AbstractAimsDespite medical therapy for heart failure (HF) having proven benefits of improving quality of life and survival, many patients remain under‐treated. This may be due to a combination of under‐prescription by medical professionals and poor adherence from patients. In HF, as with many other chronic diseases, adherence to medication can deteriorate over time particularly when symptoms are well controlled. Therefore, detecting and addressing non‐adherence has a crucial role in the management of HF. Significant flaws and inaccuracies exist in the methods currently used to assess adherence such as patient reporting, pill counts, and pharmacy fill records. We aim to use high‐performance liquid chromatography–tandem mass spectrometry (HPLC‐MS) to detect metabolites of HF medications in the urine samples of chronic HF patients.Methods and resultsUrine samples were collected from 35 patients in a specialist HF clinic. Patients were included if they had an ejection fraction <45% and were taking at least two disease‐modifying HF medications. They were excluded if they had been admitted to hospital for HF in the 3 months preceding clinic attendance. These samples were sent for HPLC‐MS and tested for all HF medications prescribed for that patient. A high rate of complete adherence of 89% was detected in these patients, with 94% being partially adherent (at least one HF medication detected) to therapy (at least one HF medication detected). This analysis also highlighted that mineralocorticoid antagonists represent both the most under‐prescribed (67%) and poorly adhered (75%) medication class.ConclusionsThis analysis revealed a surprisingly high level of adherence to disease‐modifying therapy in chronic HF patients and highlights that most of our ‘total’ under‐treatment is likely to be from a failure to prescribe rather than a failure to adhere. Testing for metabolites of disease‐modifying HF drugs in urine using HPLC‐MS is feasible and is a useful adjunct to a specialist HF service. At present, the distinction between treatment failure and failure to take treatment is not always clear, which is important because the investigation and potential solutions are different. The former needs initiation of additional therapies and consideration of additional diagnoses, whereas the latter requires strategies to understand reasons underlying poor adherence and collaborative working to improve this: the wrong strategy will be ineffective.

Background and Aims: Evaluate premature morbidity and mortality among patients with potentially undiagnosed Familial Hypercholesterolemia (FH).

ischaemic heart disease remains the leading cause of death worldwide. 1decades of research have established that the accumulation of the cholesterol cargo carried by low density lipoprotein particles within the arterial wall is the initiating factor in atherogenesis and its clinical manifestation as coronary artery disease.large scale epidemiological studies, mendelian randomisation genetic studies and trials of therapeutic interventions have established that low density lipoprotein cholesterol (ldl-C) is a causal factor in developing atherosclerotic heart disease. 2-5the mainstay of therapy for reducing ldl-C has so far been with statin therapy initially followed by add-on therapy.despite current lipid lowering therapies, a proportion of patients either fail to reach their target ldl-C with statins or are intolerant to statins thus limiting treatment options.While ezetimibe can be used as an add-on or alternative to statins, the modest 20% reduction in ldl-C precludes more widespread use.there is therefore, an unmet need for further ldl-C reduction with new treatments, among those with high atherosclerotic cardiovascular disease risk such as those with prevalent disease or with familial hypercholesterolaemia.