PubMed · 3989130
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T N James. 1985. Crib death.. https://doi.org/10.1016/s0735-1097(85)80023-1
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BACKGROUND: Abnormal atrial automaticity in young patients with structurally normal hearts is often located around the pulmonary veins and in sinus venosus-related parts of the right atrium. We hypothesize that these ectopic pacemaker sites correspond to areas of embryonic myocardium with an early phenotypic differentiation, as indicated by differences in antigen expression during normal cardiac development. METHODS AND RESULTS: In human embryos ranging in age from 42 to 54 days of gestation, the development of the cardiac conduction system was studied with the use of HNK-1 immunohistochemistry. HNK-1 stains the developing atrioventricular conduction system, ie, the bundle branches, His bundle, right atrioventricular ring, and retroaortic ring. In addition, the myocardium around the common pulmonary vein showed transient HNK-1 antigen expression. In the right atrium, 3 HNK-1-positive connections were demonstrated between the sinoatrial node and the right atrioventricular ring. An anterior tract through the septum spurium connects the sinoatrial node with the anterior right atrioventricular ring, and 2 posterior tracts connect the sinoatrial node with the posterior right atrioventricular ring through the right venous valve (future crista terminalis) and sinus septum, encircling the coronary sinus. The medioposterior part of the right atrioventricular ring connected to the His bundle and the medioanterior part form 2 node-like structures. CONCLUSIONS: In patients with abnormal atrial automaticity, the distribution of left and right atrial pacemaker foci correspond to areas of the embryonic myocardium that temporarily express the HNK-1 antigen.
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We tested the hypothesis that in some patients affected by typical AVNRT, successful catheter ablation treatment may be achieved independently of specific measurable electrophysiological modifications of antegrade AV node conducting properties. Standard electrophysiological parameters and comparable antegrade AV node function curves were obtained, before and after successful ablation, in 104 patients (mean age 52 +/- 16 years; 69 women and 35 men) affected by the common form of AVNRT. The end point of the ablation procedure was noninducibility of AVNRT and of no more than one echo beat. For the purpose of this study, AV node duality was defined as an increase of > or = 50 ms in the A2H2 interval in response to a 10 ms decrease of the A1A2 coupling interval. Before ablation, AV node duality was present in 65 patients (62%) and absent in 39 patients (37%). Ablation caused measurable modifications of electrophysiological properties of the AV node in most patients with elicited AV node duality, but not in most patients without demonstrable AV node duality. After ablation, AV node duality persisted in 20 patients who had it before, whereas a new duality that could not be elicited before appeared in 5 patients. During 19 +/- 6 months of follow-up, clinical AVNRT recurred in 1 of 45 patients who had disappearance of AV node duality after ablation, in 1 of 34 patients who did not show AV node duality before and after ablation, and in 1 of 20 patients who had persistence of AV node duality after ablation. In conclusion, modifications of antegrade conduction properties of the AV node are not crucial for the cure of AVNRT in many patients.