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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood loss and the incidence of emetic sequelae were assessed in 148 patients undergoing midcavity forceps delivery under continuous lumbar extradural analgesia. Five units of oxytocin i.v. was found to be as effective as ergometrine 0.5 mg i.v. in reducing blood loss at delivery. Nausea, retching or vomiting occurred in 35 (46%) of the mothers who received ergometrine and in none of those who received i.v. oxytocin. The cardiovascular side-effects of ergometrine and oxytocin are reviewed and compared with special reference to patients with hypertension and heart disease. It is suggested that 5 units of oxytocin i.v. should be preferred in these high-risk patients. Because of the absence of an emetic action, i.v. oxytocin is preferable to i.v. ergometrine for patients receiving extradural analgesia.
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PMID:Ergometrine, oxytocin and extradural analgesia. 95 92

The forms of administration, mechanisms of action, side effects and complications, and other aspects of female hormonal contraception are set forth in this "lesson" for medical students. Female hormonal contraception has been in use for over 30 years and is used by more than 150 million women worldwide. Oral contraceptives suppress the preovulatory peak of follicle stimulating hormone and luteinizing hormone, preventing ovulation and follicular maturation. Progestins render the cervical mucus impermeable to sperm and modify the endometrium so that it will no longer support implantation. The synthetic estrogen ethinyl estradiol is used in most combined oral contraceptives (OCs). Among the numerous progestins in use are the newer desogestrel, gestodene, and norgestimate, which have fewer androgenic and metabolic effects than did the 1st generation. the different forms of administration of hormonal methods include combined OCs, oral preparations containing low doses of progestin continuously administered or high doses continuously or discontinuously administered. Intramuscular injection of progestins and the so-called "morning after" postcoital pills are less often prescribed. The combined preparations may be monophasic, biphasic, triphasic, or sequential. Sequential preparations should be avoided because of the hyperestrogenic climate they induce. The low-dose progestin preparations are indicated for women with contraindications to synthetic estrogen. They must be taken at the same time each day and have a relatively high rate of side effects, especially ovarian and breast cysts and irregular bleeding. High-dose progestin preparations have significant metabolic effects and are indicated primarily for patients with gynecological problems such as fibromas and endometriosis. Intramuscular injection of medroxyprogesterone acetate every 3 months is effective but has the same side effects as high-dose progestins. It is indicated primarily for patients unable to control their own behavior. The hormonal methods are all highly effective in preventing pregnancy when correctly administered. Side effects may be minor problems, such as nervousness and nausea, that are usually of short duration. the more serious side effects, including modifications of lipid or carbohydrate metabolism, hemostasis, blood pressure, or hepatic functioning and cardiovascular effects, have been reduced with the new lower dosed formulations. Absolute contraindications to hormonal contraception include undiagnosed vaginal bleeding or amenorrhea, history of thromboembolic or cerebral vascular accidents, severe cardiopathy or hypertension, hyperlipidemia, hepatopathy, hormonodependent cancer, pituitary tumors, porphyria, and severe mental problems. Relative contraindications impose the need for careful monitoring and follow-up. The practitioner should be aware of the possibility of interactions between OCs and certain other drugs.
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PMID:[Hormonal contraception]. 160 74

Digitalis intoxication is among the most common serious adverse drug reactions in clinical medicine. While the recent development of a radioimmunoassay to accurately measure serum concentrations of digoxin has been of assistance, digitalis intoxication remains a difficult diagnosis to make with certainty. The difficulty in diagnosing digitalis intoxication arises from the nonspecificity of its associated signs and symptoms. The most common symptoms include fatigue, weakness, nausea, and anorexia. These symptoms can occur with many illnesses other than digitalis intoxication. Similarly, the electrocardiographic disturbances caused by cardiac glycosides may be nondiagnostic. The arrhythmias commonly associated with digitalis toxicity are often nonspecific and can be a reflection of the patient's underlying heart disease. The measurement of serum digoxin levels is useful, but studies have demonstrated overlap of the levels between groups with and without toxicity. Due to the modulation of the cardiac effects of digitalis glycosides by such clinical variables as underlying myocardial or renal disease, electrolyte and acid-base imbalances, and other factors, the correlation of toxicity with particular serum digoxin concentrations may vary. Because of the inherent difficulties in confirming the diagnosis of digitalis intoxication in some cases, digoxin-specific Fab antibodies may play a role as a diagnostic tool. Certainly, digoxin-specific Fab antibodies play a significant part in the treatment of digitalis intoxication. Fab antibodies have been successfully used to reverse the effects of digoxin, digitoxin, and oleander poisoning. These antibodies are useful in the treatment of acute and chronic digitalis intoxication in all age groups, including geriatric and pediatric populations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Recognition and management of digitalis intoxication: implications for emergency medicine. 199 19

In a multicentre study efficacy and safety of propafenone 450 mg day-1 and 750 mg day-1 was studied in 97 patients with frequent ventricular premature beats (VPB greater than 30 h-1). 70 patients suffered from organic heart disease, in 27 patients no organic heart disease was present during an initial work-up. After a 1-week washout period, all patients underwent 24 h Holter monitoring. Patients were then treated by propafenone 450 mg day-1 and controlled for 24 h Holter, ECG, blood pressure, blood chemistry and side-effects after 1 week of treatment. At this time, 35 patients were responders (reduction of VPB greater than 84%, of ventricular pairs greater than 90% and of ventricular tachycardia 100%). The mean reduction of VPB in all patients was 60%, of ventricular pairs 88% and of ventricular tachycardia 100%. When treatment was continued for 3 weeks 20/35 patients (56%) were still responders. The mean reduction of VPB was 83%. In 42 non-responders to 450 mg day-1 the dose was increased to 750 mg day-1. Of these patients, 17 (41%) became responders after 3 weeks of treatment; the mean reduction of VPB increased from 17% (first week, 450 mg day-1) to 63% (750 mg day-1). Ventricular pairs were reduced by 80%, ventricular tachycardia by 100%. Side-effects occurred in 11/97 patients and limited therapy in six patients. The most frequent complaints were dryness of the mouth, nausea, tiredness, headache and gastrointestinal upset. In conclusion, propafenone in a dose of 450-750 mg day-1 seems to be an effective and safe antiarrhythmic agent in the majority of patients.
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PMID:Antiarrhythmic efficacy and tolerance of oral propafenone in patients with frequent ventricular arrhythmias: experience of a multicentre study. 268 May 6

Experimental and clinical experience with compounds containing antimony have shown that the trivalent compounds are generally more toxic than the pentavalent ones. APT can cause severe pain and tissue necrosis and is therefore not given by intramuscular or subcutaneous injection. APT has the actions and uses of AST, but it is less soluble and more irritating than the sodium salt which is therefore more suitable for intravenous use. Trivalent antimony compounds are toxic when used topically. Adverse effects are similar for all trivalent compounds, and include nausea, vomiting, weakness and myalgia, abdominal colic, diarrhoea, and skin rashes, including pustular eruptions. Hypersensitivity reactions also occur. Respiratory symptoms include cough, dyspnoea, and chronic lung changes. Cardiotoxicity is the most important and may produce arrhythmias, myocardial depression and damage, Stokes-Adams attacks, heart failure, and cardiac arrest. Hepatic damage and necrosis, as well as blood dyscrasias, may occur. Toxic effects on the kidney may follow chronic use. Continuous treatment with small doses of antimony may give rise to symptoms of subacute poisoning, similar to those of chronic arsenic poisoning, due to accumulation of antimony in the body, especially if trivalent compounds are used, because of their long biological half-lives. Reproductive disorders and chromosome damage have been reported; antimony compounds are, therefore, potentially toxic to reproduction and have mutagenic, and oncogenic potential. Antimony compounds should, therefore, not be used during pregnancy or in the presence of hepatic, renal, or heart disease. Pentavalent antimony preparations especially the organic compounds, together with non-metallic synthetic preparations, such as the diamidines, have now replaced APT for use in leishmaniasis. Because of the toxicity of antimony compounds, investigations have been undertaken to reduce their adverse effects by combining them with chelating agents. These preparations appear to have reduced the toxic effects of antimony without affecting the efficacy of the preparations. Liposome-encapsulated antimony products have, more recently, been shown to be much less toxic because of the reduced dose of the antimony compound required for effective therapy. The historical uses of antimony were based on the belief that the topical and systemic adverse effects, for example, skin eruptions and diarrhoea and vomiting, were signs that the condition being treated was responding by being brought to the surface to relieve congestion at the diseased area. There is no evidence in topical use, but there is evidence that such use can cause severe reactions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Toxicity of antimony and its compounds. 330 36

A 55-year-old Caucasian woman suddenly developed substernal chest pain at rest accompanied by pallor, diaphoresis, nausea, and vomiting. Physical examination was otherwise unremarkable. The resting ECG showed T-wave inversion in all anterior leads which returned to normal 24 h after the onset of the symptoms. The pain was eliminated promptly by sublingual isosorbide dinitrate. "Impending" acute myocardial infarction was diagnosed. Coronary arteriography, however, failed to reveal any change in any major coronary artery but an apical aneurysm of the left ventricle was detected. As the complement-fixation test for Chagas' disease was positive, the diagnosis of chronic Chagas' heart disease was then established. This unusual clinical manifestation of Chagas' disease is thought to be the consequence of a transient imbalance in the cardiac autonomic nervous system, which is considered to play a central role in the pathogenesis of chronic Chagas' heart disease. In addition, the present case may alert clinicians to the thus far neglected atypical chest pain, which is frequently seen in chagasic patients but whose etiology remains obscure.
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PMID:Chronic Chagas' heart disease presenting as an impending myocardial infarction: a case favoring the neurogenic pathogenesis concept. 359 60

Programmed ventricular stimulation was used to test oral bethanidine sulfate in 10 patients with life-threatening ventricular arrhythmias. These patients had previously documented, recurrent, sustained ventricular tachycardia (VT) and/or ventricular fibrillation (VF) complicating stable heart disease. During control electrophysiologic studies, VT could be induced in all 10 patients: 6 with nonsustained VT, 3 with sustained VT, and 1 with VT/VF. After control, bethanidine 20-30 mg/kg was administered orally and beginning 60 minutes later, programmed ventricular stimulation was repeated. After bethanidine administration, VT could be induced in nine patients; in four, the VT was essentially unchanged from that induced during control studies. In four others, worse VT was induced after bethanidine. The remaining two patients had a potentially beneficial response to the drug. Bethanidine was poorly tolerated: seven patients had symptomatic orthostatic hypotension that persisted for several days despite concurrent protriptyline therapy. Furthermore, in four patients, spontaneous VT or VT/VF occurred 3-8 hours after the last dose. Nausea, vomiting, flushing, and blood pressure elevation were also noted. Bethanidine sulfate in the dosages used usually does not prevent the induction of VT by programmed ventricular stimulation and frequently causes serious toxicity. These findings suggest that the drug would be ineffective and poorly tolerated for long-term therapy in patients with serious ventricular arrhythmias.
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PMID:Bethanidine sulfate in paroxysmal ventricular tachycardia: toxicity and antifibrillatory actions. 377 63

We questioned 113 patients with subsequently diagnosed sustained ventricular tachycardia (VT) regarding the symptoms that prompted their seeking hospital treatment, eliciting the following: 15% of patients had lost consciousness, 15% had near syncope, 35% had mild lightheadedness and 35% had no cerebral symptoms. Patients with preexisting congestive heart failure or a VT rate of 200 beats per minute or greater more often lost consciousness. Other symptoms included palpitations in 57% of patients, chest pain in 27%, dyspnea in 25%, weakness in 6%, nausea or diaphoresis in 3% each and flushing in 2%. In approximately 50% of patients who had mild lightheadedness or no cerebral symptoms, their condition was incorrectly diagnosed as supraventricular tachycardia based on the absence of severe symptoms during the tachycardia. In some patients, VT may be associated with mild or atypical symptoms. The differentiation of supraventricular from ventricular tachycardia should be based on electrocardiographic criteria and should not be influenced by the nature or severity of a patient's symptoms. The severity of cerebral symptoms is at least partially related to the VT rate and a patient's underlying heart disease.
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PMID:Clinical symptoms in patients with sustained ventricular tachycardia. 399 9

The majority of sudden cardiac deaths in children occur in patients with prior arrhythmias and an abnormal heart. Amiodarone was given to 39 young patients (35 with an abnormal heart) with arrhythmias unresponsive to conventional treatment. Their age ranged from 6 weeks to 30 years with nine patients younger than 2 years of age. Atrial flutter was present in 16 patients, ventricular tachycardia in 14 patients and supraventricular tachycardia in 9 patients. The most common diagnosis (14 patients) was postoperative repair of congenital heart disease. The dose ranged from 2.5 to 21.6 mg/kg per day (mean 8.2). Elimination of arrhythmia (on 24 hour electrocardiography) occurred in 15 of 16 patients with atrial flutter, 11 of 14 with ventricular tachycardia and 5 of 9 with supraventricular tachycardia. Symptomatic side effects were: rash (three patients), headache (two patients), nausea (one patient) and peripheral neuropathy (one patient); seven patients had asymptomatic corneal microdeposits which normalized in all after the drug was discontinued. No side effects occurred in patients younger than 10 years of age. The following changed with treatment (p less than 0.05): heart rate decreased (three patients with atrial flutter and sick sinus syndrome required pacemaker implantation for bradycardia) and QTc increased; thyroxine (T4) and serum reverse triiodothyronine (T3) increased. During follow-up study (range 6 months to 3 years), 21 of the 39 patients continued to take amiodarone with complete control of arrhythmias, 9 were no longer taking the drug and 9 died (7 nonsudden and 2 sudden deaths). Amiodarone is an extremely effective treatment for infants and children with tachyarrhythmias resistant to conventional treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amiodarone treatment of critical arrhythmias in children and young adults. 638 28

Abrupt clonidine withdrawal may be associated with sharp marked increases in catecholamine levels, heart rate, and blood pressure, which may induce nausea, vomiting, and palpitations. Relatively little information is available on the incidence of cardiac arrhythmias in this setting. With continuous ambulatory ECG recordings, we determined the incidence of arrhythmias in seven male hypertensive patients (without active heart disease) after abrupt clonidine withdrawal. Serious ventricular arrhythmias, including brief ventricular tachycardia, developed in two patients who had greater increases in mean systolic blood pressure (28 +/- 3 vs 10 +/- 8 mm Hg) and double product (552 +/- 681 vs 333 +/- 195) than the others. The differences were not significant. Ventricular arrhythmias were not related to age, dose, withdrawal symptoms, initial blood pressure, urinary norepinephrine levels, or ECG abnormalities. We conclude that serious ventricular arrhythmias may be relatively common but unpredictable during clonidine withdrawal, even in patients with no clinically apparent heart disease. The triggering of ventricular arrhythmias should be added to the list of components of clonidine withdrawal syndrome.
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PMID:Cardiac arrhythmias after abrupt clonidine withdrawal. 661 64


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