Basis and Treatment of Cardiac Arrhythmias by Robert E. Kass, Colleen E. Clancy

By Robert E. Kass, Colleen E. Clancy

This ebook contains the main up-to date details with regards to mechanisms and remedy of cardiac arrhythmia. some of the subject matters mentioned during this textual content mirror very lately undertaken examine instructions together with genetics of arrhythmias, mobile signalling molecules as strength healing ambitions and trafficking to the membrane. those new techniques and implementations of anti-arrhythmic treatment derive from many a long time of analysis as defined within the first bankruptcy through distinct Professors Michael Rosen (Columbia college) and Michiel Janse (University of Amsterdam). The textual content covers adjustments in techniques to treatment through the years, arrhythmias in a number of cardiac areas and over many scales, from gene to protein to mobilephone to tissue to organ.

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Blackwell Scientific Publications, Oxford Scherf D (1947) Studies on auricular tachycardia caused by aconitine administration. Proc Soc Exp Biol Med 64:233–239 Scherf D, Cohen J (1964) The atrioventricular node and selected arrhythmias. Grune and Stratton, New York Scherf D, Schott A (1953) Extrasystoles and allied arrhythmias. Heinemann, London Scherlag BJ, Kosowsky BD, Damato AN (1976) Technique for ventricular pacing from the His bundle of the intact heart. J Appl Physiol 22:584–587 Scherlag BJ, Lau SH, Helfant RH, et al (1979) Catheter technique for recording His bundle activity in man.

60 60 61 62 5 Conclusions . . . . . . . . . . . . . . . . . . 63 References . . . . . . . . . . . . . . . . . . . . 64 . . . . . . . . . . Abstract The ionic basis of automaticity in the sinoatrial node and His–Purkinje system, the primary and secondary cardiac pacemaking regions, is discussed. Consideration is given to potential targets for pharmacologic or genetic therapies of rhythm disorders. An ideal target would be an ion channel that functions only during diastole, so that action potential repolarization is not affected, and one that exhibits regional differences in expression and/or function so that the primary and secondary pacemakers can be selectively targeted.

1994; Schuessler et al. 1997). However, several observations revived the “focus” theory combined with fibrillary conduction, even though the “focus” was in itself re-entrant in nature. Thus, in isolated canine atria exposed to large doses of acetylcholine, which shortened the refractory period to about 95 ms, and in which fibrillation became stable, the “focus” consisted of a small, single and stable re-entrant circuit which activated the rest of the atrium by fibrillatory conduction (Schuessler et al.

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