BackgroundIn chronic obstructive pulmonary disease (COPD), functional and structural impairment of lung function can negatively impact heart rate variability (HRV); however, it is unknown if static lung volumes and lung diffusion capacity negatively impacts HRV responses. We investigated whether impairment of static lung volumes and lung diffusion capacity could be related to HRV indices in patients with moderate to severe COPD.MethodsSixteen sedentary males with COPD were enrolled in this study. Resting blood gases, static lung volumes, and lung diffusion capacity for carbon monoxide (DLCO) were measured. The RR interval (RRi) was registered in the supine, standing, and seated positions (10 minutes each) and during 4 minutes of a respiratory sinus arrhythmia maneuver (M-RSA). Delta changes (Δsupine-standing and Δsupine-M-RSA) of the standard deviation of normal RRi, low frequency (LF, normalized units [nu]) and high frequency (HF [nu]), SD1, SD2, alpha1, alpha2, and approximate entropy (ApEn) indices were calculated.ResultsHF, LF, SD1, SD2, and alpha1 deltas significantly correlated with forced expiratory volume in 1 second, DLCO, airway resistance, residual volume, inspiratory capacity/total lung capacity ratio, and residual volume/total lung capacity ratio. Significant and moderate associations were also observed between LF/HF ratio versus total gas volume (%), r=0.53; LF/HF ratio versus residual volume, %, r=0.52; and HF versus total gas volume (%), r=−0.53 (P<0.05). Linear regression analysis revealed that ΔRRi supine-M-RSA was independently related to DLCO (r=−0.77, r2=0.43, P<0.05).ConclusionResponses of HRV indices were more prominent during M-RSA in moderate to severe COPD. Moreover, greater lung function impairment was related to poorer heart rate dynamics. Finally, impaired lung diffusion capacity was related to an altered parasympathetic response in these patients.

Worldwide, binge drinking is a major public health problem. The popularized health risks associated with binge drinking include physical injury and motor vehicle crashes; less attention has been given to the negative effects on the cardiovascular (CV) system. The primary aims of this review were to provide a summary of the adverse effects of binge drinking on the risk and development of CV disease and to review potential pathophysiologic mechanisms. Using specific inclusion criteria, an integrative review was conducted that included data from human experimental, prospective cross-sectional, and cohort epidemiological studies that examined the association between binge drinking and CV conditions such as hypertension (HTN), myocardial infarction (MI), stroke, and arrhythmias. Studies were identified that examined the relationship between binge drinking and CV outcomes. Collectively, findings support that binge drinking is associated with a higher risk of pre-HTN, HTN, MI, and stroke in middle-aged and older adults. Binge drinking may also have adverse CV effects in young adults (aged 18 to 30). Mechanisms remain incompletely understood; however, available evidence suggests that binge drinking may induce oxidative stress and vascular injury and be proatherogenic. Public health messages regarding binge drinking need to include the effects of binge drinking on the CV system.

BackgroundCardiac autonomic modulation (CAM) is impaired in patients with stable COPD. Exacerbation aggravates the patients’ health status and functional capacity. While the clinical and functional effects of exacerbation are known, no studies investigated CAM during exacerbation and whether there is a relationship between CAM and functional capacity and dyspnea.MethodsThirty-two patients with moderate to severe COPD were enrolled into two groups: stable COPD (GSta, n=16) and acute exacerbation of COPD (GAE, n=16). The GAE patients were evaluated 24–48 hours after starting standard therapy for COPD exacerbation during hospitalization; the GSta patients were evaluated in an outpatient clinic and included in the study if no decompensation episodes had occurred during the previous month. The heart rate (HR) and R-wave peak detection intervals in ms (RRi) were registered using a heart rate monitor (Polar® system) at rest in seated position during 10 minutes. CAM was assessed by heart rate variability (HRV) linear and non-linear analysis. Functional capacity was evaluated by handgrip strength test, performed by Jamar® dynamometer, and dyspnea was scored using the modified scale of the Medical Research Council.ResultsGAE presented higher parasympathetic CAM values compared with GSta for square root of the mean squared differences of successive RRi (RMSSD; 17.8±5.6 ms vs 11.7±9.5 ms); high frequency (HF; 111.3±74.9 ms2 vs 45.6±80.7 ms2) and standard deviation measuring the dispersion of points in the plot perpendicular to the line of identity (SD1; 12.7±3.9 ms vs 8.3±6.7 ms) and higher CAM values for standard deviation of the mean of all of RRi (STD RRi; 19.3±6.5 ms vs 14.3±12.5 ms); RRi tri (5.2±1.7 ms vs 4.0±3.0 ms); triangular interpolation of NN interval histogram (TINN; 88.7±26.9 ms vs 70.6±62.2 ms); low frequency (LF; 203±210.7 ms2 vs 101.8±169.7 ms2) and standard deviation measuring the dispersion of points along the line of identity (SD2; 30.4±14.8 ms vs 16.2±12.54 ms). Lower values were observed for the complexity indices: approximate entropy (ApEn; 0.9±0.07 vs 1.06±0.06) and sample entropy (SampEn; 1.4±0.3 vs 1.7±0.3). Significant and moderate associations were observed between HF (nu) and handgrip strength (r=−0.58; P=0.01) and between LF (ms2) and subjective perception of dyspnea (r=−0.53; P=0.03).ConclusionCOPD exacerbated patients have higher parasympathetic CAM than stable patients. This should be interpreted with caution since vagal influence on the airways determines a narrowing and not a better clinical condition. Additionally, functional capacity was negatively associated with parasympathetic CAM in COPD exacerbation.

Systolic heart failure is a common and disabling co-morbidity of chronic obstructive pulmonary disease (COPD) which may increase exercise ventilation due to heightened neural drive and/or impaired pulmonary gas exchange efficiency. The influence of heart failure on exercise ventilation, however, remains poorly characterized in COPD. In a prospective study, 98 patients with moderate to very severe COPD [41 with coexisting heart failure; 'overlap' (left ventricular ejection fraction < 50%)] underwent an incremental cardiopulmonary exercise test (CPET). Compared to COPD, overlap had lower peak exercise capacity despite higher FEV. Overlap showed lower operating lung volumes, greater ventilatory inefficiency and larger decrements in end-tidal CO (PETCO) (P < 0.05). These results were consistent with those found in FEV-matched patients. Larger areas under receiver operating characteristic curves to discriminate overlap from COPD were found for ventilation ([Formula: see text]E)-CO output [Formula: see text]CO) intercept, [Formula: see text]E-[Formula: see text]CO slope, peak [Formula: see text]E/[Formula: see text]CO ratio and peak PETCO. Multiple logistic regression analysis revealed that [Formula: see text]CO intercept ≤ 3.5 L/minute [odds ratios (95% CI) = 7.69 (2.61-22.65), P < 0.001] plus [Formula: see text]E-[Formula: see text]CO slope ≥ 34 [2.18 (0.73-6.50), P = 0.14] or peak [Formula: see text]E/[Formula: see text]CO ratio ≥ 37 [5.35 (1.96-14.59), P = 0.001] plus peak PETCO ≤ 31 mmHg [5.73 (1.42-23.15), P = 0.01] were indicative of overlapping. Heart failure increases the ventilatory response to metabolic demand in COPD. Variables reflecting excessive ventilation might prove useful to assist clinical interpretation of CPET responses in COPD patients presenting heart failure as co-morbidity.