Heart block as a complication of acute myocardial infarction: the anatomical and physiological mechanisms

Heart block (HB) frequently forms part of the clinical picture of patients suffering acute myocardial infarction (AMI) (Gamon et al, 2007). Identifying the type of HB associated with AMI is important in determining treatment strategies and predicting its likely clinical course (Fowler, 2002). This is reliant on a sound understanding of relevant anatomy and physiology (Moran and Gunnar, 1975). Although many of the original pathological studies investigating HB were conducted almost half a century ago, their results are still of value in highlighting the role of anatomical and physiological variations in the clinical presentation of HB in the context of AMI.

The heartbeat is initiated by an intrinsic electrical system composed of modified myocytes. These myocytes are organised into a group of spontaneously discharging pacemaker cells, situated in the sinoatrial (SA) node, and a series of elongated conduction fibre cells, responsible for propagating electrical impulses throughout the heart (Levick, 2010). The SA node is situated close to the superior vena cava on the posterior wall of the right atrium. It is suggested that impulses originating from the SA node are transmitted throughout the atria via anterior, middle and posterior pathways (Figure 1), named Bachmans, Wenkebachs and Thorels bundles respectively (Katz, 2006).