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)

The experience of three institutions in the management of atrial flutter in infants under 2 years of age without associated heart disease is reviewed. Five babies with neonatal onset were treated with digoxin and had uncomplicated resolution of their arrhythmia, although one continued to have episodes of paroxysmal supraventricular tachycardia for six years. Two of the three older infants required DC cardioversion for complications after quinidine was substituted for digoxin therapy. Digoxin continues to be the preferred initial therapy for non-acutely ill patients; those showing signs of cardiac decompensation should be converted with DC countershock.
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PMID:Idiopathic atrial flutter in infancy: a review of eight cases. 26 74

Digoxin serum and urine levels were determined by radioimmunoassay in 6 subjects (4 patients with heart disease and 2 volunteers without heart disease) who had been maintained on oral digoxin (0.25 or 0.5 mg daily). Observations were made during a 3-day control period and then during 8 days of concomitant digoxin and oral furosemide (40 mg daily) therapy. Serum digoxin levels determined 10 and 24 hr after each dose of digoxin averaged 1.2+/-0.1 ng/ml (M+/-SE) during control and 1.3+/-0.1 during the last 3 days on digoxin and furosemide. The daily urinary excretion of digoxine averaged 51+/-6% of the oral dose during control and 52+/-6 during the entire period of furosemide administration. The renal clearance of digoxin and creatinine averaged 94+/-7 and 87+/-11 ml/min, respectively, during control; corresponding values were 88+/-8 and 85+/-9 for urine collections demonstrating a distinct diuretic effect of furosemide and 87+/-8 and 75+/-10 for urine collections not demonstrating such an effect during diuretic therapy. The results suggest that the diuretic effect of furosemide does not significantly affect the excretion of digoxin
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PMID:Effect of furosemide on the renal excretion of digoxin. 97 15

In view of their potentially dangerous proarrhythmic effects, antiarrhythmic drugs should only be prescribed for patients with poorly tolerated symptomatic supraventricular arrhythmias. The choice of a suitable preparation depends not only on the type of arrhythmia, but also on the underlying heart disease and left-ventricular function. Digoxin, verapamil, sotalol and quinidine remain first-line drugs, while in view of recent trials the type-1c antiarrhythmics (flecainide) should only be given in cases resistant to other agents. Amiodarone is also an important and efficacious "reserve" antiarrhythmic, which has to be utilized at low doses to avoid its well-known side effects.
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PMID:[Drug therapy in supraventricular arrhythmia]. 159 45

Cardiac diseases of cattle may involve valvular structures, myocardium, pericardium, or blood vessels and are manifested by the clinical signs of cardiac dysrhythmias, cardiac murmurs, generalized edema, muffled heart sounds, jugular venous distention, jugular venous pulsations, pulmonary edema, pleural effusion, or ascites. Digoxin, quinidine, and furosemide can be used effectively to control signs of CHF and cardiac arrhythmias. Combination antimicrobial therapy can be successful for cows with infective endocarditis and thrombophlebitis. Pericardial fluid drainage may temporarily improve cattle with traumatic pericarditis or lymphosarcoma so that short-term goals may be reached.
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PMID:Treatment of cardiovascular disease in cattle. 176 Jul 59

We have reviewed the records of 65 children with paroxysmal supraventricular tachycardia (PST) without congenital heart disease followed a mean of 4 years, with a total of 121 episodes. PST appeared before 6 months of age in 42 (64.6%) children. Thirteen patients (20%) had a present factor which might predispose to PST in 66.2% of the patients who were younger than 6 months of age, and in only 4.3% of those over 6 months. Wolff-Parkinson-White syndrome was present on surface ECG during sinus rhythm in 26.1% of children younger than 6 months, and in 39.1% of those over 6 months. Digoxin was the initial treatment in 84.3% of the episodes with a success rate of 75% when were employed alone and of 84.2% when were employed in combination of quinidine. PST recurred at least once in 35 children (53.8%), the 90% within three months of the first episode. All patients were alive and 63 (96.9%) doing well. One patient developed cerebral anoxia and now has hemiparesia and another patient has incessant PST. We conclude that children with PST without congenital heart disease and without delay in diagnosis had a good outcome.
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PMID:[Supraventricular paroxysmal tachycardia without congenital heart disease: clinical, therapeutic aspects and course in 65 children]. 179 89

Digoxin excess can produce characteristic bradyarrhythmias, tachyarrhythmias, and hyperkalemia. The bradyarrhythmias, which consist of disturbances in conduction and block at the level of the atrioventricular and sinus nodes, are mediated by a direct and vagotonic effect. The vagotonic effect of excess digoxin may also result in a marked slowing of the sinus rate in the setting of severe toxicity. Digoxin increases automatic and triggered electrical activity in atrial muscle, His-Purkinje system, and ventricular muscle, which predisposes to tachycardias. Many of the tachyarrhythmias are relatively specific for the toxic effects of digoxin. Atrial tachycardias with variable atrioventricular block, accelerated junctional rhythms (especially in the setting of atrial fibrillation), and fascicular tachycardias are characteristic digoxin toxic rhythms. Digoxin-specific antibody fragments should be considered the treatment of choice for any digoxin toxic arrhythmia associated with hemodynamic compromise or the threat of hemodynamic compromise. Hyperkalemia, when due to acute severe digoxin toxicity, is also an appropriate indication for digoxin-specific Fab fragment therapy. When assessing the risk:benefit ratio for using digoxin-specific Fab fragment therapy, one needs to determine, in addition to the electrocardiographic manifestations and patient's hemodynamic status (1) the severity of toxicity, as indexed by the amount ingested and/or the serum digoxin concentration; (2) the expected time course for reversal of toxicity, which is usually determined by the status of renal function; (3) the need for digoxin to provide ventricular rate control or improved ventricular contractility and therapeutic alternatives to digoxin; (4) the presence of a strong allergy history; (5) the presence of such factors as increased age and severity of heart disease that may predispose to digoxin toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Which cardiac disturbances should be treated with digoxin immune Fab (ovine) antibody? 199 18

In this study, the lymphocytes and erythrocytes from peripheral venous blood were used as the study model from which were measured the cellular contents of potassium, sodium, calcium and magnesium in 50 patients with chronic congestive heart failure and 39 control patients. Levels of endogenous digoxin-like substance in the plasma and activities of Na/K ATPase in red cell membrane wer monitored simultaneously. In the patients with heart failure, the intracellular contents of potassium and magnesium were decreased while those of sodium and calcium were increased significantly. The levels of endogenous digoxin-like substance were much higher in the plasma than those either in healthy controls or in patients with heart disease but without congestive failure (273.7 +/- 35.5 vs 23.3 +/- 2.2 and vs 32.9 +/- 3.6 pg/ml, respectively, P less than 0.001 for both). The activities of Na/K-ATPase were much lower in the patients with heart failure than in the controls. Values for intracellular electrolytes were significantly correlated with the rising levels of digoxin-like substance in the plasma. Non-digitalis inotropic therapy was associated with the recovery of these alterations of heart function, with the levels of the digoxin-like substance decreasing and activity of Na/K-ATPase going up. We conclude that endogenous digoxin-like substance might play a role in the imbalance of intra-cellular electrolytes seen in patients with congestive heart failure. Digoxin may exacerbate the loss of intracellular potassium.
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PMID:Intra-cellular electrolyte changes and levels of endogenous digoxin-like substance within the plasma in patients with congestive heart failure. 215 46

Eighty six patients (48 males and 38 females) with W-P-W diagnosed before the age of 15 years had a maximum follow-up of 20 years. The mean age at diagnosis was 3 y and 5 m., most cases being concentrated in the first 6 months of life (37%). Twenty seven (31.4%) had associated heart disease, the more common being: ventricular septal defect (6 cases), Ebstein malformation (5 cases) and transposition of the great arteries (4 cases). Supraventricular tachycardia (SVT) was the commonest form of clinical presentation, followed by examination because heart murmur or heart disease. Fifty patients (58%) had SVT along the follow-up. SVT was more frequent in W-P-W type A than in type B (p less than 0.05). There was a statistically significant correlation (p less than 0.001) between the association of SVT and the absence of heart disease, but the finding must be questioned because the true incidence of W-P-W in normal population is unknown. There also were a significant correlation (p less than 0.05) between the association of W-P-W type B and the presence of heart disease. An electrophysiologic study was performed in 11 patients, 6 of them being concealed W-P-W. Four patients were operated upon because of SVT. We have studied a total of 154 SVT episodes in the 50 patients with SVT. The treatment more frequently used to finish the SVT included: verapamil, DC-Countershock and Digoxin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Wolff-Parkinson-White syndrome: long-term follow up study in a pediatric population (86 cases)]. 222 29

A case report is presented of supraventricular tachycardia (SVT) associated with metoclopramide administration in the early postpartum period in a 37-year-old woman. The patient was scheduled for elective laparoscopic tubal ligation 4 hours after an uncomplicated spontaneous vaginal delivery. The preoperative evaluation revealed that the patient's only significant past medical history was a total of 4 spontaneous vaginal deliveries. A review of systems was noncontributory, and the patient denied any untoward effects from drugs. Metoclopramide, 10 mg, was administered intravenously to facilitate gastric emptying and as an anti-emetic. Within 1 minute, the heart rate rose to 170 bpm. She was in no distress, being unaware of any change in her status. Arterial blood pressure remained in the 130-140 mmHg (systolic) range throughout the ensuing period. Various approaches, i.e., valsalva, carotid sinus massage, ocular pressure, were used to increase vagal tone without a decrease in the heart rate. After determining that the PR interval was grossly normal, she received 2 boluses of verapamil (10 mg intravenously) over a 10-minute period without change in heart rate. She then was given alphaprodine and droperidol for sedation. The patient then was administered Digoxin approximately 20 minutes after the administration of metoclopramide. This was followed by a gradual decrease in her heart rate to 130 bpm over the next 5 minutes. The patient was transferred to a telemetry unit for a 24-hour period, where her arterial blood pressure remained stable and her heart rate was noted to be in the 90-110 range. 12-lead EKG revealed sinus tachycardia with "nonspecific" ST changes. PR, QRS, and QTC intervals were within normal limits. Chest radiograph was without pathology. The patient was reinterviewed on several occasions and continued to deny a history of SVT, palpitations, syncope, or any other cardiac symptomatology. 2 days following the initial episode, she underwent successful laparoscopic tubal ligation under spinal anesthesia and sedation. In sum, a stable postpartum patient without history of SVT or evidence of structural heart disorder developed SVT immediately following metoclopramide administration. This may be because of the cardioactive properties of metoclopramide or to an underlying predisposition from her peripartum state, or a combination of factors.
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PMID:Supraventricular tachycardia associated with postpartum metoclopramide administration. 333 65

An acute ingestion of 6 to 7 mg digoxin as a suicidal gesture in a 76-year-old man with chronic heart disease is presented. The patient arrived in the emergency department approximately 5 hours after ingestion with a normal serum potassium and increasing numbers of multifocal premature ventricular contractions. Digoxin-specific antibody fragments were administered. The patient developed ventricular tachycardia and ventricular fibrillation and was eventually stabilized 35 minutes after the Fab fragments were infused. A review of the pharmacology and indications for use of digoxin-immune Fab fragments is also presented.
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PMID:Acute digoxin overdose: use of digoxin-specific antibody fragments. 341 42


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