Manuel R. Estioko

Primary sick sinus syndrome as an indication for chronic pacemaker therapy in young adults: Incidence, clinical features, and long-term evaluation

Of 1484 pacemakers placed at our institution between 1970 and 1980, there were 18 patients between the ages 20 and 40 years who were not postoperative congenital heart disease cases. Twelve of these patients had primary sick sinus syndrome (SSS) as the indication for pacing. Eleven of 12 patients were markedly symptomatic with syncope, near syncope, or lightheadedness. Ambulatory monitoring revealed evidence of sinus node disease in all patients studied. Electrophysiologic studies were falsely negative in the five patients in whom they were performed. Patients tolerated pacemaker therapy well and became asymptomatic with pacing. We conclude that SSS in young adults is uncommon, but still represents the most common indication for permanent pacemaker therapy in this age group. The decision for pacemaker therapy should depend on symptoms and results of ambulatory monitoring. These patients can expect symptomatic improvement with pacing.

Left ventricular to left atrial communication secondary to a paraaortic abscess: Color flow doppler documentation

Aortic root abscess occurs frequently in aortic prosthetic valve infective endocarditis. The present echocardiographic report documents a ruptured abscess that led to a direct communication between the left ventricular outflow tract and the left atrium confirmed by real-time (color flow) Doppler imaging.

Accidental placement of the Greenfield filter in the heart: Report of two cases

The Greenfield filter has become the most popular device for interruption of the inferior vena cava; however, a potential for lethal complications exists. We report two cases in which this filter was accidentally released in the heart. To avoid this problem, it is recommended that the guide wire be positioned in the inferior vena cava before the introducer is inserted into the venous system.

Myopotential interference with DDD pacemakers: Endocardial electrographic telemetry in the diagnosis of pacemaker-related arrhythmias

Skeletal myopotentials may inhibit the output of unipolar demand ventricular pacemakers, resulting in protracted episodes of asystole in susceptible patients. The new DDD-mode pacemakers have, in addition to a unipolar ventricular lead, a unipolar atrial lead to enable atrioventricular sequential or atrial synchronous function. During clinical investigation of a new dual-unipolar cardiac pacing system programmed to operate in the DDD mode (Pacesetter AFP models 281 and 283), 6 patients were noted (5 men and 1 woman, aged 22 to 68 years) who manifested paroxysmal acceleration of ventricular pacing rate approaching the maximal tracking rate. Two patients also had abrupt slowing or cessation of ventricular output. With the use of atrial electrographic recordings (obtained with telemetry), the following mechanisms of rate change were found: myopotential tracking, myopotential inhibition, interference-mode asynchronous operation, sudden increases in sinus rate, and pacemaker-mediated reentrant tachycardia. In all patients, reprogramming of the implanted devices, based on telemetered atrial electrography, resulted in disappearance of the arrhythmias and loss of symptoms while maintaining the DDD pacing mode. Thus, several mechanisms of rhythm disturbances are peculiar to dual-chamber cardiac pacing systems that use unipolar electrodes. Endocardial telemetry combined with extensive programming capability offers the best opportunity for proper diagnosis and management of these problems.

Clinical and electrophysiologic determinants, treatment and survival of patients with sustained malignant ventricular tachyarrhythmias occurring late after myocardial infarction.

To assess the clinical and electrophysiologic determinants, treatment and survival of patients with sustained malignant ventricular tachyarrhythmias late after myocardial infarction, a total of 108 patients (mean age 61 +/- 10 years) were studied. Thirty-two patients (Group I) had sustained ventricular tachyarrhythmias 8 to 60 days (mean 13 +/- 9) after acute myocardial infarction. The remaining 76 patients (Group II), who served as a control group, had no sustained ventricular tachyarrhythmias less than or equal to 60 days after infarction. The most significant independent determinants of sustained ventricular tachyarrhythmias late after infarction were the presence of late potentials (chi square = 16.07, p = 0.0001), defined as an abnormal signal-averaged QRS complex in association with an abnormal root-mean-square voltage in the terminal 40 ms of the QRS complex, and an abnormal ejection fraction of less than 40% (chi square = 10.09, p = 0.001). Sustained ventricular tachycardia was induced in 27 (96%) of 28 Group I patients. Among the 32 patients in Group I, antitachycardia therapy included antiarrhythmic drug therapy as the sole preventive measure in 14 (44%); map-guided surgery or coronary artery bypass surgery, or both, in 14 (44%) and the automatic cardioverter-defibrillator in 4 (12%). The arrhythmias were rendered noninducible in 83% of patients after map-guided surgery and in 41% after drug therapy. During a follow-up period of 20 +/- 14 months, five Group I patients (15%) had an arrhythmic event and four (9.3%) had a cardiac-related death. All five patients who had an arrhythmic event were receiving antiarrhythmic drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

A Comparative Analysis of Signal Averaging of the Surface QRS Complex and Signal Averaging of Intracardiac and Epicardial Recordings in Patients with Ventricular Tachycardia

To test the hypothesis that late potentials may be more enhanced by signal processing of intracardiac and epicardial electrograms, we performed a comparative analysis of signal averaging (SA) of the surface QRS complex (method I), signal averaging of an endocardial electrode catheter recording (method II), and epicardial recording (method III) in 24 patients (mean age = 55 ± 14 years). Sixteen of (he 24 patients (66%) had spontaneous as well as induced sustained ventricular tachycardia (VT), whereas the remaining 8 patients (33%) had spontaneous non‐sustained VT. SA by the three methods was performed within ≤24 hours of each other, utilizing a band pass jilter frequency of 25 to 250 Hz. The duration of the SA‐QRS complex, low amplitude signals (LAS) of <40 μV and the RMS‐voltage (V) of the terminal 40 ms were determined for the three methods. There was a significant correlation between method I and methods II and III for the SA‐QfiS duration (r = .928, p < .001), RMS‐V(r = .634. p < .002) and LAS (r = .783, p < .001). There was no significant difference in the quantitative signal‐averaged parameters between the three methods. The incidence of the RMS‐V of <25 μV (37.5% vs 21%); LAS of >32 ms (46% vs 37.5%) and SA‐QRS of >120 ms (54% vs 42%) was higher but statistically non‐significant by methods II and III when compared to method I. We concluded that: (1) SA of intracardiac electrograms correlate well with SA of the surface QKS. This observation further validates the technique of surf ace SA to detect delayed ventricular activation. (2) SA of intracardiac electrograms may provide additional information on quantitative SA parameters relative to surface QRS in some patients with VT.