[Chronic obstructive pulmonary disease and cardiovascular disease].
Servicio de Neumología, Hospital Universitario, Guadalajara, España.Archivos de Bronconeumología (Impact Factor: 1.82). 01/2010; 46 Suppl 3:18-22.
In the last decade, various studies have suggested that chronic obstructive pulmonary disease (COPD) could favor the development of ischemic heart disease. Several observational and case-control studies have confirmed that patients with COPD have a higher risk of cardiovascular disorders. However, this increased risk could be largely explained by a greater prevalence of classical risk factors. Currently, there are no data to indicate a causal relation between COPD and cardiovascular disease and the concept of systemic inflammation as a common pathogenic mechanism has not been demonstrated. Equally, there is insufficient evidence to conclude that some drugs, such as statins or inhaled corticoids, could decrease cardiovascular risk in patients with COPD by reducing systemic inflammation. Currently, these drugs should only be recommended if patients show specific indications for their use.
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ABSTRACT: We aimed to compare the cardiovascular risk in biomass-using women with or without chronic obstructive pulmonary disease (COPD). A total of 22 biomass-using married women with COPD and 24 matched controls with normal lung function were enrolled for this purpose. Platelet P-selectin (P-sel) expression and platelet–leukocyte aggregation were determined using flow cytometry. Platelet aggregation by collagen was measured by aggregometer. Soluble P-selectin (sP-sel), tumor necrosis factor-alpha (TNF-α), interleukin-8, -6, -10 (IL-8, IL-6, IL-10), neutrophil-activating protein-2 (NAP-2), C-reactive protein (CRP), oxidized low density lipoprotein (oxLDL) in plasma were measured by enzyme-linked immunosorbent assay. Generation of reactive oxygen species (ROS) by leukocytes was measured by flow cytometry, and erythrocyte content of superoxide dismutase (SOD) was measured by spectrophotometry. Particulate matter with a diameter of less than 2.5 μm (PM2.5) in indoor air was measured by real-time aerosol monitor. Compared with control, biomass users with COPD had increased expression of platelet P-selectin, elevated levels of sP-sel, oxLDL, TNF-α, IL-8, IL-6, NAP-2, CRP, lowered IL-10 and more circulating platelet-neutrophil (p < 0.0001) and platelet–monocyte (p < 0.0001) aggregates. ROS generation was increased by 19.5% while SOD was depleted by 32% in women with COPD. Biomass smoke-induced COPD is associated with excess cardiovascular risk via oxidative stress, platelet activation, and inflammation.Air Quality Atmosphere & Health 03/2012; 6(1). DOI:10.1007/s11869-012-0173-8 · 1.80 Impact Factor
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ABSTRACT: Patients with chronic obstructive pulmonary disease (COPD) can experience 'exacerbations' of their conditions. An exacerbation is an event defined in terms of subjective descriptors or symptoms, namely dyspnoea, cough and sputum that worsen sufficiently to warrant a change in medical management. There is a need for reliable markers that reflect the pathological mechanisms that underlie exacerbation severity and that can be used as a surrogate to assess treatment effects in clinical studies. Little is known as to how existing study variables and suggested markers change in both the stable and exacerbation phases of COPD. In an attempt to find the best surrogates for exacerbations, we have reviewed the literature to identify which of these markers change in a consistent manner with the severity of the exacerbation event. We have searched standard databases between 1966 to July 2004 using major keywords and terms. Studies that provided demographics, spirometry, potential markers, and clear eligibility criteria were included in this study. Central tendencies and dispersions for all the variables and markers reported and collected by us were first tabulated according to sample size and ATS/ERS 2004 Exacerbation Severity Levels I to III criteria. Due to the possible similarity of patients in Levels II and III, the data was also redefined into categories of exacerbations, namely out-patient (Level I) and in-patient (Levels II & III combined). For both approaches, we performed a fixed effect meta-analysis on each of the reported variables. We included a total of 268 studies reported between 1979 to July 2004. These studies investigated 142,407 patients with COPD. Arterial carbon dioxide tension and breathing rate were statistically different between all levels of exacerbation severity and between in out- and in-patient settings. Most other measures showed weak relationships with either level or setting, or they had insufficient data to permit meta-analysis. Arterial carbon dioxide and breathing rate varied in a consistent manner with exacerbation severity and patient setting. Many other measures showed weak correlations that should be further explored in future longitudinal studies or assessed using suggested mathematical modelling techniques.Respiratory research 02/2006; 7(1):74. DOI:10.1186/1465-9921-7-74 · 3.09 Impact Factor
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ABSTRACT: The chronic systemic inflammation and oxidative stress are important features in chronic obstructive pulmonary disease (COPD). Atherosclerosis is accepted as an inflammatory disease. Both local and systemic inflammation and oxidative stress negatively affect the atherosclerotic process. Metabolic alterations, systemic inflammation, and neurohormonal activation frequently occur in patients with COPD. However, the impact of COPD on intensity and severity of atherosclerosis and morphology of stenotic lesions in patients with established coronary artery disease by coronary angiography is unknown. Eighty-eight patients who were diagnosed with COPD disease were enrolled in the study. Eighty-two patients without any pulmonary disease were included in the control group. Coronary angiography and blood gases analysis were performed in all patients. Gensini score and Extent score were used to evaluate the intensity and severity of atherosclerosis. Lesion morphologies were defined in all patients. The mean number of affected coronary arteries was 2.5 +/- 0.6 in the COPD group and 2.1 +/- 0.7 in the control group (P = 0.004). The mean Extent score was 37 +/- 16 in the COPD group and 23 +/- 11 in the control group (P = 0.001). The Gensini score in the COPD group was significantly higher than that in the control group (respectively 10.9 +/- 6.3 vs 6.6 +/- 4.1, P = 0.01). The number of critical lesions, and type B and C lesions were higher in the COPD group. Multivariate analysis demonstrated that COPD was independently predictive for Gensini score (odds ratio 1.371; 95% confidence interval 1.682-9.228; P = 0.002) and Extent score (odds ratio 1.648; 95% confidence interval 2.023-13.339; P = 0.001). Severity and intensity of atherosclerosis increases in COPD and atherosclerotic lesions have worse morphological properties in COPD.Heart and Vessels 06/2009; 24(3):164-8. DOI:10.1007/s00380-008-1103-4 · 2.07 Impact Factor