Association between cardiac autonomic dysfunction and inflammation in type 1 diabetic patients: effect of beta-blockade

• Published in: European heart journal 2007-04, Vol.28 (7), p.814-820
• Main Authors: Lanza, Gaetano Antono, Pitocco, Dario, Navarese, Eliano Pio, Sestito, Alfonso, Sgueglia, Gregory Angelo, Manto, Andrea, Infusino, Fabio, Musella, Tittania, Ghirlanda, Giovanni, Crea, Filippo
• Format: Article
• Language: English
• Subjects: Adrenergic beta-Antagonists - therapeutic use; Arrhythmias, Cardiac - drug therapy; Atenolol - therapeutic use; Autonomic Nervous System Diseases - drug therapy; Biological and medical sciences; C-Reactive Protein - metabolism; Cardiology. Vascular system; Diabetes Mellitus, Type 1 - drug therapy; Diabetes. Impaired glucose tolerance; Diabetic Neuropathies - drug therapy; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Female; Humans; Male; Medical sciences; Middle Aged; Myocarditis - complications
• ISSN: 0195-668X; 1522-9645
• DOI: 10.1093/eurheartj/ehm018

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 C-reactive protein serum levels suggest that autonomic nervous system may have significant modulator effects on inflammation.