Abstract
Background.In patients with extensive myocardial bridging, evaluation of its clinical significance remains a challenge.
Hypothesis.Sequential invasive testing is feasible and gives more insight into the pathophysiological mechanism of bridging-related angina.
Methods.Twelve patients with chest pain, proven ischaemia and extensive myocardial bridging were assessed. Myocardial bridging was evaluated at rest, during intracoronary acetylcholine infusion, through coronary flow velocity and flow reserve measurements, and during dobutamine stress.
Results.The mean length of the bridging segment was 24.9 mm (QCA; range 8.4-48.0 mm). Acetylcholine infusion caused severe vasospasm in two patients. In these two patients anginal symptoms were related to vasospasm and sequential testing was discontinued. In the remaining ten patients sequential testing was continued. Coronary flow reserve was normal in all patients: 3.3±0.6. In six patients reliable quantitative measurements could be performed during dobutamine stress. The mean systolic diameter of the bridging segment was 1.6±0.4 at baseline and 1.3±0.3 during dobutamine stress (mean of differences 0.38 (95% CI 0.1-0.7)). The difference between the diastolic and systolic diameter in the bridging segment increased from 0.3±0.2 mm at baseline to 1.0±0.5 mm during dobutamine infusion (mean of differences 0.6 (95% CI 0.3 to 0.9)).
Conclusion.Sequential testing for bridging is feasible and may disclose endothelial dysfunction or spasm as an underlying mechanism in a minority of patients. Coronary flow reserve was preserved. Dobutamine stress unmasked further lumen reduction and may give further insight into the clinical significance of myocardial bridging in individual patients. (Neth Heart J 2008;16:10-5.)
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Department of Cardiology, Groningen University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands
Correspondence to: R.A. Tio Department of Cardiology, Thoraxcentre, University Medical Centre Groningen, University of Groningen, PO Box 30.001, 9700 RB Groningen, the Netherlands
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Hazenberg, A.J.C., Jessurun, G.A.J. & Tio, R.A. Mechanisms involved in symptomatic myocardial bridging. NHJL 16, 10–15 (2008). https://doi.org/10.1007/BF03086110
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DOI: https://doi.org/10.1007/BF03086110