title: ST-elevation myocardial infarction following heart transplantation as an unusual presentation of coronary allograft vasculopathy: a case report.
abstract: BACKGROUND
  The presentation, mechanisms, and incidence of ST elevation myocardial infarction (STEMI) in heart transplant recipients have been characterized only to a limited degree in the current literature. Herein, we present a unique case of STEMI years after heart transplantation with a focus on the salient features of its diagnosis and interventions. We also provide a review of the epidemiology of this phenomenon.
  
  
  METHODS
  A 33-year-old woman who was status post cardiac transplantation for dilated cardiomyopathy presented to the clinic with mild nonspecific fatigue and concern after having noticed relative bradycardia compared with her posttransplantation baseline heart rate. Electrocardiogram (ECG) showed junctional rhythm and inferior ST elevations, likely reflecting nodal ischemia. Troponins were grossly positive and echocardiogram showed marked right ventricular dysfunction.
  
  
  RESULTS
  Successful percutaneous coronary intervention (PCI) with aspiration thrombectomy and drug-eluting stent placement was emergently performed. The heart's rhythm soon returned to sinus tachycardia. Right ventricular wall-motion abnormalities resolved. The patient suffered no clinical sequelae of her STEMI.
  
  
  CONCLUSIONS
  This case illustrated that "classic" symptoms of STEMI may not occur at all in the setting of heart transplantation. To our knowledge, this is the first case of posttransplantation STEMI presenting as asymptomatic bradycardia, and highlights the importance of maintaining high clinical suspicion for ischemia in transplant recipients with subtle changes. In reviewing the epidemiology of this case, we locate and bundle different types of studies that have directly or indirectly looked at STEMI in heart transplantation. For a variety of putative pathophysiological reasons, STEMI is indeed a rare manifestation of the common transplant phenomenon of coronary artery vasculopathy (CAV).
authors.affiliation: Stanford University Hospital, Stanford, Calif 94305-5110, USA.
authors.forename: S
authors.initials: S
authors.lastname: Peter
authors.forename: O
authors.initials: O
authors.lastname: Hulme
authors.forename: T
authors.initials: T
authors.lastname: Deuse
authors.forename: B
authors.initials: B
authors.lastname: Vrtovec
authors.forename: W F
authors.initials: WF
authors.lastname: Fearon
authors.forename: S
authors.initials: S
authors.lastname: Hunt
authors.forename: F
authors.initials: F
authors.lastname: Haddad
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D001919:Bradycardia / Q000209:etiology / Q000503:physiopathology; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D018618:Echocardiography, Doppler, Color; D004562:Electrocardiography; D005260:Female; D006339:Heart Rate; D016027:Heart Transplantation / Q000009:adverse effects*; D006801:Humans; D009203:Myocardial Infarction / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D062645:Percutaneous Coronary Intervention / Q000295:instrumentation; D015607:Stents; D017131:Thrombectomy; D013997:Time Factors; D016896:Treatment Outcome; D014336:Troponin / Q000097:blood; D018497:Ventricular Dysfunction, Right / Q000209:etiology / Q000503:physiopathology; D016278:Ventricular Function, Right
chemical_list: D015415:Biomarkers; D014336:Troponin