The first reports of electrical multisite ventricular activation in humans.
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Biomedical subjects
Publications and source records attributed to S S Barold.
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Discordant ST elevation > 5 mm was recently described as an electrocardiographic sign with good specificity and moderate sensitivity for the diagnosis of acute myocardial infarction during right ventricular pacing. This report shows that the same sign may occur transiently during myocardial ischemia and also serve as a diagnostic marker.
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The Medtronic Minix pacemaker during normal function in the VVT mode was found to exhibit a Wenckenbach upper rate response similar to that of dual chamber devices. This behavior occurred only when the upper rate interval was longer than the pacemaker refractory period. In a single chamber device this response may simulate pacemaker malfunction.
The consequences of a short 160 ms postventricular atrial refractory period (PVARP) were studied in 27 patients with Medtronic Elite series of pacemakers (programmed to the unipolar mode) by using chest wall stimulation and myopotential interference. Because the ventricular refractory period is nonprogrammable at 230 ms, appropriately timed signals produced As-Vr combinations where As is an atrial sensed event and Vr is a ventricular event detected in the ventricular refractory period. The As-Vr combination inhibited the release of the atrial stimulus at the completion of the atrial escape interval in the DDI, DDIR, DDD, and DDDR modes. A paced ventricular beat (Vp) was documented to initiate automatic PVARP extension in circumstances where Vp was preceded by a Vr event and the pacemaker interpreted the Vr-Vp sequence as 2 ventricular events without an intervening atrial event and Vp as a ventricular premature beat. Knowledge of these eccentricities should facilitate the interpretation of complex pacemakers responses to interference.
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Biventricular (BV) pacing is a promising treatment of end-stage heart failure. This article describes our experience with a strictly endocardial BV pacing system in patients with severe congestive heart failure. Three women and eight men (age 65 +/- 9 years) with drug-resistant end-stage CHF underwent implantation of an endocardial BV pacing system. In the first seven patients, the left ventricular lead was placed via a combined femoral and internal jugular approach. In the last four patients, the transseptal puncture was directly performed via the right internal jugular vein with a dedicated kit. The procedure was successful in all 11 patients. The acute left ventricular and BV thresholds were 1.3 +/- 0.6 V and 2.4 +/- 1 V, respectively. The QRS duration decreased from 214 +/- 57 to 176 +/- 25 ms. A functional improvement was noted in ten patients with a decrease in mean NYHA functional class from 3.7 +/- 0.5 before, to 2.6 +/- 0.9 after system implantation. A significant decrease in pulmonary capillary wedge pressure and increase in cardiac output were measured in eight patients. During follow-up, four patients died from CHF (n = 3) or ventricular fibrillation (n = 1). Under oral anticoagulation, no thromboembolic event was observed but one transient ischemic attack occurred in one patient whose anticoagulation was interrupted. Endocardial BV pacing is technically feasible and appears safe, though further studies are needed before it is used on a longer scale.
Lone atrial fibrillation (AF) is defined by the absence of identifiable causes of AF, but its hemodynamics have not been investigated. Twenty-eight patients with lone AF were compared with 14 control patients referred for Wolff-Parkinson-White ablation. Transthoracic and transesophageal echocardiography were performed to rule out structural heart disease, followed by transseptally performed complete hemodynamic evaluation of the left heart systolic and diastolic function. There was no evidence of diastolic dysfunction according to echocardiographic criteria in AF and control patients. There was no difference in echocardiographic measurements, except for a significantly higher inferosuperior left atrial dimension seen in the four-chamber apical view in AF patients (51+/-10 vs 40+/-6 mm, P = 0.03). Hemodynamic evaluation showed that end-diastolic left ventricular pressure and the nadir of the left atrial Y descent were significantly higher in lone AF patients versus controls: 13+/-5 versus 8+/-3 mmHg (P = 0.001) and 6.7+/-3 versus 4.6+/-2.7 mmHg (P = 0.05). Our results demonstrated the presence of diastolic left heart dysfunction in patients with so-called lone AF.
OBJECTIVE: To assess the effect of adding propafenone to atrial overdrive for the prevention of atrial arrhythmia episodes in patients with DDD pacemakers. DESIGN: 22 patients (8 female, 14 male, mean (SD) age 67 (9) years, range 48 to 77) with DDD pacemakers and frequent paroxysmal atrial arrhythmia episodes were evaluated in a randomised crossover study. SETTING: University hospital. METHODS: Atrial overdrive was defined as a paced rate of 10 paced beats/min above the mean ventricular rate stored for the last 24 hours in the pacemaker memory function. The protocol consisted of two phases of one month each. The first phase consisted of atrial overdrive alone, while in the second phase, propafenone (600 mg/day) was added to atrial overdrive (atrial overdrive + propafenone). All 22 patients underwent the two phases in random order. RESULTS: Mean ventricular rate was 72 (8) beats/min with atrial overdrive v 73 (6) with atrial overdrive + propafenone (NS). With atrial overdrive, 14 patients (64. 6%) had no recorded atrial arrhythmia v 15 (68.2%) with atrial overdrive + propafenone (NS). There was no statistical difference between the atrial overdrive and atrial overdrive + propafenone phases with regard to the number of atrial arrhythmia episodes (14 (27) v 13 (28)), their total duration (30 (78) v 29 (63) h), and their maximum duration (41 (72) v 31 (58) min). However, in the brady-tachy subgroup with persistent atrial arrhythmias, atrial overdrive + propafenone produced a shorter mean cumulative duration of atrial arrhythmia than atrial overdrive (104 (115) v 178 (149) h, p = 0.04), with a significant decrease in the number of atrial arrhythmia episodes (134 (98) v 102 (83), p = 0.05). The proportion of asymptomatic atrial arrhythmia episodes increased only in the AV block group during atrial overdrive + propafenone (p = 0.03). Three patients had atrial arrhythmias during atrial overdrive + propafenone but not with atrial overdrive alone. CONCLUSIONS: In DDD paced patients, the overall effect of propafenone during atrial overdrive is variable. Propafenone may increase the proportion of asymptomatic atrial arrhythmia episodes. A proarrhythmic effect of propafenone was documented (aggravation of atrial arrhythmias). These results need to be confirmed by further larger randomised studies.
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Atrial fibrillation (AF), the most common of all sustained cardiac arrhythmias, is frequently resistant to antiarrhythmic drugs, and physicians have seen limited success with catheter ablation limited to the right atrium. As a result, the safety and efficacy of systematic biatrial linear ablation for drug resistant AF was investigated. Forty-four patients (54 +/- 7 years) underwent catheter ablation of daily drug-resistant AF. Two right-atrial lines (1 septal and 1 cavotricuspid) and 3-4 left-atrial lines were transseptally performed: 2 joining each superior pulmonary vein to the posterior mitral annulus and 1 interconnecting them. An additional left-atrial septal line from the right superior pulmonary vein (RSPV) to the foramen ovalis was performed in 23 patients. Radiofrequency was delivered with a conventional thermocouple-equipped ablation catheter or with an irrigated tip ablation catheter for resistant cases and for sparing the endocardium. Of the 44 patients, 25 (57%) were successfully treated without antiarrhythmic drugs. Twelve patients (27%) improved (<6 hours of AF per trimester under a previously ineffective drug) and 7 (16%) were considered treatment failures. Multiple sessions were required to ablate new left-atrial macro-reentry and initiating foci (2.7 +/- 1.3 procedures per patient). Five patients had a pericardial effusion and 1 each a pulmonary embolism, an inferior myocardial infarction, and a reversible cerebral ischemic event. One patient had thrombosis of the 2 left pulmonary veins. Despite a relatively high success rate, this procedure is too long, and the safely and efficacy need to be improved and applied to a broader range of patients.
The gold standard for rate modulation is the sinus node. To improve the rate modulation provided by artificial sensors, new sensors have to be developed or 2 different sensor systems can be combined within a single device. Association combination of a sensor with a rapid-response fast-rate increase sensor (activity) and a progressive, more specific sensor (QT ventilation) is generally used. Sensor combinations require adequate sensor blending for signal production and prioritization during rate modulation. However, in the new devices, some other aspects of rate modulation could be taken into consideration, particularly circadian rate variations to obtain lower rates at nighttime than during daytime, and automatic adaptation of the slope of rate increase during exercise, according to the patient's fitness, heart function, age, etc. Despite the need for automaticity, manual programming could continue to be useful to adapt rate modulation with data from sensor trending memories.
The relation between left ventricular electromechanical delay and the acute hemodynamic effect of right ventricular pacing was studied in heart failure patients with and without complete left bundle branch block. Whereas right ventricular pacing provided a shorter electromechanical delay that correlated with an improvement in left ventricular function in patients with left bundle branch block, the converse was observed in patients without left bundle branch block.
This report describes two patients with atrial fibrillation in whom an implanted CHORUS DDD pacemaker programmed to the DDI mode produced an irregular ventricular stimulation rate. The lower rate timing of these devices is atrial-based only when an atrial event opens an AV interval shorter than the programmed AV delay. In the DDI mode, if Api represents the time when an atrial paced event (Ap) would have occurred if it had not been inhibited by a previous atrial sensed event (As), then Api-Vp constitutes the implied AV interval where Vp is a paced ventricular event. Although the As-Vp interval (As-Api + Api-Vp) generates an atrial refractory period during its entire duration, the pacemaker can sense an atrial event (AR) during the implied AV interval. AR cannot start another AV delay, but it can initiate the atrial-based lower rate interval. This timing mechanism can cause irregular prolongation of Vp-Vp intervals to a value longer than the programmed lower interval with a maximal extension equal to the programmed AV delay. Such behavior of the CHORUS pacemaker should not be interpreted as malfunction.
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A patient with a Pacesetter Paragon III DDD pacemaker exhibited sustained pacemaker inhibition at rates below the programmed lower rate during sinus rhythm with marked first degree AV block. In this device, a pacemaker defined ventricular extrasystole initiates automatic extension of the postventricular atrial refractory period to 480 ms and the atrial escape interval to 830 ms regardless of the programmed lower rate. Sustained pacemaker inhibition at rates below the programmed lower rate occurred because the P wave fell continually in the extended postventricular atrial refractory period, and the conducted QRS complex initiated a pacemaker ventricular extrasystole response with atrial escape interval extension. This process continued as long as the P wave stayed within the extended postventricular atrial refractory period, no ventricular extrasystole disrupted the sequence, and the R-R interval of spontaneous beats was shorter than the extended atrial escape interval. Such a pacemaker response should not be misinterpreted as device malfunction.
RF catheter ablation is highly effective in eliminating atrioventricular nodal reentrant tachycardia by targeting the slow pathway in the posteroinferior part of Koch's triangle in the right atrium. We report here a patient in whom "slow-fast" atrioventricular nodal reentrant tachycardia was eliminated only by ablation of the slow pathway in the left atrial posteroseptal region at the level of the mitral annulus after unsuccessful attempts at the traditional site on the right side.
Concise and complete guidelines of indications for permanent pacemakers are critical for the clinician involved in permanent pacing. A critical appraisal of the American College of Cardiology/American Heart Association 1998 guidelines on indications for permanent pacing clarifies inconsistencies and expands on information within the current guidelines.