Relationship between central sympathetic drive and magnetic resonance imaging-determined left ventricular mass in essential hypertension

Joanna Burns, Mohan U Sivananthan, Stephen G Ball, Alan F Mackintosh, David A S G Mary, John P Greenwood, Joanna Burns, Mohan U Sivananthan, Stephen G Ball, Alan F Mackintosh, David A S G Mary, John P Greenwood

Abstract

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.

Figures

Figure 1
Figure 1
LV short axis images taken from the base of the heart to the apex, using a standard SSFP multi-phase, multi-slice MRI sequence. Endocardial and epicardial contours are shown outlined in end diastole enabling accurate calculation of LV mass.
Figure 2
Figure 2
Within subject groups there is no direct relationship between sympathetic nerve activity (SNA) and mean arterial pressure (MBP) (A & B). Also in normal control subjects there is no relationship between SNA and left ventricular mass index (LVMI) (C & D). However in LVH[−] and LVH[+] there is a direct linear relationship between SNA and LVMI (C & D).
Figure 3
Figure 3
For any of the individual subject groups (NC, LVH[−], and LVH[+]) there are no direct relationships between mean arterial pressure (MBP) and left ventricular mass index (LVMI).

Source: PubMed

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