Blunted sympathetic response in diabetic patients with decompensated congestive heart failure.
BACKGROUND
The risk for congestive heart failure is strongly increased in diabetes, and the prognosis of diabetic patients with established heart failure is worse compared to nondiabetic patients. Heart failure entails complex alterations in autonomic and neurohormonal responses, which exert a direct deleterious effect on the heart and contribute to progressive circulatory failure. Altered neurohumoral physiology may underlie the poor prognosis of diabetic patients with heart failure.


METHODS
We studied 88 patients (mean age 61+/-13 years) admitted for decompensated heart failure. Neurohormonal and cytokine profiles, including plasma renin activity, aldosterone, norepinephrine, endothelin-1, tumor necrosis factor-alpha, and interleukin-6, were obtained in all patients. In addition, a 24-h Holter recording was performed, and time and frequency domain heart rate variability indices were calculated.


RESULTS
Of 88 patients, 48 were classified as having diabetes based on history, diet therapy, or use of oral hypoglycemic agents or insulin. The only difference in the neurohormonal and cytokine profile between the diabetic and nondiabetic groups was a significantly lower norepinephrine level in diabetic patients (668+/-64 vs. 489+/-50 pg/ml, P=0.009). Heart rate variability analysis revealed that the low-frequency power in normalized units (an index of sympathetic modulation) was significantly lower in diabetic patients (4.7+/-1.4 vs. 5.9+/-0.9, P=0.04). No significant differences occurred in any of the time (the percentage of RR intervals with >50 ms variation and the square root of mean squared differences of successive RR intervals) or frequency domain (high frequency power) indices of parasympathetic modulation between the two groups.


CONCLUSIONS
Patients with diabetes mellitus exhibit a blunted sympathetic response during heart failure decompensation. Blunted sympathetic activation in the setting of symptomatic heart failure may impair the ability of the myocardium to compensate and contribute to the high incidence of symptomatic heart failure among diabetic patients.
Burger
A J
AJ
Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, West Campus Noninvasive Cardiology Laboratory, Baker-3 1 Deaconess Road, Boston, MA 02215, USA. aburger@caregroup.harvard.edu
Aronson
D
D
D000368:Aged; D002940:Circadian Rhythm / Q000502:physiology; D016207:Cytokines / Q000378:metabolism; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000378:metabolism; D015716:Electrocardiography, Ambulatory; D005260:Female; D006333:Heart Failure / Q000150:complications* / Q000175:diagnosis; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000378:metabolism; D011379:Prognosis; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D016207:Cytokines; D009638:Norepinephrine