Atrioventricular and intraventricular conduction disorders in acute myocardial infarction: a reappraisal in the thrombolytic era.
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Biomedical subjects
Publications and source records attributed to A Natale.
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The objective of this study was to assess the safety and efficacy of transvenous low energy cardioversion of atrial fibrillation in patients with ventricular tachycardia and atrial fibrillation and to study the mechanisms of proarrhythmia. Previous studies have demonstrated that cardioversion of atrial fibrillation using low energy, R wave synchronized, direct current shocks applied between catheters in the coronary sinus and right atrium is feasible. However, few data are available regarding the risk of ventricular proarrhythmia posed by internal atrial defibrillation shocks among patients with ventricular arrhythmias or structural heart disease. Atrial defibrillation was performed on 32 patients with monomorphic ventricular tachycardia and left ventricular dysfunction. Shocks were administered during atrial fibrillation (baseline shocks), isoproterenol infusion, ventricular pacing, ventricular tachycardia, and atrial pacing. Baseline shocks were also administered to 29 patients with a history of atrial fibrillation but no ventricular arrhythmias. A total of 932 baseline shocks were administered. No ventricular proarrhythmia was observed after well-synchronized baseline shocks, although rare inductions of ventricular fibrillation occurred after inappropriate T wave sensing. Shocks administered during wide-complex rhythms (ventricular pacing or ventricular tachycardia) frequently induced ventricular arrhythmias, but shocks administered during atrial pacing at identical ventricular rates did not cause proarrhythmia. The risk of ventricular proarrhythmia after well-synchronized atrial defibrillation shocks administered during narrow-complex rhythms is low, even in patients with a history of ventricular tachycardia. The mechanism of proarrhythmia during wide-complex rhythms appears not to be related to ventricular rate per se, but rather to the temporal relationship between shock delivery and the repolarization time of the previous QRS complex.
The physiology of the escape rhythm (ER) and its response to pharmacological modulation under varying autonomic conditions were studied 48 patients undergoing radiofrequency ablation of the atrioventricular junction (AVJ) for refractory atrial fibrillation. The QRS morphology and cycle length (CL) of the baseline ER were measured 15 minutes postablation. The CL of the ER was measured in response to doses of isoproterenol, atropine, adenosine, lidocaine, and verapamil. The ER QRS was narrow (QRS < 120 ms) in 20 patients and wide (QRS > 120 ms) in 28 patients. Of the 28 patients with wide QRS ER, 11 patients had a new bundle branch block (8 patients new right bundle branch block [RBBB] and 2 patients new left bundle branch block [LBBB]). The ERCL was similar in both narrow and wide ERs (1,593 +/- 376 ms and 1,516 +/- 296 ms, P = 0.44). In 23 patients receiving isoproterenol infusion, the ER CL decreased with increasing doses from 1 mcg/min to 2 mcg/min (1,378 +/- 200 to 1,240 +/- 229 ms, P < 0.001), but did not decrease further at 3 mcg/min (1,201 +/- 192 ms, P = 0.48 vs 2 mg/min). Seven patients received 0.02 mg/kg of atropine, and ER decreased significantly (1,572 +/- 408 ms to 1,319 +/- 333 ms, P = 0.028). In 30 patients who received intravenous boluses of adenosine (6-18 mg), the ER did not change significantly. In 28 patients who received 150 mg of lidocaine, the ER increased from 1,462 +/- 286 ms to 1,715 +/- 467 ms (P < 0.001), and one patient developed transient asystole. Nineteen patients received 7.5 mg of verapamil, and the ER did not change (1,488 +/- 313 ms to 1,513 +/- 666 ms, P = 0.80). There was no significant difference in response to isoproterenol, adenosine, lidocaine, or verapamil between the patients with wide and narrow QRS ERs. We conclude that patients may have stable ERs immediately following AVJ ablation even when a wide complex ER results. The ER is responsive to sympathetic stimulation and vagal blockade. The ER is prolonged after lidocaine but not after verapamil, suggesting response to sodium but not to calcium channel blockade. These data are consistent with an ER originating in the distal compact AV node or proximal His bundle.
This study was designed to evaluate the ability to distinguish between supraventricular tachycardias (SVTs) and ventricular tachycardias (VTs) based on onset, stability, and width criteria in an implantable defibrillator. Inappropriate detection of atrial fibrillation and sinus tachycardia is a common problem in patients with implantable defibrillators. The onset, stability, and width criteria were studied in 17 patients who underwent implantation of a Medtronic 7218C implantable defibrillator by inducing sinus tachycardia and atrial fibrillation. Additional data on the width criteria was obtained by pacing at separate sites in both the left and right ventricle. Patients were studied at different times for up to 6 months to determine any changes in the criteria. The onset and stability criteria caused inappropriate detections in 36% and 12% of the episodes, respectively. The addition of the width criteria decreased the inappropriate detection using the onset and stability criteria to 5% and 2%, respectively. Pacing from the RV apex, RV outflow tract, and LV apex was appropriately detected as wide in 76%, 41%, and 94%, respectively. The width criteria changed over time in individual patients, but was stable by 6 months in all but one patient. No single criterion is satisfactory for distinguishing between SVT and VT in this patient population, but the combination of criteria seems to provide better discrimination. The width criteria can change dramatically over time and needs to be monitored carefully. Newer algorithms will need to be developed to allow better detection of supraventricular tachycardias.
Little data is available comparing the efficacy of the Transvene, Endotak C 70 series, and the active CAN configuration on defibrillation success. In addition, the impact of the superior vena cava (SVC) electrode surface area and length on the active CAN system is unknown. Therefore, we compared the defibrillation efficacy of the Transvene and Endotak C 70 series lead systems with and without the active CAN in dogs. Defibrillation threshold (DFT) testing was randomly performed in 20 dogs. In protocol I (10 dogs), DFT energy was compared in three RV/SVC lead systems with an SVC electrode defibrillating surface area of 90 mm2 (Transvene-90), 160 mm2 (Transvene-160), 617 mm2 (Endotak), and an RV/CAN configuration. In protocol II (10 dogs), DFT comparison was performed in the Transvene-90/CAN, Transvene-160/CAN, Endotak/CAN, and RV/CAN configurations. In protocol I, increasing the SVC surface area from 90 to 160 mm2 and from 160 to 617 mm2 significantly lowered DFT energy. The Endotak and the RV/CAN systems provided the lowest DFT energy requirements. In protocol II, the Endotak/CAN system significantly lowered DFT energy compared to the other three lead configurations. In both protocols, the impedance decreased as the SVC surface area increased from 90 to 160 mm2. However, no significant reduction in DFT impedance occurred as the SVC surface area increased from the Transvene-160 to the Endotak lead. Increasing the SVC surface area from 90 to 617 mm2 in a two coil lead system lowered DFT energy to similar levels provided by the RV/CAN configuration. The addition of an SVC electrode with a surface area of 90 or 160 mm2 did not reduce DFT energy compared to the RV/CAN configuration. The Endotak/CAN system, however, provided the lowest DFT requirements.
Radiofrequency (RF) catheter modification of the sinus node appears to be a promising therapeutic modality for the treatment of inappropriate sinus tachycardia. Modification, as opposed to total obliteration, of the atrial pacemaker requires precise localization of the sinus node. This has been successfully achieved with a multicatheter approach guided by intracardiac echocardiography. This article describes the first clinical use of a tridimensional nonfluoroscopic mapping system to guide successful RF modification of the sinus node in two cases of inappropriate sinus tachycardia. This system simplifies the current approach and greatly reduces the fluoroscopy time.
BACKGROUND: The purpose of this investigation was to evaluate the outcome of pregnancy in women with implantable cardioverter-defibrillators (ICDs). METHODS AND RESULTS: A multicenter retrospective analysis was performed on women with an ICD who became pregnant. Data were collected on 44 patients. The mean age and ejection fraction at the time of the initial ICD implant were 25.6+/-4.9 years and 49.8+/-9.7%, respectively. The mean follow-up after the ICD implant was 4.8+/-2.8 years. Forty-two women had abdominally implanted generators, and 2 had a prepectoral device. Thirty had epicardial lead sensing systems, and 14 had transvenous. Thirty-six (82%) experienced no complications, and 8 (18%) had a medical or device-related complication. The ICD-related problems included tenderness at the ICD pocket scar (2 patients), generator migration (1), and pericarditis secondary to the epicardial patches (1). Medical complications were pulmonary embolism (1), therapeutic abortion (1), worsening hyperthyroidism (1), congestive heart failure (1), and weight loss (1). Thirty-seven women delivered vaginally, and 7 underwent cesarean section. Thirty-nine babies were born healthy, 1 was stillborn, 2 were small for gestational age, 1 had transient hypoglycemia, and 1 woman had a therapeutic abortion unrelated to the ICD. During pregnancy, 33 women received no ICD therapy, 8 had 1 shock, 1 had 5 discharges, 1 had 11 shocks, and 1 had 5 shocks. The total number of shocks during pregnancy ranged from 0 to 11, with an average of 0.66+/-1.9 discharges. Five women had 7 additional pregnancies without an ICD shock. CONCLUSIONS: The mere presence of an ICD should not defer a women from becoming pregnant unless she has an underlying structural cardiac disease that is considered a contraindication. Pregnancy does not increase the risk of major ICD-related complications or result in a high number of ICD discharges.
BACKGROUND: Recent studies have shown that specifically shaped biphasic waveforms can lower energy requirements for ventricular defibrillation. We prospectively compared the defibrillation efficacy of three different biphasic wave shapes incorporated in three commercially available implantable defibrillators. The results led to the development of a second protocol in which the importance of negative-phase peak voltage and duration was investigated. METHODS AND RESULTS: Defibrillation threshold (DFT) testing using different biphasic waveforms was performed randomly on 42 patients undergoing implantation of a cardioverter-defibrillator for ventricular arrhythmias. In 23 patients (group 1), 3 waveforms were tested: a CPI waveform with 60% positive-phase (P1) tilt and 50% negative-phase (P2) tilt, a Medtronic waveform with 65% fixed tilt in both P1 and P2, and a Ventritex waveform with 60% P1 tilt and a P2 leading edge voltage equal to half of the P1 trailing edge voltage. In 19 patients (group 2), 3 biphasic waveforms with equal P1 tilt at 65% but shorter P2 duration or smaller P2 peak voltage were tested. The Endotak C 60 series lead system (CPI) was used in 11 patients in group 1 and 10 patients in group 2. A Transvene lead system (Medtronics) was used in the remaining patients. Stored energy required for defibrillation was significantly lower with the CPI waveform compared with the Ventritex waveform. In group 2, energy requirements were significantly increased for the waveform with a smaller P2 peak voltage, whereas a short P2 duration did not influence defibrillation success. CONCLUSIONS: Our results suggest that specifically shaped biphasic waveforms delivered from commercially available devices can affect energy requirements for defibrillation. More importantly, the amplitude of the P2 peak voltage may be a more critical determinant than the P2 duration for defibrillation success of biphasic waveforms in humans.
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Whether the presence of abnormal PR before selective slow pathway ablation for AV node reentrant tachycardia increased the risk of complete heart block remains controversial. We report our experience in seven patients with prolonged PR intervals undergoing catheter ablation for AV reentry tachycardia. Their mean age was 66 +/- 12 years; four patients were female and three were male. RF ablation was performed using an anatomically guided stepwise approach. In six patients, common type AV node reentry was induced and uncommon type was observed in the remaining patient. In all seven patients, successful selective slow pathway ablation was associated with no occurrence of complete heart block and was followed by shortening of the AH interval in five patients. In all seven patients, successful ablation was achieved at anterior sites (M1 in two patients and M2 in five patients). Despite AH shortening after ablation, the 1:1 AV conduction was prolonged after elimination of the slow pathway, excluding either sympathetic tone activation or parasympathetic denervation. In conclusion, selective slow pathway ablation can be performed safely in the majority of patients with prolonged PR interval before the procedure. Because successful ablation is achieved at anterior sites in most patients, careful selection and monitoring of catheter position is required.
UNLABELLED: Several procedures performed in the electrophysiology laboratory (EP lab) require surgical manipulation and are lengthy. Patients undergoing such procedures usually receive general anesthesia or deep sedation administered by an anesthesiologist. In 536 consecutive procedures performed in the EP lab, we assessed the safety and efficacy of deep sedation administered under the direction of an electrophysiologist and in the absence of an anesthetist. Patients were monitored with pulse oximetry, noninvasive blood pressure recordings, and continuous ECGs. The level of consciousness and vital signs were evaluated at 5-minute intervals. Deep sedation was induced in 260 patients using midazolam, phenergan, and meperidine, then maintained with intermittent dosing of meperidine at the following mean doses: midazolam 0.031 +/- 0.024 mg/kg; phenergan 0.314 +/- 0.179 mg/kg; and meperidine 0.391 +/- 0.167 mg/kg per hour. In the remaining 276 patients, deep sedation was induced with midazolam and fentanyl and maintained with a continuous infusion of fentanyl at a mean dose of 2.054 +/- 1.43 micrograms/kg per hour. Fourteen patients experienced a transient reduction in oxygen saturation that was readily reversed following administration of naloxone. An additional 11 patients desaturated secondary to partial airway obstruction, which resolved after repositioning the head and neck. Fourteen patients experienced hypotension with fentanyl. All but one returned to baseline blood pressures following an infusion of normal saline. No patient required intubation and no death occurred. Only three patients had recollection of periprocedure events. No patient remembered experiencing pain with the procedure. Hospital stays were not prolonged as a result of the sedation used. IN CONCLUSION: (1) deep sedation during EP procedures can be administered safely under the guidance of the electrophysiologist without an anesthetist present; (2) the drugs used should be readily reversible in case of respiratory depression; and (3) this approach may reduce the overall cost of the procedures in the EP lab, maintaining adequate patient comfort.
The active can defibrillator has been designed for implantation in the left prepectoral region. Whether this system can be successfully implanted on the right side is unknown. We describe six cases in which placement of the unipolar single lead defibrillation system was successfully attempted in the right prepectoral region due to impediments on the left side. The mean age of the patients was 62 +/- 12 years. Five patients had ischemic heart disease and one idiopathic dilated cardiomyopathy. The endocardial defibrillation electrode was placed in the right ventricle through the right subclavian vein and positioned at the apex in two patients and in the septal position in four patients. Defibrillation threshold testing was performed using a step-up/step-down protocol beginning at 12 J with 3-J increments or decrements. Defibrillation threshold was defined as the lowest energy of the first shock able to terminate ventricular fibrillation. The generator models used were the Medtronic 7218C in 1 patient, the Medtronic 7219C in 3 patients, and the Ventritex Cadet 115 AC in 2 patients. The mean defibrillation threshold was 15 +/- 3 J. The defibrillation thresholds were retested at 1, 3, and 6 months, and showed no significant change in five patients but decreased from 15 J to 12 J in one patient. The presence of impediments on the left side should not preclude attempts to place the unipolar active can system in the right prepectoral region.
Limited information is available regarding potential adverse interactions between transvenous nonthoracotomy cardioverter defibrillators and pacemakers. We describe our experience with 37 patients who have undergone successful implantation of both a transvenous defibrillator and pacemaker. The patients' mean age was 64 +/- 12.9 years. Thirty-three were male and four were female. The mean LVEF was 30.8% +/- 11.8%. The indications for pacemaker implantation included sick sinus syndrome in 13 patients, complete heart block in 15 patients, sinus bradycardia secondary to medications in 8 patients, and neurocardiogenic syncope in 1 patient. The indications for insertion of a defibrillator included medically refractory VT in 27 patients and sudden cardiac death in 10 patients. Twenty-three patients received an Endotak lead and 14 patients received a Transvene lead. Eighteen patients had a pacemaker prior to an ICD, 14 patients had an ICD prior to a pacemaker, and 4 patients had both devices placed simultaneously. Interaction was evaluated at implant of the second device and 1-3 days after both devices were placed. Detection of VF/VT was analyzed during asynchronous pacing (DOO/VOO) with maximum pacing output. In addition, in six patients, DFT was determined before and after pacemaker implantation. In 14 patients (38%), device interactions that could not always be optimally corrected were observed. In five patients, the pacemaker was reset to the "noise reversion" mode after high energy ICD discharge. Oversensing of atrial pacemaker stimuli resulted in inappropriate ICD firings in four patients. This was observed only with a specific device and could not be prevented by atrial lead repositioning in two of them, but required reprogramming of the pacemaker to the VVI mode. An increase in DFT was observed in five patients who had a pacemaker implanted after an ICD. Compared with previously published studies, a greater frequency of transvenous ICD and pacemaker interactions were observed. Considering that almost 50% of the patients already have a pacemaker at the time of ICD implant, the availability of defibrillators with dual chamber pacing capability will not eliminate the potential for this problem.
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Limitations of pharmacological therapy for VT have led to great interest in alternative nonpharmacological therapies. The appeal of a curative therapy for VT initially led to the search for operative techniques to identify and destroy the underlying substrate, and more recently, has resulted in the development of catheter techniques to achieve the same goal in the electrophysiology laboratory. Investigations into the pathophysiology of VT have resulted in the recognition that this arrhythmia reflects a mechanistically and anatomically heterogeneous set of disorders. Recent growth in our understanding of these distinctions has both led to, and resulted from, simultaneous advances in catheter ablation techniques. The clinical electrophysiology laboratory has served as a testing ground for theories derived from in vitro and animal experiments while also providing its own set of human experimental data regarding the pathophysiology and treatment of VT. As a result of this process, several distinct forms of VT that are amenable to catheter ablation have been characterized. This article will summarize current knowledge of the pathophysiology of various VT subtypes and of techniques for catheter mapping and ablation.
The aims of this study were to identify whether tissue renin is regulated by a negative-feedback mechanism produced by locally generated angiotensin (Ang II) in the adrenal cortex and to detect the pathway of Ang II modulation. For this purpose, in 36 12-week old, salt-restricted, nephrectomized Sprague-Dawley rats, we studied the effects of the Ang II AT1-subtype receptor antagonist losartan and of the Ang II AT2-subtype receptor antagonist PD123319 on renin mRNA and activity, aldosterone synthase mRNA, and AT1a-, AT1b-, and AT2-subtype receptor expression in the adrenal cortex. Ten additional rats, kept on a regular diet and then nephrectomized, were also studied. In salt-restricted, nephrectomized rats, losartan administration caused increases of adrenal renin mRNA (P<.05) and activity (P<.05) and a concomitant reduction of aldosterone synthase mRNA (P<.05). In addition, after losartan AT1b, receptor mRNA was reduced (P<.05), AT1a receptor mRNA was unchanged, and AT2 mRNA was increased (P<.05). PD123319 did not significantly modify any of these parameters. In conclusion, in salt-restricted, nephrectomized rats, selective antagonism of AT1-subtype receptors stimulates the expression and the activity of renin in the adrenal cortex. This observation demonstrates that Ang II locally formed in the adrenal cortex exerts a modulatory negative-feedback action on adrenal renin biosynthesis independent of the influence of the circulating renin-Ang system; this action is largely mediated through the AT1b-subtype receptors.
We assessed left ventricular function and quality of life after atrioventricular junction ablation and pacemaker implant in 14 patients with chronic atrial fibrillation and normal ventricular response. A significant improvement in left ventricular ejection fraction, fractional shortening, and functional capacity were observed at follow-up, suggesting that in patients with chronic atrial fibrillation a regular heart beat may be preferable over rate control.
We measured left atrial function during sinus rhythm before and after ventricular tachycardia was induced in an electrophysiology laboratory, using peak transmitral A-wave velocity from pulsed-Doppler transthoracic echocardiography as a marker of left atrial mechanical function. The results of this prospective study do not support the hypothesis that a transthoracic shock of mild to moderate energy diminishes atrial mechanical function.