PubMed · 5346964
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D Berman. 1969. Electronic pacemakers.. https://pubmed.ncbi.nlm.nih.gov/5346964/
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AIMS: Identification of implantable cardioverter/defibrillator (ICD) recipients at higher risk of future therapies may assist in pre-empting future shocks. Native QRS duration is an established predictor of overall mortality, but the role of this parameter as a clinical predictor of arrhythmic events warrants further investigation. METHODS AND RESULTS: In an analysis of a single-centre, 13-year ICD implantation experience (1990-2002), multiple clinical parameters including QRS duration were analysed using a multiple logistic regression model. Of 562 patients followed for at least 1 year, 98 (17%) did not receive ICD therapies (event-free, group A). Comparisons were made with a randomly selected sample of 123 patients who received ICD therapies (arrhythmic events, group B). There were no significant differences in age, gender, frequency of coronary artery disease, and degree of left ventricular dysfunction. However, QRS duration was a significant determinant of arrhythmic events (> or =100 vs. <100 ms: adjusted OR 2.75, 95% CI 1.37-5.51; > or =120 vs. <120 ms: adjusted OR 1.77, 95% CI 0.97-3.23). QRS duration was also a predictor of overall mortality in the logistic regression models (> or =100 ms: adjusted OR 3.72, 95% CI 1.17-11.9; > or =120 ms: adjusted OR 3.09, 95% CI 1.39-6.85). CONCLUSION: In this ICD population, consisting largely of secondary prevention ICD recipients, longer QRS duration predicted higher likelihood of arrhythmic events. Extent of QRS prolongation could guide the decision to initiate prophylactic anti-arrhythmic therapy in ICD patients.
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Spatially discordant alternans, where the action potential duration (APD) and intracellular calcium transient (Ca(i)) alternate with opposite phase in different regions of tissue, is known to promote wave break and reentry. However, this phenomenon is not completely understood. It is known that alternans at the cellular level can be caused by dynamical instabilities arising from either membrane voltage (V(m)) attributable to steep APD restitution or to calcium (Ca) cycling. Here, we used a mathematical model of intracellular Ca cycling, coupled with membrane ion currents, to investigate the dynamics of V(m) and Ca(i) transient alternans in an isolated cell, in two electrotonically coupled cells, and in 1D spatially homogeneous tissue. Our main finding is a novel instability mechanism in which the bidirectional coupling of V(m) and Ca(i) can drive the Ca(i) transient of two neighboring cells to be out of phase. This instability is manifested in cardiac tissue by the dynamical formation of spatially discordant alternans. In this case, Ca(i) transient alternans can reverse phase over a length scale of one cell, whereas APD alternans reverses phase over a much longer length scale set by the electrotonic coupling. We analyze this mechanism in detail and show that it is a robust consequence of experimentally established properties of the bidirectional coupling between Ca cycling and V(m) dynamics. Finally, we address the experimental relevance of these findings and suggest physiological conditions under which these patterns can be observed.