Pacing and implantable cardioverter-defibrillator leads can safely, effectively, and predictably be extracted. Open-heart extractions can be limited to special cases. The results indicate that the traditional policy of abandoning redundant leads, instead of removing them, may be obsolete in many patients.
Background: In humans, atrial fibrillation (AF) induces electrical, contractile, and structural remodeling leading to AF stabilization. Little is known about AF-induced atrial remodeling in horses.Hypothesis: Induced AF produces rapid atrial electrical and contractile remodeling in horses. Animals: Six horses, 5 animals completed the study. Methods: Each horse was instrumented with a pulse generator and pacemaker to maintain AF by burst pacing and to study atrial and ventricular electrophysiology (AF cycle length [AFCL], AF duration, and atrial/ventricular effective refractory period [AERP/VERP] at different pacing cycle lengths [PCL]). Left atrial and ventricular contractile remodeling were assessed echocardiographically by calculation of fractional changes in atrial and ventricular dimensions, respectively, during the cardiac cycle. Measurements were performed at baseline, a 7-day AF period and a 2-day recovery period.Results: Atrial electrical and contractile remodeling could be demonstrated after 4 and 12 hours of AF, respectively. A progressive shortening of the AERP (261 AE 39-171 AE 18 ms at a PCL of 1,000 ms, P o .0001), an attenuation of the AERP rate adaptation, a decrease in AFCL (239 AE 39-194 AE 7 ms, P o .0001), and a decrease in atrial FS (12 AE 3% to 0 AE 2%, P o .05) occurred. AF duration increased progressively and became persistent in 2 animals. VERP did not change significantly. Upon restoration of sinus rhythm, values returned to baseline within 48 hours.Conclusions and Clinical Importance: Atrial electrical and contractile remodeling appears rapidly. After 7 days of AF, reverse remodeling occurred within 2 days. These observations suggest that early conversion of AF might be beneficial for success rate and early return to training.
Objective-To study the outcome of patients with arrhythmogenic right ventricular dysplasia treated with an implantable cardioverter-defibrillator (ICD) for ventricular tachyarrhythmias complicated by haemodynamic collapse. Design-Observational study. Setting-University hospital. Patients-Nine consecutive patients (eight male, one female; mean (SD) age, 36 (18) years) with arrhythmogenic right ventricular dysplasia presenting with ventricular tachycardia and haemodynamic collapse (n = 6) or ventricular fibrillation (n = 3), treated with an ICD. Main outcome measures-Survival; numbers of and reasons for appropriate and inappropriate ICD interventions. Results-After a mean (SD) follow up of 32 (24) months, all patients were alive. Six patients received a median of 19 (range 2-306) appropriate ICD interventions for events detected in the ventricular tachycardia window; four received a median of 2 (range 1-19) appropriate ICD interventions for events detected in the ventricular fibrillation window. Inappropriate interventions were seen for sinus tachycardia (18 episodes in three patients), atrial fibrillation (three episodes in one patient), and for non-sustained polymorphic ventricular tachycardia (one episode in one patient). Conclusions-Patients with arrhythmogenic right ventricular dysplasia and malignant ventricular arrhythmias have a high recurrence rate requiring appropriate ICD interventions, but they also often have inappropriate interventions. Programming the device is diYcult because this population develops supraventricular and ventricular tachyarrhythmias with similar rates. (Heart 2001;85:53-56)
This is the first observation that the use of lipid lowering drugs is associated with a reduction of recurrences of VA in patients with CAD and ICD implants. These data require confirmation in a prospective randomized trial.
Intravenous digoxin offers no substantial advantages over placebo in recent onset atrial fibrillation with respect to conversion, and provides weak rate control.
Timothy syndrome type 1 (TS-1) is a rare disorder that affects multiple organ systems and has a high incidence of sudden death due to profound QT prolongation and resultant ventricular arrhythmias. All previously described cases of TS-1 are the result of a missense mutation in exon 8A (p.G406R), an alternatively spliced variant of the L-type calcium channel gene (Ca(v)1.2, CACNA1C). Most patients reported in the literature represent highly affected individuals who present early in life with severe cardiac and neurological manifestations. Here, we describe somatic mosaicism in TS-1 patients with less severe manifestations than the typical TS-1 patient. These findings suggest that the TS prognosis may not be as dismal as previously reported. Moreover, our findings have implications for genetic counseling in that previously described de novo TS mutations may represent cases of parental mosaicism and warrant careful genotyping of parental tissue other than peripheral blood lymphocytes.
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