Initial clinical experience with a fully automatic in-hospital external cardioverter defibrillator.

Sudden cardiac death due to ventricular tachyarrhythmia remains a significant problem in the in-hospital setting. Although the probability of survival is closely correlated with the rapidity of a response by qualified personnel, response times can be prolonged, even in specialized care units. In an effort to decrease response time, a fully automatic external cardioverter defibrillator was recently devised. This device was evaluated in the in-hospital setting to assess safety and efficacy. A total of 79 patients were studied in a multicenter trial. Patients were monitored with fully functional devices in the electrophysiology laboratory (51 patients) and in the cardiac care unit (28 patients). Performance of the device was assessed by comparing automatic responses to any sustained change in cardiac rhythm, either spontaneous or induced, to a retrospective review of stored ECG data and programmed parameters. During a total duration of 964 hours of monitoring, there were 99 episodes of sustained tachycardia. Therapy was appropriately delivered or advised in all episodes. Therapy was advised in one episode of supraventricular tachycardia. There were no episodes of inappropriate therapy delivery. There were no complications or adverse events. The device performed with a sensitivity of 100% and specificity of 98.8% with an average response time of 22 seconds. In conclusion, this automatic external defibrillator was safe, effective, and functioned as designed. Significant improvement in response time to life-threatening ventricular tachyarrhythmia in the in-hospital setting would be expected if this technology was widely adopted.

Multicenter comparison of truncated biphasic shocks and standard damped sine wave monophasic shocks for transthoracic ventricular defibrillation. Transthoracic Investigators.

BACKGROUND: The most important factor for improving out-of-hospital ventricular fibrillation survival rates is early defibrillation. This can be achieved if small, lightweight, inexpensive automatic external defibrillators are widely disseminated. Because automatic external defibrillator size and cost are directly affected by defibrillation waveform shape and because of the favorable experience with truncated biphasic waveforms in implantable cardioverter-defibrillators, we compared the efficacy of a truncated biphasic waveform with that of a standard damped sine monophasic waveform for transthoracic defibrillation. METHODS AND RESULTS: The principal goal of this multicenter, prospective, randomized, blinded study was to compare the first-shock transthoracic defibrillation efficacy of a 130-J truncated biphasic waveform with that of a standard 200-J monophasic damped sine wave pulse using anterior thoracic pads in the course of implantable cardioverter-defibrillator testing. Pad-pad ECGs were also examined after transthoracic defibrillation. After the elimination of data for 24 patients who did not meet all protocol criteria, the results from 294 patients were analyzed. The 130-J truncated biphasic pulse and the 200-J damped sine wave monophasic pulse resulted in first-shock efficacy rates of 86% and 86%, respectively (P = .97). ST-segment levels measured 10 seconds after the shock in 151 patients in sinus rhythm were -0.26 +/- 1.58 and -1.86 +/- 1.93 mm for the 130- and 200-J shocks, respectively (P < .0001). CONCLUSIONS: We found that 130-J biphasic truncated transthoracic shocks defibrillate as well as the 200-J monophasic damped sine wave shocks that are traditionally used in standard transthoracic defibrillators and result in fewer ECG abnormalities after the shock.

Long-term prognosis after myocardial infarction. Who is at risk for sudden death?

Patients who have survived myocardial infarction may be at risk for recurrent infarction or sudden death within the first year. Clinical factors that identify high-risk patients include the following: Poor left ventricular function Presence of spontaneous ventricular ectopy Abnormal signal-averaged electrocardiogram Decreased heart rate variability Exercise-induced depression of the ST segment Inducible ventricular tachyarrhythmia When these high-risk patients are identified, appropriate strategies (eg, use of antiarrhythmic agents or an implantable cardioverter-defibrillator) may improve outcome.

Reproducibility of programmed electrical stimulation responses in patients with ventricular tachycardia or fibrillation associated with coronary artery disease.

Invasive electrophysiologic studies were performed in 102 patients with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) using an aggressive programmed electrical stimulation (PES) protocol. The study was repeated after 2.0 +/- 2.9 days in all patients with no intercurrent changes in antiarrhythmic therapy. Patients with coronary artery disease (n = 72) were identified and PES results of these patients were analyzed and compared with results of patients without coronary artery disease. Multiple clinical and electrophysiologic factors were analyzed to determine any association with concordance of PES responses. No significant difference in concordance of PES responses was found in the 2 groups of patients. PES responses were groups into 3 categories: (1) noninducible, (2) nonsustained VT, and (3) sustained VT. Kappa values of PES responses of noninducible and sustained VT in both groups were higher and therefore the PES responses were more reproducible than nonsustained VT. The induction of sustained monomorphic VT was more reproducible than a PES response of nonsustained or sustained polymorphic VT. Inducible sustained VT with a rate of greater than or equal to 250 beats/min was less reproducible than induction of sustained VT with a rate less than 250 beats/min. Induction of VT by 3 extrastimuli was less reproducible than with any other mode. This short-term variability may account for false negatives associated with PES-directed antiarrhythmic therapy. Because of these findings, it is recommended that nonsustained VT and sustained polymorphic or rapid polymorphic VT should not be used as PES end points to guide antiarrhythmic therapy.

Concurrent myocardial and cerebral infarctions after intranasal cocaine use.

BACKGROUND AND PURPOSE: Cardiac and cerebrovascular complications associated with cocaine abuse have increasingly been reported, but concurrent development of cocaine-induced cardiac disease and stroke has rarely been reported. CASE DESCRIPTION: A 37-year-old man with a remote history of intravenous heroin and amphetamine use, cardiomyopathy, and recent cocaine use developed chest pain and ventricular tachycardia 30 minutes after intranasal cocaine hydrochloride use and jogging on a cold winter morning. Ventricular tachycardia was converted to atrial fibrillation. He was proven to have a small myocardial infarction. Within 6 hours of cocaine use he suffered a left hemisphere stroke. Cardiac electrophysiologic evaluation revealed inducible ventricular tachycardia. CONCLUSIONS: To our knowledge, this is the first report of concurrent myocardial infarction, life-threatening ventricular arrhythmias, and cerebral infarction temporally related to cocaine use. It is probable that one mechanism by which cocaine use causes stroke is to trigger expression of a known cardiac source of embolism.

Safety and efficacy of sotalol in patients with drug-refractory sustained ventricular tachyarrhythmias.

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)

Amiodarone in patients with previous drug-mediated torsade de pointes. Long-term safety and efficacy.

The safety and efficacy of long-term amiodarone therapy were examined in 12 patients who had previously developed torsade de pointes as a complication of previous antiarrhythmic therapy. The QTc intervals were determined at the time of torsade de pointes (570 +/- 40 ms), after 7 days of amiodarone loading (490 +/- 70 ms), and after 3 months of chronic amiodarone administration (580 +/- 80 ms). Compared to a drug-free control period, QTc was significantly prolonged (P less than 0.05) at the time of torsade de pointes, after amiodarone loading, and after 3 months of amiodarone therapy. The QTc intervals at the time of torsade de pointes and after chronic amiodarone treatment were not significantly different. At 16 +/- 7 months of follow-up, all patients remained free of subsequent torsade de pointes, syncope, or sudden death. In addition, 5 of 6 patients with a history of sustained ventricular tachycardia remained free from arrhythmic recurrence despite persistence of inducible ventricular tachycardia during programmed stimulation studies done before discharge. We conclude that amiodarone can often be used safely and effectively in patients who have previously had an episode of drug-mediated torsade de pointes. Amiodarone-induced QTc prolongation, even when marked, does not predict recurrent torsade de pointes. These observations also suggest that the propensity for a drug to produce this arrhythmia is dependent on other electrophysiologic effects in addition to its ability to simply lengthen repolarization.

Long-term arrhythmic outcome in survivors of ventricular fibrillation with absence of inducible ventricular tachycardia.

While programmed electrical stimulation of the heart is useful in directing therapy in cardiac arrest survivors who exhibit inducible ventricular tachycardia (VT), controversy exists as to the risk of recurrent ventricular fibrillation (VF) and need for antiarrhythmic therapy in patients without inducible VT during drug-free control programmed stimulation studies. In this study, the clinical features and arrhythmic outcome of 43 survivors of VF without inducible VT at control programmed stimulation were examined. In 38 patients, factors that may have played a potentiating role in the genesis of VF included ischemia in 15, proarrhythmia in 18, rapid rate response to atrial fibrillation in 3 and acute alcoholism in 2. Three patients required antiarrhythmic drugs for supraventricular tachyarrhythmia and 40 patients were discharged without antiarrhythmic therapy. At 32 +/- 21 months (range 1 to 82), 37 (92%) have remained free of arrhythmic recurrence while 3 have had sustained subsequent major arrhythmic events (syncope 1 patient, VF 1, sudden cardiac death 1). Thus, survivors of VF without inducible VT at drug-free control programmed stimulation are characterized by (1) potentiating factors--often identifiable and correctable--that may be important to the genesis of VF; (2) generally low risk of arrhythmic recurrence; and (3) effective long-term management often achieved without the use of additional antiarrhythmic drugs or antitachycardia/defibrillation devices.

Phrenic nerve conduction studies: a new technique and its application in quadriplegic patients.

Although a few reports of phrenic nerve stimulation have appeared over the past dozen years, electromyographers have not readily accepted these methods. Perhaps this is because the techniques are considered unreliable, or because there is a major element of patient discomfort. In this study a simple, safe, and relatively painless procedure was devised for placing a needle near the phrenic nerve for use as a stimulating electrode. Also, the positions of the recording electrodes were relocated until a site was found that consistently provided a response with an initial negative deflection in all subjects. Emphasis has been on improving technique. A group of 60 nerves in 30 normal subjects was studied. The mean latency was 7.44 +/- 0.59msec, and the mean difference between right and left was 0.08 +/- 0.42msec. A response was obtained in all nerves examined. In addition, 13 patients with quadriplegia due to spinal cord injury were studied. This method now permits reliable analysis of localized phrenic nerve lesions and abnormalities induced in either the phrenic nerve or diaphragm by generalized disease processes.