Assessment of Medication Adherence Using Pharmacy Data Before and After Percutaneous Coronary Intervention.

Objective: Adherence to anti-platelet medications is critical following coronary stenting, but prior studies indicate that clinician assessment and patient self-assessment of adherence are poorly correlated with future medication-taking behavior. We therefore sought to determine if integrated pharmacy data can be used to identify patients at high risk of non-adherence after percutaneous coronary interventions (PCI). Methods: Using Veteran Affairs (VA) Clinical Assessment, Reporting, and Tracking (CART) data linked with pharmacy records, we assessed adherence to cardiovascular medications from 2012 to 2018. Adherence was defined as the proportion of days covered (PDC) ≥ 0.80. We assessed the association of pre-PCI adherence with post-PCI adherence to P2Y12 inhibitors and clinical outcomes using logistic regression and Cox proportional hazard models, respectively. Results: Among 56,357 patients, 66.0% filled at least 1 cardiovascular medication within VA for the year prior to PCI and were evaluable for adherence. Pre-PCI non-adherence was 20.7%, and non-adherent patients were more likely to be younger and present non-electively. Non-adherent patients were less likely to adhere to P2Y12 inhibitor therapy after PCI (Adjusted OR 0.45 C.I. 0.41-0.46), compared with adherent patients, and had a higher adjusted risk of mortality (HR 1.17 C.I. 1.03-1.33). Conclusion: Adherence to cardiovascular medications prior to PCI can be assessed for most patients using pharmacy data, and past adherence is associated with future adherence and mortality after PCI. Use of integrated pharmacy data to identify high-risk patients could improve outcomes and cost-effectiveness of adherence interventions.

Disordered Toll-like receptor 2 responses in the pathogenesis of pulmonary sarcoidosis.

In this study, we hypothesized that the granulomatous disorder sarcoidosis is not caused by a single pathogen, but rather results from abnormal responses of Toll-like receptors (TLRs) to conserved bacterial elements. Unsorted bronchoalveolar lavage (BAL) cells from patients with suspected pulmonary sarcoidosis and healthy non-smoking control subjects were stimulated with representative ligands of TLR-2 (in both TLR-2/1 and TLR-2/6 heterodimers) and TLR-4. Responses were determined by assessing resulting production of tumour necrosis factor (TNF)-α and interleukin (IL)-6. BAL cells from patients in whom sarcoidosis was confirmed displayed increased cytokine responses to the TLR-2/1 ligand 19-kDa lipoprotein of Mycobacterium tuberculosis (LpqH) and decreased responses to the TLR-2/6 agonist fibroblast stimulating ligand-1 (FSL)-1. Subsequently, we evaluated the impact of TLR-2 gene deletion in a recently described murine model of T helper type 1 (Th1)-associated lung disease induced by heat-killed Propionibacterium acnes. As quantified by blinded scoring of lung pathology, P. acnes-induced granulomatous pulmonary inflammation was markedly attenuated in TLR-2(-/-) mice compared to wild-type C57BL/6 animals. The findings support a potential role for disordered TLR-2 responses in the pathogenesis of pulmonary sarcoidosis.