title: Time course of sympathetic neural hyperactivity after uncomplicated acute myocardial infarction.
abstract: BACKGROUND
  Little information is available on sympathetic activity after acute myocardial infarction (AMI), despite the belief that sympathetic drive is important in relation to morbidity and mortality. Indirect indices such as plasma catecholamines are transiently elevated after uncomplicated AMI, whereas other prognostically important autonomic indices may be affected longer. We planned to quantify central sympathetic output to the periphery after uncomplicated AMI and to investigate its progress over time.
  
  
  RESULTS
  After uncomplicated AMI, 13 patients had muscle sympathetic nerve activity (MSNA) assessed from multiunit discharges and from single units with defined vasoconstrictor properties (s-MSNA). Measurements were obtained 2 to 4 days after AMI and were repeated after 3 and 6 months. We also examined 3 matched control groups comprising normal subjects, patients with coronary artery disease, and hospitalized patients without AMI. MSNA and s-MSNA after AMI (84+/-4.6 bursts/100 beats and 95+/-5.8 impulses/100 beats) were unchanged at 3 months but decreased (P<0.01 and P<0.001) after 6 months (75+/-4.0 bursts/100 beats and 80+/-4.4 impulses/100 beats). These were still greater (at least P<0.01) than values in normal subjects, patients with coronary artery disease, and hospitalized patients without AMI (51+/-3.9 bursts/100 beats, 58+/-4.7 impulses/100 beats; 56+/-2.2 bursts/100 beats, 61+/-2.2 impulses/100 beats; and 55+/-3.6 bursts/100 beats, 61+/-3.3 impulses/100 beats, respectively). This sympathetic hyperactivity was inversely correlated to left ventricular ejection fraction but not to changes in blood pressure.
  
  
  CONCLUSIONS
  A protracted state of sympathetic hyperactivity was shown to occur after uncomplicated AMI. It is suggested that this hyperactivity may explain delayed cardiovascular morbidity and mortality and that it arises because of an impairment of reflexes from cardiac receptors.
authors.affiliation: Department of Cardiology, St James's University Hospital, Leeds, UK. lee@graham93.fsnet.co.uk
authors.forename: Lee N
authors.initials: LN
authors.lastname: Graham
authors.forename: Paul A
authors.initials: PA
authors.lastname: Smith
authors.forename: John B
authors.initials: JB
authors.lastname: Stoker
authors.forename: Alan F
authors.initials: AF
authors.lastname: Mackintosh
authors.forename: David A S G
authors.initials: DA
authors.lastname: Mary
mesh_terms: D000200:Action Potentials; D000208:Acute Disease; D000704:Analysis of Variance; D001794:Blood Pressure; D001835:Body Weight; D003402:Creatine Kinase / Q000097:blood; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006334:Heart Function Tests; D006339:Heart Rate; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology*; D010543:Peroneal Nerve / Q000503:physiopathology; D011187:Posture; D012815:Signal Processing, Computer-Assisted; D013318:Stroke Volume; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D044465:White People
chemical_list: D003402:Creatine Kinase