Hypertensive left ventricular hypertrophy: relation to peripheral sympathetic drive
John P. Greenwood, PhD, MBChB*,a,
Eleanor M. Scott, BS, BM, BMedScia,
John B. Stoker, BSc, MBChBa and
David A. S. G. Mary, PhD, MBChBa
a Department of Cardiology, St. James’s University Hospital, Leeds, United Kingdom
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Figure 1 Example of recordings from a patient with hypertension. From above and moving down are shown the electrocardiogram (ECG), respiratory movements (Resp), Finapress blood pressure (FBP), multiunit muscle sympathetic nerve activity (Bursts) and action potentials (AP in µV). The single-unit muscle sympathetic nerve activity is counted from APs of the same profile and amplitude (tallest unit in this example) to derive the mean frequency of central vasoconstrictor sympathetic neural discharge. The burst count may include a variable number of units with different profiles.
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Figure 2 Scatter-graph showing the mean frequency of single-unit muscle sympathetic nerve activity (s-MSNA) in essential hypertensives with left ventricular hypertrophy (LVH) (triangles) and without LVH (squares). Open triangles = those subjects receiving therapy; bars = the group mean. *p < 0.001 (two-way analysis of variance). NS = nonsignificant.
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Figure 3 Scatter-graph showing the mean frequency of multiunit muscle sympathetic nerve activity (MSNA) in essential hypertensives with left ventricular hypertrophy (LVH) (triangles) and without LVH (squares). Open triangles = those subjects receiving therapy; Bars = the group mean.  p < 0.05 (two-way analysis of variance). NS = nonsignificant.
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