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Biomedical subjects

E V Platia

Publications and source records attributed to E V Platia.

At least 19 recordsLinked to original sources

Comparison of a novel rectilinear biphasic waveform with a damped sine wave monophasic waveform for transthoracic ventricular defibrillation. ZOLL Investigators.

OBJECTIVES: We compared the efficacy of a novel rectilinear biphasic waveform, consisting of a constant current first phase, with a damped sine wave monophasic waveform during transthoracic defibrillation. BACKGROUND: Multiple studies have shown that for endocardial defibrillation, biphasic waveforms have a greater efficacy than monophasic waveforms. More recently, a 130-J truncated exponential biphasic waveform was shown to have equivalent efficacy to a 200-J damped sine wave monophasic waveform for transthoracic ventricular defibrillation. However, the optimal type of biphasic waveform is unknown. METHODS: In this prospective, randomized, multicenter trial, 184 patients who underwent ventricular defibrillation were randomized to receive a 200-J damped sine wave monophasic or 120-J rectilinear biphasic shock. RESULTS: First-shock efficacy of the biphasic waveform was significantly greater than that of the monophasic waveform (99% vs. 93%, p = 0.05) and was achieved with nearly 60% less delivered current (14 +/- 1 vs. 33 +/- 7 A, p < 0.0001). Although the efficacy of the biphasic and monophasic waveforms was comparable in patients with an impedance < 70 ohms (100% [biphasic] vs. 95% [monophasic], p = NS), the biphasic waveform was significantly more effective in patients with an impedance > or = 70 ohms (99% [biphasic] vs. 86% [monophasic], p = 0.02). CONCLUSIONS: This study demonstrates a superior efficacy of rectilinear biphasic shocks as compared with monophasic shocks for transthoracic ventricular defibrillation, particularly in patients with a high transthoracic impedance. More important, biphasic shocks defibrillated with nearly 60% less current. The combination of increased efficacy and decreased current requirements suggests that biphasic shocks as compared with monophasic shocks are advantageous for transthoracic ventricular defibrillation.

Aged↗

Intravenous amiodarone for recurrent sustained hypotensive ventricular tachyarrhythmias. Intravenous Amiodarone Multicenter Trial Group.

OBJECTIVES: We sought to determine the response rate and safety of intravenous amiodarone in patients with ventricular tachyarrhythmias refractory to standard therapies. BACKGROUND: Numerous small retrospective reports suggest a response of refractory ventricular tachyarrhythmias to intravenous amiodarone, yet no controlled prospective trials exist. METHODS: Two hundred seventy-three patients with recurrent hypotensive ventricular tachyarrhythmias refractory to lidocaine, procainamide and bretylium were randomized to receive one of three doses of intravenous amiodarone: 525, 1,050 or 2,100 mg/24 h (mean [+/- SE] dose 743.7 +/- 418.7, 1,175.2 +/- 483.7, 1,921.2 +/- 688.8 mg, respectively) by continuous infusion over 24 h. RESULTS: Of the 273 patients, 110 (40.3% response rate) survived 24 h without another hypotensive ventricular tachyarrhythmic event while being treated with intravenous amiodarone as a single agent (primary end point). A significant difference in the time to first recurrence of ventricular tachyarrhythmia (post hoc analysis) over the first 12 h was observed when the combined 1,050- and 2,100-mg dose groups were compared with the 525-mg dose group (p = 0.046). The number of supplemental (150 mg) infusions of intravenous amiodarone (given for breakthrough destabilizing tachyarrhythmias) during hours 0 to 6 (prespecified secondary end point) was significantly greater in the 525-mg dose group than in the 2,100-mg dose group (1.09 +/- 1.57 vs. 0.51 +/- 0.97, p = 0.0043). However, there was no clear dose-response relation observed in this trial with respect to success rates (primary end point), time to first recurrence of tachyarrhythmia (post hoc analysis) or mortality (secondary end point) over 24 h. CONCLUSIONS: Intravenous amiodarone is a relatively safe therapy for ventricular tachyarrhythmias refractory to other medications.

Amiodarone↗

Dose-ranging study of intravenous amiodarone in patients with life-threatening ventricular tachyarrhythmias. The Intravenous Amiodarone Multicenter Investigators Group.

BACKGROUND: Oral amiodarone effectively suppresses ventricular arrhythmias; however, full activity may take days or weeks. In patients with frequent, life-threatening ventricular arrhythmias, this delay is not acceptable. Thus, in these patients, the speed and dosing accuracy of an intravenous formulation would be beneficial. The goal of this study was to demonstrate the efficacy of intravenous amiodarone in patients with refractory, recurrent hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation by determining a dose response among three regimens. METHODS AND RESULTS: A total of 342 patients were enrolled at 46 medical centers in the United States. Patients received one of three randomized, double-blind dose regimens delivering 125, 500, or 1000 mg during the first 24 hours. Supplemental infusions (150 mg) of intravenous amiodarone could be given to treat breakthrough ventricular arrhythmias. The key efficacy end points were the arrhythmia event rate, time to first arrhythmic event, and number of supplemental infusions administered. The event rate decreased with increasing doses: median values were 0.07, 0.04, and 0.02 events per hour for the 125-, 500-, and 1000-mg dose groups, respectively, representing a significant decrease from baseline event rates (P = .043), and approached significance in the overall test for trend (P = .067). There was a significant dose-related increase in the time to first event (trend test P = .025) and a significant dose-related decrease in the number of supplemental boluses per hour (trend test P = .043). Hypotension was the most common (26%) treatment-emergent adverse event during intravenous amiodarone therapy; there was no dose-response relationship. Seventy-eight percent of the patients survived to at least 48 hours. CONCLUSIONS: Intravenous amiodarone is effective for the treatment of recurrent, life-threatening ventricular tachyarrhythmias.

Amiodarone↗

Interaction of baseline characteristics with the hazard of encainide, flecainide, and moricizine therapy in patients with myocardial infarction. A possible explanation for increased mortality in the Cardiac Arrhythmia Suppression Trial (CAST).

BACKGROUND: The Cardiac Arrhythmia Suppression Trial (CAST) was designed to test the hypothesis that suppression of ventricular ectopy with antiarrhythmic drugs after a myocardial infarction reduces the incidence of sudden arrhythmic death. Patients in whom ventricular ectopy could be suppressed with encainide, flecainide, or moricizine were randomly assigned to receive either active drug or placebo. The encainide and flecainide arms of the study were discontinued in 1989 (CAST-I) and the moricizine arm in 1991 (CAST-II) because of excess mortality. To explore the mechanisms of these adverse outcomes, we examined the interaction of baseline characteristics with the hazard of therapy with encainide, flecainide, or moricizine compared with their respective placebos. METHODS AND RESULTS: CAST-I comprised 755 patients assigned to flecainide or encainide and 743 patients assigned to placebo, whereas in CAST-II, 502 patients received moricizine and 491 patients received placebo. Clinical and laboratory baseline variables of patients receiving active drug and those receiving placebo were similar. In CAST-I patients, there was a significant interaction of active therapy with both all-cause death/cardiac arrest and arrhythmic death/cardiac arrest for non-Q-wave myocardial infarction (total mortality hazard ratios, 1.8 versus 7.9 for Q-wave versus non-Q-wave infarction, P = .03). Ventricular premature depolarization (VPD) frequency > or = 50/h and heart rate > or = 74 beats per minute each interacted significantly with total mortality/cardiac arrest only. In the sicker CAST-II patients (ejection fraction < or = 40%), only diuretic use at baseline interacted significantly with moricizine use for both all-cause death/cardiac arrest and arrhythmic death/cardiac arrest (total mortality hazard ratios, 1.9 versus 0.7 for diuretic use versus no use, P = .01). CONCLUSIONS: Although active treatment in CAST-I was associated with greater mortality than placebo with respect to almost all baseline variables, the therapeutic hazard was more than expected in patients with non-Q-wave myocardial infarction and (for total mortality) frequent premature VPDs and higher heart rates, suggesting that the adverse effect of encainide or flecainide therapy is greater when ischemic and electrical instability are present. The relative hazard of therapy with moricizine in the sicker CAST-II population was greater in those using diuretics. Thus, although these drugs have the common ability to suppress ventricular ectopy after myocardial infarction, their detrimental effects on survival may be mediated by different mechanisms in different populations, emphasizing the complex, poorly understood hazards associated with antiarrhythmic drug treatment.

Arrhythmias, Cardiac↗

Automatic implantable cardioverter-defibrillator: is early implantation cost-effective?

The evaluation of survivors of sudden cardiac death with serial electrophysiologic studies involves a lengthy and expensive hospitalization, especially when an automatic implantable cardioverter-defibrillator is ultimately necessary. The cost efficacy of this conventional approach was therefore compared with direct implantation of a cardioverter-defibrillator after the first electrophysiologic study. Thirty-two survivors of sudden death who had inducible ventricular tachycardia during their initial electrophysiologic study underwent serial drug trials. At discharge 12 (37%) were taking an antiarrhythmic drug found to prevent induction of ventricular tachycardia and 20 underwent cardioverter-defibrillator implantation after serial drug trials proved ineffective. The average length of hospitalization for this group that had undergone serial drug testing was 20.2 +/- 9.3 days at an average cost of $48,900 +/- $31,600. Seven survivors of sudden death had no inducible ventricular tachycardia during their initial electrophysiologic study and underwent direct cardioverter-defibrillator implantation. Their average length of hospitalization was 12.6 +/- 6.2 days at an average cost of $40,400 +/- $8,300. It is concluded that automatic implantable cardioverter-defibrillator implantation as an early intervention is not more costly and indeed may be cost-effective compared with therapy guided by serial electrophysiologic testing. As antitachycardia devices become more versatile, long lived and easier to implant, earlier implantation is likely to compare even more favorably with drug therapy.

Anti-Arrhythmia Agents↗

Esmolol versus verapamil in the acute treatment of atrial fibrillation or atrial flutter.

The effects of esmolol, an ultrashort-acting beta blocker, and verapamil were compared in controlling ventricular response in 45 patients with atrial fibrillation or atrial flutter, in a randomized, parallel, open-label study. Patients with either new onset (less than 48 hours, n = 31) or old onset (greater than 48 hours, n = 14) of atrial fibrillation or flutter with rapid ventricular rate were stratified to receive esmolol (n = 21) or verapamil (n = 24). Drug efficacy was measured by ventricular rate reduction and conversion to sinus rhythm. The heart rate declined with esmolol from 139 to 100 beats/min (p less than 0.001) and with verapamil from 142 to 97 beats/min (p less than 0.001). Fifty percent of esmolol-treated patients with new onset of arrhythmias converted to sinus rhythm, whereas only 12% of those who received verapamil converted (p less than 0.03). Mild hypotension was observed in both treatment groups. Esmolol compares favorably with verapamil with respect to both efficacy and safety in acutely decreasing ventricular response during atrial fibrillation or flutter. Moreover, conversion to sinus rhythm is significantly more likely with esmolol.

Adrenergic beta-Antagonists↗

Intravenous diltiazem for termination of reentrant supraventricular tachycardia: a placebo-controlled, randomized, double-blind, multicenter study.

To assess the efficacy and safety of intravenous diltiazem, 54 patients with inducible sustained supraventricular tachycardia received diltiazem, 0.25 mg/kg or 0.25 mg/kg, followed by 0.35 mg/kg body weight, or placebo in a double-blind, randomized study. Twenty patients had atrioventricular (AV) node reentrant tachycardia, whereas 34 had orthodromic AV reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. Supraventricular tachycardia was terminated in 24 (86%) of 28 patients given intravenous diltiazem compared with 5 (19%) of 26 given placebo (p = 0.0000014). Nineteen (95%) of 20 patients initially given placebo had termination of supraventricular tachycardia after receiving diltiazem. Overall, 43 (90%) of 48 patients receiving intravenous diltiazem had conversion of supraventricular tachycardia to sinus rhythm; the median time to tachycardia termination was 2 min after initiation of a 2 min diltiazem infusion. All 20 patients (100%) with AV node reentrant tachycardia treated with diltiazem had conversion of tachycardia to sinus rhythm as did 26 (81%) of 30 patients with AV reciprocating tachycardia treated with diltiazem. Diltiazem prolonged refractoriness and slowed conduction of the AV node and thereby provided antiarrhythmic action to cause tachycardia termination. Diltiazem had no effect on the electrophysiologic properties of accessory AV connections. Adverse effects were seen in 3 (6%) of the 48 patients given diltiazem. For paroxysmal supraventricular tachycardia initiated in the electrophysiology laboratory, it is concluded that intravenous diltiazem is safe and very effective for acute tachycardia termination when the AV node is part of the reentrant circuit.

Adolescent↗

Immediate quantitation of antiarrhythmic drug effect by monophasic action potential recording in coronary artery disease.

A contact electrode catheter, which permits clinical recording of cardiac monophasic action potentials (MAPs), was used as a means of quantifying the electrophysiologic effect of 2 antiarrhythmic drugs, procainamide and quinidine. MAP recordings were made in continuous fashion from the right ventricle in 16 patients, before and after the intravenous administration of procainamide (11 patients) or quinidine (5). Increases in the MAP duration at 90% repolarization (MAPD90) were used as indexes of drug effect and related to plasma drug level. Surface electrocardiographic (QRS duration, corrected QT interval [QTC]) and electrophysiologic (ventricular effective refractory period) measurements, in addition to MAPD90, were made at the same time as blood sampling for plasma drug level determination. Dose response curves, plotting change in MAPD90 versus plasma drug level, showed strong linear correlation for both procainamide (p less than 0.0001) and quinidine (p less than 0.0001). The variance (error of estimation) of the predictive relation, change in MAPD90 versus plasma drug level, was significantly lower than that of change in QTC (p less than 0.001), QRS duration (p less than 0.0001) or ventricular effective refractory period (p less than 0.0001) versus plasma drug level for both procainamide and quinidine. Changes in MAP duration closely correlate with plasma drug level, and as such, may serve as an immediate, quantitative indicator of myocardial drug effect during the administration of antiarrhythmic agents.

Action Potentials↗

Reuse of pacing catheters: a survey of safety and efficacy.

We surveyed 12 medical centers with regard to the reuse of pacing catheters during electrophysiologic studies. The prevalence of superficial skin infections or bacteremia related to EP studies was extremely low, and was not significantly different in the catheter reuse group compared to the single use group. We conclude that catheter resterilization and reuse is safe and cost-effective.

Cardiac Catheterization↗

Refractory symptomatic ventricular tachycardia and ventricular fibrillation in elderly patients.

The problem of refractory life-threatening ventricular tachyarrhythmias in elderly patients has not been previously studied. To determine if clinical, anatomic, or electrophysiologic variables and prognosis are significantly different in elderly subjects, 49 elderly (68 to 84 years) and 44 younger (44 to 53 years) survivors of refractory symptomatic ventricular tachycardia and/or ventricular fibrillation secondary to coronary artery disease were studied. Elderly patients displayed more extensive anatomic coronary artery disease, with 80 percent having three-vessel disease in comparison with 30 percent of the younger patients (p less than 0.001). Prior myocardial infarction, heart failure, and cardiomegaly were more common in the elderly group (p less than 0.01, p less than 0.001, and p less than 0.034, respectively), whereas angina was more common in the younger group (p less than 0.001). In 55 percent of the elderly patients and 58 percent of the younger patients, electrophysiologic testing demonstrated inducible sustained ventricular tachycardia that required treatment with an investigative antiarrhythmic drug and/or cardiac surgery, including implantation of an automatic defibrillator. Elderly patients tolerated aggressive evaluation as well as did younger patients, and despite the difference in clinical and anatomic findings, long-term survival curves were similar, although the probability of survival at 20 months was 62 percent in the elderly and 80 percent in the younger patients. This difference in early survival is explained by eight surgical deaths in the elderly group, compared with two in the younger group.

Age Factors↗

Treatment of malignant ventricular arrhythmias with endocardial resection and implantation of the automatic cardioverter-defibrillator.

Although ventricular resection guided by endocardial mapping has been a successful treatment for drug-refractory ventricular arrhythmias, 20 to 30 percent of patients still have postoperative sustained ventricular tachycardia or sudden death. To improve the outcome of the procedure, we implanted an automatic cardioverter-defibrillator in conjunction with endocardial resection in 28 patients, all of whom had had previous myocardial infarctions and between one and five cardiac arrests. There were three perioperative deaths. During follow-up of 8 to 51 months (mean, 25), 4 of the 25 survivors had recurrences of hypotensive ventricular tachycardia, which in all instances were automatically terminated by the implanted device. One patient, whose automatic cardioverter-defibrillator was not functional, died suddenly. We conclude that patients undergoing mapping-directed endocardial resection can be provided with additional protection against recurrent ventricular tachyarrhythmias or sudden death by implantation of an automatic cardioverter-defibrillator.

Adult↗

De novo refractory ventricular tachyarrhythmias after coronary revascularization.

Twelve of 1,675 patients who underwent coronary artery bypass grafting during a 2.5-year period had new onset, recurrent, sustained ventricular tachyarrhythmia a mean of 27 days (range 2 to 150) postoperatively. No patient had an intra- or perioperative myocardial infarction and all patients were hemodynamically stable and had normal metabolic and electrolytic indexes at the time of ventricular tachyarrhythmia. Preoperative ejection fraction was 39 +/- 10% (mean +/- standard deviation) and all patients had Lown grade II or less ventricular ectopic activity on ambulatory monitoring. Postoperative angiography demonstrated occluded saphenous vein grafts in 3 of 7 patients studied, none of whom had symptoms suggestive of myocardial ischemia. Treatment with conventional antiarrhythmic therapy was unsuccessful in all but 1 patient, and 10 patients were treated with amiodarone and 1 patient with propafenone. Four of these patients also received an automatic implantable defibrillator. Thus, de novo ventricular tachyarrhythmia can occur unexpectedly after coronary artery bypass grafting and may be the result of several factors related to either subclinical graft occlusion or increased dispersion of repolarization secondary to reperfusion.

Aged↗

Time course of transvenous pacemaker stimulation impedance, capture threshold, and electrogram amplitude.

To examine the time course of atrial and ventricular stimulation impedance, capture threshold, and electrogram amplitude, we obtained noninvasive telemetric data in 63 patients who underwent implantation of unipolar, endocardial pacing leads and a second-generation dual chamber pacemaker with expanded bidirectional telemetry, including stimulation impedance, endocardial electrograms, and automatic capture threshold determination. On follow-up of 9-20 months (mean, 15 months), all but six patients continued to pace in the DDD mode. To validate measurements made with telemetry, invasive measurements made directly with a pacing system analyzer at time of implant were compared with immediate postimplant telemetric measurements. Significant correlation of acute stimulation impedance was noted in both atrial (r = .7, p less than .001) and ventricular (r = .8, p less than .001) lead systems. The atrial stimulation impedance decreased from 538 ohms at implant to 471 ohms at 13 months (p less than .01); the ventricular stimulation impedance similarly declined from 545 ohms to 485 ohms at 13 months (p less than .01). Capture thresholds peaked at one month, then declined: atrial, 1.2 V at implant vs 2.2 V at 1 month (p less than .008) and 1.4 V at 13 months; ventricular, 1.1 V at implant vs 1.9 V at 1 month (p less than .001) and 1.3 V at 13 months. There were no significant changes noted in atrial or ventricular electrogram amplitude following implantation. We conclude that there is close correlation of invasive recordings with those made telemetrically with this pacemaker at time of implant.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

The characterization of human transmyocardial impedance during implantation of the automatic internal cardioverter defibrillator.

We set out to determine in a prospective fashion the characteristics of energy delivery related to defibrillation in a population of patients receiving the AICD. Specifically, we examined the characteristics of the delivered current, transmyocardial voltage, and transmyocardial impedance. Secondly, we determined the relationship between the energy delivered, the impedance encountered and the defibrillation threshold. Since the AICD will deliver a succession of shocks if the initial shock does not cardiovert, the effects of consecutive shocks at different energy levels on the transmyocardial impedance were also assessed.

Cardiac Surgical Procedures↗

The use of ambulatory monitoring in the prognostic evaluation of patients with sustained ventricular tachycardia treated with amiodarone.

We recently reported a retrospective experience with serial Holter monitoring as a guide to therapy in patients with sustained ventricular tachycardia treated with amiodarone. To confirm and substantiate these findings, a prospective study was designed that included baseline 24 hr Holter monitoring and serial Holter monitoring after 1 week of therapy with amiodarone. Fifty-two patients with documented sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring were treated with amiodarone. Thirty-four patients (group I) had nonsustained ventricular tachycardia completely suppressed and 18 patients (group II) had continued nonsustained ventricular tachycardia on serial Holter monitoring performed on days 8, 9, and 10 of therapy. At 11.6 +/- 1.0 (mean +/- SE) months follow-up, three (9%) group I patients and 12 (67%) group II patients had recurrent sustained ventricular tachycardia or sudden cardiac death (p less than .01). The sensitivity, specificity, positive and negative predictive value, and predictive accuracy of ventricular tachycardia on 24, 48, and 72 hr Holter monitoring over days 8, 9, and 10 for predicting recurrent sustained ventricular tachycardia or sudden cardiac death were analyzed. The positive and negative predictive values were 89% and 84%, 69% and 89%, and 67% and 91% for 24, 48, and 72 hr Holter monitoring, respectively. Overall predictive accuracy was 85%, 83%, and 83%, respectively. We conclude that early Holter monitoring is useful in assessing the clinical efficacy of amiodarone in patients with sustained ventricular tachycardia who manifest nonsustained ventricular tachycardia on baseline Holter monitoring.

Amiodarone↗

Ambulatory electrocardiographic recordings at the time of fatal cardiac arrest.

The relation between arrhythmias at cardiac arrest and the outcome of arrest is poorly understood. The Holter monitor tracings of 13 patients were reviewed after they sustained an in-hospital cardiac arrest during ambulatory electrocardiographic monitoring. All had a prior cardiac arrest or cardiac syncope. Twelve patients had ventricular tachycardia (VT) as their initial arrest arrhythmia and 1 patient had bradycardia followed by ventricular fibrillation (VF). VT degenerated to VF in 10 of 12 patients after a mean interval of 96 +/- 31 seconds (+/- standard error of the mean). The number of VT runs increased significantly during the hour immediately preceding arrest (p = 0.004). Despite prompt resuscitation efforts in 12 patients, only 6 survived. The 6 survivors and 6 nonsurvivors were not different with regard to age, ejection fraction, extent of coronary artery narrowing and time to first defibrillation. However, degeneration to VF within 30 seconds of arrest (5 of 6 nonsurvivors and 1 of 6 survivors, p = 0.04) and a slower rate of VT at the onset of arrest (166 beats/min in nonsurvivors and 227 beats/min in survivors, p = 0.02) were associated with unsuccessful resuscitation.

Adult↗