COPD is characterized by irreversible airflow limitation and symptoms, such as chronic cough, wheezing, expectoration and dyspnea. Although COPD is an important cause of morbidity and mortality, a large proportion of its mortality is not of pulmonary origin.
Traditionally, it was considered that patients with COPD are at special risk of cardiovascular diseases. COPD increases the risk of cardiovascular disease two- to three-fold, and it has been proposed that low-grade systemic inflammation in patients with COPD is strongly associated with their increased risk of cardiovascular injury.
The cardiovascular sequel of chronic obstructive pulmonary disease have been recognized for decade the spectrum of cardiovascular disease include right ventricular dysfunction, pulmonary hypertension, coronary artery disease and arrhythmia.
Apart from ischemic heart disease, supraventricular and ventricular arrhythmias, as well as conduction disturbances are frequently observed in COPD. Many factors have been implicated as potential triggers of COPD-related arrhythmias.
Two major hypotheses for arrhythmogenesis in COPD have been proposed: arrhythmias are a consequence of hypoxemia, hypercapnia or acid–base disturbances, arrhythmias are the result of the autonomic neuropathy that characterize COPD , p wave dispertion (heterogeneous atrial depolarization) or secondary atrial dysfunction
The hypothesis of electropathy proposes that hypoxemia, hypercapnia and acid–base disturbances are the triggers of arrhythmias, since they increase the electrical heterogeneity within the ventricular wall. This heterogeneity has been implicated in the development of potentially lethal re-entrant arrhythmias.
The second hypothesis proposes autonomic neuropathy as the arrhythmogenic trigger. Chronic hypoxemia is a significant factor in the pathophysiology of autonomic neuropathy and it has been considered to be the underlying cause of COPD autonomic neuropathy.
The third hypothesis pulmonary hypertension in COPD affect right atrial function without growth enlargement in the early stage lead to secondary atrial dysfunction and consequent atrial arrhythmia or p wave dispersion (reflect heterogeneous atrial depolarization) cause arrhythmia especially atrial fibrillation
Recent evidence suggests that autonomic neuropathy can appear even in the very early stages of the disease and there is strong evidence that, in patients with stable COPD, hypoxaemia is associated with a derangement in the autonomic nervous system, which may be partially reversed by oxygen administration. Finally, it has been observed that among patients with COPD those with autonomic neuropathy are at higher risk of sudden cardiac death.
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