In our study of symptomatic patients with a distinctive focal wall motion abnormality upon EE, we invasively confirmed the presence of an MB by IVUS, by identification of an echo lucent half‐moon sign and/or systolic compression, and also demonstrated significant hemodynamic disturbances associated with the MB, including a marked increase in flow velocity and an abnormal dFFR during dobutamine stress. Also, all patients had at least one septal branch within the MB segment in concordance with a focal abnormality seen on EE. This is the first time, to our knowledge, that a noninvasive functional abnormality for the identification of an MB has been identified and undergone extensive invasive correlation in patients with anginal symptoms.
In previous work, Escaned et al11
found that dFFR under dobutamine stress measured distal to the bridge was abnormal only in a minority of patients with angiographically confirmed MBs, leaving the question of why an abnormal value of this hemodynamic measurement of ischemia was not found more consistently in this cohort of symptomatic patients. Our observation of a focal, end‐systolic/early‐diastolic buckling of the septum with apical sparing on EE, in a similar patient population, led to the hypothesis that the hemodynamic disturbance and, thereby, ischemia was local to the MB rather than distal to it.
There is literature supportive of this concept. Klues et al14
measured diastolic blood pressure proximal to, within, and distal to the MB in 12 patients in the resting state and found a trend toward lower diastolic pressure intrabridge with pressure recovery distally. This hemodynamic change in the Pd/Pa ratio should be exacerbated under dobutamine stress within the bridge.
The most common finding in the patients in our cohort was an abnormal dFFR that was present only within the bridge. We posit a model of ischemia involving the Venturi effect (). During end‐systole to early‐diastole, the tunneled portion of a vessel resembles the constricted section of a pipe. The laws governing fluid dynamics dictate that the fluid velocity must increase when it passes through a narrowed area to satisfy the principle of continuity, while pressure must decrease to satisfy the principle of conservation of energy by Bernoulli's equation. The Venturi effect may be derived from a combination of these 2 concepts. Thus, we infer that the decrease in the pressure in the tunneled section, and thereby the perfusion pressure to the corresponding septal branch vessels, leads to focal ischemia. Conversely, distal to the bridge, the vessel area increases, resulting in a decrease in velocity and pressure recovery, and hence, resulting in a nonischemic distal dFFR. This Venturi effect serves as a model to explain the EE finding of a focal septal wall motion abnormality with apical sparing supported by our hemodynamic findings of a pressure drop in the MB, during dobutamine stress.
Figure 5. Venturi effect. With mild constriction (A), there is little change in the pressure and velocity throughout the pipe, with only a small increase in velocity and drop in pressure within the myocardial bridge (MB) segment. With marked constriction (B), velocity (more ...)
For the 3 subjects in our study who had an abnormal distal dFFR, 2 had the longest and second longest MBs, and the other harbored 2 serial MBs. It is possible that the length of arterial compression increased with dobutamine stress, a phenomenon reported previously by Escaned et al,11
thereby possibly obscuring the true velocity and pressure measurements distal to the long and serial bridges. We hypothesize that we were simply not able to extend the distal pressure measurement far enough to be truly outside of the MB during stress in these 3 cases.
Another corroborative observation of the timing of the end‐systolic to early‐diastolic wall motion abnormality is found in the cross sectional area tracings at the site of compression by IVUS, noted in this study as well as in another report.6
The smallest luminal area of the MB is in late‐systole and very early‐diastole, hence this is when flow is most restricted. The timing of this area change differs from a fixed stenosis, in which the area does not change between systole and diastole. Also, in normal coronary physiology, the proportion of coronary flow during systole increases with an elevated heart rate, to compensate for the decrease in diastolic filling time.15
With a lumen area reduction at end‐systole and early‐diastole in MBs, this adaptive mechanism for maintenance of adequate blood flow with exercise may be compromised.
Jhi et al recently reported a finding on speckle‐tracking strain echocardiography of a “bi‐phasic” or “double‐peak” radial strain with dobutamine stress associated with MBs.16
We believe that the septal buckling we have described on EE corresponds temporally to the late systolic dip in the radial strain described by Jhi et al although their invasive confirmation of MB was by CA alone. The mechanism behind this biphasic wall motion and radial strain are not known and will require further investigation. We speculate that maximum systolic compression of the MB in late systole, followed by relaxation in diastole, is related to these phenomena.
The major limitation was the lack of a control group in this proof‐of‐concept study. We could not justify these extensive invasive measurements in patients with normal EE. Thus, sensitivity, specificity, and other standard measures for validating a putative test were not estimated. These parameters will need to be established before our echocardiographic findings can be widely adopted for routine clinical care. Additionally, the sample size of this cohort was relatively small and 3 patients without the IVUS half‐moon echo‐lucent sign were not studied with dobutamine as the procedural delay to allow offline analysis for MB confirmation could not be justified for this study. Furthermore, it may not be possible to reach the distal LAD in long MBs with small distal segments. Also, with stress the optimal definition of the Doppler signal can be challenging to record when the patient is in pain and is tachycardic. Finally, we do recognize that because the constriction may not be uniform within all bridges and can change with time, there could be dynamic changes in velocity and pressure, requiring more complex modeling for further mechanistic validation.