PubMed · 6416749
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E R Sjogren. TONOCARD (tocainide HCL).. https://pubmed.ncbi.nlm.nih.gov/6416749/
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We used computer simulation to study the possible role of the dispersion of cellular coupling, refractoriness or both, in the mechanisms underlying cardiac arrhythmias. Local ischemia was first assumed to induce cell to cell dispersion of the coupling resistance (case 1), refractory period (case 2), or both (case 3). Our numerical experiments based on the van Capelle and Durrer model showed that vortices could not be induced. On the other hand, with cellular properties dispersed in a patchy way within the ischemic zone, a single activation wave could give rise to abnormal activities. This demonstrates the stability of the wave front under small inhomogeneities. Probabilities of reentry, estimated for the three cases cited above showed that a severe alteration of the coupling resistance may be an important factor in the genesis of reentry. Moreover, use of isochronal maps revealed that vortices were both stable and sustained with an alteration of the coupling alone or along with a reduction of the action potential duration. Conversely, simulations with reduction of the refractoriness alone, inducing only transient patterns, could exhibit functionally determined reentries.
Indications for permanent pacemakers have expanded in recent years. The American College of Cardiology (ACC) and American Heart Association (AHA) guidelines for implantation of cardiac pacemakers were recently updated and now include several of the newer indications. Greatest interest about newer applications of pacemaker therapy focuses on hypertrophic obstructive cardiomyopathy, dilated cardiomyopathy, and pacing for the prevention of atrial fibrillation. Pacing for neurocardiogenic syncope remains controversial despite emerging data. Pacing for long QT syndrome, pacing after cardiac transplantation, and pacing for hemodynamic improvement in the occasional patient with first-degree atrioventricular block and hemodynamic compromise also warrant attention. Available clinical data are discussed in the context of the recent ACC and AHA guidelines.
The ever-increasing complexity of pacing systems, combined with functions that vary from one manufacturer to another, can pose challenges during analysis of device function. Standard pacemaker diagnostics are measured data, electrogram telemetry, maker annotations and event counters, albeit with their current limitations. New diagnostic features discussed include time-based diagnostics, histograms of sensed amplitudes, pacing thresholds, or impedance trending. Mode-switching algorithms, combined with diagnostic features, facilitate the use of dual-chamber devices in patients with paroxysmal atrial tachyarrhythmias. The introduction of electrogram storage into pacemakers further improves diagnostic capabilities and allows a permanent validation and optimization of diagnostic and therapeutic algorithms. External diagnostic devices, which provide Holter recordings with continuous marker annotations and patient-triggered diagnostics, are additional features that will become increasingly important.