We read with great interest the recently published case report by Melão et al. (March 2014 issue of the Portuguese Journal of Cardiology) of a 56-year-old male with chronic obstructive pulmonary disease (COPD) who developed stress-induced cardiomyopathy associated with ipratropium bromide use, administered in the context of an acute exacerbation of COPD.

Although this timely and interesting case report provides important information, we would like to share some thoughts.

Acute COPD exacerbation and acute respiratory failure (hypoxemic and/or hypercapnic) have been described1,2 as potential physical triggers of takotsubo cardiomyopathy (TCM). In a study by Sharkey et al.,1 acute respiratory failure and COPD exacerbation were among the most prevalent physical triggers.

Hypoxemia and hypercapnia can induce sympathetic nerve stimulation; the effect of hypoxemia alone can produce a longer-lasting sympathetic activation than hypercapnia, however if both occur simultaneously the result may be a significant increase in sympathetic activity with concomitant increase in catecholamine release,3–5 which has been widely implicated in the etiology of TCM.

Acidosis has been associated with high levels of catecholamine release and may have negative inotropic effects secondary to decreasing calcium release from the sarcoplasmic reticulum. Acidosis-induced cardiomyocyte injury has been reported.6–8 Inhaled beta 2 agonists used in acute asthma and COPD exacerbation have also been implied as potential triggers of TCM.9

Rarely, paradoxical bronchospasm may occur in the setting of inhaled ipratropium; however, this should be carefully distinguished from inadequate response and from transient nocturnal desaturation in COPD.10

This patient had hypercapnia and respiratory acidosis and used inhaled salbutamol. We wonder why COPD exacerbation itself (especially in the context of a left paratracheal consolidation suggesting community-acquired pneumonia, which could potentially add hypoxia to this clinical scenario) was not considered the most likely trigger of TCM instead of a rare paradoxical reaction to an anticholinergic drug.