Characterising Mechanisms of Ischemia in Patients with Myocardial Bridges

Abstract

Background: Myocardial bridges (MBs) are prevalent and can be associated with acute and chronic ischemic syndromes. We sought to determine the substrates for ischemia in patients with angina, nonobstructive coronary arteries (ANOCA) and a MB in the left anterior descending artery. Methods: Patients with ANOCA underwent acquisition of intracoronary pressure and flow during rest, supine bicycle exercise and adenosine infusion. Coronary wave intensity analysis was performed, with perfusion efficiency defined as accelerating wave energy/total wave energy (%). Epicardial endothelial dysfunction was defined as a reduction in epicardial vessel diameter ≥20% in response to intracoronary acetylcholine infusion. Patients with ANOCA and a MB were compared to two ANOCA groups with no MB: one with coronary microvascular disease (CMD: coronary flow reserve, CFR, <2.5) and one with normal CFR (reference: CFR≥2.5). Results: 92 patients were enrolled in the study (30 MB, 33 CMD and 29 reference). FFR in these three groups was 0.86±0.05, 0.92±0.04 and 0.94±0.05; CFR was 2.5±0.5, 2.0±0.3 and 3.2±0.6. Perfusion efficiency increased numerically during exercise in the reference group (65±9% to 69±13%, p=0.063), but decreased in the CMD (68±10% to 50±10%, p<0.001) and MB (66±9% to 55±9%, p<0.001) groups. The reduction in perfusion efficiency had distinct causes: in CMD this was driven by microcirculation derived energy in early diastole, whereas in MB this was driven by diminished accelerating wave energy, due to the upstream bridge, in early systole. Epicardial endothelial dysfunction was more common in the MB group (54% versus 29% reference and 38% CMD). Overall, 93% of patients with a MB had an identifiable ischemic substrate. Conclusions: MBs led to impaired coronary perfusion efficiency during exercise, which was due to diminished accelerating wave energy in early systole compared to the reference group. Additionally, there was a high prevalence of endothelial and microvascular dysfunction. These ischemic mechanisms may represent distinct treatment targets.