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NSAIDs and heart failure: A dangerous relationship

Raffaele Rotunno, Igino Oppo, Gabriele Saetta, Pietro Aveta, Sergio Bruno
  • Igino Oppo
    Roccadaspide Hospital, Cardiology Department, Italy
  • Gabriele Saetta
    Roccadaspide Hospital, Cardiology Department, Italy
  • Pietro Aveta
    Roccadaspide Hospital, Cardiology Department, Italy
  • Sergio Bruno
    ASL Salerno, Italy

Abstract

One of the potential cardiotoxic action of anti-inflammatory drugs is the occurrence of heart failure (HF), due to their effects on fluid retention and blood pressure. The risk of hospitalization for HF is roughly doubled for both Coxibs, cyclooxygenase-1 (COX-1) and cyclooxygenase- 2 (COX-2) inhibitors, and all the conventional nonsteroidal anti-inflammatory drugs (NSAIDs). These drugs are also associated with a risk of vascular thrombosis, which for NSAIDs is different in relation to their different ability to inhibit COX-1 and COX-2. The cardiovascular toxicity of these drugs in the direction of HF follow different pathways respect to their related vascular thrombosis toxicity and involves, in particular, the renal prostaglandins, PGE2 and prostacyclin, mostly synthesized by COX-2. In the kidneys the PGs perform a direct vasodilatory action, e.g. by means of non-contrasting angiotensin mechanisms, and for this reason nimesulide effects on renal microcirculation are independent from the prevalence of intrarenal renin angiotensin aldosterone system (RAAS) activity. Conversely, nimesulide reduces sodium tubular urinary flow only in presence of intrarenal RAAS.

Keywords

NSAIDs; COX1; COX2; cardiotoxic action.

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Submitted: 2018-04-24 12:32:50
Published: 2018-06-07 14:54:28
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Copyright (c) 2018 Raffaele Rotunno, Igino Oppo, Gabriele Saetta, Pietro Aveta, Sergio Bruno

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