Article

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: 6.18). 03/1997; 58(3):287-92. DOI: 10.1016/S0167-5273(96)02876-8
Source: PubMed

ABSTRACT 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.

0 Bookmarks
 · 
53 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Previous large epidemiological studies reporting on the association between chronic obstructive pulmonary disease (COPD) and cardiovascular diseases mainly focussed on prevalent diseases rather than on the incidence of newly diagnosed cardiovascular outcomes. We used the UK-based General Practice Research Database (GPRD) to assess the prevalence and incidence of cardiovascular diseases in COPD patients aged 40-79 between 1995 and 2005, and we randomly matched COPD-free comparison patients to COPD patients. In nested-case control analyses, we compared the risks of developing an incident diagnosis of cardiac arrhythmias, venous thromboembolism, myocardial infarction, or stroke between patients with and without COPD, stratifying the analyses by COPD-severity, using COPD-treatment as proxy for disease severity. We identified 35,772 patients with COPD and the same number of COPD-free patients. Most cardiovascular diseases were more prevalent among COPD patients than among the comparison group of COPD-free patients. The relative risk estimates of developing an incident diagnosis of cardiac arrhythmia (OR 1.19, 95% CI 0.98-1.43), deep vein thrombosis (OR 1.35, 95% CI 0.97-1.89), pulmonary embolism (OR 2.51, 95% CI 1.62-3.87), myocardial infarction (OR 1.40, 95% CI 1.13-1.73), or stroke (OR 1.13, 95% CI 0.92-1.38), tended to be increased for patients with COPD as compared to COPD-free controls. The findings of this large observational study provide further evidence that patients with COPD are at increased risk for most cardiovascular diseases.
    European Journal of Epidemiology 02/2010; 25(4):253-60. · 5.12 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Long-acting beta2 agonist bronchodilators (e.g. formoterol, salmeterol) are a new interesting therapeutic option for patients with chronic obstructive pulmonary disease (COPD). In the short term, both salmeterol and formoterol appear to be more effective than short-acting beta2 agonists, and in patients with stable COPD they are more effective than anticholinergic agents and theophylline. Regular treatment of patients with COPD with long-acting beta2 agonists can induce an improvement in the respiratory function and certain aspects of quality of life. Moreover, salmeterol seems to be better than ipratropium and theophylline in improving lung function at the recommended doses after a long term treatment. Use of combination therapy of a long-acting inhaled beta2 agonist and an anticholinergic agent or theophylline in patients with COPD has not been sufficiently studied. Combination of usual doses of ipratropium or oxitropium with usual doses of salmeterol or formoterol does not appear to improve pulmonary function, but this lack of improvement with the combination should not, in itself, prevent implementation of further therapeutic steps in patients responsive to an anticholinergic agent and/or salmeterol or formoterol administered singly. Neither formoterol nor salmeterol elicit significant cardiovascular effects in healthy individuals and patients with reversible airway obstruction. However, adverse cardiac events might occur in patients with COPD with pre-existing cardiac arrhythmias and hypoxaemia if they use long-acting 12 agonists, although the recommended single dose of salmeterol 50 microg or formoterol 12 microg ensures a relatively higher safety margin than formoterol 24 microg. The bronchodilatory effect of long-acting beta2 agonists seems to be fairly stable after regular treatment with these bronchodilators. Moreover, pre-treatment with a conventional dose of formoterol or salmeterol does not preclude the possibility of inducing further bronchodilation with salbutamol in patients with partially reversible COPD. All these findings support the use of long-acting beta2 agonist bronchodilators as first-line bronchodilator therapy for the long term treatment of airflow obstruction in patients with COPD. However, since physicians must always choose a drug that is highly efficacious, well tolerated and inexpensive, the cost-effectiveness analysis in relation to other bronchodilators will determine the proper place of long-acting beta2 agonists in the long term therapy of stable COPD.
    Drugs 09/2000; 60(2):307-20. · 4.13 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND.: QT dispersion (QTd) is increased in patients with dilated cardiomyopathy. Increased QTd has been associated with the risk of sudden death. We studied: a) the relation between QTd on 12-lead ECG and QTd-ECG Holter; b) the relation between QTd apex (QTda) and QTd end (QTde) on ECG Holter and the risk of ventricular arrhythmias in patients with dilated cardiomyopathy. METHODS AND RESULTS: 65 patients with dilated cardiomyopathy (33 idiopathic and 32 post-ischemic etiology; NYHA II-III) were studied. We divided the patients into: Group A -patients with not-sustained ventricular arrhythmias-; and Group B -patients without arrhythmias-. A significant direct correlation between QTd calculated from 12-lead ECG and from ECG Holter was found in all patients. QTda/24h was not significantly different in the two groups (Gr.A 59.9±7.8 msec vs Gr.B 53.6±8.4 msec p=ns) while QTde/24h was significantly higher in Group A (Gr.A 81.9±5.9 msec vs Gr.B 44.5±6.8 msec; p<0.005). In post-ischemic etiology (32 pts; 17 with arrhythmias) the correlation between QTde/24h and ventricular arrhythmias was confirmed (Gr.A 81.4±7.8 msec vs Gr.B 42.6±6.2 msec p<0.002). CONCLUSIONS: ECG Holter recordings can evaluate QTd as well as the QTd on 12-lead ECG. An increased QTde/24h seems to be correlated with the occurence of ventricular arrhythmias in patients with dilated cardiomyopathy and can then be a useful tool to select patients at high risk for sudden death.
    Heart International 01/2006; 2(1):33.