Effect of blood gas derangement on QTc dispersion in severe chronic obstructive pulmonary disease: Evidence of an electropathy?

Seconda Università degli Studi di Napoli, Facoltà di Medicina e Chirurgia, Italy.
International Journal of Cardiology (Impact Factor: 4.04). 03/1997; 58(3):287-92. DOI: 10.1016/S0167-5273(96)02876-8
Source: PubMed


Cardiac arrhythmias are common in patients with respiratory failure from chronic obstructive pulmonary disease (COPD). Several factors may be potentially arrhythmogenic in these patients, including hypoxemia and hypercapnia, acid-base disturbances, cor pulmonale and the use of digitalis, methylxanthines, and sympathomimetic drugs. The aim of this study was to examine the effect of hypoxemia and hypercapnia on QTc dispersion (QTcD) in COPD patients, and to evaluate the effect of a partial correction of one of these pro-arrhythmic factors, the hypoxemia, on Qtc dispersion, as QTcD has been proposed as a marker of heterogeneous repolarization and, hence of ventricular electrical instability. We showed that in 15 hypoxemic/hypercapnic COPD patients, compared to 20 controls, the QTcD was significantly higher (49.7 +/- 10.6 vs. 22.9 +/- 9.8 ms; P = 0.0001); furthermore, after only 24 h of oxygen therapy, and hence after a partial correction of hypoxemia, there was a significant reduction in QTcD in COPD patients (49.7 +/- 10.6 vs. 36.3 +/- 10.1 ms; P = 0.018). The data of the present study suggest that the increase in QTcD may be an early marker of a blood gas mediated electropathy in COPD patients.

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    • "There are some previous studies examining possible factors leading to an alteration in cardiac repolarization in COPD patients, however, the COPD patients in these studies [16,31-33] were free from comorbidities. Zulli et al. [31] found a significant univariate association between QT dispersion with FEV1% pred. "
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    ABSTRACT: Altered cardiac repolarization and increased dispersion of repolarization have been identified as risk factors for sudden cardiac death (SCD). The prevalence of and the mechanisms contributing to altered cardiac repolarization are currently unknown in COPD. In 91 COPD patients, 32 controls matched for age, cardiovascular risk and medication, and 41 healthy subjects, measures of cardiac repolarization and dispersion of repolarization (QTc interval, QT dispersion) were derived from 12-lead electrocardiography (ECG). Prevalence rates of heart rate corrected QT (QTc) >450ms and QT dispersion >60ms were determined to assess the number of subjects at risk for SCD. Univariate and multivariate analyses were used to identify possible factors contributing to altered cardiac repolarization. QTc was found to be prolonged in 31.9% and QT dispersion in 24.2% of the COPD patients compared to 12.5% in matched controls and 0% in healthy subjects. The QTc interval was longer in COPD patients compared to matched and healthy controls respectively (437.9 +/- 29.5 vs. 420.1 +/- 25.3 ms, p = 0.001 and vs. 413.4 +/- 18.2 ms, p < 0.001). QT dispersion was significantly increased in COPD patients compared to healthy subjects (45.4 (34.8 , 59.5) vs. 39.7 (29.3 , 54.8) ms, p = 0.049). Only oxygen saturation was independently associated with QTc duration in multivariate analysis (beta = -0.29, p = 0.015). One third of a typical COPD population has altered cardiac repolarization and increased dispersion of repolarization, which may be related to hypoxia. Altered cardiac repolarization may expose these patients to an increased risk for malignant ventricular arrhythmias and SCD.
    BMC Pulmonary Medicine 04/2014; 14(1):55. DOI:10.1186/1471-2466-14-55 · 2.40 Impact Factor
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    ABSTRACT: Objective: Hypoxia is one of the major concerns in aviation. Clinical hypoxia has been shown to increase QT dispersion (QTd). We aimed to examine QTd during hypobaric chamber training to observe the effect of hypobaric hypoxia on QT dispersion. Methods: A total of 38 healthy male aviators volunteered to take part in this longitudinal study. Subjects' electrocardiograms were recorded by 12-lead digital Holter device before, during, and after hypobaric exposure at simulated altitude of 30,000ft. Data from 23 of the subjects, aged 27.91±6.02 years (range 22-39) was used. QT intervals were measured manually. QT dispersion and heart rate adjusted QTd (QTcd) were calculated for each subject. Statistical significance of changes in parameters was analyzed using the Friedman test. Comparison of pre-post exposure clusters was made using Dunn's test. Results: QT dispersion values were as following: prehypoxic 64.09±8.39 ms, hypoxic 50.35±11.06 ms and posthypoxic 59.83±9.06 ms (Median: 64, 50, 60; Mean rank: 2.65, 1.28, 2.07) (p=0.0001 for prehypoxic-hypoxic, p=0.046-prehypoxic-posthypoxic, and p=0.002 for posthypoxic-hypoxic). Heart rate values were as following: prehypoxic 74.09±6.43 beats/min, hypoxic 127.1±17.39 beats/min, and posthypoxic 95.17±11.35 beats/min (Median: 75, 122, 92; Mean rank: 1, 3, 2) (p=0.0001 for prehypoxic-hypoxic, prehypoxic-posthypoxic, and posthypoxic-hypoxic). The change in QTd and HR during hypobaric chamber exposure was statistically significant but, the change in QTcd was not (p
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