PubMed · 13977888
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
R B SKELTON, E CORDAY. 1962. Ectopic atrial rhythms.. https://pubmed.ncbi.nlm.nih.gov/13977888/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Controlling cardiac chaos is often achieved by applying a large damaging electric shock-defibrillation. It removes all waves, without differentiating reentries and normal waves, anatomical and functional reentries. Anatomical reentries can be removed by anti-tachycardia pacing (ATP) as well. But ATP requires the knowledge of the position of the reentry, and an access to it with an invasive stimulating electrode. We show that the physics of electric field distribution between cardiac cells permits one to deliver an electric pulse exactly to the core of an anatomical reentry, without knowing its position and even to locations where access with a stimulating electrode is not possible. The energy needed is two orders of magnitude less than defibrillation energy. The results are insensitive to both a detailed ionic model and to the geometry of the fibers.
Myocardial calcium signalling is a vital component of the normal physiological function of the heart. Key amongst the many roles calcium plays is its use as the primary signalling component of excitation-contraction coupling, the intracellular process that links cardiomyocyte depolarisation to contraction. Defective cellular calcium handling, due to abnormalities of the various components which mediate and control excitation-contraction coupling, is widely recognised as a significant patho-physiological event in the contractile dysfunction of the failing heart. In addition, similar defects also appear to be increasingly recognised as mediators of certain forms of cardiac arrhythmias. Such defects include single gene defects in excitation-contraction coupling components that lead to inherited sudden death arrhythmia syndromes. Alternatively, arrhythmogenesis occurring within the context of acquired cardiac disease, in particular heart failure, also appears to be highly dependent on abnormal calcium homeostasis. In this article we review the defects in cardiomyocyte calcium homeostasis that lead to particular pro-arrhythmogenic phenomena and discuss recent insights gained into a variety of inherited and acquired arrhythmia syndromes that appear to involve defective calcium signalling as a central component of their patho-physiology. Potential opportunities for new anti arrhythmic therapeutic strategies based on these recent insights are also discussed.
The advent of gene therapy and cell therapy has led to reconsideration of standard therapies for cardiac disease. One such area of reconsideration is that of the cardiac pacemaker, which has been the mainstay of treatment for high-degree heart block and sinoatrial node dysfunction. Over the past five years, gene therapy has been used to explore the overexpression of beta(2)-adrenergic receptors, the down-regulation of inward rectifier current, and the overexpression of pacemaker current as potential sources of biological pacemakers. Cell therapy approaches have explored the "forcing" of embryonic stem cells to evolve along cardiac (and specifically pacemaker) cell lines and the use of adult mesenchymal stem cells as platforms for delivery of specific gene therapies. This review considers the strengths and weaknesses of each of the approaches used to date and attempts to look to the future of biological alternatives to electronic pacemakers.