Letter by Schlaich et al Regarding Article, “Relationship Between Central Sympathetic Drive and Magnetic Resonance Imaging–Determined Left Ventricular Mass in Essential Hypertension”
To the Editor:
The demonstration of a relation between left ventricular (LV) hypertrophy and the risk of cardiovascular morbidity and mortality both in hypertensive patients and in the general population1 evoked a large series of investigations into the mechanisms underlying the development of LV hypertrophy. Clearly, hemodynamic factors, in particular systolic blood pressure, play a crucial role.2 Convincing evidence also exists of a close relation between cardiac norepinephrine release and LV hypertrophy.3 A recent report by Burns and colleagues4 confirms previous reports and supports the concept of an association between sympathetic activation and the development of LV hypertrophy. In their recent study, LV mass was quantified with cardiac magnetic resonance imaging, which gave a new level of rigor to the testing of the relationship of LV hypertrophy to sympathetic nervous activity in essential hypertension.
We do have some concerns with the data presented and their interpretation. First, we feel that the influence of blood pressure has not been adequately addressed as a confounding factor. Ambulatory blood pressure measurement would have been more appropriate, particularly in the nonhypertensive range. Furthermore, we found it somewhat surprising that a difference in systolic blood pressure of 9 mm Hg between the 2 hypertensive groups with and without LV hypertrophy did not yield a statistically significant result. Such a difference in blood pressure would have been expected to influence LV mass.
A second concern is the neglect of the importance of regionalization of sympathetic activity. The sympathetic outflow to individual organs is not homogenous; sympathetic outflow to the skeletal muscle vasculature, as measured by Burns et al,4 gives only inferential information about sympathetic outflow to the heart. This point is underscored by our previous demonstration that the increase in sympathetic nerve activity in the kidneys in essential hypertension, not surprisingly, is unrelated to the presence of LV hypertrophy.3 However, a positive correlation between cardiac sympathetic drive and LV mass index has been reported previously in a cohort of normotensive and hypertensive subjects.3
The work by Burns and colleagues is interesting and provides further information about the relationship between sympathetic activity and LV hypertrophy. Although we are convinced that sympathetic activation is a major contributor to LV structural changes in hypertension, to definitively test this question, prospective studies involving the measurement of cardiac sympathetic activity and its relation to LV mass, with due consideration of other confounding factors, such as blood pressure, will be needed.
Schlaich MP, Kaye DM, Lambert E, Sommerville M, Socratous F, Esler MD. Relation between cardiac sympathetic activity and hypertensive left ventricular hypertrophy. Circulation. 2003; 108: 560–565.
Burns J, Sivananthan MU, Ball SG, Mackintosh AF, Mary DASG, Greenwood JP. Relationship between central sympathetic drive and magnetic resonance imaging–determined left ventricular mass in essential hypertension. Circulation. 2007; 115: 1999–2005.