Myocardial Infarction and Atrial Fibrillation

Abstract

Background— Myocardial infarction (MI) is associated with the development of atrial fibrillation (AF). We aimed to characterize the atrial abnormalities because of MI and determine the role of ischemia to the AF substrate. Methods and Results— Forty-four sheep were studied. MI was induced by occlusion of the left circumflex artery (LCX) or left anterior descending artery (LAD). Excluding 11 with fatal arrhythmias, equal groups of animals (LCX; LAD; and sham-operated) underwent sequential electrophysiology study for 45 minutes to determine atrial effective refractory periods, conduction velocity, conduction heterogeneity index, and AF inducibility. Postmortem evaluation was performed with 2,3,5 triphenyl tetrazolium chloride staining. MI resulted in greater left ventricular dysfunction ( P <0.05), LA pressure ( P <0.0003), and reduction in atrial effective refractory periods ( P <0.0001) compared with control. 2,3,5 triphenyl tetrazolium chloride staining demonstrated that the left circumflex artery, and not the LAD, group had atrial infarction. The left circumflex artery group demonstrated the following compared with the LAD or control groups: greater slowing in atrial conduction velocity ( P <0.0001 and P <0.001); increased absolute range of conduction phase delay ( P <0.001 and P <0.001); increased conduction heterogeneity index ( P <0.0001 and P <0.001); greater AF vulnerability ( P <0.05 for both); and longer AF duration ( P <0.05 for both). LAD group had modest but significant slowing in conduction velocity ( P <0.01) but no change in conduction heterogeneity index or AF duration compared with control. Conclusions— Left ventricular infarction, which is known to result in atrial stretch, hemodynamic change, and neurohumoral activation, contributes partially to the atrial abnormalities in MI. Atrial ischemia/infarction results in greater atrial electrophysiological changes and propensity for AF forming the dominant substrate for AF in MI.

Electrophysiological Effects of Selective Atrial Coronary Artery Occlusion in Humans

“…15,16 Direct characterization of the atrial ischemic electrophysiological substrate has been attempted in a restricted number of experimental studies in animals submitted to selective ligature of atrial coronary arterial branches. [3][4][5][6] In these experimental models, mapping of local electrograms over the atrial surface revealed a significant slowing of local conduction in the ischemic zone creating conditions for increased inducibility and maintenance of atrial fibrillation. 3,5 The local conduction delay will therefore explain the changes in the duration and shape of the P wave in our patients with atrial branch occlusion.…”

“…2 However, a direct link between atrial myocardial ischemia and atrial fibrillation has been demonstrated only in experimental animal models submitted to selective occlusion of atrial coronary branches. [3][4][5][6] These studies revealed that atrial ischemia induced local atrial conduction slowing and favored the electric induction and maintenance of atrial fibrillation.…”

Selective downregulation of mitochondrial electron transport chain activity and increased oxidative stress in human atrial fibrillation

“…The incidence and prevalence of AF increase with advancing age and aging-associated diseases such as hypertension, ischemic heart disease, and heart failure (2,40) and contribute to increased morbidity, particularly an increased risk for stroke, heart failure, and death (25,52). Although the pathophysiology of AF has been well characterized, the underlying mechanisms that contribute to the progression of AF in human atria have not been fully defined (33,35,57,58,60).…”

Effect of rosuvastatin on atrial structural remodeling in rabbits with myocardial infarction

“…Atrial structural remodeling can not only impair atrial systolic and diastolic function but also provide a matrix for impulse reentry, leading to AF and other atrial arrhythmias. In addition, a number of studies have also shown that the excessively high pressure and sharp dilatation of the left atrium following MI increases the susceptibility to AF (11,12). A previous study has also confirmed that statins have anti-arrhythmia effects and can improve post-MI cardiac remodeling (13).…”