To the Editor:
In the article on myocardial bridging by Lauer and Carlson,1 the patient was evaluated by an adenosine thallium SPECT study. This showed a fairly small, reversible anterior wall perfusion defect.
Adenosine causes vasodilation and actually decreases intramural myocardial pressure. The reason a reversible defect appears is that more time is spent in systole per minute owing to the adenosine-caused heart rate increase. I would suggest that either exercise or dobutamine stress would have been more appropriate, because by raising intramural pressure (as well as heart rate), the submerged segment would more likely be compressed, giving a more sensitive quantification of the amount of myocardium at risk.
- Copyright © 1999 by American Heart Association
We appreciate Dr Elson’s insightful comments on our article.R1 To the best of our knowledge, there have been no published studies comparing the use of stress modalities in myocardial bridging. Because she was unable to tolerate exercise, our patient was stressed with the use of adenosine as a preoperative evaluation without knowledge of her bridging a priori. We agree that when possible, an exercise stress study is preferable, because it provides functional data and correlates perfusion defects with physiological stress.
Within a bridged coronary segment, intravascular ultrasound and intracoronary Doppler have shown that there is not only a systolic luminal diameter reduction, but also a persistent diastolic diameter reductionR2 with delayed relaxation in diastole and a subsequent prominent peak in coronary flow velocities in early diastole.R3 With an increase in heart rate, a decrease in diastolic filling time, or an increase in contractility, there is a decrease of flow through the bridge segment (for example, with exercise or dobutamine). Furthermore, short-term β-blocker therapy has been demonstrated to significantly decrease diameter reductions during both systole and diastole.R2
Adenosine, by its dilation of intramyocardial resistance vessels and a slight increase in heart rate, may theoretically decrease flow across a bridge segment by a “steal” phenomenon similar to that seen in significant fixed stenoses. However, because of the dynamic nature of a bridged segment stenosis within the cardiac cycle, adenosine may, in fact, underestimate perfusion defects compared with exercise.
Lauer WJ, Carlson TA. Myocardial bridging. Circulation. 1998;98:821.
Schwarz ER, Klues HG, vom Dohl J, Klein I, Krebs W, Hanrath P. Functional, angiographic and intracoronary Doppler flow characteristics in symptomatic patients with myocardial bridging: effect of short-term intravenous beta-blocker medication. J Am Coll Cardiol. 1996;27:1637–1645.
Ge J, Erbel R, Rupprecht HJ, Koch L, Kearney P, Gorge G, Haude M, Meyer J. Comparison of intravascular ultrasound and angiography in the assessment of myocardial bridging. Circulation. 1994;89:1725–1732.