title: Heart rate variability during the acute phase of myocardial infarction.
abstract: BACKGROUND
  After acute myocardial infarction (AMI), several abnormalities of the autonomic control to the heart have been described. Heart rate (HR) variability has been used to explore the neural control to the heart. A low HR variability count measured 7-13 days after AMI is significantly related to a poor outcome. Little information is available on HR variability early after AMI and its relation to clinical and hemodynamic data.
  
  
  RESULTS
  We studied 54 consecutive patients (42 men and 12 women; mean age, 60.4 +/- 11 years) with evidence of AMI by collecting the 24-hour HR SD from Holter tapes recorded on day 2 or 3. We also measured HR variability in 15 patients with unstable angina and in 35 age-matched normal subjects. HR variability was lower in AMI than in unstable angina patients (57.6 +/- 21.3 versus 92 +/- 19 msec; p less than 0.001) and controls (105 +/- 12 msec; p less than 0.001). Also, HR variability was greater in non-Q-wave than in Q-wave AMI (p less than 0.0001) and in recombinant tissue-type plasminogen activator-treated patients with respect to the rest of the group (p less than 0.02). No difference was found for infarct site. HR variability was significantly related to mean 24-hour HR, peak creatine kinase-MB, and left ventricular ejection fraction (all p less than 0.0001). Patients belonging to Killip class greater than I or who required the use of diuretics or digitalis had lower counts (p less than 0.004, p less than 0.001, and p less than 0.024, respectively). Six patients died within 20 days after admission to the hospital. In these patients, HR variability was lower than in survivors (31.2 +/- 12 versus 60.9 +/- 20 msec; p less than 0.001), and a value less than 50 msec was significantly associated with mortality (p less than 0.025).
  
  
  CONCLUSIONS
  HR variability during the early phase of AMI is decreased and is significantly related to clinical and hemodynamic indexes of severity. The causes for the observed changes in HR variability during AMI may be reduced vagal and/or increased sympathetic outflow to the heart. It is suggested that early measurements of HR variability during AMI may offer important clinical information and contribute to the early risk stratification of patients.
authors.affiliation: Clinica Medica I, University of Florence, Italy.
authors.forename: G C
authors.initials: GC
authors.lastname: Casolo
authors.forename: P
authors.initials: P
authors.lastname: Stroder
authors.forename: C
authors.initials: C
authors.lastname: Signorini
authors.forename: F
authors.initials: F
authors.lastname: Calzolari
authors.forename: M
authors.initials: M
authors.lastname: Zucchini
authors.forename: E
authors.initials: E
authors.lastname: Balli
authors.forename: A
authors.initials: A
authors.lastname: Sulla
authors.forename: S
authors.initials: S
authors.lastname: Lazzerini
mesh_terms: D000789:Angina, Unstable / Q000503:physiopathology; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D001341:Autonomic Nervous System / Q000503:physiopathology; D003325:Coronary Care Units; D015716:Electrocardiography, Ambulatory; D005260:Female; D006321:Heart / Q000294:innervation; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D010959:Tissue Plasminogen Activator