Effect of diurnal variability of heart rate on development of arrhythmia in patients with chronic obstructive pulmonary disease.

We examined the possible effect of diurnal variability of heart rate on the development of arrhythmias in patients with chronic obstructive pulmonary disease (COPD). Forty-one COPD patients (M/F: 39/2, mean age: 59+/-8.5 years) and 32 (M/F: 27/5, mean age: 57+/-11 years) healthy controls were included. Twenty-four hour ECG recordings were analyzed for atrial fibrillation (AF) or ventricular premature beats (VPB), and circadian changes in heart rate variability (HRV) were assessed by dividing the 24-h period into day-time (08:00-24:00 h) and night-time (24:00-08:00 h) periods. Night-time total (TP), low frequency (LF) and high frequency (HF) powers were similarly lower from day-time parameters in AF(-) COPD patients (HF 3.91+/-1 vs. 4.43+/-1.04 ms(2), P=0.001) and controls (HF 3.95+/-0.72 vs. 4.82+/-0.66 ms(2), P<0.001). The LF/HF ratios were also significantly reduced in the same patient groups (AF(-) COPD 1.35+/-0.21 vs. 1.27+/-0.19, P=0.04, controls 1.43+/-0.14 vs. 1.24+/-0.09, P<0.001). Night-time TP and LF were increased, HF unchanged and LF/HF significantly increased (1.11+/-0.25 vs. 1.19+/-0.27, P<0.05) in AF(+) COPD patients. Frequency of VPB was correlated with corrected QT dispersion (QTc(d)) (r=0.52, P=0.001) and the day-time/night-time HF ratio (r=0.43, P=0.02). Patients with QTc(d)>or=60 ms did not have the expected increase in night-time HF and had a statistically insignificant increase in LF/HF ratio. In COPD patients with QTc(d)<60 ms, circadian changes in HRV parameters were parallel with the controls. We concluded that COPD patients with arrhythmia had circadian HRV disturbances such as unchanged night-time parasympathetic tone and disturbed sympatho-vagal balance in favor of the sympathetic system all day long, which may explain the increased frequency of arrhythmia.

Ventricular arrhythmias in patients with COPD are associated with QT dispersion.

STUDY OBJECTIVE: QT dispersion (QTd) and late potentials derived from signal-averaged ECG (SAECG) have been proposed as noninvasive predictors of cardiac arrhythmias that occur in patients with COPD. In this study, we aimed to investigate QTd and SAECG in patients with COPD. DESIGN: Cross-sectional study. SETTING: Teaching chest disease hospital and cardiology center in a university hospital. PATIENTS: Thirty patients with COPD (28 men and 2 women; mean +/- SD age, 60 +/- 9 years) and 31 age- and sex-matched control subjects (28 men and 3 women; mean age, 57 +/- 7 years) were included. MEASUREMENTS AND RESULTS: Respiratory function tests, arterial blood gas analyses, echocardiographic examinations, rhythm Holter recordings, and heart rate variability (HRV) analyses were performed in addition to the measurements of QT intervals and SAECG. Patients with COPD had higher rate of ventricular premature beats (VPBs) as compared to control subjects (924 +/- 493 beats vs 35 +/- 23 beats, p = 0.009). Eight patients with COPD (27%) had nonsustained runs of ventricular tachycardia (VT). QTd rates were significantly increased in patients with COPD as compared to control subjects (57.7 +/- 9.9 ms vs 37.5 +/- 8.2 ms, p < 0.001). On comparing patients with COPD with and without runs of VT, patients with VT had longer QTd (67 +/- 10 ms vs 55 +/- 8 ms, p = 0.001). However no difference in any HRV and late potential parameters were found between patients with COPD with and without runs of VT. VPB rates were strongly correlated with QTd in patients with COPD (r = 0.61, p < 0.001). On SAECG analysis, patients with COPD had significantly increased total QRS duration as compared to control subjects. Nine of the 30 patients with COPD (30%) had positive late potentials. However, QTd and VPB rates were also similar between patients with COPD with and without late potentials. CONCLUSIONS: The development of ventricular arrhythmia in patients with COPD was associated with increased QTd. Increased QTd may be associated with autonomic changes seen in patients with COPD.

Factors associated with the development of atrial fibrillation in COPD patients: the role of P-wave dispersion.

BACKGROUND: Supraventricular tachyarrhythmia is a common problem in chronic obstructive pulmonary disease (COPD) patients. The purpose of this study is to analyze the factors associated with paroxysmal atrial fibrillation (AF) in COPD patients. METHODS: Forty COPD patients (38 male, 2 female, mean age 60 +/- 9 years) and 33 healthy controls (29 male, 4 female, mean age: 58 +/- 10 years) were included in this study. Echocardiography, 24-hour ambulatory and 12-lead ECG, pulmonary function tests, arterial blood gases, and serum electrolytes were measured. On ECG, maximum (P(max)) and minimum (P(min)) duration of P wave and its difference, P-wave dispersion (PWd), were measured. RESULTS: On echocardiography, diastolic dysfunction was found in 14 of the 40 (35%) COPD patients. Heart rate variability analysis revealed that COPD patients had decreased SDANN, SDNN, SDNNIDX in time-domain, and decreased LF in frequency domain parameters. Fourteen of the 40 COPD patients (35%) had AF. Patients with AF were older (57 +/- 10 vs 64 +/- 5 years, P = 0.03) and had lower SDANN, SDNN, and LF/HF ratio as compared to patients without AF in univariate analysis. All P-wave intervals (P(max), P(min,) and PWd) were increased in COPD patients compared to controls. P-wave dispersion was significantly increased in COPD patients with AF, as compared to patients without AF (57 +/- 11 vs 44 +/- 7 ms, P = 0.001). In logistic regression analysis PWd was found to be the only factor associated with the development of AF (P = 0.04). CONCLUSIONS: The presence of AF was significantly related to the prolongation of PWd, but not with pulmonary function, arterial blood gasses, and left and right atrial function.

Effects of losartan on the blood-brain barrier permeability in long-term nitric oxide blockade-induced hypertensive rats.

Hypertension is closely associated with vascular endothelial dysfunction. The aim of this study was to investigate the effects of Angiotensin II (ANG II) receptor antagonist losartan on the blood-brain barrier (BBB) permeability in L-NAME-induced hypertension and/or in ANG II-induced acute hypertension in normotensive and hypertensive rats. Systolic blood pressure was measured by tail cuff method before, during and following L-NAME treatment (1 g/L). Losartan (3 mg/kg) was given to the animal for five days. Acute hypertension was induced by ANG II (60 microg/kg). Arterial blood pressure was directly measured on the day of the experiment. BBB disruption was quantified according to the extravasation of the albumin-bound Evans blue dye. Losartan significantly reduced the mean arterial blood pressure from 169 +/- 3.9 mmHg to 82 +/- 2.9 mmHg in L-NAME and from 171 +/- 2.9 mmHg to 84 +/- 2.9 in L-NAME plus losartan plus ANG II groups (p < 0.05). The content of Evans blue dye in the cerebral cortex significantly increased in L-NAME (p < 0.01). Moreover, the content of Evans blue dye markedly increased in the cerebellum (p < 0.001) and slightly increased in diencephalon region (p < 0.05) in L-NAME plus ANG II. Losartan reduced the increased BBB permeability to Evans blue dye in L-NAME (p < 0.01) and L-NAME plus ANG II (p < 0.001). These results indicate that L-NAME and L-NAME plus ANG II both lead to an increase in microvascular Evans blue dye efflux to brain, and losartan treatment attenuates this protein-bound dye transport into brain tissue presumably due to its protective effect on endothelial cells of brain vessels.