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Short bowel syndrome after extensive surgical resection of the intestine is characterised by inadequate digestion and absorption of nutrients. Additional clinical problems include impaired absorption and metabolism of diverse drugs requiring individualised medical therapy or alternative treatments. We report a case of individualised dual antiplatelet therapy in a patient who underwent an extensive intestinal resection complicated by acute myocardial infarction requiring percutaneous coronary intervention and stent implantation. Genetic testing of CYP2C19 gene polymorphisms and platelet aggregation testing were used to assess responses to aspirin, clopidogrel, prasugrel and ticagrelor. Given its unique pharmacokinetics with good absorption and without need of metabolism to an active substance, ticagrelor appears to be the best for patients with short bowel syndrome who require dual antiplatelet therapy after coronary stent implantation., (2015 BMJ Publishing Group Ltd.)

Antiplatelet therapy is the cornerstone of the treatment for patients with coronary artery disease (CAD). Dual therapy with clopidogrel and aspirin is currently the standard treatment after percutaneous coronary interventions. However, despite the use of clopidogrel, a considerable number of patients continue to suffer major adverse cardiac events. There is a growing degree of evidence supporting high on-treatment platelet reactivity (HPR) as a predictive factor for recurrent ischemic complications. Numerous studies have shown an interindividual variability of responsiveness to clopidogrel and aspirin, which is one of the reasons for HPR. There is yet to be established an assay for antiplatelet drug response as the gold standard. This paper provides a background to the current controversies surrounding the issue of testing for the effectiveness of antiplatelet therapy and reviews the various genetic and phenotype-based laboratory tests to measure aspirin and clopidogrel response and their correlation with clinical outcomes. On the basis of the current evidence and trying to be cost-effective, testing should be considered on a case-by-case basis, especially in patients who present with an acute coronary syndrome or stent thrombosis. In the case of stable CAD, we think that testing might be helpful in particular risk groups of patients to avoid ischemic or bleeding complications.

Objectives: This study was designed to identify the multivariate effect of clinical risk factors on high on-treatment platelet reactivity (HPR) and 12 months major adverse events (MACE) under treatment with aspirin and clopidogrel in patients undergoing non-urgent percutaneous coronary intervention (PCI). Methods: 739 consecutive patients with stable coronary artery disease (CAD) undergoing PCI were recruited. On-treatment platelet aggregation was tested by light transmittance aggregometry. Clinical risk factors and MACE during one-year follow-up were recorded. An independent population of 591 patients served as validation cohort. Results: Degree of on-treatment platelet aggregation was influenced by different clinical risk factors. In multivariate regression analysis older age, diabetes mellitus, elevated BMI, renal function and left ventricular ejection fraction were independent predictors of HPR. After weighing these variables according to their estimates in multivariate regression model, we developed a score to predict HPR in stable CAD patients undergoing elective PCI (PREDICT-STABLE Score, ranging 0-9). Patients with a high score were significantly more likely to develop MACE within one year of follow-up, 3.4% (score 0-3), 6.3% (score 4-6) and 10.3% (score 7-9); odds ratio 3.23, P=0.02 for score 7-9 vs. 0-3. This association was confirmed in the validation cohort. Conclusions: Variability of on-treatment platelet function and associated outcome is mainly influenced by clinical risk variables. Identification of high risk patients (e.g. with high PREDICT-STABLE score) might help to identify risk groups that benefit from more intensified antiplatelet regimen. Additional clinical risk factor assessment rather than isolated platelet function-guided approaches should be investigated in future to evaluate personalized antiplatelet therapy in stable CAD-patients. [ABSTRACT FROM AUTHOR]