Related Articles

Triggers and mechanisms of skeletal muscle wasting in chronic obstructive pulmonary disease.

Int J Biochem Cell Biol. 2013 Jul 1;

Authors: Langen RC, Gosker HR, Remels AH, Schols AM

Abstract
Skeletal muscle wasting contributes to impaired exercise capacity, reduced health-related quality of life and is an independent determinant of mortality in chronic obstructive pulmonary disease. An imbalance between protein synthesis and myogenesis on the one hand, and muscle proteolysis and apoptosis on the other hand, has been proposed to underlie muscle wasting in this disease. In this review, the current understanding of the state and regulation of these processes governing muscle mass in this condition is presented. In addition, a conceptual mode of action of disease-related determinants of muscle wasting including disuse, hypoxemia, malnutrition, inflammation and glucocorticoids is provided by overlaying the available associative clinical data with causal evidence, mostly derived from experimental models. Significant progression has been made in understanding and managing muscle wasting in chronic obstructive pulmonary disease. Further examination of the time course of muscle wasting and specific disease phenotypes, as well as the application of systems biology and omics approaches in future research will allow the development of tailored strategies to prevent or reverse muscle wasting in chronic obstructive pulmonary disease. This article is part of a Directed Issue entitled: Muscle wasting.

PMID: 23827718 [PubMed - as supplied by publisher]

Related Articles

Right ventricular dysfunction and remodeling in COPD without pulmonary hypertension.

J Am Coll Cardiol. 2013 Jul 3;

Authors: Hilde JM, Skjørten I, Grøtta OJ, Hansteen V, Melsom MN, Hisdal J, Humerfelt S, Steine K

Abstract
OBJECTIVES: The present study aimed to elucidate RV function and structure in COPD patients without PH.
BACKGROUND: There is little knowledge of RV function and remodeling in COPD without PH.
METHODS: Thirty-four controls and 98 patients with COPD were included. The patient population was divided in two groups by right heart catheterization, no-PH (mPAP) <25 mmHg) and PH (mPAP≥25 mmHg). Echocardiographic TDI variables as RV isovolumic acceleration, peak systolic strain and RV myocardial performance index were measured at basal free wall, and RV wall thickness and RV internal dimension in the RV outflow tract.
RESULTS: The increase of RV wall thickness and RV dimension were more evident from controls to no PH, 3.5±0.5 to 5.5±1.0 mm (p<0.01) and 1.5±0.2 to 2.0±0.5 cm (p<0.01), than from no-PH to PH, 5.5±1.0 to 6.6±1.1mm (p<0.01) and 2.0±0.5 to 2.1±0.3 cm (NS), respectively. Similarly, RV isovolumic acceleration, performance index and strain deteriorated significantly from controls to no-PH and from no-PH to PH (p<0.01). Significant correlations were observed between mPAP and RV isovolumic acceleration, performance index and strain and RV wall thickness (p<0.01). RV impairment and increased RV wall thickness and RV dimensions were present even at slight elevations of mPAP, 18±3mmHg, in no-PH.
CONCLUSION: The present study has demonstrated that impaired RV systolic function, hypertrophy and dilatation were present even at slight increase of mPAP, which indicates early impact on RV function and structure in patients with COPD. RV isovolumic acceleration, performance index and strain could detect subclinical disease and separate controls from no-PH.

PMID: 23831444 [PubMed - as supplied by publisher]

Heart failure and chronic obstructive pulmonary disease: the challenges facing physicians and health services.

Eur Heart J. 2013 Jul 5;

Authors: Hawkins NM, Virani S, Ceconi C

Abstract
Pulmonary disease is common in patients with heart failure, through shared risk factors and pathophysiological mechanisms. Adverse pulmonary vascular remodelling and chronic systemic inflammation characterize both diseases. Concurrent chronic obstructive pulmonary disease presents diagnostic and therapeutic challenges, and is associated with increased morbidity and mortality. The cornerstones of therapy are beta-blockers and beta-agonists, whose pharmacological properties are diametrically opposed. Each disease is implicated in exacerbations of the other condition, greatly increasing hospitalizations and associated health care costs. Such multimorbidity is a key challenge for health-care systems oriented towards the treatment of individual diseases. Early identification and treatment of cardiopulmonary disease may alleviate this burden. However, diagnostic and therapeutic strategies require further validation in patients with both conditions.

PMID: 23832490 [PubMed - as supplied by publisher]

Related Articles

Asthma, Chronic Obstructive Pulmonary Disease (COPD), and the Overlap Syndrome.

J Am Board Fam Med. 2013 Jul-Aug;26(4):470-7

Authors: Nakawah MO, Hawkins C, Barbandi F

Abstract
Asthma and chronic obstructive pulmonary disease (COPD) are highly prevalent chronic diseases in the general population. Both are characterized by heterogeneous chronic airway inflammation and airway obstruction. In both conditions, chronic inflammation affects the whole respiratory tract, from central to peripheral airways, with different inflammatory cells recruited, different mediators produced, and thus differing responses to therapy. Airway obstruction is typically intermittent and reversible in asthma but is progressive and largely irreversible in COPD. However, there is a considerable pathologic and functional overlap between these 2 heterogeneous disorders, particularly among the elderly, who may have components of both diseases (asthma-COPD overlap syndrome). The definitions for asthma and COPD recommended by current guidelines are useful but limited because they do not illustrate the full spectrum of obstructive airway diseases that is encountered in clinical practice. Defining asthma and COPD as separate entities neglects a considerable proportion of patients with overlapping features and is largely based on expert opinion rather than on the best current evidence. The presence of different phenotypes or components of obstructive airway diseases, therefore, needs to be addressed to individualize and optimize treatment to achieve the best effect with the fewest side effects for the patient. Although specific interventions vary by disease, the treatment goals of obstructive airway diseases are similar and driven primarily by the need to control symptoms, optimize health status, and prevent exacerbations.

PMID: 23833163 [PubMed - in process]