title: Inverse relation of C-reactive protein levels to heart rate variability in patients after acute myocardial infarction.
abstract: BACKGROUND
  Inflammation has a major role in atherosclerosis and the acute phase C-reactive protein (CRP) is elevated after acute myocardial infarction. Inflammation is also implicated in autonomic nervous system control. Heart rate variability (HRV) has been used as a marker of abnormal autonomic activity after myocardial infarction. Our purpose was to investigate the relation between CRP levels and autonomic tone in patients after acute ST-segment elevation myocardial infarction.
  
  
  METHODS
  We studied prospectively 98 patients. CRP and the cardiac enzymes CK, CK-MB, and troponin-I were measured for a total of 72 hours and 24-hour Holter ECG recordings for HRV analysis were acquired before hospital discharge.
  
  
  RESULTS
  The natural logarithm of CRP levels was inversely correlated with the following logarithmic transformed indices of HRV in the time and in the frequency domain: SDNN, standard deviation of all normal R-R intervals, (r = -0.40, p < 0.001); SDANN index, standard deviation of the average normal R-R intervals for 5-minute segments, (r = -0.46, p < 0.001); SDNN index, mean of the standard deviation of all normal R-R intervals for 5-minute segments (r = -0.41, p < 0.001); total power (TP) (r = -0.38, p < 0.001); high frequency power (HF) (r = -0.31, p < 0.01); low frequency power (LF) (r = -0.45, p < 0.001). The strong inverse relation between CRP and SDNN, SDANN, SDNN index, LF and TP persisted after adjustment for left ventricular function.
  
  
  CONCLUSIONS
  Increased levels of circulating CRP after acute myocardial infarction are associated with attenuated HRV indices, suggesting a possible relationship between inflammation and cardiac autonomic balance.
authors.affiliation: 2nd Department of Cardiology, Nikea General Hospital, Athens, Greece. tglyras@ath.forthnet.gr
authors.forename: Stavroula N
authors.initials: SN
authors.lastname: Psychari
authors.forename: Thomas S
authors.initials: TS
authors.lastname: Apostolou
authors.forename: Efstathios K
authors.initials: EK
authors.lastname: Iliodromitis
authors.forename: Petros
authors.initials: P
authors.lastname: Kourakos
authors.forename: Georgios
authors.initials: G
authors.lastname: Liakos
authors.forename: Dimitrios T
authors.initials: DT
authors.lastname: Kremastinos
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form / Q000097:blood; D015716:Electrocardiography, Ambulatory; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology; D006339:Heart Rate; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000503:physiopathology*; D011446:Prospective Studies; D012107:Research Design; D013318:Stroke Volume; D019210:Troponin I / Q000097:blood; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; D019210:Troponin I; D002097:C-Reactive Protein; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form