Can we assess the efficacy of therapy in neurocardiogenic syncope?
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Biomedical subjects
Publications and source records attributed to J S Sra.
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BACKGROUND: The long-term efficacy of atrial fibrillation (AF) detection and R-wave synchronization are critical safety requirements for the development of an implantable atrial defibrillator (IAD) for treatment of AF. METHODS AND RESULTS: The long-term efficacy of the Metrix IAD for AF detection and R-wave synchronization was tested in 51 patients. The mean duration of follow-up was 259+/-138 days (72 to 613 days). AF detection tests were performed 2240 times during observed operation with 100% specificity and 92.3% sensitivity for differentiation between sinus rhythm and AF; 2219 episodes and their electrograms stored in the device during AF detection were analyzed. The positive predictive value of the AF detection algorithm was 97.4% (lower 95% confidence limit [CL], 94.5%) in the out-of-hospital setting. A total of 242 435 R waves were analyzed for R-wave synchronization. Of these, 49% were marked for synchronized shock delivery, 82% of sinus rhythm and 36% of AF R waves, respectively. All shock markers were properly synchronized and within the R wave (overall synchronization accuracy, 100%; lower 95% CL, 99.999%). Overall, 3719 shocks have been delivered via the IAD with no instance of unsynchronized shock delivery or any episode of proarrhythmia. The observed proarrhythmic risk was 0%, with an estimated maximum proarrhythmic risk of 0.084% per shock (95% upper CL). CONCLUSIONS: The Metrix IAD can appropriately detect AF with a high specificity and sensitivity and reliably synchronize within a suitable R wave for shock delivery to minimize the risk of ventricular proarrhythmia.
The effect of initial phase polarity on the DFT of two pectorally implanted biphasic ICDs was tested in a randomized, prospective manner at the time of implantation. Twenty-two consecutive patients with VT-VF who received either the Medtronic PCD 7219C Jewel device (10 patients) or PCD 7219D Jewel device (12 patients) were studied. DFT testing was performed in a standard step-down manner. Both initial phase polarities--initial defibrillation current flowing from active can/SVC coil +/- subcutaneous patch) to the RV coil (RV coil to active can/SVC (RV+)--were tested in random order. The mean DFT achieved with RV+ compared with RV-was lower for the 7219C patient group (6.6 +/- 3.1 vs 10.8 +/- 5.5 J; P = 0.007). A similar trend was observed for the 7219D group, though the difference did not reach statistical significance (12.0 +/ 4.0 vs 16.3 +/- 7.3 J; P = 0.07). Seven of the 10 patients in the 7219C group had a lower DFT with RV+, while the initial phase polarity made no difference in 3. In the 7219D group, 7 patients had a lower DFT using RV+, 2 patients had a lower DFT using RV-, and the initial phase polarity made no difference in 3. In conclusion, this study demonstrates that changing the polarity of the initial phase of a biphasic shock waveform can have a significant impact on the DFT achieved at the time of ICD implantation.
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OBJECTIVES: This study assessed the feasibility of detecting atrial fibrillation (AF) and delivery of appropriately timed R wave shocks using an implantable atrial defibrillator. BACKGROUND: For atrial defibrillation therapy to be feasible in an implantable form, AF must be detected in a specific fashion, and the risk of ventricular proarrhythmia should be minimized. METHODS: Eleven patients with AF underwent testing with an implantable atrial defibrillator (METRIX 3000 Automatic Atrial Defibrillator, InControl, Inc.). Wideband electrograms (EGMs) were recorded from the right ventricular (RV) bipolar catheter and from the multipolar catheters located in the right atrium (RA) and coronary sinus (CS). Atrial fibrillation detection was performed using two serial algorithms-quiet interval analysis and baseline crossing analysis-that detect atrial activity on the RA-CS channel. Ventricular sensing using a minimal preceding synchronization interval of 500 ms as a criterion for synchronous shock delivery was performed from filtered RV and RV-CS EGMs. RESULTS: The AF detection algorithms were applied to 53 AF data segments and 18 normal sinus rhythm data segments. Atrial fibrillation was detected appropriately in 49 instances, and the specificity for detecting AF and normal sinus rhythm was 100%. Synchronization criterion efficacy was assessed by delivering shock markers and shocks. Of the 2,025 R waves processed, 557 (27.5%) were marked as suitable for shock delivery. In addition, 69 therapeutic and 11 test shocks were delivered during AF. All shock markers and shocks were delivered synchronously with the R wave, and the synchronization criterion was never violated. CONCLUSIONS: Atrial fibrillation can be detected in a specific fashion using the RA-CS lead configuration and serial detection algorithms for atrial sensing. The delivery of properly timed shocks is feasible and should minimize the risk of ventricular proarrhythmia.
BACKGROUND: Head-up tilt test is increasingly being used to evaluate patients with syncope. This study was designed to evaluate the specificity of head-up tilt testing using different tilt angles and isoproterenol infusion doses in normal volunteers with no prior history of syncope or presyncope. METHODS AND RESULTS: One hundred fifty volunteers were randomized to two groups of 75 each. In group 1, subjects were further randomized to have head-up tilt testing at a 60, 70, or 80 degree angle at baseline followed by repeat tilt testing during a low-dose isoproterenol infusion that increased the heart rate by an average of 20%. In group 2, after having a baseline head-up tilt test at a 70 degree angle for a maximum of 20 minutes, subjects were randomized to have a repeat tilt table testing at a 70 degree angle during a low-dose, 3 micrograms/min, or 5 micrograms/min isoproterenol infusion. In group 1, syncope or presyncope along with hypotension developed in 2 subjects during the baseline test at 60 and 70 degrees of tilt and in 5 subjects during tilting at 80 degrees. The addition of low-dose isoproterenol reduced the specificity minimally from 92% to 88% at both 60 and 70 degrees of tilt but substantially to 60% at an 80 degrees angle. However, 6 of the 10 subjects with a positive test at an 80 degree angle had an abnormal response after 10 minutes of tilt testing. In group 2, using various isoproterenol doses with tilt table testing at a 70 degree angle, low-dose (mean infusion dose, 1.5 +/- 0.45 microgram/min), 3 micrograms/min, and 5 micrograms/min isoproterenol infusions elicited an abnormal response in 1 (4%), 5 (20%), and 14 (56%) of the subjects, respectively. Using multiple logistic regression analysis, head-up tilt testing at an 80 degree angle (P = .01) or during 3 micrograms/min (P = .02) and 5 micrograms/min isoproterenol infusion rates (P < .001) was the most significant predictor of an abnormal response. CONCLUSIONS: Head-up tilt testing at a 60 or 70 degree angle with or without low-dose isoproterenol infusion provides an adequate specificity. Caution is needed, however, in interpreting the results if the head-up tilt test at 80 degrees is extended beyond 10 minutes or if high doses of isoproterenol are used.
Implantable cardioverter defibrillators have an established role in the management of life-threatening tachyarrhythmias. These devices use sophisticated sensing circuitry to detect and promptly treat a vast majority of these arrhythmias. However, they are not foolproof. We report one case where the device failed to sense every other QRS complex during induced ventricular fibrillation due to marked electrical alterans. Thus, undersensing can be a potentially fatal problem despite the use of auto adjustable gain.
Head-up tilt testing is increasingly being used as a diagnostic modality in patients with unexplained syncope who are thought to have neurocardiogenic (vasovagal) mechanisms of syncope. Although large-scale placebo-controlled trials are still awaited, pharmacologic therapy is usually effective in preventing syncope or presyncope in this patient population. However, the role of permanent pacemaker therapy remains controversial. Because hypotension is usually associated with paradoxical bradycardia and occasionally asystole, it has been argued that permanent pacemaker therapy may be useful in preventing syncope and, thus, injury, in the so-called "malignant vasovagal cardioinhibitory response" in which the onset of syncope is thought to be abrupt. The onset of hypotension, however, usually precedes bradycardia during neurocardiogenic syncope, and pacing may thus not prevent syncope or presyncope in these patients. The role of cardiac pacing in patients with neurocardiogenic syncope is reviewed.
Changes in heart rate, arterial pressure, norepinephrine and epinephrine levels were compared in 19 consecutive patients (10 men and 9 women, mean age 46 +/- 16 years) with neurocardiogenic syncope and 11 age- and sex-matched control subjects (5 men and 6 women, mean age 49 +/- 15 years) during head-up tilt testing. Norepinephrine and epinephrine levels were measured at the baseline supine position, in the initial upright position, every 90 seconds during the 70 degrees upright tilt, at the time of termination due to hypotension and syncope (or at 15 minutes in control subjects), and at 40 seconds and 1 minute and 40 seconds in the supine position after terminating the head-up tilt test. Baseline norepinephrine, epinephrine and heart rate were slightly higher in patients. Despite a significant decrease in mean arterial pressure during head-up tilt testing in patients (51 +/- 20 mm Hg; p < 0.001), norepinephrine levels in patients and control subjects at the time of terminating the head-up tilt test were comparable (459 +/- 204 vs 473 +/- 172 pg/ml). A fivefold increase in epinephrine levels (73 +/- 53 to 345 +/- 260 pg/ml; p < 0.01) were seen in patients, whereas control subjects had insignificant change (38 +/- 16 to 65 +/- 44 pg/ml). It is concluded that diminished neuronal sympathetic activity and enhanced adrenomedullary activity is demonstrated during head-up tilt testing in patients with neurocardiogenic syncope.
OBJECTIVES: We sought to assess the safety and efficacy of selective slow pathway ablation using radiogfrequency energy and a transcatheter technique in patients with a prolonged PR interval and atrioventricular (AV) node reentrant tachycardia. BACKGROUND: Although both fast and slow AV node pathways can be ablated in patients with AV node reentrant tachycardia, slow pathway ablation, by obviating the risk of AV block, appears to be safer. However, the safety and efficacy of selective slow pathway ablation using transcatheter radiofrequency energy in patients with a prolonged PR interval during sinus rhythm are unclear. METHODS: The seven study patients with a prolonged PR interval (mean +/- SD 237 +/- 26 ms) comprised three women and four men with a mean age of 31 +/- 15 years. The slow pathway was targeted in all seven patients at the posterior/inferior interatrial septal aspect of the tricuspid annulus. Two patients presented with the uncommon variety of AV node reentrant tachycardia after initial fast pathway ablation; in the remaining five patients, the AV node reentrant tachycardia was of the common variety. RESULTS: A single radiofrequency pulse at 30 W successfully abolished the slow pathway in both the anterograde and the retrograde direction in the two patients with uncommon AV node reentrant tachycardia. A mean of 5 +/- 3 radiofrequency pulses were required in the remaining five patients with reentrant tachycardia of the common variety. The postablation PR interval and AH interval remained unchanged. The shortest cycle length of 1:1 AV conduction was prolonged significantly (from 327 +/- 31 to 440 +/- 59 ms, p < 0.01, as was the AV node effective refractory period (from 244 +/- 35 to 344 +/- 43 ms, p < 0.01). During a mean follow-up interval of 20 +/- 6 months, no patient developed symptoms suggestive of AV node reentrant tachycardia or had evidence of second- or third-degree AV block. CONCLUSIONS: These data suggest that the AV node slow pathway can be ablated in patients with AV node reentrant tachycardia who demonstrate a prolonged PR interval during sinus rhythm.
Implantation of a nonthoracotomy system (Medtronic PCD or CPI Endotak) was attempted in 170 patients with ventricular tachycardia (VT) or ventricular fibrillation (VF) not requiring concomitant cardiac surgery. A nonthoracotomy system could be successfully implanted in 95 of the 115 patients with the PCD system and 49 of 55 patients receiving the Endotak lead system. In 26 patients with failed nonthoracotomy system because of defibrillation threshold (DFT) > 25 joules (J), an epicardial system was implanted at the same setting. Patients receiving the two lead systems were comparable with regard to age, sex, and ejection fraction. However, since the PCD system offers tiered therapy multiprogrammable options, all attempts were made to implant this lead system in patients with VT that could be pace terminated. Mean DFT (15 +/- 4.7 vs 17 +/- 4.6 J; P = 0.03) and implant time (2.5 +/- 0.6 vs 3.3 +/- 0.7 hours; P = 0.02) were less with the Endotak lead system. There was no perioperative mortality. During a mean follow-up of 20 +/- 4 months, there were eight instances of lead dislodgment in patients receiving the PCD system. There were four nonsudden cardiac deaths and one sudden death in the Endotak group and three nonsudden deaths in the PCD group. Sudden cardiac death and total survival using the intention-to-treat analysis during this follow-up period were 99% and 95%, respectively. In conclusion, successful implantation, perioperative mortality, and survival rate are comparable with both lead systems; however, incorporating two defibrillating electrodes in one lead minimizes lead dislodgment and reduces implant time.
INTRODUCTION: Transcatheter ablation of the left free-wall atrioventricular accessory pathways (AP) by delivery of radiofrequency current at the ventricular insertion site has been shown to be effective. The efficacy of such a technique targeting the atrial insertion site of the AP was evaluated. METHODS AND RESULTS: One hundred consecutive patients with left free-wall APs and symptomatic supraventricular tachyarrhythmias were included. APs were manifest in 55 patients and concealed in 45. There were 55 men and 45 women with a mean age of 35 years. A total of 107 left free-wall APs were identified in these patients. In these 100 patients, successful ablation was accomplished in all by using a transseptal (45 patients) or transaortic (54 patients) technique. In one patient, ablation was accomplished from within the coronary sinus. Seven patients required a repeat ablative procedure, which was performed successfully. During 107 ablative procedures, six were associated with nonfatal complications including pericardial effusion (hemopericardium) in two patients, mild mitral regurgitation in two patients, swelling of the left arm in one patient, and staphylococcal bacteremia in one patient. Eighty-two (82%) patients underwent a repeat electrophysiologic study 6 to 8 weeks after successful ablation and were found to have no functioning AP or inducible supraventricular tachycardia. During a mean follow-up of 20 +/- 8 months, none of the 100 patients had a recurrence of tachyarrhythmias. CONCLUSION: These data indicate that the atrial insertion site of the AP can be successfully ablated in the majority of patients with left free-wall APs by using either a transseptal or transaortic approach. Furthermore, both techniques are associated with minimal morbidity and no mortality.
BACKGROUND: The efficacy of transcatheter ablation of atrioventricular (AV) accessory pathways (APs) located in the posteroseptal region using a right atrial approach and radiofrequency energy was evaluated. METHODS AND RESULTS: Fifty consecutive patients with APs in the posteroseptal region underwent radiofrequency catheter ablation. Manifest preexcitation was present in 36 patients and a concealed AP in 14. In 18 patients (group 1), the ventriculoatrial (VA) interval during orthodromic tachycardia was prolonged by 21 +/- 7 milliseconds (range, 10 to 30 milliseconds) with functional left bundle-branch block. In 16 patients (group 2), functional left bundle-branch block caused no VA interval prolongation. The remaining 16 patients (group 3) had no inducible left bundle-branch block during orthodromic tachycardia. Functional right bundle-branch block was induced in 30 patients with no effect on the VA interval. In group 1, of 14 patients with manifest preexcitation during sinus rhythm, 10 patients had a positive delta wave in lead V1. Of 10 group 2 patients with manifest preexcitation, only 5 had a positive delta wave in lead V1. In group 3, of 12 patients with manifest preexcitation, 7 exhibited a positive delta wave in lead V1. All posteroseptal APs were successfully ablated, and this was achieved via a right atrial approach in 48 patients and left ventricular approach in only 2. Successful sites were at the posteroseptal region of the tricuspid annulus (30 patients), within the terminal 1 cm of the coronary sinus including its ostium (16 patients), and at the inferomedial aspect of the right atrium posterior to the coronary sinus ostium (2 patients). The posteroseptal region of the left ventricle was the site of successful ablation in 2 patients. Six patients with a recurrence of AP conduction required a repeat ablation, with successful results in 5. Thirty-five patients had a complete electrophysiological evaluation 2 to 3 months after their successful ablation and were found to have no functioning AP. In 49 patients with a final successful ablation, no recurrence of symptoms was noted during a mean follow-up period of 12 +/- 9 months. Complications occurring in 3 patients were cardiac tamponade requiring surgical drainage and repair of a right ventricular tear, pericardial effusion with no hemodynamic consequence that spontaneously resolved, and a transient 2:1 atrioventricular block. CONCLUSIONS: These data suggest that posteroseptal APs are amenable to successful ablation using a right atrial approach. Success was achieved in 47 cases (94%) in this series even though the ECG and/or electrophysiological characteristics of the posteroseptal APs of some patients were suggestive of "left-sided" pathways.
BACKGROUND: The efficacy of permanent cardiac pacing in patients with neurocardiogenic (or vasovagal) syncope associated with bradycardia or asystole is not clear. We compared the efficacy of cardiac pacing with that of oral drug therapy in the prevention of hypotension and syncope during head-up tilt testing. METHODS: Among 70 patients with a history of syncope in whom hypotension and syncope could be provoked during head-up tilt testing, 22 had bradycardia (a heart rate < 60 beats per minute, with a decline in the rate by at least 20 beats per minute) or asystole along with hypotension during testing. There were 9 men and 13 women, with a mean (+/- SD) age of 41 +/- 17 years. Head-up tilt testing was repeated during atrioventricular sequential pacing (in 20 patients with sinus rhythm) or ventricular pacing (in 2 patients with atrial fibrillation). Regardless of the results obtained during artificial pacing, all the patients subsequently had upright-tilt testing repeated during therapy with oral metoprolol, theophylline, or disopyramide. RESULTS: During the initial tilt test, 6 patients had asystole and 16 had bradycardia along with hypotension. Despite artificial pacing, the mean arterial pressure during head-up tilt testing still fell significantly, from 97 +/- 19 to 57 +/- 19 mm Hg (P < 0.001); 5 patients had syncope, and 15 had presyncope. By contrast, 19 patients who later received only medical therapy (metoprolol in 10, theophylline in 3, and disopyramide in 6), 2 patients who received both metoprolol and atrioventricular sequential pacing, and 1 patient who received only atrioventricular sequential pacing had negative head-up tilt tests. After a median follow-up of 16 months, 18 of the 19 patients who were treated with drugs alone (94 percent) remained free of recurrent syncope or presyncope, whereas the patient treated only with permanent dual-chamber pacemaker had recurrent syncope. CONCLUSIONS: In patients with neurocardiogenic syncope associated with bradycardia or asystole, drug therapy is often effective in preventing syncope, whereas artificial pacing is not.
INTRODUCTION: The objective of this report is to delineate the atrioventricular (AV) nodal electrophysiologic behavior in patients undergoing fast or slow pathway ablation for control of their AV nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: One hundred sixteen consecutive patients with symptomatic AVNRT were included. Twenty-two patients underwent fast pathway ablation with complete abolition of AVNRT in all and development of complete AV block in five patients. Of 17 patients with intact AV conduction postablation, 12 had demonstrated antegrade dual pathway physiology during baseline study, which was maintained in three and lost in nine patients postablation. Two patients with successful fast pathway ablation developed uncommon AVNRT necessitating a slow pathway ablation. Twenty-one patients demonstrated both common and uncommon forms of AV nodal reentry during baseline study. The earliest site of atrial activation was close to the His-bundle recording site (anterior interatrial septum) during common variety and the coronary sinus ostium (posterior interatrial septum) during the uncommon AV nodal reentry in all 21 patients. Ninety-six patients underwent successful slow pathway ablation. Among these, the antegrade dual pathway physiology demonstrable during baseline study (60 patients) was maintained in 25 and lost in 35 patients postablation. CONCLUSION: These data suggest that: (1) dual pathway physiology may persist after successful ablation, which might be a reflection of multiple reentrant pathways in patients with AVNRT; and (2) the retrograde pathways during common and uncommon AVNRT have anatomically separate atrial breakthroughs. These findings have important electrophysiologic implications regarding the prevailing concept of the AV nodal physiology in patients with AVNRT.
A 40-year-old man undergoing electrophysiologic study for recurrent palpitations was found to have a right bundle branch block during sinus rhythm and right bundle potentials occurring after ventricular activation. The sequence of activation of the proximal and distal right bundle potentials was suggestive of a retrograde invasion of the right bundle during sinus rhythm. This transseptal activation of the right bundle via the left bundle exhibited decremental conduction characteristics during atrial as well as ventricular stimulation. Observations made in this case may provide some important information concerning the electrophysiologic behavior of transseptal impulses.
Over the past several decades there has been enormous progress in the understanding of many electrophysiologic characteristics of the AVNRT circuit. Although a great number of questions have been resolved, several pertinent issues require further investigation. Medical treatment remains the most widely used therapeutic intervention for acute or short-term management of patients with recurrent AVNRT. However, nonpharmacologic approaches, particularly transcatheter modification of the AV node, have increasingly become popular for long-term management. Radiofrequency energy has been safe and effective for transcatheter ablative techniques. It seems highly likely that in the next several years, selective transcatheter ablation of the AV nodal (slow or fast) pathway, by providing permanent cure, will become the modality of choice in symptomatic patients with AVNRT.
Neurocardiogenic syncope is a common medical problem that can be identified easily by history and the findings of the head-up tilt test. Depressor reflexes from the heart causing sympathetic withdrawal that, in turn, lead to peripheral vasodilatation and hypotension may have an important role in the pathogenesis of neurocardiogenic dysfunction. Once a diagnosis of neurocardiogenic syncope has been made, specific therapeutic strategies can usually prevent recurrent syncope. However, the natural history of neurocardiogenic syncope has not been studied. Double-blind placebo-controlled studies or drug withdrawal trials are needed to assess whether all patients with neurocardiogenic syncope need lifelong therapy.