Inferior myocardial infarction scars could be more arrhythmogenic than anterior ones

Pascale et al.1 reported that the scars of old inferior infarctions without areas of potential ischaemia and accompanied by, on average, even better left ventricular systolic function were significantly more associated with the occurrence of ventricular arrhythmias than anterior scars. The authors proposed that the right ventricle damage and sympathetic hyperactivity due to the destruction of afferent vagal fibres in the inferior infarctions may be underlying mechanisms. However, there is an observation 2 suggesting a temporary 6-week impairment of cardiac parasympathetic activity associated with anterior infarctions and preserved parasympathetic function in inferior infarctions which conflicts with the latter mechanism Pascale et al. have proposed. Several additional mechanisms should also be considered. It has been generally accepted that vagal fibres are mainly located in the inferoposterior cardiac wall, whereas the distribution of sympathetic fibres is less well determined. Although there is a report suggesting that sympathetic nerves are distributed equally to the inferoposterior and anterior left ventricular wall, 3 a body of evidence suggests that sympathetic endings follow coronary arteries and are preferentially distributed across the anterior wall. 4–6 At least part of these fibres are destroyed by anterior infarctions. This may reduce sympathetic efferent activity and abolish its arrhythmogenic consequences, particularly when cardiac vagal fibres are preserved. In inferior infarctions, preserved sympathetic endings in the anterior wall may be the loci of significantly increased catecholamine release, favouring initiation of ventricular arrhythmias in the local myocardium. In severe acute emotional stress, such a hypercatecholaminaemia may produce a cytotoxic effect on surrounding myocytes and even cause contraction band necroses like those seen with the left ventricular ballooning syndrome. 7 , 8 Further mechanisms may involve papillary muscles. The surviving muscle bundles within zones of prior infarction may be an origin of ventricular arrhythmia based on a re-entry mechanism. 9 , 10 It has been estimated that damage of the posteromedial papillary muscle, commonly involved in inferoposterior infarctions, occurs 6–10 times more often than damage of the anterolateral muscle secondary to anterolateral infarction. 11–13 The posteromedial muscle is more subject to dysfunction and damage because in the majority of cases it is perfused either by the right coronary artery or by the third obtuse marginal branch of the left circumflex artery. In contrast, the anterolateral muscle more often receives blood by two separate arteries; the first diagonal branch of the left anterior descending artery and the first obtuse marginal branch of the circumflex artery. In case of the occlusion of one, the remaining artery supplies the muscle and prevents the damage. 11 , 12 , 14 Lacroix et al.15 reported that ventricular tachycardias associated with inferior infarctions are more complex than with anterior infarctions because of a shorter tachycardia total activation time, frequent intramural re-entrant or monoregional activation patterns, and involvement of papillary muscles. They suggested that the proximity and relationship among anatomic structures such as the mitral annulus, papillary muscles, posterior septum, and posteroseptal space may be responsible for this complexity. Both the authors 1 and Hiukuri 16 in the accompanying editorial noted that the inclusion of only patients who survived a life-threatening arrhythmia and those with stable sustained ventricular tachycardia did not allow a significant advance in risk assessment in the present study. 1 Further study of the pathophysiological differences and electromechanical consequences of anterior and inferior infarctions, stratification of post-infarction patients and reliable tools for identification of arrhythmogenic loci are required for a better definition of high-risk subgroups for sudden cardiac death. Conflict of interest: none declared.