3 research outputs found
Smoking cessation can improve quality of life among COPD patients: Validation of the clinical COPD questionnaire into Greek
<p>Abstract</p> <p>Background</p> <p>Chronic obstructive pulmonary disease (COPD) remains a major public health problem that affects the quality of life of patients, however smoking cessation may emeliorate the functional effects of COPD and alter patient quality of life.</p> <p>Objective-design</p> <p>The aim of this study was to validate the Clinical COPD Questionnaire (CCQ) into Greek and with such to evaluate the quality of life in patients with different stages of COPD, as also assess their quality of life before and after smoking cessation.</p> <p>Results</p> <p>The internal validity of questionnaire was high (Cronbach's a = 0.92). The reliability of equivalent types in 16 stabilized patients also was high (ICC = 0.99). In general the domains within the CCQ were strongly correlated with each other, while each domain in separate was strongly correlated with the overall CCQ score (r<sup>2 </sup>= 0.953, r<sup>2 </sup>= 0.915 and r<sup>2 </sup>= 0.842 in regards to the functional, symptomatic and mental domain, respectively). The CCQ scores were also correlated with FEV<sub>1, </sub>(r<sup>2 </sup>= -0.252, p < 0.001), FEV<sub>1</sub>/FVC, (r<sup>2 </sup>= -0.135, p < 0.001) as also with the quality of life questionnaire SF-12 (r<sup>2 </sup>= -0.384, p < 0.001). Smoking cessation also lead to a significant reduction in CCQ score and increase in the SF-12 score.</p> <p>Conclusions</p> <p>The self administered CCQ indicates satisfactory validity, reliability and responsiveness and may be used in clinical practice to assess patient quality of life. Moreover the CCQ indicated the health related quality of life gains attributable to smoking cessation among COPD patients, projecting smoking cessation as a key target in COPD patient management.</p
Inflammatory Mechanisms in Atherosclerosis: The Impact of Matrix Metalloproteinases
Inflammatory process is essential for the initiation and progression of
vascular remodeling, entailing degradation and reorganization of the
extra-cellular matrix (ECM) scaffold of the vessel wall, leading to the
development of atherosclerotic lesions. Matrix metalloproteinases (MMPs)
are zing dependent endo-peptidases found in most living organisms and
act mainly by degrading ECM components. Most MMPs are formed as inactive
proenzymes and are activated by proteolysis. This process depends and is
regulated by other proteases and endogenous MMP inhibitors (TIMPs). MMPs
and TIMPs play a major role not only in ECM degradation but also in
mediating cell migration, proliferation, tissue remodeling; acting as a
signal for the production and secretion of growth factors and cytokines.
More importantly MMPs through proteolysis and degradation of ECM
contribute in many physiological and pathological processes including
organ development, wound healing, tissue support, vascular remodeling
and restenosis, atherosclerosis progression, acute coronary syndromes,
myocardial infarction, cardiomyopathy, aneurysms remodeling, cancer,
arthritis, and chronic inflammatory diseases. A substantial body of
evidence support the notion that imbalance between the activity of MMPs
and their tissue inhibitors (TIMPs) contribute to the pathogenesis of
cardiovascular diseases such as atherosclerosis, vascular remodeling and
progression of heart failure. In this review, we will discuss the
relationship between MMPs, inflammation and atherosclerosis under the
topic of cardiovascular disease
Circulating Biomarkers Determining Inflammation in Atherosclerosis Progression
Atherosclerosis is the main underlying pathology of cardiovascular
disease and is precipitated by various hereditary and non-hereditary
risk factors. Inflammation is considered an important step in the
progression of atherosclerosis and involves numerous cells, mediators
and cellular procedures. Therefore, a biomarker able to determine the
vascular inflammatory status is imperative as the combination of
inflammatory biomarkers with the classic risk factors might provide
further information about atherosclerosis progression and cardiovascular
risk. The identification of novel inflammatory molecules and the
improvement in analytical methods allows the potential implementation of
these tests in every day clinical practice. In the current article, we
focus on the role of established and novel biomarkers in atherosclerosis
progression and in the determination of cardiovascular risk. We also
present recent data concerning the risk stratification of patients
according to their inflammatory status and the possible
anti-inflammatory treatment strategies