Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the factors relating to prognosis, the records of 15 neonates with persistent prolongation of the QT interval on the electrocardiogram after the fourth day of life were reviewed. Patients were admitted for symptoms (syncope, cardiac failure, or seizures), abnormal auscultation with an irregular heart rate or bradycardia, or because of a family history of a long QT syndrome. All infants had a long QTc, ranging from 0.46 to more than 0.70 second. Eight patients who had a QTc over 0.60 second developed severe ventricular arrhythmias (torsades de pointes, ventricular tachycardia) or second-degree AV block. Twelve of 15 were treated with beta-blocking agents, combined with ventricular pacing in five cases. Four infants died in the first month of life; they all had a very long QT interval and had experienced ventricular arrhythmias and AV block. Six children are still being treated with beta-blocking agents for the long QT syndrome and are doing well. In five infants, electrocardiographic abnormalities were transient and the QT interval returned to normal within 1 year. Therefore (1) prolongation of the QT interval in neonates may be transient or may represent an early form of the long QT syndrome and (2) the length of the QT interval may provide data on prognosis: those with a QTc less than 0.50 second returned to normal; those with a QTc greater than 0.60 second were associated with severe arrhythmias and four of eight infants died.
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PMID:Prolonged QT interval in neonates: benign, transient, or prolonged risk of sudden death. 135 80

Catheter ablation using direct current (DC) shock has proved invaluable in the management of a variety of tachycardias. However, sporadic reports of fatal arrhythmias following ablation have raised the question of the proarrhythmic potential of DC shock ablation. The present study was undertaken in 45 patients to assess prospectively any proarrhythmia related to DC shock ablation, using matched pre- and postablation Holter monitors and programmed electrical stimulation (PES). Nineteen of these patients had Holter monitors for three successive postablation days to observe trends. There was unmatched data in 11 additional patients. All 56 patients provided prospective follow-up for clinical events. There was no immediate sustained VT/VF at the time of the ablation. Four patients had sustained VT in the first 72 hours after ablation; three episodes were similar to the preablation clinical arrhythmias; one patient had torsades de pointes interrupting bradycardia. Twelve patients met Holter, PES, or clinical criteria for proarrhythmia; none were treated on the basis of these findings. On Holter monitoring, there were significant increases in VPCs/hour and couplets/hour in patients undergoing atrial or atrioventricular junctional ablations; and an increase in couplets after accessory pathway ablations. Increases in these categories were not significant for VT patients; nor were increases in episodes of VT/hour or atrial arrhythmias significant in any group. Patients were followed for 44 +/- 33 months, with an actuarial survival of 95% at 1 year, 88% at 3 years, and 85% at 4 years. There were six deaths during follow-up. Two patients had sudden death: one at 2 months had early evidence of proarrhythmia; the other at 32 months may have represented later myocardia deterioration. One patient died of heart failure at 77 months; and there were three noncardiac deaths. DC shock ablation in humans is much less proarrhythmic than in dogs. The low incidence of clinical proarrhythmic events during prolonged follow-up after discharge resulted in low sensitivity, specificity, and positive predictive values for Holter and PES, although the negative predictive values of these tests were greater than 90%. Only one of 12 patients who met criteria for proarrhythmia in the days immediately following ablation had subsequent clinical events consistent with proarrhythmia. These results may be useful as standards for comparison with results of radiofrequency or other ablation modalities.
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PMID:Direct current shock ablation: quantitative assessment of proarrhythmic effects. 172 98

Oral sotalol was given to 64 patients (78% postinfarction) with recurrent, reentrant ventricular tachycardia (VT) during an average follow-up period of 19.7 months. Fifty-nine (92%) patients had previously experienced recurrent ventricular tachycardia, in spite of having received an average of three conventional antiarrhythmic drugs (13 had previously failed on other Class III drugs). The nature and mechanism of the VT was proved with electrophysiologic testing (EPS), and the chronic sotalol dosage was determined by repeated EPS at 3- to 4-day intervals until the VT was no longer inducible. Sotalol failed in five patients and was discontinued in six patients because of severe side effects (three proarrhythmic effects, including two with torsades de pointes)--a total of 18%. Sotalol was successful alone in 42 patients (65%) and in combination with another antiarrhythmic drug in 11 patients (18%). The average dose of sotalol required for success was 589 mg; 658 mg was the mean daily dose when given alone and 486 mg when given in combination. Side effects were common and were due mainly to the beta-blocking effects of sotalol. Dual chamber pacing was required by 11 patients because of poorly tolerated bradycardia, and 14 patients remained symptomatic from worsening of the cardiac failure in spite of pacing, increased diuretics, or vasodilator therapy. The average drug dosage was the same for symptomatic (680 mg) and asymptomatic (627 mg) patients. Sotalol is a valuable antiarrhythmic drug for reentrant ventricular tachycardia. High doses are needed, and at these doses the beta-blocking activity is responsible for most of the side effects.
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PMID:Efficacy of oral sotalol in reentrant ventricular tachycardia. 227 91

The safety and efficacy of oral sotalol, an investigational beta-adrenergic blocker with class III antiarrhythmic drug properties, were examined in a multicenter study in 236 patients with sustained ventricular tachyarrhythmias. In 104 patients, the index arrhythmia was a cardiac arrest, and all patients had undergone at least 3 previous unsuccessful antiarrhythmic trials (mean = 5 per patient). In the 106 patients assessed by programmed electrical stimulation, sotalol completely suppressed induction of ventricular tachycardia (VT) in 33 (31%) and rendered VT slower (greater than 100 ms prolongation of cycle length) or more difficult to induce in 29 (27%). Using continuous 24-hour ambulatory monitoring methods, sotalol complete- and partial-response rates were 51 and 12%, respectively. Of the 236 acute-phase patients, 151 were discharged receiving long-term sotalol therapy. The median sotalol dose was 480 mg/day. At a mean follow-up of 346 +/- 92 days, 27 patients (18%) had recurrence of sustained arrhythmia; 9, sudden death; 11, sustained VT; 5, automatic defibrillator discharge; and 2, syncope. Adverse effects forced discontinuation of therapy in 10 patients (7%): 6 secondary to symptomatic bradyarrhythmia, 2 due to refractory heart failure, 1 due to torsades de pointes, and 1 from bronchospasm. Life-table analysis of sotalol's overall long-term efficacy at 6, 12 and 18 months were 80, 76 and 72%, respectively. Although mean follow-up was short (less than 1 year), neither acute-phase programmed stimulation nor 24-hour ambulatory monitoring responses were significantly predictive of subsequent arrhythmic outcome. Proarrhythmia was documented in 18 patients (7%), 17 during the acute phase and 1 during long-term follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety and efficacy of sotalol in patients with drug-refractory sustained ventricular tachyarrhythmias. 229 89

Key safety parameters of sotalol were examined in 1,288 patients entered into recent controlled trials of ventricular (85% of patients) or supraventricular arrhythmias (15%). Most patients were middle-aged male Caucasians with significant heart disease. The most serious adverse event was proarrhythmia, occurring in 56 patients (4.3%). Of these, 27 had hemodynamic compromise due to malignant ventricular arrhythmias. Most had a history of sustained ventricular tachycardia, myocardial infarction, congestive heart failure (CHF) or cardiomyopathy, or a combination of these. The other 29 had nonsevere events; 38% continued taking sotalol. Proarrhythmia was manifested by torsades de pointes in 24 of the 56 patients. No universal causal relation was found with commonly associated factors such as bradycardia, hypokalemia and long QT interval. The mean QT and QTc at baseline within 1 week of a severe proarrhythmic event were greater than those of patients not having proarrhythmia. Nineteen patients (1%) discontinued therapy with sotalol because of drug-related CHF. Predisposing conditions included low initial baseline ejection fraction, history of CHF, cardiomyopathy or cardiomegaly, or both, male gender and age greater than 65 years. Heart failure usually occurred within 7 to 30 days of initiating therapy. The most common reason for premature discontinuation of the drug in patients treated for sustained ventricular tachycardia was ineffectiveness (39%), whereas adverse effects were the most common reasons among patients treated for complex ventricular ectopy (21%). Dyspnea and bradycardia were the most common cardiovascular effects, and fatigue, dizziness and asthenia the most common noncardiac, adverse effects. Although frequently reported, these adverse effects resulted in discontinuation of only 1 to 4% of the patients at risk.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical safety profile of sotalol in patients with arrhythmias. 240 37

A patient with acute monocytic leukemia and fibrosis presented with severe hypocalcemia producing tetany, myocardial failure, and ventricular tachycardia with torsades de pointes configuration. Hypophosphatemia, hypomagnesemia, an elevated alkaline phosphatase level, and osteosclerosis were also present. Bone marrow biopsy samples showed fibrosis and thickened bony trabeculae lined with large osteoblasts. Tetracycline labeling showed an increased rate of calcification. Complete remission of the leukemia and fibrosis was achieved with a single 3-week course of low-dose cytarabine and hydroxyurea, with resolution of the hypocalcemia and hypophosphatemia. Calcitriol and etidronate disodium were also administered. The calculated left ventricular ejection fraction increased from 15% to 55% with correction of the hypocalcemia. The hypocalcemia and hypophosphatemia in this patient probably resulted from accelerated bone formation stimulated by the leukemic cells. The high dose of calcitriol that this patient received may have contributed to the remission of the leukemia.
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PMID:Accelerated bone formation causing profound hypocalcemia in acute leukemia. 346 37

The prevalence of arrhythmia increases with age. Considered as an "ordinary" event in elderly patients, these arrhythmias may nevertheless have serious consequences. This study was undertaken to determine the clinical, aetiological and prognostic features of serious arrhythmias in a population of elderly subjects (> or = 70 years) hospitalised over a 20 months period and comprising 202 patients (103 women, 99 men, mean age 79.6 +/- 5.9 years). Supraventricular arrhythmias are the most common by far (84.2%): 51.4% of patients had atrial fibrillation, 15.3% had atrial flutter; 12.9% had focal atrial tachycardia, 4.5% had junctional tachycardia. Of the ventricular arrhythmias (15.8%), there were 12 sustained ventricular tachycardias, 4 torsades de pointes and 1 ventricular fibrillation. The increased duration of hospital stay (10 +/- 6 days on average) is related not to age but to the type of arrhythmia (longer for ventricular arrhythmias) and to left ventricular dysfunction. The main complications of arrhythmias were cardiac failure (52.4%), neurological deficits (37.4%) and angina (18.6%). Electrocardiographic signs of atrioventricular block were present in 62% of cases and QRS changes in 47.3% of cases. Ventricular arrhythmias were more commonly associated with intraventricular conduction defects, signs of myocardial necrosis and prolongation of the QT interval; they were also common in patients with left ventricular dysfunction and when the left ventricle was dilated. The aetiology of ventricular arrhythmias was mainly iatrogenic (50%) and ischaemic (21.8%), whereas the aetiologies of the supraventricular arrhythmias were varied, 14.7% of cases being idiopathic. Conversion to stable sinus rhythm was obtained in half the patients. A pacemaker was implanted in 10.8% of cases. The hospital mortality was 4.9%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Severe arrhythmia in the elderly: a prospective hospital study]. 764 46

Amiodarone is considered to be safe in patients with prior QT prolongation and torsades de pointes taking class I antiarrhythmic agents who require continued antiarrhythmic drug therapy. However, the safety of amiodarone in advanced heart failure patients with a history of drug-induced torsades de pointes, who may be more susceptible to proarrhythmia, is unknown. Therefore, the objective of this study was to assess amiodarone safety and efficacy in heart failure patients with prior antiarrhythmic drug-induced torsades de pointes. We determined the history of torsades de pointes in 205 patients with heart failure treated with amiodarone, and compared the risk of sudden death in patients with and without such a history. To evaluate the possibility that all patients with a history of torsades de pointes would be at high risk for sudden death regardless of amiodarone treatment, we compared this risk in patients with a history of torsades de pointes who were and were not subsequently treated with amiodarone. Of 205 patients with advanced heart failure, 8 (4%) treated with amiodarone had prior drug-induced torsades de pointes. Despite similar severity of heart failure, the 1-year actuarial sudden death risk was markedly increased in amiodarone patients with than without prior torsades de pointes (55% vs 15%, p = 0.0001). Similarly, the incidence of 1-year sudden death was markedly increased in patients with prior torsades de pointes taking amiodarone compared with such patients who were not subsequently treated with amiodarone (55% vs 0%, p = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amiodarone and torsades de pointes in patients with advanced heart failure. 765 52

We present a case provoked life-threatening ventricular arrhythmias probably due to psychotropic drugs. The patient was a 55-year-old man who had previously twice operations of aortic valve replacement (AVR). The signs of cardiac failure were recurrently appeared from the end of 1991, and he had received promethazine and sulpiride for his depressive state. From cardiac catheterization, we planned his third AVR. The electrocardiographic (ECG) QTc interval was prolonged to 0.48 seconds on this admission. In March 1992 syncopal attack appeared suddenly, and his monitor ECG revealed frequent polymorphous ventricular tachycardia (VT) and Torsade de Pointes (Tdp). These arrhythmias stopped by emergent cardiac pacing. After discontinuing these psychotropic drugs, no ventricular arrhythmias appeared. Since the patient complained severe insomnia one month before operation, the diminished dose of psychotropic drugs (promethazine and levomepromazine) was readministered. Ten days after the operation, syncopal attack reappeared and his ECG recorded frequent VT and Tdp. During both syncopal attacks his serum potassium and magnesium were within normal limits. Two days later, he died from multi-organ failure. We concluded that life-threatening arrhythmias such as VT and Tdp might develop under the administration of mild psychotropic drugs (promethazine or levomepromazine), therefore, must better take a care of ECG changes in cases of using any psychotropic drugs.
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PMID:[A case of life-threatening ventricular arrhythmias probably due to psychotropic drugs]. 825 55

Certain drugs can induce ventricular tachycardia (VT) by creating reentry, ventricular after potentials or exaggerating the slope of phase 4. These may or may not be symptomatic, sustained or non-sustained and have variable ECG appearances: monomorphic or polymorphic, bidirectional, torsades de pointes. They risk degenerating into ventricular flutter of fibrillation and have been held responsible for the increased mortality observed unexpectedly in some long-term treatments. The drugs responsible are mainly those used in cardiology, probably due to predisposing circumstances (cardiomegaly, cardiac failure, previous severe ventricular arrhythmias, therapeutic associations, metabolic abnormalities). These include primarily the antiarrhythmic drugs (IA, IC, sotalol and bepridil), digitalis, sympathomimetics and phosphodiesterase inhibitors. These complications may be toxic or idiosyncratic, in patients with or without cardiac disease, and may also occur with other drugs: vasodilators and anti-anginal drugs (lidoflazine, vincamine, fenoxedil), psychotropic agents (phenothiazine and imipramine), antimitotics, antimalarials (chloroquine) or antibiotics (erythromycin, pentamidine). The prognosis is severe and the treatment is often difficult which makes prevention, helped by repeated surface ECG (or Holter monitoring), very important with careful assessment of patients at risk.
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PMID:[Drug-induced ventricular tachycardia]. 826 4


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