Rate smoothing with cardiac pacing for preventing torsade de pointes.

Cardiac pacing remains one of the most effective means for preventing torsade de pointes in patients with long QT syndrome (LQTS). However, fatal arrhythmias may occur despite combined therapy with beta blockers and pacing, and it is possible that failure of cardiac pacing for preventing arrhythmias in the long run is related (at least in part) to suboptimal pacemaker programming. Preventing sudden pauses may be especially important for preventing arrhythmias in the LQTS because such pauses are highly proarrhythmic in this patient population. Unfortunately, properly functioning pacemakers cannot be expected to prevent postextrasystolic pauses. The use of a pause-prevention pacing algorithm-rate smoothing-for preventing pause-dependent torsade de pointes is described in 12 patients with cardiac arrest or syncope due to congenital LQTS who were followed for 21 +/- 11 months.

Prevention of torsade de pointes in the congenital long QT syndrome: use of a pause prevention pacing algorithm.

Torsade de pointes in the congenital long QT syndrome (LQTS) is often pause dependent. Thus, the main goal of pacemaker treatment in the LQTS may be the prevention of pauses that facilitate the onset of torsade de pointes. A pause prevention pacing algorithm (rate smoothing) was used for arrhythmia prevention in a 14 year old girl with congenital LQTS. By temporarily increasing the pacing rate after spontaneous premature beats, rate smoothing down of 18% prevented postextrasystolic pauses, pause related T-U changes, and recurrence of pause induced torsade de pointes. Rate smoothing is a potentially useful tool that ought to be evaluated for the prevention of torsade de pointes in the LQTS.

Pacemaker endocarditis. Report of 44 cases and review of the literature.

We conducted a retrospective study to characterize the clinical course, microbiologic spectrum, and risk factors for endocarditis and for associated mortality in a large series of patients with documented pacemaker endocarditis. Using a computerized search through the medical records of 10 major hospitals in Israel from 1982 to 1992, and carefully reviewing the charts, we identified 44 patients with pacemaker endocarditis. The cases were categorized as definite (n = 25), probable (n = 12), or possible (n = 7) infective endocarditis based on strict case definition. Fever and chills were the most common symptoms. Increased ESR, leukocytosis, microscopic hematuria, and anemia were the most common laboratory findings. A relatively high proportion of the patients were diabetic. The most common source of endocarditis was infection acquired by the placement procedure or infection of the pacemaker pouch. Demographic, clinical, and laboratory features were similar to those of endocarditis patients of a similar age range without pacemakers, although the frequency of fever and chills was higher in our patients than in those patients and splenomegaly, vascular embolic phenomena, and new or changing murmurs were rare in our patients. The major pathogens were Staphylococcus aureus and Staphylococcus epidermidis, similar to other series of pacemaker-associated bacteremia and similar to the microbiologic findings of early prosthetic-valve endocarditis. However, this microbiologic profile is different from that of native-valve endocarditis. Although the present series did not show a statistically significant advantage to electrode removal over conservative treatment, when analyzed together with pooled data from other studies, it suggests that the surgical approach is preferable.(ABSTRACT TRUNCATED AT 250 WORDS)

The use of transcranial Doppler in the hemodynamic assessment of implanted pacemakers.

Twenty patients with DDD pacemakers had their intracranial cerebral circulation assessed in different pacing modes, using transcranial Doppler. The studies were performed at the vertebral artery in a sitting position. Although DDD pacing was preferred to VVI pacing in 18 of the 20 patients, the figures did not reach statistical significance. There was no statistical difference in maximal blood flow velocity between DDD pacing at 60 and 80 beats/min. Varying the AV interval from 150-250 msec also demonstrated no clear difference in maximal peak Doppler velocity, in the group as a whole, though there was a greater individual preference for 150 msec. Transcranial Doppler assessment of the hemodynamics of the cerebral circulation is of limited value as an indicator of mode or rate preference in the pacemaker population.

Traumatic heart block.

Penetrating chest wounds have only occasionally been reported as a cause of permanent atrioventricular block. A case is presented in which a nail, fired from a power operated device, passed through the chest, causing complete atrioventricular block and requiring permanent pacing.

The effect of metal detector gates on implanted permanent pacemakers.

The effect of metal detector security gates, such as are used in airports, was tested in 103 nonselected pacemaker patients. Various types of single and dual chamber units were examined, using telemetry during the test. Pulse rate and duration were measured immediately before and after the procedure. No ill effect was seen on any of the units tested, pacemaker inhibition was not observed, and programmability was not affected. Metal detector security gates have no effect on implanted permanent pacemakers.

Mechanisms of syncope in glossopharyngeal neuralgia.

Syncope is a rare presentation of glossopharyngeal neuralgia (GN). The mechanisms of the syncope were studied in a patient with recurrent episodes comprising prolonged cardiac standstill and arterial hypotension. During attacks, no supraventricular or ventricular potentials were recorded in the ECG. Atropine prevented the cardiac arrest without affecting the pain, indicating the vagus as the efferent limb of the reflex asystole. Following atropine blood pressure continued to fall during GN attacks, suggesting abolition of sympathetic tone. Indeed, serum norepinephrine levels fell during these attacks. Infiltration of either vagus above the clavicle with local anesthetics did not abolish the cardiac asystole. Carbamazepine and a dual chamber pacemaker were effective in controlling the symptoms of the patient. The results suggest that, during a neuralgic attack, the stimulation excites both vagi, causing asystole and simultaneously abolishes sympathetic tone.