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Much evidence indicates an involvement of the sympathetic nervous system in the genesis of silent myocardial ischemia. The authors assessed autonomic system activity by power spectrum analysis of heart rate variability in 21 elderly hypertensive men with and without angiographically confirmed coronary artery disease and compared the results with those from an age-matched control group. In the analysis an autoregressive algorithm was used to determine the power spectrum from an electrocardiographic recording of 512 consecutive RR intervals. The autonomic nervous system induces two distinct sinusoids: a low-frequency signal attributable to sympathetic activity and a high-frequency vagal response. In the hypertensive patients with coronary disease the authors also evaluated sympathetic activation after double-blind, placebo-controlled administration of metoprolol (100 mg/day), followed by amlodipine (10 mg/day), quinapril (20 mg/day), and amlodipine (5 mg/day) plus quinapril (10 mg/day). (continued on next page) Spectrum analysis showed significantly increased sympathetic activity in the hypertensive patients with coronary disease (low frequency: 58.4 ±2.0, P < 0.001) as compared with controls (36.21 ± 1.0, P < 0.001) and hypertensive subjects without coronary disease (low frequency: 25.2 ±0.6 , P < 0.001) but significantly reduced parasympathetic activity (39.4 ±2.0, P < 0.001) with respect to hypertensive patients without heart disease (42.5 ±2.0, P < 0.001) and controls (60.3 ±2.0). Treatment with metoprolol, quinapril, and amlodipine plus quinapril significantly reduced sympathetic tone (P < 0.05).

Background: Cardiovascular diseases are prevalent in people with chronic obstructive pulmonary disease (COPD). We hypothesized that endothelial dysfunction could be a marker of the proatherogen status in COPD. Methods and results: We measured endothelial dysfunction by flow-mediated dilation (FMD) and after sublingual administration of nitroglycerin (nitrate-mediated dilation: NMD) in 44 COPD patients and 48 controls. Compared with controls COPD patients had worse mean FMD (5.4% vs 8.2%, P < .001) and NMD (12.0% vs 13.9%, P = .007). FMD was inversely related to FEV1/VC ratio ( r = −0.327, P = .030). The negative association between COPD and FMD was confirmed after correction for potential confounders in a multiple linear regression model (β = −0.019, P = .002). In the same model NMD (β = 0.396, P < .001) was positively associated with FMD. Conclusions: Endothelial-dependent and, to a lesser extent, endothelial-independent dilations are significantly impaired in COPD, and the impairment is proportional to the severity of bronchial obstruction.