title: Disturbed intracoronary hemodynamics in myocardial bridging: early normalization by intracoronary stent placement.
abstract: BACKGROUND
  The purpose of this study was to evaluate the hemodynamic mechanisms leading to myocardial ischemia in patients with myocardial bridging. Myocardial bridging is known to induce angina and even severe myocardial ischemia.
  
  
  RESULTS
  In 12 symptomatic patients with myocardial bridges, quantitative coronary angiography was performed to obtain systolic/diastolic vessel diameters within the bridged segments. Coronary flow velocities, flow reserve, and pressures were determined with a 0.014-in Doppler and a 0.014-in pressure microtransducer. In 3 symptomatic patients, coronary stents were implanted and hemodynamic measurements were repeated immediately and after 7 weeks. An in vitro validation of the pressure measurements was performed. Angiography revealed a systolic diameter reduction of 80.6+/-9.2% and a persistent diastolic reduction of 35.3+/-11% within the bridged segment. Diastolic flow velocities (cm/s) were increased (31.5+/-14.3 within versus 17.3+/-5.7 proximal and 15.2+/-6.3 distal, P<.001). Coronary flow reserve distal to the bridge was 2.5+/-0.5. There was an increased peak systolic pressure within the bridged segment (171+/-48 versus 113+/-10 mm Hg proximal, P<.001). Stent placement abolished the phasic lumen compression, the diastolic flow abnormalities, the intracoronary peak systolic pressure, and clinical symptoms. Coronary flow reserve improved to 3.8+/-0.3.
  
  
  CONCLUSIONS
  Coronary hemodynamics in myocardial bridges are characterized by a phasic systolic vessel compression with a localized peak pressure, persistent diastolic diameter reduction, increased blood flow velocities, retrograde flow, and a reduced flow reserve. These alterations may explain the occurrence of symptoms and ischemia in these patients. Intracoronary stent placement abolished all hemodynamic abnormalities and may improve clinical symptoms in otherwise unsuccessfully treated patients with myocardial bridges.
authors.affiliation: Medical Clinic I, University Hospital, Rheinisch Westfälische Technische Hochschule, Aachen, Germany.
authors.forename: H G
authors.initials: HG
authors.lastname: Klues
authors.forename: E R
authors.initials: ER
authors.lastname: Schwarz
authors.forename: J
authors.initials: J
authors.lastname: vom Dahl
authors.forename: T
authors.initials: T
authors.lastname: Reffelmann
authors.forename: H
authors.initials: H
authors.lastname: Reul
authors.forename: K
authors.initials: K
authors.lastname: Potthast
authors.forename: C
authors.initials: C
authors.lastname: Schmitz
authors.forename: J
authors.initials: J
authors.lastname: Minartz
authors.forename: W
authors.initials: W
authors.lastname: Krebs
authors.forename: P
authors.initials: P
authors.lastname: Hanrath
mesh_terms: D000328:Adult; D001794:Blood Pressure; D017023:Coronary Angiography; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology* / Q000628:therapy; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D015607:Stents