title: Association between discharge heart rate and left ventricular adverse remodelling in ST segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention.
abstract: OBJECTIVE
  Left ventricular (LV) adverse remodelling is an important determinant of mortality after ST segment elevation myocardial infarction (STEMI). Recently, discharge heart rate (DHR) has been associated with long-term outcomes after STEMI. Whether DHR is related to the development of LV remodelling after STEMI remains unknown. The present study evaluated the association between DHR after STEMI and the occurrence of LV remodelling at 6 months. DESIGN, SETTING, PATIENTS AND INTERVENTIONS: In 964 STEMI patients (60±11 years, 77% male) treated with primary percutaneous coronary intervention, DHR was derived from predischarge 12-lead electrocardiograph. LV volumes were measured with two-dimensional transthoracic echocardiography at baseline and 6-month follow-up. Variables independently associated with the occurrence of LV remodelling were investigated.
  
  
  METHODS
  LV remodelling, defined as ≥20% increase in LV end-diastolic volume at 6 months follow-up.
  
  
  RESULTS
  LV remodelling occurred in 30.7% of patients. Compared with patients without remodelling, these patients had higher DHR (72±11 bpm vs 68±12 bpm, p<0.001), higher levels of peak troponin T (5.6 (2.7, 11) ug/L vs 3.7 (1.6, 7.4) ug/L, p<0.001) and creatine kinase (2083 (960, 4045) U/L vs 1469 (669, 2750) U/L, p<0.001), lower LV ejection fraction (45±10 vs 48±9%, p<0.001) and more frequently displayed left anterior descending artery as culprit (52% vs 44%, p=0.02). Median DHR was 69 bpm. DHR >69 bpm (OR 1.5, 95% CI 1.10 to 2.04, p=0.01) and higher peak troponin T (OR 1.06, 95% CI 1.03 to 1.09, p<0.001) were independently associated with LV remodelling at follow-up.
  
  
  CONCLUSIONS
  DHR is independently associated with LV remodelling after STEMI, underlining the importance of heart rate as an early risk marker in this contemporary population.
authors.affiliation: Department of Cardiology, Leiden University Medical Center, Albinusdreef 2, Leiden, The Netherlands.
authors.forename: Emer
authors.initials: E
authors.lastname: Joyce
authors.forename: Georgette E
authors.initials: GE
authors.lastname: Hoogslag
authors.forename: Darryl P
authors.initials: DP
authors.lastname: Leong
authors.forename: Kim
authors.initials: K
authors.lastname: Fox
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Schalij
authors.forename: Nina Ajmone
authors.initials: NA
authors.lastname: Marsan
authors.forename: Jeroen J
authors.initials: JJ
authors.lastname: Bax
authors.forename: Victoria
authors.initials: V
authors.lastname: Delgado
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D016009:Chi-Square Distribution; D015150:Echocardiography, Doppler; D004562:Electrocardiography; D005260:Female; D006339:Heart Rate; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D016017:Odds Ratio; D010351:Patient Discharge; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects; D011237:Predictive Value of Tests; D012189:Retrospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D013318:Stroke Volume; D013997:Time Factors; D016896:Treatment Outcome; D020107:Troponin T / Q000097:blood; D015854:Up-Regulation; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers; C545568:TNNT2 protein, human; D020107:Troponin T