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)

Three cases of symptomatic bradycardia due to topical ocular timolol administration are reported. Two patients had syncope related to atrioventricular block, and the other one complained of dizziness due to sinus bradycardia. Heart disease was not present in any case, although a right bundle branch block was observed in one patients. A normal sinus rhythm resumed in all patients after discontinuation of timolol.
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PMID:[Bradyarrhythmias secondary to the use of ophthalmic timolol. A report of 3 cases]. 154 65

An 18-yr-old college freshman basketball player at a Division I university suffered chest pain, dyspnea, and dizziness followed by syncope while running a 400-m dash. After an extensive multidisciplinary workup that eliminated all organic causes, the patient, an only child from a remote rural area, was found to be suffering from panic attacks with mild features of agoraphobia. Exertional chest pain is a common complaint in young athletes. The etiologies are myriad and can be referable to many organ systems; however, the cause is usually benign. Psychogenic origin is uncommon but must be considered when organic causes have been ruled out and the patient's social history is suggestive.
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PMID:Chest pain and shortness of breath in a collegiate basketball player: case report and literature review. 156 45

20 patients with WPW syndrome and recurrent tachyarrhythmias were studied clinically and electrophysiologically. The localization and electrophysiological properties of accessory pathways and other heart structures were estimated before the surgical treatment. 13 patients (pts) suffered syncope in the course of atrial flutter or atrial fibrillation with heart rate greater than 300/min, often proceeding into ventricular fibrillation or atrioventricular tachycardia greater than 260/min, which sometimes proceeds into atrial/ventricular fibrillation. 6 pts experienced dizziness or fainted during tachyarrhythmias or rhythm changes. In 15 pts antiarrhythmic drugs in monotherapy or various combinations did not prevent recurrence of tachyarrhythmias. In 4 of 5 other pts only amiodarone was effective but the drug was discontinued due to serious adverse effects. The lack of good effect of antiarrhythmic drug therapy can be based on mutually unfavorable electrophysiologic properties of the accessory pathways and other heart structures. Pts who experienced syncope had a particularly short effective refractory period (ERP) of the accessory pathways in ante- and retro-grade direction and short ERP of the ventricle muscle. Additionally, there were multiple accessory pathways, heart muscle impairement and frequent ventricular premature beats--factors triggering the tachyarrhythmias.
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PMID:[Clinical and electrophysiological indications for surgical treatment in patients with Wolff-Parkinson-White syndrome]. 160 82

We report a 52-year-old male patient with Shy-Drager syndrome (SDS) complicated by an occurrence of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The patient first developed impotence at the age of 48, accompanied by urinary incontinence, and episodes of dizziness while standing. The following year, the patient had developed a staggering gait and speech became monotonous. At age 52, the patient was admitted to the hospital after experiencing frequent episodes of syncope associated with complete loss of consciousness. Upon examination, blood pressure was 100/70 in a recumbent position, and 80/60 when standing. The pulse rate varied from 60 per minute to 62. The patient was alert. The alternating Horner sign was observed, and a paucity of facial movements was visible. His speech was slow and monotonous. Muscle tone was increased bilaterally. There was incoordination. A laboratory examination revealed reduced serum sodium levels of 127 mEq/L and increased sodium excretion with plasma hypoosmolality (262 mOsm/kg/H), urine hyperosmolality and low serum renin activity (0.2 ng/ml/h). Renal functions were normal and the levels of adrenocortical and thyroid hormones were normal. There were no abnormalities observed in the chest roentgenogram taken. The level of antidiuretic hormone (ADH) was unreasonably high (5.74 pg/ml). A water-load test demonstrated failure of both water diuresis and inhibition of ADH secretion. These data suggested that hyponatremia in this case was caused by SIADH. The correlation between plasma osmolality and the concentration of ADH suggested that osmolality that initiates ADH release appeared to have been reset to around 230 mOsm/kg lower than normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Shy-Drager syndrome and the syndrome of inappropriate secretion of antidiuretic hormone]. 161 76

Progressive or primary autonomic failure (AF) is a disease of unknown-etiology, and presents generalized and extensive autonomic disturbances because of selective neuronal degeneration in the whole of autonomic nervous system. AF is classified into three categories; (1) pure autonomic failure, without associated neurological disorders, (2) AF with Parkinson's disease (PD), and (3) AF with multiple system atrophy (Shy-Drager syndrome) (Bannister, 1988). AF with PD is pathologically characterized by neuronal cell degeneration in the intermediolateral column and the substantia nigra, together with Lewy bodies mainly in the pigmented nuclei in the brain stem. Patients with PD occasionally develop syncope or dizziness due to orthostatic hypotension and/or postprandial hypotension as well as urorectal disturbances as the initial symptoms, and are followed by parkinsonism. Levodopa is usually effective for parkinsonism but the prognosis is rather poor. AF with PD could be regarded as a form of 'the Lewy body disease' according to Kosaka's clinicopathological entity (1984).
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PMID:[Progressive autonomic failure with Parkinson's disease]. 161 62

Ten patients, who were admitted to the Intensive Coronary Care Unit during a one year period with symptomatic bradycardia while on combination therapy with oral diltiazem and beta-blocker agents, are described. The important features of this adverse reaction to drug combination were that it appeared mainly in a relatively elderly age group and with presenting symptoms of lethargy, dizziness, syncope, chest pain, and (in one patient with poor left ventricular function) pulmonary edema. It was not dose dependent and occurred even in very low doses of each drug. Electrophysiologic abnormalities were localized to the sinus node in all 10 patients and the primary rhythm disorders were junctional escape rhythm, sinus bradycardia, and sinus pause. These rhythm abnormalities resolved within 24 h following withdrawal of the offending drugs. Temporary pacemaker insertion was necessary in four patients. The duration of drug combination used before the acute episode range from within hours to up to 2 years. In conclusion, although combination diltiazem/beta blocker therapy is very effective in ischemic syndrome, caution is advised when this combination is used especially in the elderly or in patients with left ventricular dysfunction or antecedent sinoatrial or atrioventricular conduction abnormality.
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PMID:Symptomatic bradycardia induced by the combination of oral diltiazem and beta blockers. 168 24

Increased sympathetic tone is one physiopathological mechanism of vasovagal syncope. In this case, betablocker therapy is logical. The reports in the literature suggest that the head-up tilt test can reliably reproduce vasovagal syncope. Ten patients (4 men and 6 women, mean age 59 +/- 18 years) who suffered from recurrent vasovagal syncopes (2 to 10 attacks in 6 patients and more than 10 in the other 4) with a positive initial head-up tilt test (syncope or severe dizziness with marked hypotension after a maximum of 40 minutes at 60 degrees) were treated with atenolol (200 mg daily in 7 cases and 100 mg daily in the other 3). A second head-up tilt test was performed 15 +/- 6 days later under betablocker therapy; this test was negative in 7 and remained positive in 3 cases. Irrespective of the result, the 10 patients followed the same therapy at the same dosage. After 9 +/- 5 months, 3 patients had another syncopal attack; 2 stopped taking their medication and the third patient continued the betablocker because there was a marked reduction in the frequency of his attacks. There were no further syncopal episodes during follow-up of the other 7 patients. The medium-term efficacy could not be predicted from the results of the second head-up tilt test. The following conclusions may be drawn from this study: The head-up tilt test becomes negative in 70% of cases after introducing betablocker therapy, assuming a 100% reproductivity. This treatment is effective in over half the patients at medium term and should be considered in patients with recurrent vasovagal syncope.
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PMID:[Evaluation of beta-adrenergic blockader therapy in vasovagal syncope reproduced by head-up tilt test]. 168

Ventricular couplets may be a risk factor for sudden death in adults, but their prognosis in children is unknown. From 1981 to 1987 104 patients, mean age 13.2 years (0.2 to 37 years), had ventricular couplets on a 24-hour electrocardiogram (ECG) (Holter monitor) and on follow-up with a second Holter (mean, 2.5 years). Of the 104 patients, 22 had a normal heart and 82 had an abnormal heart. Patients with a normal or an abnormal heart did not differ in incidence or severity of symptoms (patients with a normal heart had 17 instances of palpitations and none of syncope; patients with an abnormal heart had 49 instances of palpitations, six of dizziness, and none of syncope). Number of ventricular couplets was higher in patients with a normal heart (33 +/- 50/day: mean +/- 1 SD) than in those with an abnormal heart (17 +/- 15/day; p less than 0.05). Of the 22 patients with a normal heart, 11 underwent an electrophysiologic study (EPS); none had inducible ventricular tachycardia. After mean follow-up of 29.7 months, all 22 patients with a normal heart were alive without ventricular tachycardia; 6 of 22 were treated for palpitations, with complete suppression of couplets in two. In 11 of 16 untreated patients with a normal heart, ventricular couplets disappeared spontaneously. Of the 82 patients with an abnormal heart, 32 had an EPS: nine (28%) had sustained ventricular tachycardia, 16 (50%) had nonsustained ventricular tachycardia, and seven (22%) had no inducible ventricular tachycardia. ECG criteria and hemodynamic status were of limited value in predicting inducibility of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventricular couplets in the young: prognosis related to underlying substrate. 168 31

We examined the hypothesis that a greater than or equal to 2 second pause detected on 24-hour Holter monitoring in patients with persistent atrial fibrillation and complaints of syncope or dizziness lacked sufficient specificity to warrant implantation of a permanent pacemaker. We retrospectively reviewed cases from our 24-hour electrocardiographic (Holter) monitoring data base. A total of 411 consecutive Holter monitoring records demonstrating persistent atrial fibrillation obtained during a 5-year period (1982 to 1987) were examined. One hundred and five (26%) patients had cerebral symptoms (dizziness or syncope) as a primary indication for monitoring 80 (76%) patients were identified with documented ventricular pauses of greater than or equal to 2 seconds. Three hundred and six patients (74%) underwent 24-hour monitoring without cerebral symptoms as an indication and 209 (68%) patients had greater than or equal to 2-second pauses. Clinical information was available in 164 (50 symptomatic and 114 asymptomatic) patients. There were no significant differences in the clinical or Holter findings between the two groups. Of the 50 symptomatic patients, 15 (30%) underwent permanent pacemaker placement and the remaining 35 (70%) were managed conservatively during a mean follow-up of 23 +/- 5 months. Eleven of 15 paced (73%) and 31 of 35 (89%) nonpaced patients experienced resolution of their cerebral symptoms (NS). The sensitivity of Holter monitoring in detecting pauses of greater than or equal to 2 seconds in patients with cerebral symptoms was high (76%), but the specificity (32%) and positive predictive values (28%) were low.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Permanent pacemaker placement in chronic atrial fibrillation associated with intermittent AV block and cerebral symptoms. 169 52

The follow-up and characteristics of 20 patients with ventricular tachycardia (VT) and no detectable heart disease is reported. These were 16 men and four women with a mean age of 44 years. Symptoms were present in 18 patients (eight had syncope and ten palpitations or dizziness), VT was sustained in 11 patients and a left bundle branch block morphology with inferior axis was found in 17 patients. In three patients, VT had a right bundle branch block morphology and left-axis deviation. The VT was inducible in 13 patients during the electrophysiological testing (EP) and was sustained in five patients. Medical treatment was introduced in 19 patients. During a mean follow-up of 10 years from the onset of the symptoms and 6 years from the EP testing, one patient died suddenly. He had stopped taking amiodarone 5 months before. In seven patients symptoms recurred and were due to discontinuation of therapy in two cases and inefficacy of previous effective treatment in five patients. After modification of the treatment (three cases), implantation of a pacemaker (one case) and catheter ablation (one case), all patients became asymptomatic. Eleven patients became asymptomatic with the first administered antiarrhythmic therapy. One patient continues to be asymptomatic in spite of discontinuation of his medical therapy. We conclude that patients with VT and no detectable heart disease have a good long-term prognosis and that appropriate therapy can be found in almost all patients.
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PMID:Ten-years follow-up of 20 patients with idiopathic ventricular tachycardia. 170 11


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