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Cited by 459Blood Pressure and Hypertension StudiesCardiovascular Function and Risk FactorsHeart Rate Variability and Autonomic Control

Relation Between Cardiac Sympathetic Activity and Hypertensive Left Ventricular Hypertrophy

Schlaich, Markus P., Kaye, David M., Lambert, Elisabeth, Sommerville, Marcus, Socratous, Flora, Esler, Murray D.·2003·Circulation
DOI 10.1161/01.cir.0000081775.72651.b6
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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. 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/m 2 in NT, 106±11g/m 2 in EH−, and 138±17g/m 2 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.

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  • Microneurographic studies almost universally show that sympathetic nerve traffic is potentiated in established hypertension in middle age and in elderly as well as young patients.

    “As far as the second issue is concerned, microneurographic studies almost universally shown that sympathetic nerve traffic is potentiated in established hypertension in middle age and in elderly as well as young patients38–46.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [42]

  • Adrenergic neural factors may contribute to the development and progression of target organ damage, as documented by pronounced increases in sympathetic nerve traffic and cardiac norepinephrine spillover rate in patients with hypertension complicated by left ventricular hypertrophy or left ventricular diastolic dysfunction.

    “Adrenergic neural factors may also contribute to the development and progression of target organ damage, as documented by the pronounced increase in sympathetic nerve traffic and cardiac norepinephrine spillover rate in patients in which hypertension is complicated by left ventricular hypertrophy or left ventricular diastolic dysfunction40,42,44,45.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [42]

  • The sympathetic neural outflow is commonly activated also to the heart and skeletal muscle vasculature, but renal sympathetic activation is central to hypertension pathogenesis.

    “The sympathetic neural outflow is commonly activated also to the heart, shown with selective cardiac norepinephrine spillover measurements28, and to the skeletal muscle vasculature, demonstrated with microneurographic nerve traffic recording32,33,38–46, but it is the renal sympathetic activation which is central to hypertension pathogenesis96–97.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [42]

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Authors
Schlaich, M. P., Kaye, D. M., Lambert, E., Sommerville, M., Socratous, F., & Esler, M. D.
Affiliations
  • The Alfred Hospital (AU)
  • From Baker Heart Research Institute and Cardiovascular Medicine, Alfred Hospital, Melbourne, Australia.
ORCID
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2003-08-05
Volume
108
Issue
5
Pages
560-565
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/01.cir.0000081775.72651.b6
OpenAlex
W2041691782
Cited by
459
References
32
Citations by year
2026: 14 · 2025: 10 · 2024: 21 · 2023: 21 · 2022: 15 · 2021: 21 · 2020: 17 · 2019: 17 · 2018: 20 · 2017: 19 · 2016: 16 · 2015: 29 · 2014: 23 · 2013: 26 · 2012: 37
FWCI
9.70
Type
journal article
Language
en
Open access
closed
Locations
  • Circulation (publishedVersion)
  • PubMed (publishedVersion)
Funders
Deutsche Forschungsgemeinschaft
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
Keywords
left ventricular hypertrophy, hypertension, cardiac sympathetic activity, norepinephrine spillover, left ventricular mass, sympathetic nervous system, microneurography
MeSH terms
Adult, Blood Pressure, Echocardiography, Female, Heart, Humans, Hypertension, Male, Middle Aged, Myocardium, Norepinephrine, Peroneal Nerve, Reference Values, Sympathetic Nervous System, Tritium, Cohort Studies, Hypertrophy, Left Ventricular, Sympathetic Fibers, Postganglionic

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