Drs. Otte and Whooley Reply -- OTTE and WHOOLEY 165 (1): 137 -- Am J Psychiatry
MARY A. WHOOLEY, M.D. Hamburg, Germany To The Editor: We enjoy the considerate comments by Mister Bayles et al. We buy that sympathetic excitable activation may contribute to the evolvement of left ventricular hypertrophy and that this could be a likely mechanism by which s allele carriers of the 5-HTTLPR might be at increased risk for worse cardiovascular outcome.
This suggests that worthier 24-hour urinary norepinephrine in s allele carriers did not contribute to left ventricular hypertrophy in this study. However, as Dr.
Indeed, 24-hour urinary norepinephrine as a wide degree of overall sympathetic edgy transaction bustle might want the sensitivity to detect associations between sympathetic basket case animation and resident processes, such as the manner of left ventricular hypertrophy. Inured the bulky symbol of participants in our epidemiological cohort study, we were unable to apply deeper localized measures of norepinephrine, such as cardiac catheterization techniques coupled with norepinephrine isotope dilution methodology.
Certainly, still added duty has to be done to elucidate the mechanisms by which 5-HTTLPR, depression, stress, and catecholamine secretion are linked and how they might induce outcome in cardiovascular disease. Footnotes The authors" disclosures accompany the first article. A. Depression Impress data approximately faster international access.
