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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two cases of acute blindness due to quinine poisoning are presented. In both cases, the diagnosis was initially unsuspected. In addition, tinnitus, decreased hearing, vomiting, abdominal pain, and confusion were noted in one patient, and the other experienced decreased hearing, headache, confusion, tachycardia, later bradycardia, and first-degree atrioventricular block. The onset of blindness was delayed more than 12 hours after ingestion in both cases. Quinine levels of 13.6 micrograms/mL and 18.6 micrograms/mL were demonstrated (therapeutic = 1 to 3 micrograms/mL). One patient developed marked constriction of visual fields and some residual decreased acuity, while the other regained normal visual acuity.
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PMID:Acute toxic blindness: unrecognized quinine poisoning. 380 84

1. The antihypertensive effects of the new phenylacetylguanidine compound, guanfacine, a sympathetic inhibitor with a central site of action, were compared with methyldopa in 20 out-patients with essential or renal hypertension (WHO grade I-II). 2. During a 6-week period in randomized cross-over conditions, guanfacine 3.5 mg daily caused a mean decrease of 24% in mean arterial blood pressure (MAP). A normalization of blood pressure (BP < 145/95 mm Hg) was achieved in 50% of the patients and a 'good control' (BP < 160/100 mm Hg; > 145/95 mm Hg) in 90%. 3. Methyldopa 1.2 g daily led to a mean decrease in MAP of 12%. Normalization of blood pressure occurred in 15% and a 'good control' was achieved with 45% of the patients. Failure due to intolerance or ineffectiveness was observed in 40% of patients. 4. During therapy with guanfacine the following side-effects were noted: dryness of the mouth (n = 5), marked sedation (n = 2), constipation (n = 2), orthostasis (n = 1), collapse (n = 1) and atrioventricular block grade I on ECG (n = 1). Methyldopa caused headaches (n = 4), gastrointestinal disturbances (n = 4) and dryness of the mouth (n = 1). 5. The experience so far available seems to indicate that guanfacine is an effective antihypertensive drug which is more active than methyldopa in the doses used in this study.
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PMID:Comparative studies of guanfacine and methyldopa. 699 79

A 23-year-old black female was referred to the University Hospital of Oklahoma because of "sleep trouble." She complained of falling asleep easily during the daytime. A sleep study was performed which showed prolonged apnea, up to 35 seconds, and prolonged asystole, up to seven seconds, with second-degree heart block. A tracheostomy was performed. She had lost some weight and did well until six months later, when she developed severe throbbing headache with visual blurring. She came to the emergency room and an ECG showed sinus bradycardia with prolonged sinus pauses, up to 2.6 seconds, and first- and second-degree AV block. She had no hypoxia and atropine was ineffective. Electrophysiologic studies were performed. Details of the case are described and mechanisms of the arrhythmias are discussed.
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PMID:Arrhythmias in sleep apnea. 699 64

A 34-year-old man with AIDS was admitted to the hospital with a one-week history of cough, chest pain, and fever. Radiography revealed a cavitating left upper lobe lesion. Two weeks later he developed a headache associated with a contrast enhancing lesion in the right parietal lobe. The patient had a progressive downhill course, developing atrioventricular block and hypernatremia. Neuro-ophthalmologically, there was a mild facial droop, "hand motions" vision with presumed bilateral cytomegalic inclusion retinitis, and signs of a mesencephalic syndrome, including lid retraction. Discussions center on the differential diagnosis of the central nervous system disease and the obligative recommendations the neuro-ophthalmologist must be willing to make.
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PMID:Ophthalmoplegia associated with AIDS. 797 90

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of sotalol hydrochloride are reviewed. The chemical name of sotalol hydrochloride is 4'-[1-hydroxy-2-(isopropylamino)ethyl]methanesulfonanilide monohydrochloride. Sotalol is a class III antiarrhythmic that prolongs the action potential and refractoriness of cardiac tissue and has potent nonselective beta-blocking activity. Sotalol is well absorbed after oral administration. The pharmacokinetics of sotalol can be described by an open, linear, two-compartment model. The drug is eliminated primarily by the kidneys; mean elimination half-life is 12 hours. Sotalol has been found to be effective in controlling life-threatening ventricular arrhythmias, including sustained ventricular tachycardia, ventricular fibrillation, and premature ventricular complexes. Although sotalol has FDA-approved labeling for use in the treatment of ventricular arrhythmias only, it is also effective against a variety of supraventricular arrhythmias. Noncardiac adverse effects include fatigue, impotence, depression, headache, nausea, diarrhea, and increased triglyceride levels. Cardiovascular adverse effects include atrioventricular block, bradycardia, hypotension, exacerbation of heart failure, and polymorphic ventricular tachycardia. Overall, 11-21% of patients experience adverse effects; 6-18% of these patients have reactions serious enough to warrant the discontinuation of sotalol therapy. The initial dosage of oral sotalol hydrochloride in adults is 80 mg twice daily or 160 mg once daily; the dosage can be increased every three to four days in increments of 40-160 mg/day to a maximum of 480 mg/day. Sotalol is useful in the control of intractable, life-threatening ventricular arrhythmias, as well as a variety of supraventricular arrhythmias, in patients who do not respond to or are intolerant of more conventional antiarrhythmics.
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PMID:Sotalol: a new class III antiarrhythmic agent. 813 5

A total of 44 patients referred for Tc-99m MIBI myocardial imaging for detection of coronary artery disease (CAD) were studied to compare the differences in heart beat, blood pressure, electrocardiographic changes and side effects during intravenous infusion of dipyridamole (ID) and adenosine (IA) and also to determine the degree of concordance between ID and IA Tc-99m MIBI imaging. These patients were divided into two groups: 20 suspected CAD patients constituted group I and 24 proven CAD patients formed group II. All patients received ID 0.56 mg/kg for 4 min and within about 10 days IA 0.14 microgram/kg/min for 6 min with Tc-99m MIBI imaging. The results revealed that maximal heart beat increased and maximal systolic blood pressure decreased in both IA and ID patients with no statistically significant differences. Transient second-degree AV block occurred with IA in 3 patients. Side effects, such as, chest pain, headache, dizziness and shortness of breath occurred more often and were in general more intense in IA patients, but they were typically mild and resolved spontaneously within 1 or 2 min of discontinuation of IA. Both IA and ID Tc-99m MIBI imaging were normal in 18 of 20 group I patients and were concordant for the presence of perfusion defects in the other 2 patients. Of 24 group II patients, all had myocardial perfusion defects on both tests and were concordant for the severity of the perfusion abnormalities. However, in other 2 patients. Of 24 group II patients, all had myocardial perfusion defects on both tests and were concordant for the severity of the perfusion abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of intravenous dipyridamole and adenosine Tc-99m MIBI myocardial imaging for detection of coronary artery disease. 817 73

Diltiazem is a benzothiazepine derivative calcium antagonist available in several formulations, some of which enable once daily administration. The drug as monotherapy has demonstrated similar efficacy to diuretics in older patients with hypertension. Data comparing diltiazem with beta-blockers and angiotensin converting enzyme inhibitors are more limited, but available studies suggest at least comparable antihypertensive efficacy. Diltiazem as monotherapy or in combination with a beta-adrenoceptor-antagonist, isosorbide dinitrate, or another calcium antagonist, has demonstrated efficacy in patients with effort angina. The drug has also been used intravenously to terminate supraventricular tachycardias and to control the ventricular response to atrial fibrillation or flutter; it also appears to reduce the rate of early reinfarction in patients with non-Q-wave myocardial infarction. The most common adverse events during diltiazem therapy include headache, flushing, peripheral oedema and hypotension. Atrioventricular block although rare, is the most frequent serious adverse event related to diltiazem therapy and may be exacerbated by coadministration of beta-adrenoceptor antagonists, especially in the elderly. Thus, diltiazem appears to be an effective and well tolerated treatment for hypertension and angina in older patients and has shown promise as therapy for supraventricular tachycardias and as prophylaxis against early reinfarction in patients with non-Q-wave myocardial infarction.
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PMID:Diltiazem. A review of its pharmacology and therapeutic use in older patients. 836 96

The use of dobutamine stress echocardiography for the evaluation of coronary artery disease is rapidly expanding. Despite its widespread use, the feasibility and safety of dobutamine stress echocardiography has not been sufficiently documented. Between November 1992 and June 1995, we performed 1000 dobutamine stress echocardiographies. There were 744 men and 256 women with a mean age of 59 +/- 11 years. Anti anginal medication was not routinely withdrawn before the test. The mean maximal dobutamine dose was 41,4 +/- 10 mu g/kg center dot min(-1). Atropine was given additionally in 440 patients, with a mean dose of 0.5 mg. In patients receiving beta-blockers additional atropine was more often necessary as compared to those not receiving beta-blockers (278/457 = 61% versus 162/543 = 30 %, p < 0.0001). Reasons for discontinuing dobutamine infusion were achievement of target heart rate (64 % of cases) and maximal dose (12 % of cases). In 791 (79,1 %) patients no side-effects of dobutamine stress echocardiography were noticed. Termination of the study because of adverse side-effects occurred in 6.6 %. A total of 103 (10,3 %) noncardiac side-effects were observed: dizziness or nausea 6.4 %, headache 1.7 %. In one patient a focal cerebral seizure occurred. 156 cardiac side-effects occurred: blood pressure decrease of more than 20 mm Hg in 25 patients, extreme palpitations in 16 patients and pulmonary edema in one case. Most common cardiac side-effects consisted of arrhythmias (11.4 %): 9.1 % ventricular and 2.3 % supraventricular arrhythmias. Most ventricular arrhythmias were less severe (uniform and multiform premature ventricular beats, ventricular bigeminy or couplets in 71 patients). Nonsustained ventricular tachycardia, with a maximum duration of 20 s, occurred in 18 patients. In one patient sustained ventricular tachycardia developed and progressed towards ventricular fibrillation. This patient could be successfully defibrillated. Supraventricular arrhythmias presented as new atrial fibrillation in 10 patients, supraventricular tachycardia in three patients, junctional rhythm with a short decline in heart rate in nine patients and a second-degree AV block in another case. Dobutamine stress echocardiography has proven to be a safe and feasible method in the diagnosis of coronary heart disease. Minor side-effects are common and sometimes unpleasant for the patient, but do not often require termination of the study. Severe side-effects are seldom (< 1 %), but nevertheless, adequate medical and technical (defibrillator) support should be rapidly available.
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PMID:[Feasibility and safety of dobutamine stress echocardiography: experiences with 1,000 studies]. 871 45

The safety and tolerability of mibefradil, a selective T-type calcium channel antagonist, were evaluated in 3,430 patients with essential hypertension and chronic stable angina pectoris treated in 15 double-blind placebo and active-controlled clinical trials and 2 open-label, long-term safety studies. Of these patients, 2,636 were treated with the recommended doses of mibefradil (50 and 100 mg) and form the basis of this report. With the 50-mg dose of mibefradil, the incidence of each adverse event was similar to, or lower than, that observed in the placebo-treated patients. Treatment with the 100-mg dose was associated with a slightly higher incidence compared to placebo of dizziness (2.1% vs 1.8%), leg edema (3.5% vs 1.4%), fatigue (2.1% vs 1.4%), and lightheadedness (2.1% vs 0.4%). The incidence of headache (4.6%) and angina pectoris (1.1%) was more frequent in patients treated with placebo. In active-controlled trials, a lower incidence of pedal edema (5.1%) was observed with mibefradil compared to amlodipine (25.7%), diltiazem SR/CD (9.4%), or nifedipine SR/GITS (17.4%). Overall, mibefradil was better tolerated than amlodipine and nifedipine SR/GITS and was as well tolerated as diltiazem SR/CD. Rates of premature discontinuation due to clinically adverse experiences with the 50- and 100-mg doses were 2.5% and 3.5%, respectively, compared with placebo (3.5%). No consistent pattern of laboratory adverse experiences were observed for mibefradil. Sinus bradycardia (heart rate <45 beats/minute) and first-degree atrioventricular block were the only relevant treatment-emergent electrocardiographic changes that occurred more frequently with mibefradil than with placebo. No evidence of first-dose effects was observed in mibefradil-treated patients, and withdrawal effects were not observed in clinical trials. There were no clinically important differences in safety profiles in the demographic subgroups for age, gender, or race. The results of this comprehensive safety analysis indicate that treatment with the recommended doses of mibefradil is well tolerated and safe.
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PMID:Safety of mibefradil, a new once-a-day, selective T-type calcium channel antagonist. 928 53

Whether phosphodiesterase inhibitors increase the heart rate in patients with bradyarrhythmias is not known. We attempted to determine whether the oral phosphodiesterase inhibitor cilostazol exhibits beneficial chronotropic effects in patients with symptomatic bradyarrhythmias. Twenty patients comprising eight with bradycardic atrial fibrillation, eight with sick sinus syndrome, and four with Wenckebach-type atrioventricular block, whose 24-h total heart-beat count was < or =70,000 beats and whose maximal RR interval was > or =2.5 s, were enrolled. Holter recordings (24-h) were made before and 2 weeks after oral daily administration of 200 mg of cilostazol. Cilostazol increased the 24-h total heart-beat count from 77,429 +/- 11,168 to 107,981 +/- 13,536 (95% confidence interval, 24,605-36,497; p < 0.0001), the minimal heart rate from 33 +/- 9 47 +/- 13 beats/min (95% confidence interval, 9-19 beats/min; p < 0.0001), and the maximal RR interval from 3,149 +/- 1,018 to 2,087 +/- 601 ms (95% confidence interval, -1,517 to -608 ms; p = 0.0001). Only two patients had headaches as adverse effects. In conclusion, cilostazol had a beneficial positive chronotropic effect in patients with bradyarrhythmias, especially with bradycardic atrial fibrillation and sick sinus syndrome.
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PMID:Chronotropic effects of cilostazol, a new antithrombotic agent, in patients with bradyarrhythmias. 955 1


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