To characterize the pattern of pacemaker dominance in the ventricular specialized conduction system (VSCS), escape ventricular pacemakers were localized and quantified in vivo and in virto, in normal hearts and in hearts 24 hours after myocardial infarction. Excape pacemaker foci were localized in vivo during vagally induced atrial arrest by means of electrograms recorded from the His bundle and proximal bundle branches and standard electrocardiographic limb leads. The VSCS was isolated using a modified Elizari preparation or preparations of each bundle branch. Peacemakers were located by extra- and intracellular recordings. Escape pacemaker foci in vivo were always in the proximal conduction system, usually the left bundle branch. The rate was 43+/-11 (mean+/-SD) beats/min. After beta-adrenergic blockade, the mean rate fell to 31+/-10 beats/min, but there were no shifts in pacemaker location. In the infarcted hearts, pacemakers were located in the peripheral left bundle branch. The mean rate was 146+/-20 beats/min. In isolated normal preparations, the dominant pacemakers usually were in the His bundle, firing at a mean rate of 43+/-10 beats/min. The rates of pacemakers diminished with distal progression. In infarcted hearts, the pacemakers invariably were in the infarct zone. The mean firing rates were not influenced by beta-adrenergic blockade. The results indicate that the dominant pacemakers are normally in the very proximal VSCS, but after myocardial infarction pacemaker dominance is shifted into the infarct. Distribution of pacemaker dominance is independent of sympathetic influence. (+info)
Electrophysiological effects of mexiletine in man.
(2/1706)
The electrophysiological effects of intravenous mexiletine in a dose of 200 to 250 mg given over 5 minutes, followed by continuous infusion of 60 to 90 mg per hour, were studied in 5 patients with normal conduction and in 20 patients with a variety of disturbances of impulse formation and conduction, by means of His bundle electrography, atrial pacing, and the extrastimulus method. In all but 2 patients the plasma level was above the lower therapeutic limit. Mexiletine had no consistent effects on sinus frequency and atrial refractoriness. The sinoatrial recovery time changed inconsistently in both directions; however, of the 5 patients in whom an increase was evident, 3 had sinus node dysfunction. In most patients mexiletine increased the AV nodal conduction time at paced atrial rates and shifted the Wenckebach point to a lower atrial rate. The effective refractory period of the AV node was not consistently influenced, while the functional refractory period increased in 12 out of 14 patients. The HV intervals increased by a mean of 11 ms in 8 patients and were unchanged in 17. Both the relative and effective refractory period of the His-Purkinje system increased after mexiletine. Non-cardiac side effects occurred in 7 out of 25 patients, and cardiac side effects, including one serious, in 2. The results indicate that mexiletine shares some electrophysiological properties with procainamide and quinidine, when given to patients with conduction defects, and that the drug should not be used in patients with pre-existing impairment of impulse formation or conduction. It has additional effects on AV nodal conduction which may be of value in the treatment of re-entrant tachycardias involving the AV node. (+info)
Chronic His bundle block. Clinical, electrocardiographic, electrophysiological, and follow-up studies on 16 patients.
(3/1706)
This report describes 16 patients with block within the His bundle seen over a period of 55 months. Ten were women and 6 men, with an average age of 76 years, range, 42 to 98 years. All patients had His bundle recordings showing split His bundle potentials (H and H) (13 patients) or narrow QRS with block distal to the His bundle potential (3 patients). Of the 16 patients, 10 had complete heart block, 4 second degree AV block (2 patients with Mobitz type II, and 2 with 2:1), and 2 first degree AV block. Ten patients had a narrow QRS in the conducted beats or escape rhythms. Intravenous atropine (1 to 2 mg) had a variable effect on AV conduction and the rate of the escape rhythm. Twelve patients have had a permanent pacemaker implanted. During the follow-up period, 10 patients died 1 to 31 months from the time of initial examination. The remaining 6 patients (5 with pacemaker) are alive 3 to 58 months later. (+info)
Fatal outcome arising from use of a sutureless "corkscrew" epicardial pacing electrode inserted into apex of left ventricle.
(4/1706)
A 59-year-old man is described in whom the insertion of an epicardial sutureless "corkscrew" electrode resulted in fatal ventricular perforation. Fatal myocardial perforation can occur with this electrode and the apex of the left ventricle should never be used as the site of insertion. Necropsy also showed that the transvenous right ventricular electrode, inserted one year previously, had penetrated a tricuspid leaflet. This could have accounted for the ensuing pacing failure. (+info)
Effects of varying pacemaker sites on left ventricular performance.
(5/1706)
The hemodynamic effects of the site of the artificial cardiac stimulation were studied in 17 open chest dogs. The right atrium and five ventricular sites (the inflow and outflow tracts and apex of the right ventricle, apex and lateral wall of the left ventricle) were stimulated electronically at a given rate, ranging from 130 to 190 per min. When cardiac performance during ventricular pacing was compared with those during right atrial pacing, the former uniformly caused a diminution of cardiac output and systemic blood pressure, without reduction of left ventricular end-diastolic pressure. Ventricular function curves, in which left ventricular stroke work was related to left ventricular end-diastolic pressure, shifted downwards and to the right during ventricular pacing. Stimulation frequency did not alter these variables. It was considered that the left ventricular dysfunction in ventricular pacing resulted from the absence of atrial contribution to ventricular filling, mitral regurgitation present and asynchronous ventricular contraction. No significant difference of cardiac performance was demonstrated by changing the site of ventricular pacing, suggesting that the mode of ventricular depolarization itself was not relevant to a decrease in cardiac performance. (+info)
Pacemaker lead infection: echocardiographic features, management, and outcome.
(6/1706)
OBJECTIVE: To compare transthoracic and transoesophageal echocardiography (TTE, TOE) in patients with permanent pacemaker lead infection and to evaluate the safety of medical extraction in cases of large vegetations. METHODS: TTE and TOE were performed in 23 patients with definite pacemaker lead infection. Seventeen patients without previous infection served as a TOE reference for non-infected leads. RESULTS: TTE was positive in seven cases (30%) whereas with TOE three different types of vegetations attached to the leads were visualised in 21 of the 23 cases (91%). Of the 20 patients with vegetations and lead culture, 17 (85%) had bacteriologically active infection. Left sided valvar endocarditis was diagnosed in two patients. In the control group, strands were visualised by TOE in five patients, and vegetations in none. Medical extraction of vegetations >/= 10 mm was performed in 12 patients and was successful in nine (75%) without clinical pulmonary embolism. After 31.2 (19.1) months of follow up (mean (SD)), all patients except one were cured of infection; three died from other causes. CONCLUSIONS: Combined with bacteriological data, vegetations seen on TOE strongly suggest pacemaker lead infection. Normal TTE examinations do not exclude this diagnosis because of its poor sensitivity. Medical extraction of even large vegetations appeared to be safe. (+info)
Pacemaker lead infection: report of three cases and review of the literature.
(7/1706)
Pacemaker lead infection is a rare condition, most often occurring when intervention is needed after pacemaker implantation. Diagnosis is by blood cultures and confirmation by transoesophageal echocardiography; transthoracic echocardiography is often inadequate. A literature review indicated the microorganism most responsible for late lead infection is Staphylococcus epidermidis (which can grow on plastic material). A retrospective analysis of patient files from the authors' institution (1993-97) yielded three patients with proven pacemaker lead endocarditis. The diagnosis of pacemaker endocarditis was by transoesophageal echocardiography. The endocarditis appeared after a long period and in two of the three patients there was S epidermidis infection. Thoracotomy with removal of the infected system was performed because of the large dimensions of the vegetations. A new pacemaker was implanted: in one patient with endocardial leads, in the other two with epicardial leads. All three patients recovered well and follow up was uneventful for at least one year. (+info)
Pacemaker lead extraction with the laser sheath: results of the pacing lead extraction with the excimer sheath (PLEXES) trial.
(8/1706)
OBJECTIVES: The purpose of this study was to evaluate the safety and effectiveness of pacemaker lead extraction with the excimer sheath in comparison to nonlaser lead extraction. BACKGROUND: Fibrotic attachments that develop between chronically implanted pacemaker leads and to the venous, valvular and cardiac structures are the major obstacles to safe and consistent lead extraction. Locking stylets and telescoping sheaths produce a technically demanding but effective technique of mechanically disrupting the fibrosis. However, ultraviolet excimer laser light dissolves instead of tearing the tissue attachments. METHODS: A randomized trial of lead extraction was conducted in 301 patients with 465 chronically implanted pacemaker leads. The laser group patients had the leads removed with identical tools as the nonlaser group with the exception that the inner telescoping sheath was replaced with the 12-F excimer laser sheath. Success for both groups was defined as complete lead removal with the randomized therapy without complications. RESULTS: Complete lead removal rate was 94% in the laser group and 64% in the nonlaser group (p = 0.001). Failed nonlaser extraction was completed with the laser tools 88% of the time. The mean time to achieve a successful lead extraction was significantly reduced for patients randomized to the laser tools, 10.1 +/- 11.5 min compared with 12.9 +/- 19.2 min for patients randomized to nonlaser techniques (p < 0.04). Potentially life-threatening complications occurred in none of the nonlaser and three of the laser patients, including one death (p = NS). CONCLUSIONS: Laser-assisted pacemaker lead extraction has significant clinical advantages over extraction without laser tools and is associated with significant risks. (+info)