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Blunted sympathetic response in diabetic patients with decompensated congestive heart failure
1Division 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
Insights
Diabetic patients with heart failure show a reduced sympathetic response. This blunted sympathetic activation may hinder the heart
Area of Science:
- Cardiology
- Endocrinology
- Neuroscience
Background:
- Diabetes significantly increases heart failure risk and worsens prognosis.
- Heart failure involves autonomic and neurohormonal changes detrimental to the heart.
- Altered neurohumoral function may explain poor outcomes in diabetic heart failure patients.
Purpose of the Study:
- To investigate neurohormonal and autonomic differences in heart failure patients with and without diabetes.
- To explore the impact of diabetes on heart failure pathophysiology.
Main Methods:
- Studied 88 decompensated heart failure patients.
- Assessed neurohormonal profiles (norepinephrine, aldosterone, etc.) and cytokine levels.
- Performed 24-h Holter monitoring to calculate heart rate variability indices.
Main Results:
- Diabetic patients had significantly lower norepinephrine levels compared to non-diabetic patients.
- Heart rate variability showed reduced sympathetic modulation (low-frequency power) in diabetics.
- No significant differences in parasympathetic modulation indices were observed between groups.
Conclusions:
- Diabetes mellitus is associated with a blunted sympathetic response during heart failure decompensation.
- Impaired sympathetic activation in diabetic heart failure may compromise myocardial compensation.
- This blunting could contribute to the higher incidence of symptomatic heart failure in diabetic individuals.
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.
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