Übersicht HRV – Diabetes II und Diabetes I
نویسنده
چکیده
Lanza GA, Pitocco D, Navarese EP, Sestito A, Sgueglia GA, Manto A, Infusino F, Musella T, Ghirlanda G, Crea F. Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Largo A. Gemelli, 8, 00168 Roma, Italy. [email protected] AIMS: To assess the relationship between cardiac autonomic dysfunction and inflammation in patients with type 1 diabetes and whether beta-blocker therapy might improve both abnormalities in these patients. METHODS AND RESULTS: We studied 49 patients with type 1 diabetes (age 50.5 +/11 years, 33 men). Serum levels of high-sensitivity C-reactive protein, as a marker of inflammation, and frequency-domain heart rate variability (HRV) on 24 h Holter monitoring, as a measure of cardiac autonomic function, were assessed in all patients. Twenty-one patients with depressed HRV were subsequently randomized to receive atenolol (50 mg daily) or no-beta-blockade. HRV and C-reactive protein were re-assessed after 3-4 weeks from randomization. An inverse correlation was found between C-reactive protein levels and HRV parameters, with the highest r coefficient shown with low-frequency (LF) power (r = -0.38; P = 0.007). Furthermore, C-reactive protein serum levels were significantly higher in patients with bottom quartile values of LF power compared with patients with values in the three top quartiles (4.64 +/2.8 vs.1.79 +/1.6 mg/L, respectively; P = 0.003), also after adjustment for potential confounding variables (P = 0.013). HRV parameters improved significantly in patients treated with atenolol, but not in the no-atenolol group. Furthermore, C-reactive protein levels decreased in the beta-blockade group, but not in the no-beta-blockade group (P = 0.04 for changes between groups). CONCLUSION: In type 1 diabetic patients, serum C-reactive protein levels are significantly associated with depressed HRV; the favourable effects of beta-blockade on both HRV parameters and Creactive protein serum levels suggest that autonomic nervous system may have significant modulator effects on inflammation. PMID: 17371783 [PubMed in process]
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