, which is apparent in isolated tissues, is offset in vivo by peripheral vasodilation. It has a mild, noncompetitive sympathetic antagonist effect; its most important electrophysiologic action is a depression of AV nodal conduction, accounting for its effect in supraventricular tachyarrhythmias. Its hemodynamic actions are characterized by a complex interplay of changes in preload, afterload, contractility, heart rate, and coronary blood flow. It does not depress cardiac function, except in severe heart failure. The drug has a mild dilator action on coronary arteries and reverses ergonovine-induced vasoconstriction. Controlled trials have established its role in Prinzmetal's variant angina, unstable angina, and chronic stable angina. It has also been found to be effective in obstructive cardiomyopathies. The potential role of verapamil in such conditions as hypertension, cardioprotection, and Raynaud's phenomenon needs further evaluation; at present these indications have not been approved by the Food and Drug Administration. The most common side effects include constipation, skin rash, and dizziness; AV block, heart failure, and sinus arrest may occasionally be encountered, especially when ventricular function is compromised or conduction system disease is present.
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PMID:Verapamil hydrochloride: pharmacological properties and role in cardiovascular therapeutics. 676 30


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