Abstract
BackgroundAtrial coronary branch occlusion is a hardly recognizable clinical entity that can promote atrial fibrillation. The low diagnostic accuracy of the ECG could deal with the characteristics of the ischemia-induced changes in local atrial electrograms, but these have not been described.ObjectivesWe analyzed the effects of selective acute atrial branch occlusion on local myocardial structure, atrial electrograms, and surface ECG in an experimental model close to human cardiac anatomy and electrophysiology.MethodsSix anesthetized open-chest anesthetized pigs underwent surgical occlusion of an atrial coronary branch arising from the right coronary artery during 4 h. Atrial electrograms and ECG were simultaneously recorded. One additional pig acted as sham control. In all cases, the hearts were processed for anatomopathological analysis.ResultsAtrial branch occlusion induced patchy atrial necrosis with sharp border zone. During the first 30 min of occlusion, atrial electrograms showed progressive R wave enlargement (1.8 ± 0.6 mV vs. 2.5 ± 1.1 mV, p < 0.01), delayed local activation times (28.5 ± 8.9 ms vs. 36.1 ± 16.4 ms, p < 0.01), ST segment elevation (−0.3 ± 0.3 mV vs. 1.0 ± 1.0 mV, p < 0.01), and presence of monophasic potentials. Atrial ST segment elevation decreased after 2 h of occlusion. The electrical border zone was ∼1 mm and expanded over time. After 2 h of occlusion, the ECG showed a decrease in P wave amplitude (from 0.09 ± 0.04 mV to 0.05 ± 0.04 mV after 165 min occlusion, p < 0.05) and duration (64.4 ± 8.0 ms vs. 80.9 ± 12.6 ms, p < 0.01).ConclusionSelective atrial branch occlusion induces patchy atrial infarction and characteristic changes in atrial activation, R/S wave, and ST segment that are not discernible at the ECG. Only indirect changes in P wave amplitude and duration were appreciated in advanced stages of acute coronary occlusion.
Highlights
Atrial myocardial infarction is a potentially harmful disease that can provoke atrial mechanical depression, systemic embolization, atrial arrhythmias, and cardiac rupture (Lazar et al, 1988)
Using a model close to the human cardiac anatomy and electrophysiology (Cinca et al, 1980), we have found that this procedure induces patchy atrial infarction with sharp border zone and evolving changes of atrial R/S waves, ST segment, and local activation time
The atrial infarction was massive, suggesting that the interruption of coronary flow affected most of the atrial branches that ordinarily arise from the proximal segment of the RCA or left circumflex (LCX) (Baroldi et al, 1956; James and Burch, 1958)
Summary
Atrial myocardial infarction is a potentially harmful disease that can provoke atrial mechanical depression, systemic embolization, atrial arrhythmias, and cardiac rupture (Lazar et al, 1988) It is caused by occlusion of the atrial coronary branches ordinarily emerging from the proximal segments of the right (RCA) or the left circumflex (LCX) coronary arteries (Baroldi et al, 1956; James and Burch, 1958). Selective occlusion of an atrial coronary branch may result from a rupture of a local atherosclerotic plaque or, accidentally, during percutaneous coronary interventions (Álvarez-García et al, 2013, 2016) This condition predisposes to arrhythmia reentry as evidenced in the canine model (Sinno et al, 2003; Nishida et al, 2011) but is hardly recognized at the surface ECG. The low diagnostic accuracy of the ECG could deal with the characteristics of the ischemia-induced changes in local atrial electrograms, but these have not been described
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