Pacing and clinical electrophysiology : PACE
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Pacing Clin Electrophysiol · Jun 1994
Systolic arterial pressure recovery after ventricular fibrillation/flutter in humans.
Although the elective induction of cardiac arrest for implantable defibrillator insertion under general anesthesia is widely used, the hemodynamics of recovery of arterial blood pressure after cardiac arrest is not well-defined. Accordingly, the time course of recovery of systolic arterial pressure was studied in seven patients during the repetitive induction of ventricular fibrillation (n = 6) or ventricular flutter (n = 1). The mean number of episodes of cardiac arrest was 7 +/- 2, and the mean drop in systolic pressure was 84 +/- 16 mmHg. ⋯ A linear relation between the time for systolic pressure recovery and duration of asystole was also defined. These results are consistent with the view that prolongation of ventricular fibrillation or flutter increases the duration of arterial pressure recovery through a negative effect on left ventricular contractility. Increased understanding of these relations may lead to increased safety of implantable defibrillator insertion.
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Pacing Clin Electrophysiol · May 1994
Short- and long-term reproducibility of QT, QTc, and QT dispersion measurement in healthy subjects.
The study investigated interobserver and intrasubject reproducibility of QT interval duration and dispersion measured in standard 12-lead ECGs recorded at 25 mm/sec. Twenty-eight healthy volunteers were studied. Each underwent four ECG recordings, which were performed 1, 7, and 30 days apart. ⋯ The interobserver and short-term (1 day) and long-term (1 week and 1 month) reproducibility of individual indices was assessed by computing the relative errors and comparing them by a standard sign test. In addition, the distributions of maximum and minimum QTc values among electrocardiographic leads, and the differences between QT-end and QT-peak based measurements were investigated. The results showed that: (1) the measurement of the QT interval from standard ECG recordings is feasible and not operator dependent (interobserver relative error < 4%); (2) the duration of the QT interval in healthy volunteers is stable and its short- and long-term reproducibility is high (intrasubject relative error < 6%); (3) parameters that characterize dispersion of the QT interval in the 12-lead ECG are highly nonreproducible, both between subsequent recording (relative error of 25%-35%) and between observers (relative error 28%-33%), the reproducibility of QT dispersion is significantly lower than that of QT duration (P < 0.01); and (4) the duration of the entire QT interval correlates only weakly with the duration of the Q-peak of T interval.
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Pacing Clin Electrophysiol · Apr 1994
Case ReportsPermanent ventricular pacing via the great cardiac vein.
Two cases of left ventricular pacing via the great cardiac vein are presented. A 64-year-old female with a mechanical prosthetic tricuspid valve and slow atrial fibrillation had a failed attempt at pacing from the middle cardiac vein. ⋯ In both cases, successful pacing via the great cardiac vein was achieved but with an elevated stimulation threshold. These cases illustrate an alternate transvenous route when difficulties occur using standard ventricular pacing sites.
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Pacing Clin Electrophysiol · Feb 1994
Comparative StudyEffect of low dose aspirin on augmented plasminogen activator inhibitor type 1 activity in patients with permanent pacemakers.
To clarify the activity states of coagulation and fibrinolysis in patients with a permanent pacemaker, we studied 29 patients more than 4 months after operation. They were divided into a single pacemaker lead group (S, n = 14) and a double lead group (D, n = 15). Prothrombin time, activated partial thromboplastin time, fibrinogen, antithrombin III, tissue-type plasminogen activator (tPA) activity, plasminogen activator inhibitor type-1 (PAI-1) activity, and platelet aggregation were measured and compared to those in an age-matched control group (C, n = 7). ⋯ Other parameters were not significantly different. In the patients, low dose aspirin significantly suppressed collagen induced platelet aggregation (71.8 +/- 20.3% vs 41.7 +/- 28.3%; P < 0.005), but not PAI-1 activity. tPA activity was increased significantly by the low dose aspirin administration (3.94 +/- 1.85 ng/mL vs 2.48 +/- 1.19 ng/mL; P < 0.005). Thus, PAI-1 activity in patients with a permanent pacemaker is elevated, and the activity is not suppressed by low dose aspirin unlike the platelet aggregation.