Author + information
- Jennifer A. Tremmel, MD, MS∗ ( and )
- Ingela Schnittger, MD
- ↵∗Department of Medicine (Cardiovascular), Stanford University School of Medicine, 300 Pasteur Drive, Room H2103, Stanford, California 94305-5218
We were pleased to see a state-of-the-art review on myocardial bridging (1), but were surprised by the authors’ failure to highlight several contemporary advances in the field.
First, it has become clear that traditional adenosine fractional flow reserve (FFR) is inadequate in testing the hemodynamic significance of a myocardial bridge (2). Because myocardial bridging creates a dynamic stenosis brought on by chronotropic and inotropic stimulation, simply dilating the artery with adenosine is insufficient, and will underestimate the hemodynamic significance of most bridges. Likewise, myocardial bridges cause significant diastolic pressure gradients, but normal or negative systolic pressure gradients (systolic distal pressure, Pd is greater than systolic proximal pressure, Pa) as a result of systolic pressure overshooting. This produces an artificial elevation in the mean pressure used by traditional FFR, again resulting in an underestimation of hemodynamic significance. Therefore, diastolic FFR with dobutamine challenge is currently the technique of choice in testing for hemodynamically significant myocardial bridging. Of note, the tracings used by the authors to demonstrate hemodynamics in myocardial bridging (Figure 7 in the paper by Corban et al.) (1), are actually not consistent with expected pressure tracings because the Pd is reduced compared with the Pa. This suggests either an element of coronary spasm or fixed stenosis, rather than a significant myocardial bridge.
Second, as a novel noninvasive diagnostic technique, stress echocardiography has been shown to identify myocardial bridges (3). Specifically, one sees a unique wall motion abnormality of mid septal buckling during peak stress, which distinguishes itself from a fixed left anterior descending (LAD) artery stenosis by not involving the apex. We have demonstrated that this finding of focal septal buckling with apical sparing mirrors the hemodynamics seen within and distal to the bridge. The most significant increases in flow velocity and decreases in diastolic pressure are almost invariably located within the myocardial bridge, not distal to it as is traditionally thought. We have postulated a Venturi-like effect within the bridge, resulting in local (mid septal) ischemia rather than distal ischemia.
Third, there is an ongoing misconception about the location of plaque in relation to the myocardial bridge. The maximal plaque burden is not at the entrance of the bridge, but on average 20 mm to 30 mm proximal to the entrance of the bridge (3,4). This may be attributable to the reversal of systolic flow seen on Doppler tracings, in which retrograde flow collides with antegrade flow, causing high systolic wall shear stress (WSS) upstream from the bridge entrance. The high systolic WSS referred to in Figure 1 in the paper by Corban et al. (1) is actually caused by external wall compression, not affecting WSS inside the bridge. During diastole, the WSS is low proximal and distal to the bridge, and even lower within the bridge. Recognition of the location of maximal plaque burden is important because it has been shown that stents placed proximal to or extending into bridges have higher rates of target lesion revascularization.
Finally, it should be clarified that the “half-moon” sign seen on intravascular ultrasound (IVUS) directly corresponds to muscle tissue (5), not adipose tissue, perivascular fat, or adventitia, as has been previously suggested.
Please note: Dr. Tremmel has received honoraria from Volcano Corporation, St. Jude Medical, and Boston Scientific. Dr. Schnittger has reported that she has no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation
- Corban M.T.,
- Hung O.Y.,
- Eshtehardi P.,
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- Lin S.,
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