Atrial fibrillation can directly cause ventricular oxidative stress and microcirculatory flow abnormalities, which may explain the occurrence of angina and troponin elevation in patients without significant coronary artery disease.
May explain angina or troponin rises without CAD in AF; hypothesis-generating and requires prospective trials before practice change.
Patients with atrial fibrillation (AF) often present with typical angina pectoris and mildly elevated levels of cardiac troponin (non-ST-segment elevation myocardial infarction) during an acute episode of AF. However, in a large proportion of these patients, significant coronary artery disease is excluded by coronary angiography, which suggests that AF itself influences myocardial blood flow. The present review summarizes the effect of AF on the occurrence of ventricular oxidative stress, redox-sensitive signaling pathways and gene expression, and microcirculatory flow abnormalities in the left ventricle.
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Goette et al. (2012) studied this question.
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