Response to Letter Regarding Article, “Relationship Between Central Sympathetic Drive and Magnetic Resonance Imaging–Determined Left Ventricular Mass in Essential Hypertension”
We thank Dr Schlaich and colleagues for their letter finding that our publication1 has provided further information about the relationship between sympathetic activity and left ventricular hypertrophy, and particularly that it raises the need for future studies involving cardiac sympathetic activity. Their letter also raises concerns about the potential confounding effect of blood pressure (BP) and the heterogeneous nature of regional sympathetic output.
We agree that ambulatory BP could have a closer link to left ventricular mass (LVM) than office BP. However, as discussed in our section on study limitations,1 the design required close matching of groups; this was achieved by performing repeated sphygmomanometric measurements at rest as recommended by international guidelines and relating this concurrently to resting muscle sympathetic nerve activity values. Ambulatory BP measurements also have limitations; they cannot allow for the between-subject variation in physical activity, diet, and emotional stimulation that could clearly confound studies of a mechanistic nature. We do not believe that the unavoidable group mean difference in systolic BP within the 2 hypertensive groups significantly confounded our results. We found no significant correlation between arterial pressure and LVM at a time when the pressure indices did not differ statistically. Consistently, we have shown no direct relationship between BP and LVM, even though a clear positive relationship has appeared between sympathetic nerve activity and LVM.1,2
We agree with Schlaich et al with regard to the importance of regionalization of sympathetic activity. Indeed, Schlaich et al have elegantly demonstrated no relationship between renal norepinephrine spillover and LVM index.3 However, they and others have shown a positive correlation between both cardiac norepinephrine spillover and peripheral sympathetic nerve activity with LVM index,3,4 which is thus supportive of our findings.1
Further studies are clearly required to understand the mechanisms of left ventricular hypertrophy and its regression. Cardiac magnetic resonance imaging will be fundamental to accurately quantifying LVM, to avoid the significant limitations of echocardiography in terms of observer variability and left ventricular geometric assumptions.
Drs Greenwood, Sivananthan, and Ball received research funding from the British Heart Foundation.
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.
Greenwood JP, Stoker JB, Mary DASG. Single unit peripheral sympathetic discharge: quantitative assessment in human hypertensive disease. Circulation. 1999; 100: 1305–1310.
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.