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Published on: June 14, 2016
Relation between cardiac sympathetic activity and hypertensive left ventricular hypertrophy
Markus P Schlaich1, David M Kaye, Elisabeth Lambert
1Human Neurotransmitter Laboratory, Baker Heart Research Institute and Cardiovascular Medicine, Alfred Hospital, Melbourne, Victoria 8008, Australia. markus.schlaich@baker.edu.au
Insights
Hypertension-induced left ventricular hypertrophy is linked to heightened cardiac sympathetic activity. This suggests increased norepinephrine release in the heart contributes to the development of left ventricular hypertrophy.
Area of Science:
- Cardiology
- Hypertension Research
- Autonomic Nervous System Studies
Background:
- Left ventricular (LV) hypertrophy is a significant risk factor for cardiovascular events in hypertensive individuals.
- The role of sympathetic activation in the development of LV hypertrophy in humans requires further validation.
Purpose of the Study:
- To investigate and compare systemic and regional sympathetic activity in hypertensive patients with and without left ventricular hypertrophy.
- To determine the relationship between sympathetic activity and left ventricular mass in hypertension.
Main Methods:
- Utilized radiotracer dilution methods and microneurography to assess sympathetic activity.
- Compared three groups: hypertensive with LV hypertrophy (EH+), hypertensive without LV hypertrophy (EH-), and normotensive controls (NT).
- Measured LV mass index, total body and renal norepinephrine spillover, muscle sympathetic nerve activity, and cardiac norepinephrine spillover.
Main Results:
- Muscle sympathetic nerve activity and cardiac norepinephrine spillover were significantly elevated only in the hypertensive group with LV hypertrophy (EH+).
- Cardiac norepinephrine spillover showed a positive correlation with LV mass index across all subjects.
- While total body and renal norepinephrine spillover were higher in both hypertensive groups, cardiac-specific activity was uniquely increased in EH+.
Conclusions:
- Hypertensive left ventricular hypertrophy is associated with sympathetic activity predominantly localized to the heart.
- Increased cardiac norepinephrine release appears to be a key factor in the development of left ventricular hypertrophy in hypertensive patients.
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+/-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.
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