Is routine stress ulcer prophylaxis of benefit for patients undergoing cardiac surgery?

Department of Cardiothoracic Surgery, John Radcliffe Hospital, Oxford, UK.
Interactive Cardiovascular and Thoracic Surgery (Impact Factor: 1.11). 02/2012; 14(5):622-8. DOI: 10.1093/icvts/ivs019
Source: PubMed

ABSTRACT A best evidence topic in cardiac surgery was written according to a structured protocol. We address whether routine pharmacological stress ulcer prophylaxis is of benefit for patients undergoing cardiac surgery. One hundred and fifty-six papers were found using the reported search, of which 10 represented the best evidence to answer the clinical question. The authors, journal, date, country of publication, patient group, study type, relevant outcomes and results of these papers were tabulated. The results show that the incidence of stress ulcers following cardiac surgery is low (0.45%), but remains associated with significant morbidity and mortality. Five of the 7 studies demonstrated suppression of acid secretion or decreased incidence of gastric complications in patients given pharmacological stress ulcer prophylaxis, with the remaining two suggesting no clinical benefit. One prospective study of 210 patients, randomized equally between a proton pump inhibitor (PPI), histamine antagonist and teprenone, found that PPIs were the most effective at reducing gastric complications after cardiac surgery, including ulcer formation and upper gastrointestinal bleeding (UGIB). However, a separate retrospective study suggested no difference in the outcomes between the use of a PPI and a histamine antagonist. Of the studies focused on histamine antagonists, one randomized control trial (RCT) showed that cimetidine can reduce surgical stress, augment the immune system and reduce the intubation time after cardiac surgery, although no direct association with UGIB was made. A second prospectively randomized study of histamine antagonists demonstrated superior pH control with famotidine and ranitidine, when compared with cimetidine. Furthermore, haematological and neurological side-effects were noted only with the use of cimetidine. A recent meta-analysis and systematic review of the literature associated gastric acid suppression with an increased risk of pneumonia. Two prospective cohort studies that examined the use of PPI in conjunction with clopidogrel in patients with coronary artery disease concluded that there was no association with an increase in major adverse cardiovascular events with the use of PPIs. We conclude that the current evidence is marginally in favour of the use of prophylactic PPIs. However, this is associated with an increased risk of hospital-acquired pneumonia.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The widespread use of clopidogrel alone or in combination with aspirin may result in gastrointestinal mucosal injury, clinically represented as recurrent ulceration and bleeding complications. Our recent work suggested that clopidogrel significantly induced human gastric epithelial cell (GES-1) apoptosis and disrupted gastric mucosal barrier, and that a p38 MAPK inhibitor could attenuate such injury. However, their exact mechanisms are largely unknown. The GES-1 cells were used as a model system, the effects of clopidogrel on the whole gene expression profile were evaluated by human gene expression microarray and gene ontology analysis, changes of the mRNA and protein expression were determined by real-time PCR and Western blot analysis, and cell viability and apoptosis were measured by MTT assay and flow cytometry analysis, respectively. Gene microarray analysis identified 79 genes that were differentially expressed (P<0.05 and fold-change >3) when cells were treated with or without clopidogrel. Gene ontology analysis revealed that response to stress and cell apoptosis dysfunction were ranked in the top 10 cellular events being affected, and that the major components of endoplasmic reticulum stress-mediated apoptosis pathway - CHOP and TRIB3- were up-regulated in a concentration- and time-dependent manner when cells were treated with clopidogrel. Pathway analysis demonstrated that multiple MAPK kinases were phosphorylated in clopidogrel-treated GES-1 cells, but that only SB-203580 (a p38-specific MAPK inhibitor) attenuated cell apoptosis and CHOP over-expression, both of which were induced by clopidogrel. Increased endoplasmic reticulum stress response is involved in clopidogrel-induced gastric mucosal injury, acting through p38 MAPK activation.
    PLoS ONE 01/2013; 8(9):e74381. · 3.53 Impact Factor
  • Source
    Interactive Cardiovascular and Thoracic Surgery 05/2012; 14(5):627-8. · 1.11 Impact Factor
  • Source
    Interactive Cardiovascular and Thoracic Surgery 05/2012; 14(5):628. · 1.11 Impact Factor

Full-text (2 Sources)

Available from
Jun 2, 2014