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(Circulation. 2003;108:560.)
© 2003 American Heart Association, Inc.

Clinical Investigation and Reports

Relation Between Cardiac Sympathetic Activity and Hypertensive Left Ventricular Hypertrophy

Markus P. Schlaich, MD; David M. Kaye, MBBS, PhD; Elisabeth Lambert, PhD; Marcus Sommerville; Flora Socratous; Murray D. Esler, MBBS, PhD

From Baker Heart Research Institute and Cardiovascular Medicine, Alfred Hospital, Melbourne, Australia.

Correspondence to Dr Markus P. Schlaich, Human Neurotransmitter Laboratory, Baker Heart Research Institute, PO Box 6492, St Kilda Rd Central, Melbourne, Victoria 8008, Australia. E-mail markus.schlaich{at}baker.edu.au

Received October 3, 2002; de novo received March 11, 2003; revision received May 12, 2003; accepted May 12, 2003.

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.

Methods and 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±11g/m² in EH-, and 138±17g/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.

Key Words: hypertrophy • hypertension • nervous system • sympathetic • norepinephrine

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