Relationship between central sympathetic drive and magnetic resonance imaging-determined left ventricular mass in
Joanna Burns1, Mohan U Sivananthan, Stephen G Ball
1Department of Cardiology, Leeds Teaching Hospitals NHS Trust, Leeds, UK.
Insights
Sympathetic nerve activity is linked to left ventricular hypertrophy (LVH) in hypertension. Increased sympathetic activation correlates with greater left ventricular mass (LVM), supporting its role in developing LVH.
Area of Science:
- Cardiology
- Hypertension Research
- Neurocardiology
Background:
- Sympathetic nervous system overactivity is a known factor in left ventricular hypertrophy (LVH) development.
- The precise relationship between sympathetic activation and left ventricular mass (LVM) across varying arterial pressures remains unclear.
- This study investigates the link between sympathetic activity and LVM in hypertensive individuals with and without LVH.
Purpose of the Study:
- To determine the relationship between sympathetic activation and left ventricular mass (LVM) in hypertensive patients.
- To compare sympathetic nerve activity and LVM in patients with and without LVH versus normal controls.
- To assess the correlation between sympathetic activity, LVM, and arterial blood pressure.
Main Methods:
- Compared 24 hypertensive patients without LVH (LVH[-]), 25 with LVH (LVH[+]), and 24 controls.
- Quantified resting muscle sympathetic nerve activity (SNA) using multiunit and single-unit recordings.
- Measured left ventricular mass (LVM) indexed to body surface area (LVM index) via cardiac magnetic resonance imaging.
Main Results:
- LVM index was significantly higher in LVH[+] (91 g/m2) than LVH[-] (67 g/m2) and controls (57 g/m2).
- Sympathetic activity was elevated in LVH[-] (53 bursts/100 beats) and LVH[+] (66 bursts/100 beats) compared to controls (39 bursts/100 beats).
- A strong positive correlation (r=0.76) was found between SNA and LVM index in hypertensive groups, but not controls. No consistent BP-SNA or BP-LVM relationship was observed.
Conclusions:
- Central sympathetic activation is associated with left ventricular hypertrophy (LVH) in human hypertension.
- These findings reinforce the role of sympathetic overactivity in the pathogenesis of LVH.
- Arterial pressure alone does not consistently predict sympathetic activity or LVM in this context.
Background:
Sympathetic activation has been implicated in the development of left ventricular hypertrophy (LVH). However, the relationship between sympathetic activation and LV mass (LVM) has not been clearly defined across a range of arterial pressure measurements. The present study was planned to determine that relationship, using cardiac magnetic resonance imaging to accurately quantify LVM, in hypertensive patients with and without LVH and in normal subjects.
Methods And Results:
Twenty-four patients with uncomplicated and untreated essential hypertension (LVH[-]) were compared with 25 patients with essential hypertension and left ventricular hypertrophy (LVH[+]) and 24 normal control subjects. Resting muscle sympathetic nerve activity was quantified as multiunit bursts and single units. Cardiac magnetic resonance imaging-determined LVM was indexed to body surface area (LVM index); in the LVH[-] group, LVM index was 67+/-2.1 g/m2, a value between those of the LVH[+] (91+/-3.4 g/m2) and normal control (57+/-2.2 g/m2) groups, respectively. The sympathetic activity in the LVH[-] group (53+/-1.3 bursts per 100 cardiac beats and 63+/-1.6 impulses per 100 cardiac beats) was between (at least P<0.001) those of the LVH[+] (66+/-1.7 bursts per 100 cardiac beats and 77+/-2.2 impulses per 100 cardiac beats) and normal control (39+/-3.0 bursts per 100 cardiac beats and 45+/-3.4 impulses per 100 cardiac beats) groups. Significant positive correlation existed between sympathetic activity and LVM index in the LVH[-] and LVH[+] groups (at least r=0.76, P<0.0001) but not in the normal control group. However, no consistent relationship existed between arterial blood pressure and sympathetic activity or LVM index.
Conclusions:
These findings further support the hypothesis that central sympathetic activation is associated with the development of LVH in human hypertension.
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