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Myocardial bridging is associated with alteration in coronary vasoreactivity
Joerg Herrmann1, Stuart T Higano, Ryan J Lenon
1Division of Cardiovascular Diseases, Mayo Clinic Rochester, 200 First Street S.W., Rochester, MN 55905, USA.
Insights
Myocardial bridging (MB) impairs endothelium-dependent vasoreactivity, causing vasoconstriction. This functional change, along with enhanced wall shear rate (WSR), may worsen the clinical presentation of MB.
Area of Science:
- Cardiovascular Research
- Medical Physiology
- Congenital Heart Disease
Background:
- Altered shear stress is linked to endothelial dysfunction.
- Myocardial bridging (MB), a congenital condition, alters shear stress but its effect on vasoreactivity is unknown.
Purpose of the Study:
- To investigate the impact of myocardial bridging on coronary vasoreactivity and wall shear stress.
Main Methods:
- A case-control study compared 29 MB patients with 58 controls.
- Coronary artery vasoreactivity was assessed using acetylcholine and nitroglycerine infusions.
- Wall shear rate (WSR) and coronary flow velocity reserve (CFVR) were measured.
Main Results:
- Myocardial bridging sites showed significantly greater vasoconstriction in response to acetylcholine compared to other segments and controls.
- No differences were observed in nitroglycerine response or CFVR between groups.
- Baseline and acetylcholine-stimulated WSR were higher at the myocardial bridging site.
Conclusions:
- Myocardial bridging is associated with increased WSR and impaired endothelium-dependent vasodilation.
- These functional alterations may exacerbate lumen compression and clinical symptoms in MB.
Background:
Shear stress alteration has been recognized as a predisposing factor for the impairment of endothelial function. Myocardial bridging is a congenital condition associated with alteration in shear stress, however, its impact upon vasoreactivity remains undetermined.
Methods And Results:
This was a case-control designed study with 29 patients with myocardial bridging and 58 patients without myocardial bridging. Endothelium-dependent and endothelium-independent changes in coronary artery diameters, blood flow and wall shear stress were determined after intracoronary infusion of acetylcholine (ACH, 10(-6)-10(-4) mol/L) and nitroglycerine (NTG, 200 microg). Coronary flow velocity reserve (CFVR) was determined after intracoronary injection of adenosine (18-36 microg). In response to ACH, there was more epicardial vasoconstriction at the myocardial bridging site compared with the proximal and distal segments (-29.6+/-21.7 vs. -9.6+/-22.5 and -17.4+/-21.5%, p<0.05) and compared with the control group (-29.6+/-21.7 vs. -5.9+/-36.5%, p<0.001). The response to NTG and CFVR was the same in the case and the control group. Wall shear rate (WSR) was higher in the MB site at baseline and in response to ACH.
Conclusions:
MB is characterised by enhanced WSR and impairment in endothelium-dependent vasorelaxation. These functional alterations may add to the severity of structural lumen compression and thus to the clinical presentation of this congenital abnormality.
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