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JACC VOL. 64, NO. 20, 2014

Letters

NOVEMBER 18/25, 2014:2176–82

Please note: Dr. Latib is a consultant for Medtronic and Direct Flow Medical. Dr. Colombo is a minor shareholder in Direct Flow Medical. Dr. Glauber is a consultant for Sorin. Dr. Alfieri has received royalties from Edwards; and is a consultant for Symetis. Dr. Maisano is a consultant for Edwards, Medtronic, and St. Jude Medical. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Latib and Naim contributed equally to this work.

Subselective intraluminal devices (e.g., pressure or Doppler wires, intravascular ultrasound catheters) should be generally avoided outside of experimental protocols because they can alter MB by inducing spasm and deforming the affected coronary segment (2,3). Incidentally, the “half-moon” sign associated

REFERENCES

with MB probably results from the fiberoptic probe

1. Moreillon P, Que YA. Infective endocarditis. Lancet 2004;363:139–49.

bending at the MB site; it is not a true marker of MB

2. Chu VH, Miro JM, Hoen B, et al. Coagulase-negative staphylococcal prosthetic valve endocarditis—a contemporary update based on the International Collaboration on Endocarditis: prospective cohort study. Heart 2009;95:570–6.

severity (only of its presence).

3. Lopez J, Revilla A, Vilacosta I, et al. Definition, clinical profile, microbiological spectrum, and prognostic factors of early-onset prosthetic valve endocarditis. Eur Heart J 2007;28:760–5. 4. Habib G, Thuny F, Avierinos JF. Prosthetic valve endocarditis: current approach and therapeutic options. Prog Cardiovasc Dis 2008;50:274–81. 5. Puls M, Eiffert H, Hunlich M, et al. Prosthetic valve endocarditis after transcatheter aortic valve implantation: the incidence in a single-centre cohort and reflections on clinical, echocardiographic and prognostic features. EuroIntervention 2013;8:1407–18.

Although fractional flow reserve has been advocated (1,2) as a measure of MB clinical severity and the prognosis of associated CAD, this measurement does not reveal the hemodynamic severity of MB, nor does it reflect prognosis, as it can in moderate atherosclerotic lesions. Definitive study of MB will require large, controlled, prospective, multicenter investigations with long-term, objective clinical follow-up. Anything less will only perpetuate the current state of confusion and uncertainty about this entity.

AP PEN DIX For a comprehensive list of the centers and physicians associated with this study, please see the online version of this article.

*Paolo Angelini, MD *Department of Cardiology Texas Heart Institute

Coronary Myocardial Bridges

6624 Fannin, Suite 2780

Pathophysiology and Clinical Relevance

http://dx.doi.org/10.1016/j.jacc.2014.07.992

Houston, Texas 77030 E-mail: [email protected]

REFERENCES

The recent review by Corban et al. (1) highlights the limitations of the literature on myocardial bridges (MBs) and suggests the need for clearly defined terms and protocols. For example, to clearly establish the prevalence of MB, clinical identification should require 2 angiographic views obtained after nitroglycerin

administration,

rather

than

computed

1. Corban MT, Hung OY, Eshtehardi P, et al. Myocardial bridging: contemporary understanding of pathophysiology with implications for diagnostic and therapeutic strategies. J Am Coll Cardiol 2014;63:2346–55. 2. Hazenberg AJ, Jessurun GA, Tio RA. Mechanisms involved in symptomatic myocardial bridging: value of sequential testing for endothelial function, flow reserve measurements and dobutamine stress angiography. Neth Heart J 2008;16:10–5. 3. Kim JW, Park CG, Suh SY, et al. Comparison of frequency of coronary spasm in Korean patients with versus without myocardial bridging. Am J Cardiol

tomography (whose use should probably be limited to

2007;100:1083–6.

measuring length and depth). Chest pain, myocardial

4. Nardi F, Verna E, Secco GG, et al. Variant angina associated with coronary

infarction, and sudden death are not systematically

artery endothelial dysfunction and myocardial bridge: a case report and review of the literature. Intern Med 2011;50:2601–6.

associated with MB of any anatomic severity; most MBs are benign. As Corban et al. (1) note, MBs actually prevent coronary artery disease (CAD) inside affected

Myocardial Bridging

segments. Statements regarding pathophysiology, clinical indications, and adverse effects in MB require clearly defined inclusion and exclusion criteria

We were pleased to see a state-of-the-art review on

(symptomatic or asymptomatic MB vs. MB with

myocardial bridging (1), but were surprised by the

associated comorbidities that may influence clinical

authors’ failure to highlight several contemporary

presentation, e.g., hypertrophic cardiomyopathy).

advances in the field.

To determine the cause of sporadic ischemic symp-

First, it has become clear that traditional adeno-

toms, workup must first rule out significant CAD;

sine fractional flow reserve (FFR) is inadequate in

worsening of systolic, phasic arterial narrowing at

testing the hemodynamic significance of a myocar-

MB sites (by dobutamine testing and angiography);

dial bridge (2). Because myocardial bridging creates

and, especially, spasticity or endothelial dysfunction

a dynamic stenosis brought on by chronotropic

(by acetylcholine testing) (2–4).

and inotropic stimulation, simply dilating the artery

JACC VOL. 64, NO. 20, 2014

Letters

NOVEMBER 18/25, 2014:2176–82

with adenosine is insufficient, and will underesti-

extending into bridges have higher rates of target

mate the hemodynamic significance of most bridges.

lesion revascularization.

Likewise, myocardial bridges cause significant dia-

Finally, it should be clarified that the “half-moon”

stolic pressure gradients, but normal or negative

sign seen on intravascular ultrasound (IVUS) directly

systolic pressure gradients (systolic distal pressure,

corresponds to muscle tissue (5), not adipose tissue,

Pd is greater than systolic proximal pressure, Pa)

perivascular fat, or adventitia, as has been previously

as a result of systolic pressure overshooting. This

suggested.

produces an artificial elevation in the mean pressure derestimation of hemodynamic significance. There-

*Jennifer A. Tremmel, MD, MS Ingela Schnittger, MD

fore, diastolic FFR with dobutamine challenge is

*Department of Medicine (Cardiovascular)

currently the technique of choice in testing for he-

Stanford University School of Medicine

modynamically significant myocardial bridging. Of

300 Pasteur Drive, Room H2103

note, the tracings used by the authors to demon-

Stanford, California 94305-5218

strate

E-mail: [email protected]

used by traditional FFR, again resulting in an un-

hemodynamics

in

myocardial

bridging

(Figure 7 in the paper by Corban et al.) (1), are

http://dx.doi.org/10.1016/j.jacc.2014.07.993

actually not consistent with expected pressure

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.

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

REFERENCES 1. Corban MT, Hung OY, Eshtehardi P, et al. Myocardial bridging: contemporary understanding of pathophysiology with implications for diagnostic and therapeutic strategies. J Am Coll Cardiol 2014;63:2346–55. 2. Hakeem A, Cilingiroglu M, Leesar MA. Hemodynamic and intravascular ultrasound assessment of myocardial bridging: fractional flow reserve paradox with dobutamine versus adenosine. Catheter Cardiovasc Interv 2010;75:229–36. 3. Lin S, Tremmel JA, Yamada R, et al. A novel stress echocardiography pattern for myocardial bridge with invasive structural and hemodynamic correlation. J Am Heart Assoc 2013;2:e000097. 4. Ishikawa Y, Akasaka Y, Akishima-Fukasawa Y, et al. Histopathologic profiles of coronary atherosclerosis by myocardial bridge underlying myocardial infarction. Atherosclerosis 2013;226:118–23. 5. Yamada R, Turcott RG, Connolly AJ, et al. Histological characteristics of myocardial bridge with an ultrasonic echolucent band. Comparison between intravascular ultrasound and histology. Circ J 2014;78:502–4.

within the myocardial bridge, not distal to it as is traditionally thought. We have postulated a Venturilike effect within the bridge, resulting in local (mid

REPLY: Myocardial Bridging

septal) ischemia rather than distal ischemia. Third, there is an ongoing misconception about

We appreciate the interest generated by our review

the location of plaque in relation to the myocardial

paper on myocardial bridging (1). In response

bridge. The maximal plaque burden is not at the

to comments by Dr. Tremmel and colleagues, we have

entrance of the bridge, but on average 20 mm to

attempted to describe the complex pathophysiology

30 mm proximal to the entrance of the bridge (3,4).

of myocardial bridging with emphasis on both systolic

This may be attributable to the reversal of systolic

and diastolic flow abnormalities that can coexist with

flow seen on Doppler tracings, in which retrograde

atherosclerotic plaque proximal to the bridge, nega-

flow collides with antegrade flow, causing high sys-

tive remodeling within the bridged segment, or

tolic wall shear stress (WSS) upstream from the

coronary vasospasm. We believe that it is reasonable

bridge entrance. The high systolic WSS referred to in

to begin the physiologic evaluation with fractional

Figure 1 in the paper by Corban et al. (1) is actually

flow reserve (FFR) with adenosine administration

caused by external wall compression, not affecting

measured distal to a myocardial bridge. If abnormal,

WSS inside the bridge. During diastole, the WSS is

this indicates concomitant fixed obstruction from

low proximal and distal to the bridge, and even

either plaque proximal to the bridge, negative

lower within the bridge. Recognition of the location

remodeling within the bridge, or coronary vaso-

of maximal plaque burden is important because it

spasm. It is true that mean FFR measured within the

has been shown that stents placed proximal to or

bridge may underestimate the maximal gradient as

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