LETTER TO THE EDITOR
Some questions regarding myocardial bridges still require answers
Paolo Angelini, MD*
* Texas Heart Institute, 6624 Fannin, Suite 2780, Houston, Texas 77030-2387, USA
leachman{at}ix.netcom.com
Among the first groups to investigate such coronary anomalies, Dr. Bourassa and collaborators in a recent review (1) attempted to summarize current knowledge on the difficult subject of myocardial bridges. I would like to discuss some notions that were suggested by the investigators.
First, the concept of "symptomatic" muscular bridges (which the review is said to be concerned with) is not defined and indeed is quite unlikely to be definable, especially while reviewing the literature. Such observation is fundamental when an investigator attempts to establish anatomo-clinical correlations in a matter of coronary anomalies. Indeed, one still cannot identify any consistent clinical manifestations of muscular bridges (as expected to be found, for example, in fixed severe coronary obstructions). What literature reviews can do at their best is to establish correlations in the specific cases that are being published. It is likely that some 2% of the general population (possibly 120 million people in the world) carry an angiographically recognizable muscular bridge, but only few cases are symptomatic and/or have been published. No large prospective series has yet been studied, and the problem of the denominator (the number of people with similar anatomic features of the few published) is the recurrent limit of clinical studies of patients with coronary anomalies (2). Ideally, a large population with anatomically similar anomalies and with similar functional correlates should be entered into a large multicenter database, using prospective, agreed-upon protocols that could study the natural history of such patients (2).
Second, the recent availability of newer, more refined imaging techniques (such as intravascular ultrasound) and use of functional testing (Doppler or pressure wires and coronary reserve indexes) have succeeded in improving the precision of new descriptive parameters, but they have not yet resulted in proving a necessarily ischemic implication of muscular bridges. In particular, the finding of a mildly diminished coronary flow reserve (typically by Doppler flow velocity measurements) does not explain resting nor severe angina (that can be expected only with more limited reserve) nor the probability to predict acute myocardial infarction or sudden death, the typical clinical correlates in literature reports. Such events are the real strong indicators for interventions. Doppler findings of peculiar (typical) flow patterns are possibly diagnostic of such anomalies, but they are not necessarily predictive per se of clinical events.
Finally, although the problem of establishing firm, objective criteria for indicating interventional treatment in muscular bridges remains substantially unsolved, the decision on which intervention should be contemplated as an alternative to medical treatment is not so routine, as stated by the investigators ("these interventions are not strikingly different from those of patients with single-vessel coronary disease"). Indeed, both coronary stents and mammary artery implantation were recognized to have important peculiarities when implemented in such coronary anomalies. Stents have been reported to lead to 46% restenosis rate at seven weeks’ angiographic follow-up, in a series of 11 patients (3). Besides intimal fibrocellular growth and clotting, crushing of a nonelastic metallic stent is expected in the presence of muscular bridges-related phasically active collapsing forces (4). Furthermore, mammary artery implantation has been recognized to frequently undergo atrophy when used in patients without significant baseline hemodynamic gradients (5).
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References
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1. Bourassa MG, Butnaru A, Lesperance J, Tardif JC. Symptomatic myocardial bridges: overview of ischemic mechanisms and current diagnostic and treatment strategies. J Am Coll Cardial. 2003;41:351–359[Abstract/Free Full Text]
2. Angelini P, Villason S, Chan AV, Diez JG. Normal and anomalous coronary arteries in humans. Angelini P. Coronary Artery Anomalies. Philadelphia, PA: Lippincott, Williams & Wilkins; 1999. p. 27–150
3. Haagen PK, Schwartz ER, vom Dahl J, et al. Long-term angiographic and clinical follow-up in patients with stent implantation for symptomatic myocardial bridging. Heart. 2000;84:403–408[Abstract/Free Full Text]
4. Angelini P, Velasco JA, Flamm S. Coronary anomalies. Incidence, pathophysiology, and clinical relevance. Circulation. 2002;105:2449–2454[Free Full Text]
5. Villareal RP, Mathur VS. The string phenomenon: an important cause of internal mammary artery graft failure. Texas Heart Inst J. 2000;27:346–349[Medline]
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