Anatomy of the conduction tissues 100 years on: what have we learned?

Knowledge of the anatomy of the ‘conduction tissues’ of the heart is a 20th century phenomenon. Although controversies still continue on the topic, most could have been avoided had greater attention been paid to the original descriptions. All cardiomyocytes, of course, have the capacity to conduct the cardiac impulse. The tissues specifically described as ‘conducting’ first generate the cardiac impulse, and then deliver it in such a fashion that the ventricles contract in orderly fashion. The tissues cannot readily be distinguished by gross inspection. Robust definitions for their recognition had been provided by the end of the first decade of the 20th century. These definitions retain their currency. The sinus node lies as a cigar-shaped structure subepicardially within the terminal groove. There is evidence that it is associated with a paranodal area that may have functional significance. Suggestions of dual nodes, however, are without histological confirmation. The atrioventricular node is located within the triangle of Koch, with significant inferior extensions occupying the atrial vestibules and with septal connections. The conduction axis penetrates the insulating plane of the atrioventricular junctions to continue as the ventricular pathways. Remnants of a ring of cardiomyocytes observed during development are also to be found within the atrial vestibules, particularly a prominent retroaortic remnant, although that their role has still to be determined. Application of the initial criteria for nodes and tracts shows that there are no special ‘conducting tissues’ in the pulmonary venous sleeves that might underscore the abnormal rhythm of atrial fibrillation.

The Amplatzer® Membranous VSD Occluder and the vulnerability of the atrioventricular conduction system

Transcatheter closure of ventricular septal defects with the Amplatzer® Membranous VSD Occluder has yielded promising initial results, but disturbances of conduction, including complete heart block, have been reported. We report our experience with the Amplatzer occluder in 35 patients with a median age 4.5 years, the defects being sized angiographically at 4.4 plus or minus 1.1 millimetres, with a range from 3 to 8 millimetres, and the size of the occluder varying from 4 to 12 millimetres. Over a median follow-up of 2.5 years, the rate of complete closure was 87% and 91%, at 1 and 2 years respectively, while 2 patients required surgical closure of the defect subsequent to the insertion of the device. Persistent regurgitation across the tricuspid valve related to the occluder was observed in 3 patients, and in 6 patients across the aortic valve. Abnormalities of conduction related to the procedure were noted in 7 patients, one-fifth of the cohort. The disturbances were transient in 1 patient, but permanent in 6, in one of the latter progressing after 6 months from left bundle branch block to intermittent Mobitz II second-degree atrioventricular block in association with expansion of the occluder. We conclude that transcatheter closure of perimembranous ventricular septal defects with the Amplatzer occluder is effective with limited complications, but the incidence of immediate and progressive disturbances of conduction related to the proximity of conduction tissues to the rims of the occluder stress the importance of larger and longer studies to assess the safety of this procedure.

The diverse cardiac morphology seen in hearts with isomerism of the atrial appendages with reference to the disposition of the specialised conduction system

Congenital cardiac malformations which include isomerism of the atrial appendages are amongst the most challenging of problems for diagnosis and also for medical and surgical management. The nomenclature for pathological description is controversial, but difficulties can be overcome by the use of a segmental approach. Such an approach sets out the morphology and the topology of the chambers of the heart, together with the types and modes of the atrioventricular, ventriculo-arterial, and venous connections. We have applied this method to a study of 35 hearts known to have isomerism of the atrial appendages. We have already published accounts of 27 of these cases, but these were reviewed for this study in the light of our increased awareness of the implications of isomerism, and 8 new cases were added. After examining, or re-examining, the morphology of every heart in detail, we grouped them together according to their ventricular topology and modes of atrioventricular connection. Then we studied the course of the specialised conduction system, by the use of the light microscope, first in each individual case, and then together in their groups. We conclude that the pathways for atrioventricular conduction in hearts with isomerism of the atrial appendages are conditioned both by ventricular topology, and by the atrioventricular connections. Based on our experience, we have been able to establish guidelines that direct the clinician to the likely location of the conduction tissues.