title: Role of myocardial bridging in the apical localization of stress cardiomyopathy.
abstract: BACKGROUND
  The apical ballooning syndrome is precipitated by emotional or physical stress but the underlying mechanism remains poorly understood. The contribution of myocardial bridging on the aetiology and the onset of the syndrome is not known.
  
  
  METHODS
  We observed 8 patients with chest pain, T-wave inversion in several leads of the ECG, transient left ventricular apical ballooning and no significant angiographic stenosis.
  
  
  RESULTS
  There were 7 women and I man. The median age was 67.5 years. Seven patients had an intense emotional or physical stress (87.5%). All patients presented with chest pain and aT-wave inversion in the precordial leads. The median elevation of creatine-kinase was 171 IU. In all patients, echocardiography showed an alteration of the left ventricular function with a very extensive apical akinesia. Left ventricular hypertrophy was observed in 7 patients. A myocardial bridging in the mid segment of the left anterior descending coronary artery was observed in 5 patients (62.5%). Recovery was complete in all patients. During follow-up, no patient showed recurrence.
  
  
  CONCLUSIONS
  Our data suggest that myocardial bridging possibly enhanced by catecholamines during stress may contribute, in association with left ventricular hypertrophy, to the preferential apical localization of the apical ballooning syndrome. Further investigations are necessary to confirm
authors.affiliation: Department of Cardiology, CHU Saint-Pierre, Brussels, Belgium. France_Lemaitre@stpierre-bru.be
authors.forename: France
authors.initials: F
authors.lastname: Lemaitre
authors.forename: Laurent
authors.initials: L
authors.lastname: Close
authors.forename: Nuray
authors.initials: N
authors.lastname: Yarol
authors.forename: Arsène
authors.initials: A
authors.lastname: Kemdem
authors.forename: Paul Gaël
authors.initials: PG
authors.lastname: Silance
authors.forename: Michel
authors.initials: M
authors.lastname: De Marneffe
authors.forename: Jean-Luc
authors.initials: JL
authors.lastname: Vandenbossche
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D009202:Cardiomyopathies / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging; D003402:Creatine Kinase / Q000097:blood; D004452:Echocardiography; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006329:Heart Conduction System / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology*; D012107:Research Design; D012307:Risk Factors; D013312:Stress, Physiological / Q000150:complications; D013315:Stress, Psychological / Q000150:complications; D013318:Stroke Volume; D020107:Troponin T / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000150:complications / Q000000981:diagnostic imaging; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; D020107:Troponin T; D003402:Creatine Kinase