title: Relation between cardiac sympathetic activity and hypertensive left ventricular hypertrophy.
abstract: BACKGROUND
  Left ventricular (LV) hypertrophy is an independent risk factor for cardiovascular morbidity and mortality in hypertensive subjects. Sympathetic activation has been suggested to contribute to LV hypertrophy, but this has not yet been conclusively validated in humans.
  
  
  RESULTS
  We comprehensively assessed total systemic and regional sympathetic activity by radiotracer dilution methods and microneurography in 15 untreated hypertensive subjects with echocardiographic evidence of LV hypertrophy (EH+), 11 hypertensive subjects with similar blood pressure but without LV hypertrophy (EH-), and 10 age-matched normotensive control subjects (NT). LV mass index was 87+/-15 g/m2 in NT, 106+/-11 g/m2 in EH-, and 138+/-17 g/m2 in EH+ (P<0.001). Total body and renal norepinephrine spillover were higher in both hypertensive groups compared with NT (total norepinephrine spillover, NT 223+/-145 versus EH- 418+/-135 versus EH+ 497+/-303 ng/min; renal norepinephrine spillover, NT 38.8+/-25.3 versus EH- 88.6+/-58.0 versus EH+ 103.4+/-56.2 ng/min; both P<0.05). However, muscle sympathetic nerve activity (NT 25+/-6 versus EH- 38+/-20 versus EH+ 57+/-19 bursts per 100 heartbeats; P<0.01) and cardiac norepinephrine spillover (NT 11.7+/-6.2 versus EH- 13.1+/-7.2 versus EH+ 28.6+/-17.4 ng/min; P<0.01) were only increased in EH+. Cardiac norepinephrine spillover correlated positively with LV mass index in all subjects (r=0.52; P<0.001).
  
  
  CONCLUSIONS
  Our findings demonstrate that hypertensive LV hypertrophy is associated with increased sympathetic activity largely confined to the heart, suggesting that increased cardiac norepinephrine release is related to the development of LV hypertrophy.
authors.affiliation: Human Neurotransmitter Laboratory, Baker Heart Research Institute and Cardiovascular Medicine, Alfred Hospital, Melbourne, Victoria 8008, Australia. markus.schlaich@baker.edu.au
authors.forename: Markus P
authors.initials: MP
authors.lastname: Schlaich
authors.forename: David M
authors.initials: DM
authors.lastname: Kaye
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Lambert
authors.forename: Marcus
authors.initials: M
authors.lastname: Sommerville
authors.forename: Flora
authors.initials: F
authors.lastname: Socratous
authors.forename: Murray D
authors.initials: MD
authors.lastname: Esler
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D015331:Cohort Studies; D004452:Echocardiography; D005260:Female; D006321:Heart / Q000294:innervation* / Q000502:physiology / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism / Q000493:pharmacokinetics; D010543:Peroneal Nerve / Q000502:physiology / Q000503:physiopathology; D012016:Reference Values; D017779:Sympathetic Fibers, Postganglionic / Q000502:physiology / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000502:physiology / Q000503:physiopathology*; D014316:Tritium
chemical_list: D014316:Tritium; D009638:Norepinephrine