Page and Henry1 reported a close relationship between the consumption of nonsteroidal anti-inflammatory drugs (NSAIDs) and a significant increase in hospital admissions due to worsening of chronic heart failure (CHF). This is indeed an interesting observation, particularly if one considers the possible underlying mechanisms. Conventional NSAIDs have been associated with inflammation of the small intestine, apart from aspirin and nabumetone, which seem to spare the small bowel.2 They may also contribute to increased intestinal permeability; interact with diuretics and angiotensin-converting enzyme inhibitors; and cause short-term hemodynamic effects, derangements of cellular integrity, and a reduction of the enterocyte barrier function due to chronic intestinal inflammation. Additionally, there may be abnormal bowel wall function in CHF due to venous congestion and a low cardiac output. As a plausible consequence, bacterial translocation may occur (ie, the translocation of bacteria and bacterial products such as lipopolysaccharide [endotoxin]), a phenomenon that has been proposed as an important stimulus for immune activation in CHF.3
Rauchhaus M, Sharma R, Bolger A. NSAIDs, Intestinal Cell Integrity, and Bacterial Translocation in Chronic Heart Failure. Arch Intern Med. 2000;160(19):3004–3005. doi:
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