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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac failure is a common cause of arrhythmia. Many factors predispose to the genesis of arrhythmias in these patients. A number of non-invasive methods allow stratification of the risk of arrhythmia in cardiac failure. Approximately half the deaths of these patients are due to arrhythmia. Unfortunately, most of the investigations for risk evaluation have a high negative predictive value but a lower positive predictive value. The treatment of supraventricular arrhythmias, mainly atrial fibrillation, is complex in cardiac failure. Class I antiarrhythmics are contraindicated. The only remaining options are Class II, especially Sotalol, and Class III drugs, especially Amiodarone. In some cases, non-pharmacological methods such as ablation, pacing or an implantable atrial defibrillator must be considered. The treatment of ventricular arrhythmias is also difficult. In this indication, Class I antiarrhythmic agents must also be avoided. Non-sustained ventricular tachycardia may be treated by betablockers or amiodarone. The use of an implantable defibrillator is increasingly recommended after the results of several controlled large scale trials. The indication is obvious in patients resuscitated from sudden death and these devices are also beneficial in sustained ventricular tachycardia in patients with cardiac failure. Many studies are currently under way to determine the value of this therapeutic modality in indications now considered to be "prophylactic".
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PMID:[Management of arrhythmias in patients with heart failure]. 986 6

Sudden death accounts for about 35% of the mortality of cardiac failure and its incidence does not decrease with the use of angiotensin converting enzyme inhibitors. Non-sustained ventricular tachycardia on Holter monitoring, late ventricular potentials and tachycardia induced by programmed ventricular stimulation have no formal predictive value of sudden death, underlining the varied character of the mechanisms underlying sudden death during cardiac failure. Sustained ventricular tachycardia degenerating to ventricular fibrillation is only one of the rhythmic factors implicated together with inaugural ventricular fibrillation, bradyarrhythmias and electromechanical dissociation. The underlying cardiac disease plays a role in the initiation of the fatal arrhythmia. In coronary artery disease, recurrent acute ischaemia is the principal trigger factor in patients who often have triple vessel disease. This explains the fact that classic markers of arrhythmia in the post-infarction period, which are only the reflection of the arrhythmogenic substrate of ventricular tachycardia, usually due to reentry around the fibrous scar of the infarct, are not valid in patients with progressive ischaemic cardiomyopathy. The most effective antiarrhythmic treatment in this type of patient is the prevention of ischaemia, when possible. In primary dilated cardiomyopathy, the mechanism underlying sudden death could be different at each stage. In NYHA Stages I and II, ventricular tachyarrhythmias could play a major part in unexpected sudden death in patients whose stable haemodynamic status suggested a more prolonged survival. The value of an implantable defibrillator would seem to be proved in this group of patients, at least in secondary prevention. In Stages III and IV, ventricular arrhythmias only indicate the degree of ventricular dysfunction and sudden death may follow bradyarrhythmias and electromechanical dissociation due to the precarious haemodynamic status.
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PMID:[Sudden death and chronic cardiac insufficiency]. 989 14

A 44-year-old male patient with known Becker muscular dystrophy and concomitant non-ischemic dilated cardiomyopathy presented to our department because of worsening heart failure and presyncope. Upon admission, the patient was in New York Heart Association functional class III despite optimal pharmacological treatment; his ECG showed sinus rhythm with left bundle branch block and a wide QRS complex. Non-sustained ventricular tachycardia was recorded during 24-hour Holter monitoring. A complete three-dimensional echocardiographic study was performed and documented the dilatation and concomitant hypertrabeculation of the left ventricle (LV), with severely depressed systolic LV performance (ejection fraction 20%), as well as mechanical dyssynchrony--mainly in terms of intraventricular delay. A biventricular cardioverter-defibrillator (CRT-D) was implanted in this patient, with the LV lead in a lateral vein and the right ventricular defibrillating lead in the apical part of the interventricular septum. Echocardiography-guided device programming was performed in order to achieve the optimal atrio-, inter-, and intraventricular resynchronization. The patient's clinical condition was substantially improved within one month after the implantation.
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PMID:Cardiac resynchronization therapy in becker muscular dystrophy. 2368 62