Home About us Contact
|
Home About us Contact | ||
|
|
||
Lethal Arrhythmia (lethal + arrhythmia)
Selected AbstractsAcute cardiorespiratory collapse from heparin: a consequence of heparin-induced thrombocytopeniaEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 5 2004Martha P. Mims Abstract: Background:, Heparin has rarely been reported to cause acute cardiorespiratory reactions or collapse. Some reports relate this to underlying heparin-induced thrombocytopenia. Objective:, To confirm and increase awareness of acute life-threatening cardiopulmonary events when patients with heparin-induced thrombocytopenia are re-exposed to heparin. Design:, Retrospective observational case series. Patients/setting:, Four cardiovascular surgery patients were identified in two adjacent large urban hospitals over a 2-yr-period who experienced eight episodes of cardiorespiratory collapse immediately following heparin administration. All had underlying heparin-induced thrombocytopenia. Results:, Intravenous boluses of unfractionated heparin were given to four patients with known or previously unrecognized heparin-induced thrombocytopenia. Two patients experienced severe respiratory distress within 15 min for which they required endotracheal intubation. Two other patients experienced cardiac arrest or a lethal arrhythmia within minutes of receiving intravenous heparin. Serologic tests for heparin-induced antibodies were positive in all patients. In three cases, the platelet count was normal or near normal but fell dramatically (71%) immediately following the heparin bolus. Three cases had prior diagnoses of heparin-induced thrombocytopenia, but health care workers administered heparin either unaware of the diagnosis or ignorant of its significance. No patients died, but all required some form of cardiopulmonary resuscitation and subsequent intensive care. Conclusions:, Heparin administration to patients with heparin-induced antibodies can result in life-threatening pulmonary or cardiac events. Appreciation of this phenomenon can unmask cases of heparin-induced thrombocytopenia and strengthens the mandate to avoid any heparin exposure in affected patients. Recognition is crucial to avoiding disastrous outcomes. [source] Is Defibrillation Testing Still Necessary?JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2008A Decision Analysis, Markov Model Objective: To assess the impact of defibrillation threshold (DFT) testing of implanted cardioverter-defibrillators (ICDs) on survival. Background: DFT testing is generally performed during implantation of ICDs to assess sensing and termination of ventricular fibrillation. It is common clinical practice to defibrillate ventricular fibrillation twice at an output at least 10 J below the maximum output of the device, providing a 10 J safety margin. However, there are few data regarding impact of DFT testing on outcomes. Methods: Decision analysis and Monte Carlo simulation were used to assess expected outcomes of DFT testing. Survival of a hypothetical cohort of patients was assessed according to two strategies,routine DFT testing at time of ICD implant versus no DFT testing. Assumptions in the model were varied over a range of reasonable values to assess outcomes under a variety of scenarios. Results: Five-year survival with DFT and no-DFT strategies were similar at 59.72% and 59.36%, respectively. The results were not sensitive to changing risk estimates for arrhythmia incidence and safety margin. Results of the Monte Carlo simulation were qualitatively similar to the base case scenario and consistent with a small and nonsignificant survival advantage with routine DFT testing. Conclusions: The impact of DFT testing on 5-year survival in ICD patients, if it exists, is small. Survival appears higher with DFT testing as long as annual risk of lethal arrhythmia or the risk of a narrow safety margin is at least 5%, although the incremental benefit is marginal and 95% confidence intervals cross zero. A prospective randomized study of DFT testing in modern devices is warranted. [source] Drug-Induced Torsades de Pointes and Implications for Drug DevelopmentJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2004Ph.D., ROBERT R. FENICHEL M.D. Torsades de pointes is a potentially lethal arrhythmia that occasionally appears as an adverse effect of pharmacotherapy. Recently developed understanding of the underlying electrophysiology allows better estimation of the drug-induced risks and explains the failures of older approaches through the surface ECG. This article expresses a consensus reached by an independent academic task force on the physiologic understanding of drug-induced repolarization changes, their preclinical and clinical evaluation, and the risk-to-benefit interpretation of drug-induced torsades de pointes. The consensus of the task force includes suggestions on how to evaluate the risk of torsades within drug development programs. Individual sections of the text discuss the techniques and limitations of methods directed at drug-related ion channel phenomena, investigations aimed at action potentials changes, preclinical studies of phenomena seen only in the whole (or nearly whole) heart, and interpretation of human ECGs obtained in clinical studies. The final section of the text discusses drug-induced torsades within the larger evaluation of drug-related risks and benefits. (J Cardiovasc Electrophysiol, Vol. 15, pp. 475-495, April 2004) [source] Heart rate variability , a therapeutic target?JOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 2 2002H. C. Routledge Reduced heart rate variability (HRV) is a powerful and independent predictor of an adverse prognosis in patients with heart disease and in the general population. The HRV is largely determined by vagally mediated beat to beat variability, conventionally known as respiratory sinus arrhythmia. Thus, HRV is primarily an indicator of cardiac vagal control. It is still unclear whether the relationship between measures of cardiac vagal control and mortality is causative or mere association. Possible mechanisms by which cardiac vagal activity might beneficially influence prognosis include a decrease in myocardial oxygen demand, a reduction in sympathetic activity and a decreased susceptibility of the ventricular myocardium to lethal arrhythmia. In animals, augmentation of cardiac vagal control by nerve stimulation or by drugs is associated with a reduction in sudden death in susceptible models. In humans a number of drugs which have been shown to reduce mortality and sudden death in large randomised trials can also be demonstrated to increase HRV. As a result of this evidence, it has been suggested that the effect of drugs or other therapeutic manoeuvres on HRV might be used to predict clinical efficacy. The use of HRV as a therapeutic target is discussed in this review. [source] | ||||||||||