• Cardiac function
• cardiac remodelling
• myocardial disease
• cardiomyopathy dilated
• cardiomyopathy hypertrophic
• arrhythmic right ventricular dyplasia
• genetics

The classification of cardiac conduction disease has long been dominated by concepts anchored in macroscopic anatomical structures within the heart. The sinoatrial node, atrioventricular (AV) node and proximal His-Purkinje system can each be seen with the naked eye in humans, and in the most commonly used large animal models. Early physiologic data established the distinctive cellular electrical properties of these tissues and enshrined the fundamentals of physiologic and pathophysiologic conduction.1 Clinical cases where conduction disease was the predominant presenting feature were recognised as electrocardiography spread. Painstaking postmortem histomorphometric reconstructions of hearts from such cases resulted in the concepts of focal fibrosis, or a restricted degenerative process, as the mechanisms of ‘isolated’ conduction disease.2

Parallel early work in surface electrocardiography and intracardiac recording documented the electrophysiologic correlates of proximal conduction-system pathology, but the absence of a readily defined anatomical substrate for more distal conduction abnormalities has prevented systematic reconciliation of structure and function.3 ,4 As a result, loosely defined concepts such as parietal block, hemiblocks and peri-infarct block have emerged to facilitate the retrofitting of surface electrocardiographic findings onto contemporaneous understanding of anatomy, cell biology and pathology.5 The resultant patchwork of partially overlapping clinical, electrocardiographic and pathophysiologic syndromes does not stand up to rigorous scrutiny. Structural, contractile and electrical data are rarely integrated, but rather are considered as separate entities in the individual patient. In this construct, the electrocardiographic conduction abnormalities observed in most cardiac syndromes are attributed to non-specific incidental involvement of the anatomical conduction system in the pathophysiologic processes underlying the primary disorder. There is little evidence of focal involvement of discrete anatomic structures in most cases of conduction disease, and there is substantial evidence that diffuse myocardial involvement will produce …