Abstract 12625: Characterising Mechanisms of Ischemia in Patients With Myocardial Bridges
Aish Sinha, Haseeb Rahman, Ozan Demir, Ronak Rajani, Ankur Gulati, Matthew Li Kam Wa, Holly Morgan, Saad Ezad, Howard Ellis, Dexter Hogan, Ajay M Shah, Andrew Webb, Michael Marber, Divaka Perera- Physiology (medical)
- Cardiology and Cardiovascular Medicine
Background: Myocardial bridges (MB) have been associated with ischemic syndromes. Abnormal cardiac coronary coupling is implicated but has not been systematically evaluated. 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, and perfusion efficiency defined as accelerating wave energy/total wave energy (%). Endothelial dysfunction was defined as a reduction in epicardial vessel diameter by >20% with intracoronary acetylcholine. Patients with ANOCA and a MB were compared to those with microvascular angina (CMD: coronary flow reserve, CFR, <2.5) or ANOCA with normal CFR (controls).
Results: 87 patients were enrolled (25 MB [age 56±9 years], 34 CMD [57±11 years], 28 control [57±8 years]). FFR in these 3 groups was 0.86±0.05, 0.92±0.04 and 0.94±0.05; CFR was 2.6±0.5, 2.0±0.3 and 3.3±0.6. Perfusion efficiency improved during exercise in controls (61±11% to 65±15%, p=0.044), but decreased in patients with CMD (63±11% to 44±10%, p<0.001) and MB (59±9% to 50±9%, p=0.001). In CMD, the reduction in perfusion efficiency was driven by diminished microcirculation derived accelerating energy in early diastole, whereas in MB this was driven by diminished accelerating energy arising from the upstream epicardial vessel in early systole ( Figure ). 55% of patients with MB, versus 33% of patients with CMD and 29% controls, had endothelial dysfunction.
Conclusions: MBs result in impaired coronary perfusion efficiency during exercise, which is due to diminished accelerating wave energy. Additionally, there is a high prevalence of endothelial dysfunction; both mechanisms may cause ischemia and, therefore, represent distinct treatment targets.