Left Ventricular Geometry in COPD Patients: ARE THERE ASSOCIATIONS WITH AIRFLOW LIMITATION, FUNCTIONAL CAPACITY, AND GRIP STRENGTH?

PURPOSE: Chronic obstructive pulmonary disease (COPD) and abnormalities of left ventricular (LV) geometry often coexist. This study aimed to verify whether LV geometry is associated with airflow obstruction, functional capacity, and grip strength in COPD patients. METHODS: Thirty-seven COPD patients (GOLD II, III, and IV) were allocated to three groups according to LV geometry as assessed by transthoracic echocardiography: normal (n = 13), concentric LV remodeling (n = 8), and concentric LV hypertrophy (LVH) (n = 16). Lung function was assessed using spirometry. The Duke Activity Status Index (DASI) was used to estimate functional capacity, and grip strength measurement was performed using a hydraulic hand dynamometer. RESULTS: The concentric LVH group presented lower DASI scores (P = .045) and grip strength (P = .006) when compared with the normal group. Correlations analysis showed the following: relative wall thickness negatively correlated with forced expiratory volume in the first second (r = -0.380; P = .025) and DASI score (r = -0.387, P = .018); LV mass index negatively correlated with grip strength (r = -0.363, P = .038). CONCLUSIONS: In COPD patients, LV geometry is associated with airflow limitation, functional capacity, and grip strength. Specifically, concentric LV remodeling is associated with increased airflow limitation and decreased functional capacity whereas increased LV mass is associated with decreased grip strength.

Increased parasympathetic cardiac modulation in patients with acute exacerbation of COPD: how should we interpret it?

BACKGROUND: Cardiac 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. METHODS: Thirty-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. RESULTS: GAE 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). CONCLUSION: COPD 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.