PubMed · 7591804
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G Nikolic. Left bundle branch block with right axis deviation.. https://doi.org/10.1016/s0147-9563(05)80082-2
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The histogenesis of the separation between atrial and ventricular myocardium at the atrioventricular junction in the developing human heart has been investigated immunohistochemically by using monoclonal antibodies specific for atrioventricular cushion tissue, mesenchymal cells, atrial and ventricular myocardium, and myocardium of the primary ring. It was found that the insulation between the muscle masses of atrium and ventricle is established by the fusion of the tissues of the atrioventricular sulcus (located at the epicardial side of the junctional myocardium) with those of the atrioventricular cushions (located at the endocardial side of the junctional myocardium). This process takes place at the ventricular margin of the myocardium of the atrioventricular canal. The separation of atrial and ventricular myocardium starts at approximately 7 weeks of development in the anteromedial portion of the right atrioventricular junction and is largely completed around the 12th week of development. The only remaining myocardial continuity between atrial and ventricular myocardium is the atrioventricular axis of conduction. Our findings show that the nonmuscular part of the developing leaflets of the atrioventricular valves derives from the atrioventricular cushions and that the tissues of the atrioventricular groove do not contribute to the development of these leaflets.
Atrioventricular nodal reentrant tachycardias which, for a long time, could only be treated medically, may now benefit from catheter ablation. The rapid retrograde pathway was an effective initial target but carried a risk of complete atrioventricular block of about 10%. Nowadays, most operators deliver the radiofrequency energy (endocavitary cautery) to the slow nodal pathway. Different techniques of guidance (anatomical, electrophysiological, rapid potential, slow potential) are associated with high success rates: 90 to 100%. However, experimental studies suggest that the slow potentials arise from transitional cells within the tachycardia circuit (the anatomical substrate of the slow pathway). There is still a risk of complete atrioventricular block (1 to 5%) which should be clearly explained to patients referred for ablation of this constantly benign arrhythmia.