PACE - Pacing and Clinical Electrophysiology

Thecharacteristics of radiofrequency catheter ablation induced injury in the heart are not well characterized. Since the mechanism of injury by radiofrequency energy is thermal, this study was performed to determine the temperature gradient in myocardial tissue during radiofrequency (RF) catheter ablation, and to validate a thermodynamic model derived to describe these observations. Lesions were created by RF heating in an experimental model of isolated perfused and superfused canine right ventricular (RV) free wall. RF power output was adjusted to maintain electrode tip temperature at 80°C for 120 seconds in 153 serial lesions and radial temperature gradients were measured. With increasing distance from the electrode, the temperature of the myocardium decreased in a hyperbolic form that was closely predicted by a derived thermodynamic model (P = 0.0001, r = 0.98). This gradient and resultant lesion sizes were unafected by the rate of coronary perfusion. The utility of tip temperature monitoring as a predictor of lesion size was tested in 104 serial lesions with tip temperatures that were varied between 50 and 85°C. The tip temperature correlated closely with lesion depth (P = 0.0001, r = 0.92) and width (P = 0.0001, r = 0.88), and was a better predictor of lesion size than measurements of power, current or energy. The temperature at the margin between viable and nonviable tissue was estimated to be 47.9°C. These data demonstrate that during radiofrequency catheter ablation, the radial temperature gradient is predictably hyperbolic and appears to be independent of intramyocardial perfusion if constant electrode temperature is maintained. The use of tip temperature monitoring can accurately predict the ultimate size of radiofrequency‐induced lesions.

All forms of therapy, including chronic stimulation of the thalamic relay nucleus, can provide satisfactory pain control in only 20%‐30% of cases of thalamic pain syndrome. In order to develop a more effective treatment for fhalamic pain syndrome, we investigated the effects of stimulation of various brain regions on the burst hyperactivity of thalamic neurons recorded in cats after deafferentiation of the spinothalamic pathway. Complete, long‐ term inhibition of the burst hyperactivity was induced by stimulation of the motor cortex, Based on this experimental finding, we treated seven cases of thalamic pain syndrome by chronic motor cortex stimulation employing epidural plate electrodes. Excellent or good pain control was obtained in all cases without any complications or side effects. During the stimulation, an increase in regional blood flow of the cerebral cortex and thalamus, a marked rise in temperature of the painful skin regions, and improved movements of the painful limbs were observed. These results suggest that thalamic pain syndrome can be most effectively treated by chronic motor cortex stimulation.

First introduced as a new clinical entity in 1992, the Brugada syndrome is associated with a relatively high risk of sudden death in young adults, and occasionally in children and infants. Recent years have witnessed a striking proliferation of papers dealing with the clinical and basic aspects of the disease. Characterized by a coved‐type ST‐segment elevation in the right precordial leads of the electrocardiogram (ECG), the Brugada syndrome has a genetic basis that thus far has been linked only to mutations in SCN5A, the gene that encodes the α‐subunit of the sodium channel. The Brugada ECG is often concealed, but can be unmasked or modulated by a number of drugs and pathophysiological states including sodium channel blockers, a febrile state, vagotonic agents, tricyclic antidepressants, as well as cocaine and propranolol intoxication. Average age at the time of initial diagnosis or sudden death is 40 ± 22, with the youngest patient diagnosed at 2 days of age and the oldest at 84 years. This review provides an overview of the clinical, genetic, molecular, and cellular aspects of the Brugada syndrome, incorporating the results of two recent consensus conferences. Controversies with regard to risk stratification and newly proposed pharmacologic strategies are discussed.

The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses have been shown in patients with atrial fibrillation. Recently P wave dispersion (PWD), which is believed to reflect inhomogeneous atrial conduction, has been proposed as being useful for the prediction of paroxysmal atrial fibrillation (PAF). Ninety consecutive patients (46 men, 44 women; aged 55 ± 13 years) with a history of idiopathic PAF and 70 healthy subjects (42 men, 28 women; mean age, 53 ± 14 years) were studied. The P wave duration was calculated in all 12 leads of the surface ECC. The difference between the maximum and minimum P wave duration was calculated and this difference was defined as P wave dispersion (PWD = Pmax ‐ Pmin). All patients and controls were also evaluated by echocardiography to measure the left atrial diameter and left ventricular ejection fraction (LVEF). There was no difference between patients and controls in gender (P = 0.26), age (P = 0.12), LVEF (66 ± 4% vs 67 ± 5%, P = 0.8) and left atrial diameter (36 ± 4 mm vs 34 ± 6 mm, P = 0.13). P maximum duration was found to be significantly higher in patients with a history of PAF (116 ± 17 ms) than controls (101 ±11 ms. P < 0.001). P wave dispersion was also significantly higher in patients than in controls (44 ± 15 ms vs 27 ± 10 ms, P < 0.001). There was a weak correlation between age and P wave dispersion (r = 0.27, P < 0.001). A P maximum value of 106 ms separated patients with PAF from control subjects with a sensitivity of 83%, a specificity of 72%, and a positive predictive accuracy of 79%. A P wave dispersion value of 36 ms separated patients from control subjects with a sensitivity of 77%, a specificity of 82%, and a positive predictive accuracy of 85%. In conclusion, P maximum duration and P wave dispersion calculated on a standard surface ECG are simple ECG markers that could be used to identify the patients with idiopathic paroxysmal atrial fibrillation.

The literature suggests that approximately 93% of all pacemaker lead fractures occur in the segment of the lead lateral to the venous entry, and costoclavicular compression has been implicated. While blood vessels can be compressed by movements of the clavicle, our research suggests that lead and catheter damage in that region is caused by soft tissue entrapment rather than bony contact. Dissection of eight cadavers with ten leads revealed that two entered the cephalic vein, and were not included in the study. Of the other eight leads, four passed through the subclavius muscle, two through the costoclavicular ligament, and two through both these structures before entering the subclavian, internal jugular, or brachiocephalic vein. Anatomical studies demonstrated that entrapment by the subclavius muscle or the costoclavicular ligament could cause repeated flexing of leads during movements of the pectoral girdle. Cineradiology of patients with position dependent catheter occlusion confirmed entrapment by the subclavius muscle. Soft tissue entrapment imposes a static load upon leads and catheters, and repeated flexure about the point of entrapment may be responsible for damage previously ottributed to cyclic costoclavicular compression.

A new generic pacemaker code, derived from and compatible with the Revised ICHD Code, was proposed jointly by the North American Society of Pacing and Electrophysiology (NASPE) Mode Code Committee and the British Pacing and Electrophysiology Croup (BPEC), and has been adopted by the NASPE Board of Trustees. It is abbreviated as the NBC (for “NASPE/BPEC Generic”) Code, and was developed to permit extension of the generic‐code concept to pacemakers whose escape rate is continuously controlled by monitoring some physiologic variable, rather than determined by fixed escape intervals measured from stimuli or sensed depolarizations, and to antitachyarrhythmia devices including cardioverters and defibrillators. The NASPE/BPEC Code incorporates an “R” in the fourth position to signify rate modulation (adaptive‐rate pacing), and one of four letters in the fifth position to indicate the presence of antitachyarrhythmia‐pacing capability or of cardioversion or defibrillation functions.

Atrial conduction disorders are frequent in elderly subjects and/or those with structural heart diseases, mainly mitral valve disease, hyperthrophic cardiomyopathies, and hypertension. The resultant electrophysiological and electromechanical abnormalities are associated with a higher risk of paroxysmal or persistent atrial tachyarrhythmias, either atrial fibrillation, typical or atypical flutter or other forms of atrial tachycardias. Such an association is not fortuitous because intra‐ and interatrial conduction abnormalities delays disrupt (spatial and temporal dispersion) electrical activation, thus promoting the initiation and perpetuation of reentrant circuits. Preventive therapeutic interventions induce variable, sometimes paradoxical effects as with the proarrhythmic effect of class I antiarrhythmic drugs. Similarly, atrial pacing may promote proarrhythmias or an antiarrhythmic effect according to the pacing site(s) and mode. Multisite atrial pacing was conceived to correct, as much as possible, abnormal activation induced by spontaneous intra‐ or interatrial conduction disorders or by single site atrial pacing, which are situations responsible for commonly refractory arrhythmias. Atrial electrical resynchronization can also be used to correct mechanical abnormalities like left heart AV dyssynchrony resulting from intraatrial conduction delays. (PACE 2004; 27:507–525)

Implantation of the first automatic defibrillator occurred in February 1980. Incorporation of cardioversion capability in 1982 resulted in the AICD™ automatic implantable cardioverter defibrillator. Between April 1, 1982 and April 15, 1988, 3610 patients in 236 U.S. and 84 international centers received AICD pulse generators. Patient population consisted of 2904 males and 683 females with recurrent ventricular tachycardia and/or fibrillation, mean age 59 yrs. (range 9–96 yrs.). Primary diagnoses reported for the patient group were: coronary artery disease (63.5%), nonischemic cardiomyopathy (12.9%), other (6.4%) and unspecified (17.2%). Mean reported LV ejection fraction was 32.8%. Follow‐up averaged 12.2 mo. (range 0–72 mo.). Of 385 deaths, 94 (24%) were sudden. Cumulative percentage survival (±S.E.) from sudden cardiac death (SCD) was 98.0 ± 0.3%, 96.5 ± 0.5%, 95.2 ± 0.7%, 93.7 ± 1.0%, 93.7 ± 1.0% and 89.7 ± 4.0% at 12, 24, 36, 48, 60 and 72 months, respectively. Operative mortality (30 days) was 2.5%. Reported side effects/complications were similar to those of pacemakers. To date, 33% of the patients received spontaneous device countershocks. AICD pulse generator survival from electrical and mechanical failures was 92.8 ± 0.5%, 88.4 ± 0.7%, 86.7 ± 0.8% and 86.4 ± 0.9% at 12, 18, 24 and 30 mos. Data analysis demonstrates that the AICD has had a significant impact on patient survival from SCD.