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PubMed1996

[Implantable cardioverter defibrillator].

ICD therapy has been believed to be a last resort therapy for preventing of sudden death due to VT/VF. Since 1980, when clinical use first began, ICD therapy has rapidly increased in use in Europe and in the United State. In Japan, in 1990 clinical investigation began, and in 1996 it received insurance reimbursement. From here on, it should experience a rapid rise in use. However there are many problems such as complications, inappropriate shocks, size, longevity and psychological effects etc. Therefore indication for their use should be carefully considered and it is very important to obtain the patient's informed consent.

Arrhythmias, Cardiac↗
PubMed1996

[Pseudodefects in myocardial SPECT after implantation of defibrillator patches: phantom measurement with SPECT and PET].

AIM AND METHODS: In order to estimate the effect of an epicardial or subcutan defibrillator patch electrode on the imaging of myocardium with SPET and PET we performed measurements with a body phantom and two different patch electrodes. RESULTS: We found that in 201TI-SPET with epicardial placing one electrode causes significant pseudodefects, which might lead to the impression of an infarction ("pseudoinfarction"), particularly in the case of reduced myocardial wall thickness. Measurements with 99nTc show the same pseudodefects. In case of subcutaneous placing the electrodes are much less likely to cause relevant absorption effects. With PET even epicardially placed both patch electrodes do not produce pseudodefects. Therefore the risk of false-positive findings is very small with PET. CONCLUSION: In order to avoid false positive findings in cardiovascular nuclear medicine caused by defibrillator patch electrodes, patients with patch electrodes should be referred to PET, if available.

Artifacts↗
PubMed2006

Effects of low-dose quinidine on ventricular tachyarrhythmias in patients with Brugada syndrome: low-dose quinidine therapy as an adjunctive treatment.

Quinidine is suggested as an effective agent to suppress ventricular fibrillation (VF) in the Brugada syndrome by inhibiting transient outward K(+) current (Ito) leading to the reduction and abbreviation of the disparity of repolarization in the right ventricular outflow region and ST segment elevation in the right precordial leads of electrocardiogram. We sought to assess the efficacy of low-dose (300-600 mg) quinidine sulfate on the prevention of ventricular fibrillation induction by programmed electrical stimulation (PES) and spontaneous ventricular fibrillation episodes during the subsequent follow-up period. Electrophysiologic study was performed in 14 patients with the Brugada syndrome (14 men, mean age 50 +/- 11 years, range 32-75) before and during the treatment with low-dose quinidine and evaluated the efficacy of the drug therapy. Ventricular fibrillation was induced in all the patients by programmed electrical stimulation at baseline. After oral quinidine administration (300 mg or 600 mg/d), programmed electrical stimulation was repeated. Ventricular fibrillation induction was prevented in 6 of 14 patients (44%). Serum quinidine concentration was higher in the patients with suppressed VF induction than those without (1.88 +/- 0.44 versus 1.31 +/- 0.43 microg/ml, respectively). After programmed electrical stimulation, 9 of 14 patients (64%), in whom four had implantable cardioverter defibrillator implantation, continued to receive quinidine. During a mean follow-up period of 31 months on quinidine, no side effects except one with diarrhea were observed (12.5%). There were no ventricular fibrillation recurrences in 3 of the 9 patients, who had frequent implantable cardioverter defibrillator discharges due to ventricular fibrillation attacks before treatment with quinidine. Low-dose quinidine has a potential as an adjunctive therapy for patients of the Brugada syndrome with frequent implantable cardioverter defibrillator discharges.

Adult↗
PubMed2004

Implantable cardioverter defibrillator therapy in postinfarction patients.

PURPOSE OF REVIEW: In the past few years, new clinical trials were conducted to determine the effectiveness of implantable cardioverter defibrillators (ICDs) for prevention of mortality in patients with ischemic and nonischemic cardiomyopathies. This paper aims to provide an overview of the current state of knowledge regarding ICD therapy in postinfarction patients. RECENT FINDINGS: Postinfarction patients with severe left ventricular dysfunction are at high risk of sudden cardiac death. Antiarrhythmic therapy does not improve survival in such patients and, therefore, ICDs emerged as treatment of choice for both primary and secondary prevention of mortality after MI. The MADIT (Multicenter Automatic Defibrillator Implantation Trial) and MUSTT (Multicenter Unsustained Tachycardia Trial) trials were the first primary prevention ICD trials documenting a substantial reduction in mortality with an ICD in postinfarction patients with depressed ejection fraction, nonsustained ventricular tachycardia, and inducible sustained ventricular tachycardia. The recently completed MADIT II trial broadened indications for prophylactic use of ICD in postinfarction patients with ejection fraction of 30% or less without a requirement for additional risk stratifiers. The benefit from ICD therapy in patients with low ejection fraction was recently confirmed by results from the SCD-HeFT (Sudden Cardiac Death in Heart Failure) and COMPANION (Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure) trials. SUMMARY: Recent clinical trials established ICD as an important therapeutic modality for primary and secondary prevention of mortality in postinfarction patients.

Death, Sudden, Cardiac↗
PubMed1989

Automatic implantable cardioverter defibrillator. Current status.

The automatic implantable cardioverter defibrillator was conceived by Mirowski as an implantable device for detection and termination of ventricular fibrillation. Since the initial human implant of the defibrillator in 1980, there has been a dramatic expansion of the clinical experience with more than 5000 implants. The technology of the device, which is now capable of sensing and terminating both ventricular tachycardia and fibrillation, has evolved rapidly. Although still not an ideal antiarrhythmic device, it has already had a major impact on arrhythmic mortality with a marked reduction in the sudden death rates in a high-risk patient population.

Arrhythmias, Cardiac↗