COPD Nocturnal Desaturator Patients with Obesity And Pulmonary Hypertension

Domenico Maurizio Toraldo,1 Francesco De Nuccio,2 Francesco Farì,3 Ottavio Narracci4

1. ‘V. Fazzi’ Department of Rehabilitation, Respiratory Care Unit, ASL Lecce, Regional Service Puglia, San Cesario di Lecce, Italy
2. Laboratory of Human Anatomy, Department of Biological and Environmental Sciences and Technologies, University of Salento, Lecce, Italy
3. Director Department of Rehabilitation, Regional Service Puglia, ASL Lecce, Italy
4. Health Director, Regional Service Puglia, ASL Lecce, Italy

Disclosure: No potential conflict of interest.
Received: 12.04.2013 Accepted: 26.07.2013
Citation: EMJ Respir. 2013;1:79-85.


Chronic obstructive pulmonary disease (COPD) is often accompanied by other chronic diseases associated with systemic inflammation, such as chronic heart failure, diabetes, and atherosclerosis. Nocturnal oxygen desaturation waxing and waning plays a central role in conditions leading to systemic inflammation in COPD obese patients. Obesity and metabolic syndrome (MetS) represent two different metabolic abnormalities that may be linked by the presence of underlying systemic inflammation. Alveolar hypoxia and consequent hypoxaemia increase in prevalence as the severity of COPD also increases. Chronic hypoxaemia contributes to the development of adverse sequelae of COPD such as pulmonary hypertension (PH), secondary and systemic inflammation. The innovation of COPD phenotyping is defined as COPD desaturators. These sleep-related changes predispose to nocturnal cardiac dysrhythmias, PH and potentially nocturnal death, particularly during acute exacerbations. In patients with COPD, systemic inflammatory phenotype likely reflects pulmonary inflammation, which results from lung-to-plasma spillover of inflammatory mediators. However, obesity-related hypoxia evokes local inflammatory response within adipose tissue per se, and systemic hypoxaemia likely contributes to the presence of adipose tissue inflammation. The nocturnal hypoxic insult occurring during sleep-disordered breathing may also contribute to chronic vascular remodelling. Consequently, these mechanisms may result in endothelial dysfunction and vascular damage, leading to increased risk of PH in COPD. In patients with COPD and concurrent obesity, we have proposed that three factors can play a role in the systemic inflammatory syndrome: the severity of pulmonary impairment, the degree of obesity-related adipose tissue hypoxia, and the severity of systemic hypoxia due to reduced pulmonary function.

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