Myocardial bridging of the left anterior descending coronary artery is associated with reduced myocardial perfusion reserve: a 13N-ammonia PET study

摘要

Myocardial Bridging (MB) refers to the band of myocardium that abnormally overlies a segment of a coronary artery. This paper quantitatively evaluates the influence of MB of the left anterior descending artery (LAD) on myocardial perfusion of the entire left ventricle. We studied 131 consecutive patients who underwent hybrid rest/stress ¹³N-ammonia positron emission tomography (PET) and coronary computed tomography angiography (CCTA) due to suspected myocardial ischemia. Patients with previous myocardial infarction and/or significant coronary artery disease (≥ 50% stenosis) were excluded. Myocardial perfusion measurements were compared between patients with and without LAD-MB. Additionally, we evaluated the relationship between anatomical characteristics (length and depth) of LAD-MB and myocardial perfusion measurements. 17 (13%) patients presented a single LAD-MB. Global myocardial perfusion reserve (MPR) was lower in patients with LAD-MB than in patients without LAD-MB (1.9 ± 0.5 vs. 2.3 ± 0.6, p < 0.01). Global stress myocardial blood flow (MBF) was similar in patients with and without LAD-MB (2.2 ± 0.4 vs. 2.3 ± 0.7 ml/g/min, p = 0.40). Global rest MBF was higher in patients with LAD-MB than in patients without LAD-MB (1.2 ± 0.3 vs. 1.0 ± 0.2 ml/g/min, p < 0.01). Global rest MBF, stress MBF, and MPR quantifications were similar in patients with superficial and deep LAD-MB (all p = NS). We did not find any correlation between length and global rest MBF, stress MBF nor MPR (r = − 0.14, p = 0.59; r = 0.44, p = 0.07; and r = 0.45, p = 0.07 respectively). Quantitative myocardial perfusion suggests that LAD-MB may be related to impaired perfusion reserve, an indicator of microvascular dysfunction. Anatomical characteristics of LAD-MB were not related to changes in myocardial perfusion.Electronic supplementary materialThe online version of this article (10.1007/s10554-018-1460-8) contains supplementary material, which is available to authorized users.