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Characterizing Mechanisms of Ischemia in Patients With Myocardial Bridges

Aish Sinha, BSc, MBBS, Haseeb Rahman, BMBCh, PhD, Ronak Rajani, MBBS, MD, Ozan M. Demir, MBBS, PhD, Matthew Li KamWa, BSc, MBBS, Holly Morgan, BSc, MBBS, Saad M. Ezad, BSc, MBBS, Howard Ellis, BSc, Dexter Hogan, BSc, Ankur Gulati, BMBS, MD, Ajay M. Shah, MBBS, MD, Amedeo Chiribiri, MBBS, PhD, Andrew J. Webb, MBBS, PhD, Michael Marber, MBBS, PhD, and Divaka Perera, BMBCh, MD. Circulation: Cardiovascular Interventions Volume 17, Number 1 https://doi.org/10.1161

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 with nonobstructive coronary arteries and a MB in the left anterior descending artery.

Methods:

Patients with angina with nonobstructive coronary arteries underwent the 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 angina with nonobstructive coronary arteries and a MB were compared with 2 angina with nonobstructive coronary arteries groups with no MB: 1 with coronary microvascular disease (CMD: coronary flow reserve, <2.5) and 1 with normal coronary flow reserve (reference: coronary flow reserve, ≥2.5).

Results:

Ninety-two patients were enrolled in the study (30 MB, 33 CMD, and 29 reference). Fractional flow reserve in these 3 groups was 0.86±0.05, 0.92±0.04, and 0.94±0.05; coronary flow reserve 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%–69±13%; P=0.063) but decreased in the CMD (68±10%–50±10%; P<0.001) and MB (66±9%–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 with the reference group. Additionally, there was a high prevalence of endothelial and microvascular dysfunction. These ischemic mechanisms may represent distinct treatment targets.

What is known

Myocardial bridges can be associated with microvascular dysfunction, coronary artery spasm, and proximal vessel atherosclerosis.
The hemodynamic effects of the tunneled segment during exercise are not known.

What the study adds

Patients with myocardial bridges demonstrate impaired coronary perfusion efficiency during exercise.
The tunneled segment leads to perturbation of accelerating wave energy in early systole during exercise, which is the main determinant of impaired perfusion efficiency.
Endothelial dysfunction is highly prevalent in patients with myocardial bridges, with the myocardial bridge muscle index being independently associated with it.

Angina with nonobstructive coronary arteries (ANOCA) is a common clinical problem and comprises several distinct pathophysiological entities, including coronary microvascular disease (CMD), coronary artery spasm, and myocardial bridging. Myocardial bridging due to intramyocardial passage of varying lengths of an epicardial artery is a common anatomic variant, found in up to 30% of patients on coronary computed tomography angiography (CCTA) imaging, predominantly in the left anterior descending (LAD) artery at the mid vessel. The intramyocardial segment of the vessel is known as the tunneled segment. Historically, myocardial bridges (MBs) have been considered a benign entity as myocardial perfusion predominantly occurs during diastole and MBs are thought to only alter vessel caliber during systole. However, growing evidence suggests that MBs are not always benign and have been associated with chronic intermittent angina, as well as acute ischemic presentations. Several mechanisms have been postulated, including delayed decompression of the tunneled segment in diastole leading to luminal narrowing akin to obstructive coronary artery disease, predisposition to coronary artery spasm, increased propensity to atherosclerotic coronary artery disease proximal to the bridged segment due to perturbed wall shear stress, and the venturi effect leading to reduced septal blood flow. However, while a handful of studies have assessed the physiological response to adenosine and dobutamine stress, using pressure as a surrogate of flow, coronary flow during exercise has not been specifically and systematically evaluated in patients with MBs. Our study aimed to characterize the mechanisms that lead to myocardial ischemia in patients with ANOCA and a MB (MB group) during physical exercise using wave intensity analysis to describe patterns of cardiac-coronary coupling. We compared these findings to those in patients with ANOCA but no MB, in turn classified as patients with CMD (CMD group: coronary flow reserve [CFR], <2.5) or normal CFR (reference group: CFR, ≥2.5), respectively. Better understanding of the mechanisms causing ischemia may allow the development of stratified therapies for this underserved patient population.