Peripartum cardiomyopathy (PPCM) is a potentially life-threatening condition typically presenting as heart failure with reduced ejection fraction (HFrEF) in the last month of pregnancy or in the months following delivery in women without another known cause of heart failure. This updated position statement summarizes the knowledge about pathophysiological mechanisms, risk factors, clinical presentation, diagnosis and management of PPCM. As shortness of breath, fatigue and leg oedema are common in the peripartum period, a high index of suspicion is required to not miss the diagnosis. Measurement of natriuretic peptides, electrocardiography and echocardiography are recommended to promptly diagnose or exclude heart failure/PPCM. Important differential diagnoses include pulmonary embolism, myocardial infarction, hypertensive heart disease during pregnancy, and pre-existing heart disease. A genetic contribution is present in up to 20% of PPCM, in particular titin truncating variant. PPCM is associated with high morbidity and mortality, but also with a high probability of partial and often full recovery. Use of guideline-directed pharmacological therapy for HFrEF is recommended in all patients

A low-intensity, pharmacist-led collaborative intervention in primary care resulted in modest improvements in prescribing of disease-modifying medications but did not improve clinical outcomes in a population that was relatively well treated at baseline.

Background: Patients with left ventricular systolic dysfunction (LVSD) following myocardial infarction (MI) are at high risk of developing heart failure. The addition of neprilysin inhibition to renin angiotensin system (RAS) inhibition may result in greater attenuation of adverse LV remodeling due to increased levels of substrates for neprilysin with vasodilatory, anti-hypertrophic, anti-fibrotic and sympatholytic effects. Methods: We performed a prospective, multi-center, randomized, double-blind, active-comparator trial comparing sacubitril/valsartan 97/103mg twice daily with valsartan 160mg twice daily in patients ≥3 months following MI with a LV ejection fraction (LVEF) ≤40% who were taking a RAS inhibitor (equivalent dose of ramipril ≥2.5mg twice daily), and a beta-blocker unless contraindicated or intolerant. Patients in New York Heart Association functional classification ≥II or with signs and symptoms of HF were excluded. The primary outcome was change from baseline to 52-weeks in LV end-systolic volume index (LVESVI) measured using cardiac magnetic resonance imaging (MRI). Secondary outcomes included other MRI measurements of LV remodeling, change in N-terminal prohormone of B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin I (hs-TnI), and a patient global assessment of change questionnaire. Results: From July 2018 to June 2019, 93 patients were randomized: mean age 60.7±10.4 years, median time from MI 3.6 years (IQR 1.2-7.2), mean LVEF 36.8%±7.1, median NT-proBNP 230pg/mL (124-404). Sacubitril/valsartan, compared with valsartan, did not significantly reduce LVESVI; adjusted between-group difference -1.9mL/m 2 (95%CI -4.9, 1.0); p=0.19. There were no significant between-group differences in NT-proBNP, hs-TnI, LV end-diastolic volume index, left atrial volume index, LVEF, LV mass index, or patient global assessment of change. Conclusions: In patients with asymptomatic LVSD following MI, treatment with sacubitril/valsartan did not have a significant reverse remodeling effect compared with valsartan. Clinical Trial Registration: URL: https://www.clinicaltrials.gov Unique identifier: NCT03552575

Both patients receiving and pharmacists delivering a cognitive HF service felt that it addressed a shortfall in current care. There may be a clearly defined role for pharmacists in supporting patients to address the burden of understanding and managing their condition and treatment, leading to better self management and medicines adherence. This study may inform the development of strategies or policies to improve the process of care for patients with HF and has implications for the development of other extended role services.

Polypharmacy and heart failure are becoming increasingly common due to an ageing population and the rise of multimorbidity. Treating heart failure necessitates prescribing of multiple medications, in-line with national and international guidelines predisposing patients to polypharmacy. This review aims to identify how polypharmacy has been defined among heart failure patients in the literature, whether a standard definition in relation to heart failure could be identified and to describe the prevalence. The Healthcare Database Advanced Search (HDAS) was used to search EMBASE, MEDLINE, PubMed, Cinahl and PsychInfo from inception until March 2021. Articles were included of any design, in patients ≥ 18 years old, with a diagnosis of heart failure; that explicitly define and measure polypharmacy. Data were thereafter extracted and described using a narrative synthesis approach. A total of 7522 articles were identified with 22 meeting the inclusion criteria. No standard definition of polypharmacy was identified. The most common definition was that of " ≥ 5 medications." Polypharmacy prevalence was high in heart failure populations, ranging from 17.2 to 99%. Missing or heterogeneous methods for defining heart failure and poor patient cohort characterisation limited the impact of most studies. Polypharmacy, most commonly defined as ≥ 5 medications, is highly prevalent in the heart failure population. There is a need for an internationally agreed definition of polypharmacy, allowing accurate review of polypharmacy issues. Whether an arbitrary numerical cut-off is a suitable definition, rather than medication appropriateness, remains unclear. Further studies are necessary to understand the relationship between polypharmacy with specific types of heart failure and related comorbidities.

Objectives Medication adherence is the end result of a complex set of interwoven factors. Non‐adherence with medication in heart failure patients is associated with excess mortality and morbidity. Studies describing interventions to improve adherence in heart failure are limited by a lack of robust methods and inconsistent outcomes. The aim of this evaluation was to explore the barriers to medication adherence in Scottish heart failure patients in order to inform the development of complex interventions. Methods Qualitative patient interviews. Participants were aged ≥18 years with current or previous signs or symptoms of clinical heart failure, reduced left ventricular ejection fraction ≤45% and confirmed adherence of <80% in tablet counts of heart failure therapy. Thematic analysis was employed. Key findings Eleven patients were recruited. The median age was 79 years old, and participants were typically from socially deprived communities. Participants were prescribed a mean 9.9 different medications per day. Seven distinct themes emerged around barriers to medication adherence: co‐morbidity; treatment burden; health literacy; trust in NHS; socioeconomic factors; autonomy and health expectations. Conclusions The factors affecting medication adherence in heart failure are multi‐factorial and are unlikely to be improved by one single‐faceted intervention. Future interventions need to treat patients holistically, build their trust as partners, simplify complex treatment regimens where possible and involve educational and social elements. The skill set and opportunities afforded to pharmacists may be well placed to deliver many of these aspects but this would need tested in the context of the development of complex interventions.

The framework delivers the vital first step needed to help standardise care, give pharmacists a blueprint for career progression and continuing professional development and bring clarity to the role of the pharmacist. Future collaboration between professional bodies and training providers is needed to develop structured programmes to align with the framework and facilitate training and resultant accreditation.

No abstract