Variability in the Measurement of Human Ventricular Refractoriness

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72916/1/j.1540-8159.1991.tb02885.x.pd

Management of Nonsustained Ventricular Tachycardia Guided By Electrophysiological Testing

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73206/1/j.1540-8159.1993.tb04578.x.pd

Comparison of Ventricular Refractory Periods Determined by Incremental and Decremental Scanning of an Extrastimulus

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73345/1/j.1540-8159.1989.tb02699.x.pd

Acute changes in pacing threshold and R- or P-wave amplitude during permanent pacemaker implantation

This study examines the changes in pacing threshold and R- or P-wave amplitude during the first 30 minutes after implantation of tined and screw-in leads. The leads examined were those of 1 manufacturer (Medtronic) and consisted of 3 ventricular pacing leads (model numbers 6957 unipolar screwin [11 patients], 6961 unipolar tined [12 patients] and 6962 bipolar tined [7 patients]) and 1 atrial lead (model number 6957J unipolar screw-in [10 patients]). After optimal lead position was obtained fluoroscopically in the right ventricular apex or right atrium, the pacing threshold and R- or P-wave amplitudes were measured at 5-minute intervals for 30 minutes.The acute ventricular pacing threshold with the screw-in lead was significantly higher than with the tined lead (0.84 +/- 0.17 vs 0.58 +/- 0.15 volts; p < 0.001). There was a significant (p < 0.001) acute decrease in the ventricular pacing threshold with both lead types, with the maximum decrease occurring 5 minutes after lead implantation. There was a significant acute increase in R-wave size with the ventricular screw-in lead that peaked 20 minutes after lead implantation (11.9 +/- 3.0 to 14.7 +/- 4.1 mV; p < 0.001). The atrial screw-in lead behaved in a manner identical to its counterpart in the ventricle. In conclusion, there are acute changes in the pacing threshold and R- or P-wave amplitude obtained with tined and screw-in pacing leads. In some patients, a pacing threshold or R- or P-wave amplitude that is initially unacceptable may improve to an acceptable level over 15 to 20 minutes without further lead manipulation, especially when an atrial screw-in lead is used.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28618/1/0000430.pd

Electrophysiologic effects and efficacy of recainam for sustained ventricular tachycardia

Recainam is an investigational antiarrhythmic drug recently introduced into clinical testing. It is a phenylalkyl urea derivative that produces a concentrationdependent decrease in membrane responsiveness and maximal upstroke velocity.1 The reduction in maximal upstroke velocity displays use-dependence,1 similar to the class 1A drugs. However, unlike class 1A drugs, but similar to class 1B agents, recainam does not prolong action potential duration.1 Other studies demonstrated that recainam slows conduction with minimal effect on ventricular refractoriness,2 effects consistent with a class 1C antiarrhythmic action. Thus, these preliminary investigations suggested that recainam possesses a unique electrophysiologic profile with properties of each of the 3 class 1 subclasses. Other preclinical studies have demonstrated recainam's efficacy in suppressing ventricular arrhythmias in the postinfarction dog model3 and initial clinical studies have demonstrated that it is highly effective in suppressing ventricular premature complexes.4-6 However, no studies to date have reported the electrophysiologic effects of recainam in patients with sustained ventricular tachycardia (VT). Such is the purpose of this report.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28136/1/0000587.pd

Effects of epinephrine in patients with an accessory atrioventricular connection treated with quinidine

The purpose of this study was to determine whether physiologic doses of epinephrine reverse the electrophysiologic effects of quinidine in patients with an accessory atrioventricular (AV) connection. Eighteen patients with an accessory AV connection who had inducible sustained orthodromic tachycardia underwent an electrophysiologic study in the baseline state and after at least 2 days of treatment with 1.4 to 1.9 g/day of quinidine gluconate. The effects of epinephrine were then determined. Epinephrine infusion rates of 25 and 50 ng/ kg/min were used in 9 patients each because these doses of epinephrine previously have been demonstrated to result in elevated plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. Quinidine prolonged refractoriness in the atrium and accessory AV connection and slowed conduction through the accessory AV connection. These effects were partially or completely reversed by epinephrine. Among 8 patients in whom quinidine resulted in orthodromic tachycardia becoming noninducible or nonsustained, sustained tachycardia became inducible again in 5 patients after infusion of epinephrine. After quinidine, atrial fibrillation was either non-inducible or nonsustained in 8 patients; however, sustained atrial fibrillation could be induced in 4 of these patients after infusion of epinephrine. The results of this study demonstrate that the therapeutic effect of quinidine in patients who have an accessory AV connection are often reversed by physiologic increases in circulating epinephrine.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27138/1/0000131.pd

Results of electrophysiologic testing and long-term prognosis in patients with coronary artery disease and aborted sudden death

The purpose of this study was to evaluate the results of electrophysiologic testing and the long-term prognosis of 56 patients with coronary artery disease who presented with aborted sudden death unrelated to acute myocardial infarction. The mean age of the patients was 62 +/- 8 years (+/- standard deviation) and 48 were men. The mean left ventricular ejection fraction was 0.34 +/- 0.16. During the baseline electrophysiology test, sustained monomorphic ventricular tachycardia (VT) was inducible in 22 patients who then underwent electropharmacologic testing: 11 patients were treated with antiarrhythmic drugs that suppressed the induction of VT or resulted in the VT becoming hemodynamically stable; 10 patients who failed drug testing received an automatic implantable cardioverter/defibrillator (AICD); one patient underwent endocardial resection. Among 34 patients who did not have inducible sustained VT, a precipitant of cardiac arrest (severe ischemia, proarrhythmia) was identified and was corrected in 9 of 34. An AICD was recommended in the remaining 25 patients; however, nine patients refused and were treated empirically with antiarrhythmic drugs. The mean follow-up was 22 +/- 12 months. The 2-year actuarial incidence of sudden death was 31% in patients who were treated with drugs based on the results of electropharmacologic testing, 26% in patients who were treated with antiarrhythmic drugs on an empiric basis, 0% among patients in whom a correctable etiology for the cardiac arrest was identified, and 9% among patients who underwent implantation of an AICD. The 3-year actuarial incidence of sudden death among the 20 patients treated with antiarrhythmic drugs was 53%, compared with 9% among the 26 patients who underwent AICD implantation (p = 0.03). In conclusion, antiarrhythmic therapy, whether guided by electrophysiologic testing or administered on an empiric basis, is associated with a high incidence of recurrent sudden death in patients with coronary artery disease and aborted sudden death. Implantation of an AICD may be advisable in all patients with coronary artery disease and aborted sudden death in whom a correctable precipitant cannot be identified.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/29118/1/0000157.pd

Comparison of the results of electrophysiologic testing after short-term and long-term treatment with amiodarone in patients with ventricular tachycardia

The results of electrophysiologic testing after short-term and long-term treatment with amiodarone were compared in 71 patients with ventricular tachycardia. Electrophysiologic testing was performed in the baseline state after 11 +/- 3 days of treatment with 1.2 to 2.4 gm/day of amiodarone, and after 13 +/- 4 weeks of therapy with a daily amiodarone dose of 400 mg. After short-term therapy, 62% of the patients had an adequate response to amiodarone. In 27 patients who were hemodynamically unstable, ventricular tachycardia was induced and became noninducible or hemodynamically stable after combination therapy with a class I agent. Among 18 patients who did not have inducible ventricular tachycardia after short-term therapy, eight (44%) had inducible, hemodynamically unstable ventricular tachycardia after long-term treatment with amiodarone. On the other hand, six of the 27 patients who had hemodynamically unstable ventricular tachycardia after short-term therapy had an adequate response after long-term treatment with amiodarone. Therefore an adequate electrophysiologic response after short-term therapy does not guarantee a similar response after long-term treatment, and an inadequate response after short-term therapy does not always predict a similar response after long-term therapy.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/29669/1/0000758.pd

Pharmacodynamics of intravenous procainamide as used during acute electropharmacologic testing

No previous studies have determined the pharmacodynamics of intravenous procainamide when administered in a dose of 15 mg/kg and at a rate of 50 mg/min, as is common practice during etectropharmacologic testing. In this study, 30 patients received procainamide in this fashion; the right ventricular effective refractory period and the QRS duration at a ventricular pacing rate of 120/minute were then determined every minute for 20 minutes. Ten patients received no maintenance infusion of procainamide (group A), 10 received a 4 [mu]g/min maintenance infusion (group B) and 10 received an 8 mg/min maintenance infusion (group C). Ten additional patients received no procainamide and served as control subjects (group D). The plasma procainamide concentration was measured at 1, 5, 10,15 and 20 minutes after the loading dose was administered. A stable plasma procainamide concentration was not present in group A, B, or C until 15 minutes after infusion of the loading dose. The effective refractory period and QRS duration increased compared with baseline at 1 minute, decreased between 1 and 10 minutes and then remained essentially unchanged between 10 and 20 minutes in all 3 treatment groups. Concentration-effect relation was linear in each treatment group. The plasma procainamide concentrations in group C were significantly greater than in group A; however, the effects on refractoriness and QRS duration were similar in both groups. These findings indicate that with a procainamide dosing method commonly used during electropharmacologic testing, the plasma procainamide concentration decreases significantly during the first 15 minutes after the loading dose is administered; the effects of procainamide on ventricular refractoriness and conduction parallel the changes in the plasma procainamide concentration; and an 8 mg/min maintenance infusion of procainamide results in higher plasma procainamide concentrations without an associated increase in ventricular refractoriness or slowing of conduction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27475/1/0000517.pd

Hospital Performance Trends on National Quality Measures and the Association With Joint Commission Accreditation

BackgroundEvaluations of the impact of hospital accreditation have been previously hampered by the lack of nationally standardized data. One way to assess this impact is to compare accreditation status with other evidence-based measures of quality, such as the process measures now publicly reported by The Joint Commission and the Centers for Medicare and Medicaid Services (CMS).ObjectivesTo examine the association between Joint Commission accreditation status and both absolute measures of, and trends in, hospital performance on publicly reported quality measures for common diseases.Design, setting, and patientsPerformance data for 2004 and 2008 from U.S. acute care and critical access hospitals were obtained using publicly available CMS Hospital Compare data augmented with Joint Commission performance data.MeasurementsChanges in hospital performance between 2004 and 2008, and percent of hospitals with 2008 performance exceeding 90% for 16 measures of quality-of-care and 4 summary scores.ResultsHospitals accredited by The Joint Commission tended to have better baseline performance in 2004 than non-accredited hospitals. Accredited hospitals had larger gains over time, and were significantly more likely to have high performance in 2008 on 13 out of 16 standardized clinical performance measures and all summary scores.ConclusionsWhile Joint Commission-accredited hospitals already outperformed non-accredited hospitals on publicly reported quality measures in the early days of public reporting, these differences became significantly more pronounced over 5 years of observation. Future research should examine whether accreditation actually promotes improved performance or is a marker for other hospital characteristics associated with such performance. Journal of Hospital Medicine 2011;6:458-465. © 2011 Society of Hospital Medicine