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

An experimental model of the long QT syndrome has been developed in conscious dogs. This report discusses the methods used in its preparation and the strengths and weaknesses of the model. This new model is suitable for screening the bradycardia-dependent proarrhythmic effects of drugs and for studying the electrophysiology of "torsades de pointes." Permanent bradycardia (RR: 1558 +/- 83 ms) was obtained in 37 dogs by chemically-induced complete atrioventricular block. A 10% further increase of ventricular repolarization (QT: 306 +/- 7.0 ms to 331 +/- 5.5 ms) was obtained in 28 of these dogs by diuretic-induced hypokalemia. Diuretics, despite saline replacement, induced some degree of functional renal failure and extracellular volume losses. The QT interval increased although ventricular cycle length decreased slightly. These biological and electrophysiological parameters were reproducible except for a slow increase in plasma creatinine. Cardiac failure and sudden death rarely occurred. The most severe, but reversible, renal failure occurred in some dogs given the highest diuretic doses. Hypokalemia resulted in ventricular arrhythmias in only 6 dogs, 2 of them exhibiting runs of ventricular tachycardia and even "torsade de pointes" as their potassium levels fell below 2 mmol/L. The results of studies with several drugs using the model, with or without hypokalemia, or with bradycardia worsened by propranolol are analysed.
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PMID:Methods and limitations of an experimental model of long QT syndrome. 192 6

Our study group included 12 patients (4 males, 8 females), mean age 60 yr, with symptomatic or threatening tachyarrhythmias (Lown classes IV A, B, V); 2 patients were suffering from mitral valve prolapse syndrome, 2 from ischemic heart disease; 4 from cardiac insufficiency caused by hypertensive or ischemic heart disease; 4 had no evident clinical signs of cardiopathy. Patients suffering from: cardiac insufficiency (F.C. III e IV NYHA); II and III degree BAV; atrial flutter and fibrillation; long QT syndrome; acute ischemic heart disease were excluded from the study. During short-term treatment, patients received placebo for four days and subsequently flecainide 200 mg daily for four days. During medium-term treatment patients received flecainide 200 mg daily (for six months). Several Holter/24-hour monitorings were performed for evaluation of therapy. No significant reduction in the number of ectopic ventricular beats (B.E.V.) was found with placebo whereas reductions of B.E.V. number (97% and 95%, respectively) were found during short and medium-term treatment with flecainide. Flecainide produced: changes in Lown class: from IV A, B and V to II and I; a marked reduction of subjective symptoms (dyspnea, giddiness syncope, precordial pain); ECG changes: increases in: PR: 5-25%; QRS: 11-12%; QT: 11-22%. Flecainide produced no pro-arrhythmic effects or changes in echocardiographic ventricular function index. Flecainide can be considered one of the most effective new antiarrhythmic drugs.
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PMID:[Short- and medium-term treatment of ventricular hyperkinetic arrhythmia with flecainide]. 252 12

To evaluate the mechanism of sudden death in childhood and the physical activity levels at the onset of sudden death, we studied the following items: (1) the incidence and the circumstances surrounding sudden death at school in Kanagawa Prefecture, (2) high risk heart diseases detected among healthy school children by heart disease screening, (3) sudden cardiac death or near miss seen in outpatients with heart disease except congenital heart disease. Among total 15,156,346 school children, sudden death was observed in 97 subjects (M:77, F:20). Annual incidence of sudden death was 6.4 per 10(6). Of the 97 subjects, acute heart failure of unknown etiology was found in 60 (62%), cardiovascular disease in 18 (19%), cerebral vascular accidents in 14 (14%) and heat stroke in 5 (5%). Of the 78 subjects (M:64, F:14) considered as sudden cardiac death, 62 (79%) died during sports activities, and 16 (21%) died at rest. Of the 62 subjects, 29 died during track and field activities and 7 while swimming, both in physical education classes. Eighteen died during athletic club activities and 8 during extracurricular activities. Consequently, 54 subjects (87%) died in the presence of a school teacher. Of the 18 subjects with cardiovascular disease, 9 (hypertrophic cardiomyopathy in 3, myocarditis in 3, Kawasaki disease in 2 and long QT in one) were diagnosed initially by the autopsy study. Latent high risk heart diseases, detected among presumably healthy school children by the heart disease screening program, were the following: hypertrophic cardiomyopathy, long QT syndrome, Kawasaki disease and some arrhythmias (ventricular tachycardia, sick sinus syndrome, A-V block and atrial fibrillation). Follow-up observations of outpatients with heart disease revealed the same results as the heart disease screening program. In order to prevent sudden death at school, the following recommendations should be observed: 1) sports directors should learn "sports medicine in childhood", including primary cardiovascular resuscitation, 2) an accurate heart disease screening program should be operated to detect latent high risk heart diseases, advise on adequate medical treatment, and help ensure an appropriate selection of sports activities, 3) comprehensive autopsy studies should be performed.
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PMID:Sudden cardiac death in childhood. 263 28

Seventy-seven patients with drug-refractory sustained ventricular tachycardia (VT) (28 patients) or ventricular fibrillation (VF) (49 patients) underwent implantation of an automatic cardioverter defibrillator (AICD). The 67 men and 10 women, with a mean age of 60 +/- 12 years (range 18 to 79), had coronary artery disease (60 patients), idiopathic cardiomyopathy (eight patients), mitral valve prolapse (four patients), hypertensive heart disease (one patient), Ebstein's anomaly (one patient), long QT syndrome (one patient), and primary electrical disease (two patients). The mean left ventricular ejection fraction was 35 +/- 16% (range 10% to 75%). Sustained VT/VF was induced in 64 patients (83%) at baseline electrophysiologic testing. A mean of 4.1 +/- 1.3 antiarrhythmic drugs failed to control the arrhythmia. Associated surgery at AICD implantation included coronary artery bypass in 19 patients, coronary bypass with aneurysmectomy in six patients, and aneurysmectomy alone in one patient. Five patients had only prophylactic patches implanted during aneurysmectomy or coronary bypass and the AICD device was subsequently implanted under local anesthesia to prevent arrhythmia recurrence or to control persistently inducible VT. Operative mortality was 2.6% with two deaths from intractable VF. Fifty-two patients (69%) continued receiving antiarrhythmic drugs to suppress spontaneous VT. During a mean follow-up of 15 +/- 13 months (range 1 to 63), six patients died: two suddenly due to probable pulse generator failure (greater than 2 years old), one of acute myocardial infarction, two of heart failure, and one of respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical experience in seventy-seven patients with the automatic implantable cardioverter defibrillator. 277 68

A cooperative study involving 23 centres enabled review of 69 cases of sudden death occurring less than one hour after onset of symptoms recorded by the Holter method and not related to recent, clinically documented myocardial infarction or to class IV cardiac failure. The 15 cases of asystole (22 p. cent) were observed in elderly patients (73.3 +/- 2.7 years) whose known ischaemic heart disease (12/15) was confirmed in 10 cases as the direct cause by the preceding acute ST changes. In 2 cases, death resulted from AV block presumed to be iatrogenic. The 13 episodes of torsades de point (19 p. cent) occurred mainly in younger women (58.8 +/- 6 years) without apparent cardiac disease (8 cases) and were provoked by a Group IA antiarrhythmic drug (7 cases) or by hypokalemia (3 cases). Apart from 1 case of congenital long QT syndrome, slowing of the sinus rhythm was observed (78.3 +/- 2.6 to 60.2 +/- 2.7 bpm, p less than 0.001) in the 3 hours preceding these episodes, and ventricular bigeminy with a long coupling interval was recorded in the lasts seconds before the torsades. The 41 (59 p. cent) cases of ventricular fibrillation (VF) were observed in men aged 64.9 +/- 2 years with coronary artery disease (39/41). However signs of acute ischaemia were only found in 5 cases. The VF was primary in 8 cases and secondary to ventricular tachycardia (VT in 33 cases). An acceleration of the cardiac rhythm (83.3 +/- 3.4 to 90 +/- 4.1 bpm, p less than 0.01) was recorded in the hour preceding VF and other arrhythmias were common: atrial tachycardia (4 cases), atrial extrasystoles (4 cases), a new type of ventricular extrasystoles (VES). The VF and VT were preceded by a long cycle in 17 cases. The first complex was different from previous VES in 10 cases and identical to the previous VES in 16 cases; in 4 cases this feature could not be identified and in 11 cases there were no premonitory VES. The coupling interval of the initial VES was shorter than that of the most premature preceding VES (368 +/- 13 ms vs 442 +/- 19 ms, p less than 0.001), especially in primary VF (335 +/- 9 ms, N = 8) compared to polymorphic VT (360 +/- 12 ms, N = 11) or monomorphic VT (384 +/- 18 ms N = 22).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanisms determining sudden death. A cooperative study of 69 cases recorded using the Holter method]. 309 25

Over a 2-year period, 110 patients underwent attempted implantation of an automatic cardioverter-defibrillator using the nonthoracotomy lead system. Indications included sustained monomorphic ventricular (n = 62), nonsustained with poor ventricular function (n = 7), ventricular fibrillation (n = 21), ventricular tachycardia/fibrillation (n = 18), and familial long QT syndrome (n = 2). There were 90 male and 20 female patients. Mean age was 57 +/- 15 years. Sixty percent had previous coronary bypass or valve operations, or both. Mean left ventricular ejection fraction was 30% +/- 14%, cardiac index was 2.4 +/- 0.9 L/m2, and systolic pulmonary artery pressure was 41 +/- 14 mm Hg. Under general anesthesia, the nonthoracotomy lead was introduced through the left subclavian vein. The subcutaneous patch and generator were placed posteriorly on the serratus muscle and left upper quadrant, respectively. The length of the procedure was 116 +/- 44 minutes and the mean number of defibrillation shocks for a successful implant was 8 +/- 4. Eighty-five patients (77%) had successful implantations. Failures were due to high defibrillation threshold (n = 23) and inability to place a right ventricular lead (n = 2). Predictors of failure included preoperative antiarrhythmic drugs and cardiac index of 1.8 +/- 4 L/m2 or less (p = 0.004). Three patients (2.7%) died after the operation of heart failure (n = 2) and chronic heart transplant rejection (n = 1). Complications included lead migration or dislodgment (n = 8), infection (n = 1), and hematoma (n = 3). In summary, the nonthoracotomy lead system may provide an alternative in patients undergoing cardioverter-defibrillator implantation.
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PMID:Nonthoracotomy lead system for implantable defibrillator. 824 36

The multiple facets of cardiac arrhythmias and their relationship with the autonomic nervous system can be investigated by studying the spontaneous heart rate behavior through ambulatory ECG recordings, an approach that complements the limitations of invasive electrophysiologic investigations. Information obtained from heart rate behavior is more reliable in the absence of structural heart disease and ventricular hypertrophy/failure, during which compensatory mechanisms involving the autonomic nervous system tend to limit reflex changes in heart rate. Thus, in such situations, less marked sinus rhythm variations preceding the arrhythmia onset do not imply a more limited influence of the autonomic nervous system, and the sensitivity of the electrophysiologic substrate may otherwise vary. These two factors may combine to form the basis of the "adrenergic paradox" that implies that the more marked the autonomic nervous system dependence of tachyarrhythmias, the less obvious its evidence. Assessment of the QT interval dynamicity may also allow one to evaluate the modulation of autonomic neural effects on the ventricular tissues. Finally, it may be difficult to distinguish clearly autonomic nervous system dependence from rate dependence: the latter frequently conditions the behavior of the trigger whereas the former mainly concerns the electrophysiologic substrate. There are many examples of the importance of the autonomic nervous system as a determinant of cardiac arrhythmias. In the atrium, either limb of the autonomic nervous system, particularly the parasympathetic limb, can generate atrial fibrillation. The absence of structural heart disease defines pure electrophysiologic substrates responsible for benign forms of ventricular tachycardia as well as potentially lethal tachyarrhythmias of the long QT syndrome and its variants. In both, the role of the autonomic nervous system is essential, although the therapeutic consequences are crucial only in the latter. In the presence of heart disease and, in particular, heart failure, the autonomic nervous system behavior is more difficult to assess than in the absence of structural heart disease. This does not mean that its role is less crucial. In this situation the beneficial effects of beta blockers may be as important as in normal hearts although physicians should be more cautious when heart failure is present.
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PMID:Cardiac arrhythmias and the autonomic nervous system. 826 4

To determine the risk factors for sudden deaths in hospitalized patients, 209 patients (103 men and 106 women, age 76.7 +/- 12.6 years old, mean +/- S.D.) who died in 1996 were divided into two groups and their records were analyzed. One group, the sudden death group (SD), consisted of 16 patients who had stayed in the hospital for 2 weeks or more before the onset of symptoms that led to death within 24 hours. Those who died more than 24 hours after symptoms began were placed into the non-sudden death group (NSD). Fourteen patients who died within 2 weeks of admission were not analyzed in this study. Comparing the data of the two groups led to the following findings. First, the major causes of death in the SD group were exacerbation of chronic cardiac failure (5 cases), acute cardiac failure (2 cases), exacerbation of chronic respiratory failure (2 cases) and acute respiratory failure (2 cases). Second, patients in the SD group were significantly older than those in the NSD group, and had significantly more prescriptions for digitalis. Third, patients in the SD group had higher levels of hemoglobin and hematocrit, lower levels of BUN and a higher cardiothoracic ratio. Fourth, patients in the SD group had a higher incidence of ST abnormalities and T wave abnormalities in their electrocardiograms. Brugada syndrome or long QT syndrome were not seen in either group. Taken together, these findings suggest that aged patients with cardiac failure and myocardial ischemia may be at higher risk of sudden death.
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PMID:[Risk factors for sudden death during hospitalization]. 1006 69

It has been suggested that patients be admitted for the initiation of Class I and Class III antiarrhythmic drugs to avoid serious proarrhythmic consequences. The most clinically significant proarrhythmic response to Class IC agents is likely due to an interaction with acute ischemia, and hospitalization for initiation of drug therapy has little predictive or preventive value. Amiodarone has a low risk of proarrhythmia, and any proarrhythmic reactions are generally delayed. Class IA and Class III antiarrhythmic drugs cause acquired long QT syndrome arrhythmias, which can occur soon after initiation of therapy; however, only about half of the arrhythmic events occur within 3 days of initiation of therapy. It could be argued that all patients should be hospitalized to begin Class IA or Class III drugs; however, this approach has a low yield and is extremely expensive. An alternative is to use Class IA and Class III drugs for patients at low risk of torsades de pointes (e.g., males without heart failure, ventricular tachyarrhythmias, or active coronary disease), in whom hospitalization for drug initiation is not warranted. Higher risk patients are probably better treated with other agents, such as Class IC drugs or amiodarone for women without organic heart disease and amiodarone for patients with heart failure, a history of ventricular tachycardia, or active coronary disease. When a Class IA or Class III drug is required for patient with an increased risk of torsades de pointes, hospital admission for drug initiation may be indicated.
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PMID:Optimal management with Class I and Class III antiarrhythmic drugs should be done in the outpatient setting: protagonist. 1021 May 15


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