Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Digoxin has been reported to induce feminizing effects in man. It does not compete for estradiol cytosol receptors in human breast carcinoma cells, however, and has no uterotrophic effect. We therefore investigated whether feminization might be due to digoxin action on plasma concentrations of sex steroids. Six healthy men (31.5 +/- 4 yr old) received therapeutic doses of digoxin for 43 days. We measured plasma concentrations of testosterone, androstenedione, dehydroepiandrosterone, estrone, estradiol, progesterone, 17-hydroxyprogesterone, cortisol, and aldosterone. During 35 days on digoxin levels of these steroids remained in the normal range and there was no change from before-drug values. Digoxin was in the therapeutic range of 1.9 +/- 3 nmol/l throughout. After stimulation by adrenocorticotropic hormone or human choriongonadotropin, the rise in plasma steroids was in the same range as when digoxin was given, as well as 16 wk after it had been discontinued. A normal rise in luteinizing hormone after luteinizing hormone-releasing hormone showed that the hypothalamogonadal feedback was not altered by digoxin. Free testosterone, estradiol, and cortisol concentrations under basal conditions and after stimulation were also the same before and after drug. It is concluded that the estrogen-like activity of digoxin cannot be explained by altered steroid availability from plasma. Feminizing effects attributed to digoxin may be caused by other conditions known to influence sex steroid hormones that are common in patients with heart disease. Our data suggest that digoxin may be the preferred digitalis therapy to avoid feminizing effects.
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PMID:Digoxin does not alter plasma steroid levels in health men. 628 25

As a result of overdosage a 77-year-old patient with heart disease developed digitoxin intoxication, associated with arrhythmias, extracardiac symptoms of intoxication and severe thrombocytopenia. Treatment with digoxin-specific antibody fragments relieved the signs and symptoms of intoxication within a few hours. The rise in platelet count from the pretreatment value of 26 000/mm3 to 47 000 within 12 h and to over 60 000/mm3 within 16 h of starting the antibody infusion may also be attributed to the treatment with antibodies. Such a rapid recovery from digitoxin-induced thrombocytopenia has not hitherto been described. Digoxin-specific antibodies, obtained by immunization of sheep with a digoxin-albumin conjugate, were used to treat intoxication with digitoxin, since cross-reaction had been demonstrated in vitro and in animal experiments. The present paper briefly discusses the mode of action and the general problems relating to the antibody therapy of digitalis poisoning.
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PMID:Digitoxin intoxication with severe thrombocytopenia: reversal by digoxin-specific antibodies. 640 39

One hundred and twenty-two patients with cardiac disease were compared with 250 controls with respect to the duration of pregnancy and labour, birth weight percentile and Apgar score. The babies of the patients with cardiac disease were light-for-dates (18% below the 10th percentile); the mothers, if multiparous, delivered at an earlier gestational age. The patients with cardiac disease did not have shorter labours than the control group. Digoxin administration and the severity of heart disease had no significant effect on these variables.
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PMID:The effect of maternal cardiac disease and digotoxin administration on labour, fetal weight and maturity at birth. 693 Feb 48

In a 4 1/2 year period fetal, echocardiographic studies were performed on 1600 fetuses. In 55 with arrhythmia, 44 had supraventricular ectopic beats, resolved in all, and none had heart disease. Sustained arrhythmias occurred in 11 fetuses. Atrial flutter was present in 3 all with heart disease (Ebstein disease, right atrial tumour and WPW diagnosed after birth). Another 3 fetuses had supraventricular tachycardia (SVT), all with a normal heart. In the bradycardia group, 2 had complete heart block (CHB) associated with AVSD; 2 sinus bradycardia and one had non conducted atrial ectopic beats. Digoxin was the first choice drug for tachyarrhythmia therapy; association with Verapamil, Flecainide, Quinidine and Procainamide was used in 4 of the 6. One fetus with CHB received Orciprenaline with no results. Atrial flutter resolved or improved; in SVT 2 fetuses converted to sinus rhythm and one died in utero. All fetuses with CHB died in cardiac failure. Mortality was 27% (3 cases) in utero and global 36%. In our experience most fetal arrhythmias (90%) were transitory ectopic beats or non lasting bradycardia in normal heart and did not trigger other kinds of arrhythmias. In sustained arrhythmias, heart failure and heart disease had a negative effect on prognosis.
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PMID:[Fetal arrhythmia. A case load of 4 years and a half]. 777 Dec 7

Infants and children with congenital or acquired heart disease and children with systemic disease often require pharmacological support of their failing circulation. Catecholamines may serve as inotropic (enhance myocardial contractility) or vasopressor (elevate systemic vascular resistance) agents. Noncatecholamine inotropic agents, such as the cardiac glycosides or the bipyridines, may be used in place of, or in addition to, catecholamines. Developmental changes in neonates, infants and children will affect the response to inotropic or pressor therapy. Maturation of the gastrointestinal tract, liver and kidneys alters absorption, metabolism and elimination of drugs, although there are few clear examples of this among the vasoactive drugs considered in this review. Changes in body composition affect the volume of distribution (Vd) and clearance (CL) of drugs. Developmentally based pharmacodynamic differences also affect the responses to both therapeutic and toxic effects of inotropes. These pharmacodynamic differences are based in part upon developmental changes in myocardial structure, cardiac innervation and adrenergic receptor function. For example, the immature myocardium has fewer contractile elements and therefore a decreased ability to increase contractility; it also responds poorly to standard techniques of manipulating preload. Available data suggest that dopamine and dobutamine pharmacokinetics are similar to those in adults. Wide interindividual variability has been noted. A consistent relationship between CL and age has not been demonstrated, although one investigator demonstrated an almost 2-fold increase in the CL of dopamine in children under the age of 2 years. The CL of dopamine appears to be reduced in children with renal and hepatic failure. Fewer data are available regarding the pharmacokinetics of epinephrine (adrenaline), norepinephrine (noradrenaline) and isoprenaline (isoproterenol). Digoxin pharmacokinetics have been extensively evaluated in infants and children. The Vd for digoxin is increased in infants and children. Children beyond the neonatal period display increased CL of digoxin, approaching adult values during puberty. Although it was previously thought that children both needed and tolerated higher serum concentrations of digoxin than adults, more recent studies indicate that adequate clinical response can be achieved with serum concentrations similar to those aimed for in adults, with decreased toxicity. Evaluation of studies of digoxin pharmacokinetics is complicated by the presence of an endogenous substance with digoxin-like activity on radioimmunoassay. Limited studies of amrinone pharmacokinetics in infants and children indicate a dramatically larger Vd, and a decreased elimination half-life in older infants and children, compared with values observed in adults.
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PMID:Pharmacokinetics of cardiovascular drugs in children. Inotropes and vasopressors. 785 Oct 53

Because of its prevalence in the population and its associated underlying diseases and morbidity, atrial fibrillation (AF) is an important and costly health problem. Advancing age, diabetes, heart failure, valvular disease, hypertension, and myocardial infarction predict the occurrence of AF within a population. The management of AF is complex and involves prevention of thromboembolic complications and treatment of arrhythmia-related symptoms. Stroke occurs in 4.5% of untreated patients with AF per year. Independent risk factors for stroke in nonrheumatic patients with AF are advanced age; a history of prior embolism, hypertension, or diabetes; and echocardiographic findings of left atrial enlargement and left ventricular dysfunction. Warfarin decreases stroke by two-thirds and death by one-third; aspirin is only about half as effective overall and is insufficient therapy for those with risk factors for stroke. Options for thromboembolic prophylaxis are use of warfarin for all in whom it is safe or, alternatively, warfarin for those with risk factors and aspirin for those without risk factors. One-half of the patients with AF are 75 years of age or older. The uniform applicability and relative safety of warfarin therapy in this age-group are controversial. Specific therapy for the arrhythmia should be dictated by the need to control symptoms. Symptomatic treatments include rate-control medications and strategies designed to terminate and prevent arrhythmia recurrence. Digoxin, beta-adrenergic blockers, verapamil, and diltiazem slow excessive ventricular rates in patients with AF and may favorably manage comorbid conditions. The efficacy of anti-arrhythmic medications is only 40 to 70% per year in preventing recurrences of AF, and these agents, except amiodarone, may increase the risk of sudden death in patients with certain types of organic heart disease and AF. The use of nonpharmacologic symptomatic therapies such as atrioventricular node modification or ablation with a rate-response pacemaker or surgical intervention is increasing.
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PMID:Management of atrial fibrillation in adults: prevention of thromboembolism and symptomatic treatment. 857 89

Digoxin intoxication is a common problem in the elderly. In its mildest forms it may go undiagnosed, but in severe cases it is often fatal. Altered digoxin pharmacokinetics, attributable to the physiological changes associated with aging, underlying illness, and drug-drug interactions all contribute to the occurrence of digoxin toxicity. Advanced age, male gender, initial hyperkalaemia, underlying heart disease, and advanced atrioventricular block at the time of admission are poor prognostic factors. Supportive care alone is often insufficient. Digoxin-specific Fab therapy may result in dramatic recovery from digoxin intoxication, but it must be administered early and in a an adequate dosage if reductions in mortality are to be achieved.
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PMID:Advances in the management of digoxin toxicity in the older patient. 911 5

Numerous experimental, epidemiological and clinical studies have pointed out a relevant role for magnesium deficiency in the development of many cardiovascular diseases. Some pharmacological treatments may interfere with magnesium turnover, and magnesium deficiency may alter the pharmacokinetics and pharmacodynamics of some cardiovascular drugs. Loop and thiazide-like diuretics increase magnesiuresis, and total bodily magnesium deficiency may appear during prolonged treatment with diuretically active doses of these drugs. The potassium retaining agents, such as amiloride, triamterene and spironolactone, tend to retain magnesium but they are not magnesium-retaining substances to the extent to which they are potassium-retaining diuretics. The interaction between magnesium and digitalis is complex. Magnesium, acting as an indirect antagonist of digoxin at the sarcolemma Na(+)-K(+)-ATPase pump, reduces cardiac arrhythmias due to digoxin poisoning. Recent controlled studies have shown that treatment with magnesium significantly reduces the frequency and complexity of ventricular arrhythmias in digoxin-treated patients with congestive heart failure without digoxin toxicity. Magnesium improves the efficacy of digoxin in slowing the ventricular response in atrial fibrillation. Digoxin reduces tubular magnesium reabsorption, and in patients with congestive heart failure this interaction may be cumulative with other causes of magnesium deficiency (diuretics, diet, poor intestinal absorption). The complex and potentially life-threatening interactions between magnesium and some cardiovascular drugs suggest that magnesium status should be carefully monitored in patients receiving such drugs. Therapy with magnesium is rapidly acting, has a safe toxic-therapeutic ratio, is easy to administer and titrate. The correction of magnesium deficit should therefore always be considered for patients with cardiopathy.
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PMID:Magnesium and cardiovascular drugs: interactions and therapeutic role. 1052 23

Ebstein's anomaly is a rare congenital heart disease abnormality in which the tricuspid valve leaflets do not attach normally to the tricuspid valve annulus. The effective tricuspid valve orifice is displaced apically into the right ventricle (RV), near the junction of the inlet and the trabecular parts of the RV. The authors present a retrospective study of the patients with Ebstein's anomaly admitted to a neonatal intensive care unit, in the period between January 1993 and March 2000. There were ten patients, representing 0.24% of total neonates and 1.99% of total congenital heart disease admitted to the institution in the same period. Fifty per cent were male and only one case had prenatal diagnosis. Holosystolic murmur (100%) from tricuspid regurgitation and cyanosis (80%) were the most frequent clinical findings. Chest X-ray was abnormal in 90% of the neonates, with a "balloon-shaped" enlarged heart. The main electrocardiographic findings were right atrial enlargement (70%) and arrhythmias (40%). Apical displacement of the septal leaflet of the tricuspid valve, to a maximum of 20 mm, and leaflets tethering to underlying RV myocardium were found in all patients. Tricuspid valve regurgitation was found in 90% (severe form in four cases). An atrial intracardiac shunt, mostly right-to-left, was also found in 50%. Digoxin was used (40%) to restore sinus rhythm. Fifty per cent of the neonates received intravenous prostaglandins. Two patients required a surgical procedure. Two patients died in the neonatal period. During the follow-up period (range 0.3-74.6 months), only one episode of supraventricular tachycardia was recorded. At present seven patients are clinically stable, three of them on medication.
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PMID:Ebstein's anomaly in neonates. 1176 98

We did a retrospective analysis of the clinical files of 26 neonates with arrhythmia born during the period between January 1994 and February 1999. Fourteen (53.8%) of the neonates were male and 16 (61.5%) had prenatal diagnosis. Four (15.3%) had associated congenital heart disease. Twenty-one (80.7%) had abnormal rhythm and five (19.2%) had cardiac conduction disorder. Digoxin was the therapy of first choice to restore normal rhythm, used in 66.6% of the patients, followed by adenosine (16.6%) and electrical cardioversion (16.6%). An epicardial pacemaker was used in two of the three neonates with complete atrioventricular (AV) block. One neonate died due to cerebral hemorrhage. All the neonates were discharged in a clinically stable condition and 16 (88.8%) of them were medicated with digoxin. In a follow-up period that varied from 0 to 71 months (mean of 30.8 months), two patients had an episode of supraventricular tachycardia (SVT) after treatment withdrawal. Perinatal arrhythmias, although uncommon, can be life-threatening, and hence we consider our experience with these situations worth presenting.
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PMID:Perinatal arrhythmias -- diagnosis and treatment. 1194


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