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

As children with cardiac disease grow older, atrial flutter becomes more prevalent. A collaborative study was performed in 19 institutions to determine the clinical characteristics of these children and the factors affecting prognosis. There were 380 patients with one or more electrocardiographically documented episodes of atrial flutter that first occurred between ages 1 and 25 years (mean age at onset 10.3). Episodes of flutter continued to occur for a mean of 2.5 years after the onset. Of the 380 patients, 60% had repaired congenital heart disease, 13% palliated congenital heart disease, 8% unoperated congenital heart disease, 8% an otherwise normal heart, 6% cardiomyopathy, 4% rheumatic heart disease and 2% other lesions. Overall, drugs were effective in eliminating atrial flutter in 58% of patients; specifically, amiodarone and digoxin plus quinidine were effective in 53%, digoxin alone in 44% and propranolol in 21%. Amiodarone was effective in seven (78%) of nine patients. Corrective surgery was performed after the onset of atrial flutter in 66 patients; in 52% the atrial flutter was easier to control or it resolved and in only 4% it was worse. At follow-up (mean 6.5 years), 83% of the patients were alive (49% without atrial flutter and 34% with atrial flutter) and 17% died (10% suddenly, 6% of nonsudden cardiac cause and 1% of noncardiac cause). Cardiac death occurred in 20% of those for whom an effective drug could not be found to eliminate atrial flutter compared with 5% of those who were treated with an effective drug (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial flutter in the young: a collaborative study of 380 cases. 403 2

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

Amiodarone was administered to 121 patients (82 males, 39 females; average age 59 years) with refractory atrial tachyarrhythmias. All patients had experienced recurrent atrial fibrillation, atrial flutter, or reentrant supraventricular tachycardia previously refractory to digitalis drugs, beta-adrenergic blocking agents, and an array of membrance-active preparations. Seventy-four of 121 patients (61.2%) had no evidence of organic heart disease, whereas 17 patients experienced arrhythmia as a result of coronary heart disease, nine had preexcitation syndromes, 16 had primary valvular heart disease, and five patients, had congenital heart disease. Atrial fibrillation alone or in combination with atrial flutter was the primary dysrhythmia in 95 of 121 patients (78.5%), whereas in 26 patients (21.5%) supraventricular tachycardia was the primary refractory dysrhythmia. Fifty-one patients (42%) had experienced tachyarrhythmias for more than 10 years prior to the use of amiodarone. During an average follow-up of 27.3 months, complete suppression of atrial arrhythmias occurred in 98 of 121 patients (81%), and partial suppression occurred in seven (5.8%). In 16 patients (13.2%) the drug was deemed ineffective, and in eight patients (6.6%) amiodarone was discontinued because of intolerable side effects. The average blood serum concentration among successfully treated patients was 1.9 micrograms/ml, whereas the average concentration for those with side effects was 2.3 micrograms/ml. Thus, amiodarone is an extremely effective (greater than 85%) agent for refractory atrial tachyarrhythmias. Once daily administration, generally tolerable side effects, and excellent patient tolerance render this agent an attractive option for the management of these dysrhythmias.
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PMID:Efficacy of amiodarone for refractory supraventricular tachyarrhythmias. 661 32

Twenty-five years ago clinical investigators began to appreciate that cardiomyopathy is an important and reasonably common form of heart disease. Since then, several functional classifications have been proposed, the specific myocardial diseases have been classified and chronic ischemic ventricular failure has been described. The boundary separating myocarditis from dilated cardiomyopathy remains hazy and, despite intensive research, the causes of dilated cardiomyopathy remain obscure. In particular, we still do not understand the role that may be played by viral infection and alcohol. Myocardial biopsy has proved useful in patients with specific myocardial disorders, heart transplant recipients and patients receiving Adriamycin, but is disappointing in patients with dilated cardiomyopathy. It has become increasingly evident that exercise capacity does not correlate with ventricular function, being highly dependent on peripheral factors. Measurements of oxygen consumption during exercise promise to be useful in assessing treatment of dilated cardiomyopathy. True restrictive cardiomyopathy is uncommon, and the term should be reserved for cardiomyopathies that meet strict criteria. A restrictive component to filling is common to many cardiac disorders, including some cases of cardiac amyloidosis. The concept of hypertrophic cardiomyopathy has evolved rapidly over the past 25 years, and continues to evolve. The importance of arrhythmia as a cause of sudden death is becoming increasingly clear. The place of calcium channel blocking agents in the treatment of hypertrophic cardiomyopathy will probably emerge soon. Amiodarone is finding an increasing role in the treatment of dilated and hypertrophic cardiomyopathy. Surgical treatment is still required for some patients despite unanswered questions on how it works.
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PMID:Cardiomyopathy: how far have we come in 25 years, how far yet to go? 668 23

The Authors present their experience, based on 180 patients, concerning the treatment of chronic ventricular tachycardia. According to the underlying etiology, about 1/3 of the cases were considered idiopathic (most of all in form of salvos), 1/3 were ischemic with a prior myocardial infarction (ventricular tachycardias in the setting of acute myocardial infarction were not considered) and 1/3 had miscellaneous cardiac diseases. Prophylactic treatment of ventricular tachycardia recurrences was divided in three steps: classic antiarrhythmic drugs used in monotherapy (Quinidine or Quinidine-like, betablockers, Verapamil); Amiodarone or recent class I antiarrhythmics (Flecainide, Propafenone); drug combinations. The results of medical treatment were different according to the underlying etiology: the first two steps achieved control of the arrhythmia in 2/3 of patients with idiopathic ventricular tachycardia, in 45% of ventricular tachycardia due to miscellaneous cardiopathy and only in 35% of cases with post-myocardial infarction ventricular tachycardia. Four patients were referred for antiarrhythmic surgery and 3 received a palliative electrical device. During a mean follow-up period of 5 years, there were no deaths in the group with idiopathic ventricular tachycardia, 10% of deaths in the group with miscellaneous cardiopathy and 17% in the group with post-myocardial infarction ventricular tachycardia. Idiopathic ventricular tachycardias seem to bear a minimal risk, and the need to treat them depends only on the severity of functional signs and on the frequency of arrhythmic episodes. In patients with severe underlying cardiopathy, particularly ischemic heart disease, active search for an effective treatment is mandatory, due to the high risk of death.
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PMID:[How and why treat ventricular hyperkinetic arrhythmias]. 673 20

4 children, ages 11-14 years, were diagnosed as having primary ventricular arrhythmias (3 ventricular tachycardia, 1 multifocal premature ventricular contractions) without underlying heart disease. All 4 patients were treated initially with standard antiarrhythmic drugs (quinidine, propranolol, procainamide) and either did not respond (3 patients) or experienced drug toxicity (quinidine - 1 patient) necessitating withdrawal of antiarrhythmic therapy. Amiodarone, a new antiarrhythmic agent, was initiated in a single oral daily dose of 10 mg/kg/day. All patients have shown a significant clinical response to oral amiodarone with either complete suppression of ventricular tachycardia in 2 patients, near complete suppression in 1 and abolition of multifocal premature ventricular contractions in the fourth patients. 2 patients have had corneal microdeposits detected by slitlamp examination and are receiving methylcellulose eye drops; no other adverse reactions have been encountered during the follow-up of 6 months to 3 years.
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PMID:Use of amiodarone in the therapy of primary ventricular arrhythmias in children. 686 98

The effects of Amiodarone (1000-1400 mg/week, for a period ranging from 3 to 24 months) on thyroid gland function were studied in 45 patients with heart disease, using a new method of free thyroid hormone assay. Forty-four untreated patients and 11 normal subjects were used as controls. In treated patients the prevalence of dysthyroidism was 22,2% (15,6% hypothyroidism and 6,6% hyperthyroidism); the onset of dysthyroidism ranged from 20 days to 2 years after the beginning of treatment. In control patients the prevalence of dysthyroidism was 4,4% (2,2% hypothyroidism and 2,2% hyperthyroidism). In patients with hypothyroidism (TSH greater than 7 microunits/ml) T4 levels were generally low, while T3, fT4 and fT3 levels were normal. In treated patients with hyperthyroidism (fT3 greater than 5,3 pg/ml and fT4 greater than 16 pg/ml) T4 values were high, while T3 concentrations were in the normal range. In Amiodarone-treated euthyroid patients, mean T4, fT4 and rT3 values were significantly (p less than 0,01) higher than those of control subjects; TSH levels were normal in all the groups studied. These data suggest that Amiodarone can exert both a direct effect on the thyroid gland and the peripheral metabolism of thyroid hormones. The action on the thyroid gland is suggested by the high prevalence of dysthyroidism in Amiodarone-treated patients and by the high levels of T4 and fT4 observed in patients who did not show dysthyroidism. The action on the peripheral hormonal metabolism seems to be proved by the high levels of rT3 and by the prolongation of QTc interval.
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PMID:[Thyroid function in patients chronically treated with amiodarone]. 688 52

To study the effects of class III agents on QT/QTc dispersion in patients with heart disease and cardiac arrhythmias, QT dispersion and QRS and RR intervals were compared in patients before and after treatment with amiodarone (n = 26), sematilide (n = 26), and sotalol (n = 26). QT, QRS, and RR intervals, and QTc values were calculated for each complex, and their mean values were calculated for each lead. QT and QTc dispersions were defined as differences between the minimal and maximal QT or QTc values in each of the 12 leads studied. Amiodarone, sematilide, and sotalol all significantly prolonged the QT interval and the QTc value. Significant reductions in QT and QTc dispersions were only found in the amiodarone group (QT dispersions: 79 +/- 13 vs 49 +/- 14 ms; p < 0.001; QTc dispersions: 0.08 +/- 0.02 vs 0.05 +/- 0.01 s1/2; p < 0.001). The mean RR interval was significantly increased in patients after treatment with amiodarone (p < 0.001) and sotalol (p < 0.001), but not in patients receiving sematilide treatment (p > 0.2). The baseline QT and QTc dispersions were significantly greater in patients with than without myocardial infarction before treatment (p < 0.001). The mean baseline values for QT/QTc dispersions were not significantly different among all 3 groups. However, only amiodarone significantly reduced the QT dispersion (from 76 +/- 10 to 46 +/- 11 ms; p < 0.001) and QTc dispersion (from 0.09 +/- 0.02 to 0.05 +/- 0.01 s1/2; p < 0.001) in patients with myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of amiodarone, sematilide, and sotalol on QT dispersion. 752 75

The purpose of this study was to determine the effects of chronic amiodarone treatment on systolic and diastolic function in patients with cardiac disease undergoing treatment for resistant ventricular arrhythmias. Previous studies have shown that chronic amiodarone treatment either has no effect or increases left ventricular ejection fraction, but the effects on diastolic properties of the ventricle have not been defined. Twelve male patients were given loading doses of amiodarone followed by a maintenance regimen. Serial measurements of heart rate, blood pressure, and indexes of systolic and diastolic function were measured by Doppler echocardiographic techniques at baseline conditions and at 2, 8, and 12 weeks of drug therapy. Changes in altered thyroid state were excluded by serial determinations of thyroid function. Amiodarone increased left ventricular ejection fraction (+16%, p < 0.01 by 8 weeks), decreased presystolic ejection period/left ventricular ejection time (-12%, p < 0.01 by 8 weeks), and increased velocity of circumferential fiber shortening (+22%, p < 0.05 by 8 weeks). Amiodarone decreased mitral inflow velocity peak E/peak A (-7%, p < 0.01 by 12 weeks), and increased deceleration and isovolumic relaxation times incrementally (+36% [p < 0.001] and +23% [p < 0.001], respectively, at 12 weeks). Chronically administered amiodarone can improve systolic function and exert a negative lusitropic action in patients with heart disease.
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PMID:Divergent effects of chronic amiodarone administration on systolic and diastolic function in patients with heart disease. 786 90

Atrial fibrillation is a very common arrhythmia in patients with structural heart disease, but it also occurs in patients without underlying heart disease. Acute therapy for paroxysmal atrial fibrillation is very dependent on the clinical condition of the patient. Direct current cardioversion is usually the first choice whenever the arrhythmia precipitates heart failure or severe angina, while more stable patients are normally treated with drugs. Most episodes of atrial fibrillation eventually convert to sinus rhythm even in the absence of treatment. Antiarrhythmic drugs can be used to control the ventricular response or to restore sinus rhythm, and several have been tested to assess their ability to convert recent onset atrial fibrillation. The success rate has varied, but generally flecainide and propafenone appear the most effective. Digitalis and calcium channel blockers do not increase the likelihood of reversion but they reduce ventricular rate. Amiodarone has been tested as a possible alternative to flecainide and propafenone. The pros and the cons of these and other drugs in the setting of paroxysmal atrial fibrillation will be discussed. In particular, special emphasis will be given to the differences in the design and in patient selection of the trials that tested antiarrhythmic drugs in paroxysmal atrial fibrillation.
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PMID:Clinical challenge. II. Management of recent onset atrial fibrillation. PAFIT-2 Investigators. 880 38


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