Mechanism Underlying ST-T Segment Changes Caused by Tachycardiac Atrial Fibrillation

To the Editor We would like to thank Fujimoto et al. for their case presentation demonstrating the electrocardiography changes caused by atrial fibrillation (AF). In their case, an 84-year-old woman with a history of hypertension and diabetes mellitus presented with chest discomfort, and electrocardiography (ECG) revealed AF and multilead ST-segment changes with no coronary artery stenosis (1). While this case was amazing, several concerns have been raised.

It has long been noted that arrhythmias cause ECG changes in ST-segment elevation in lead aVR (2). The main mechanism underlying these ECG changes is assumed to be relative ischemia of the coronary arteries due to tachycardia (3). Did the patient have anemia or an abnormal thyroid function? Anemia reduces the amount of oxygen in the coronary arteries, resulting in myocardial ischemia. Hyperthyroidism not only induces atrial fibrillation but also increases myocardial oxygen demand.

Another concern is elevated myocardial deviation enzymes. If there was mild-moderate stenosis in the coronary arteries, then even supraventricular tachycardia might produce a small myocardial infarction. If the patient has hypertrophic cardiomyopathy, myocardial deviator enzymes may be elevated because of too great a relative deficiency in oxygen requirements during tachycardia. Elevated troponin may also be related to tachycardia duration. Alternatively, the possibility that atrial fibrillation combined with other cardiac diseases (e.g. Takotsubo cardiomyopathy, acute myocarditis, septic cardiomyopathy, etc.) may have elevated troponin T should also be considered.

If none of the above concerns apply, then coronary microvascular dysfunction due to diabetes may have been a factor.

The authors state that they have no Conflict of Interest (COI).