By M.J. Janse, M.R. Rosen (auth.)
This ebook contains the main up-to date info on the topic of mechanisms and remedy of cardiac arrhythmia. some of the themes mentioned during this textual content mirror very lately undertaken learn instructions together with genetics of arrhythmias, mobile signalling molecules as capability healing pursuits and trafficking to the membrane. those new ways and implementations of anti-arrhythmic remedy derive from many a long time of study as defined within the first bankruptcy through amazing Professors Michael Rosen (Columbia college) and Michiel Janse (University of Amsterdam). The textual content covers adjustments in ways to treatment through the years, arrhythmias in a number of cardiac areas and over many scales, from gene to protein to phone to tissue to organ.
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Additional resources for Basis and Treatment of Cardiac Arrhythmias
1985; Cox et al. 1987; Haissaguerre et al. 1989; Epstein et al. 1989). The reason why these therapeutic interventions were attempted was that both in animals and in humans the atrial inputs to the AV node during AV conduction, and the exits during ventriculo-atrial conduction are far apart, superior and inferior to the ostium of the coronary sinus (Janse 1969; Sung et al. 1981). We therefore seem to have a very satisfactory and logical sequence of milestones on the road from understanding the mechanism of an arrhythmia to its successful therapy: Mines’ description in 1913, microelectrode studies in animal preparations in the 1960s and 1970s, experimental and clinical demonstration of termination of the tachycardia by premature stimuli, demonstration of atrial input and exit sites to and from the AV node that are wide apart, successful surgery in the 1980s and ﬁnally catheter ablation with success rates that approach 99% and with complication rates well below 1% (Strickberger and Morady 2000).
1971). In both papers, as well as in an earlier paper on AV nodal re-entry (Moe and Mendez 1966), proper credit was given to Mines. Figure 10 shows microelectrode recordings from an isolated rabbit heart preparation in which AV nodal re-entry could be induced and terminated by premature atrial stimuli. One cell (N2) belongs to the anterograde pathway, the other (N1) to the retrograde pathway. During the tachycardia, the stimulator on the atrium was switched on and accidentally the regular stimuli captured the atrium, resulting in a “premature” atrial impulse.
I was making a transverse section of the heart pretty near its base when my knife struck something so hard and gritty as to notch it. I well remember looking up to the ceiling, which was old and gritty, conceiving that some plaster had fallen down. But upon further scrutiny, the real cause appeared: the coronaries were becoming bony canals” (Parry 1799; see also Friedman and Friedland 1998). Jenner believed that coronary artery obstruction might be the cause of angina pectoris as well as of the often-associated sudden death.