Background: Guidelines recommend using multiple drugs in patients with heart failure (HF) with reduced ejection fraction, but there is a paucity of real‐world data on the simultaneous initiation of the 4 pharmacological pillars at discharge after a decompensation event. Methods and Results: A retrospective data mart, including patients diagnosed with HF, was implemented. Consecutively admitted patients with HF with reduced ejection fraction were selected through an automated approach and categorized according to the number/type of treatments prescribed at discharge. The prevalence of contraindications and cautions for HF with reduced ejection fraction treatments was systematically assessed. Logistic regression models were fitted to assess predictors of the number of treatments (≥2 versus <2 drugs) prescribed and the risk of rehospitalization. A population of 305 patients with a first episode of HF hospitalization and a diagnosis of HF with reduced ejection fraction (ejection fraction, <40%) was selected. At discharge, 49.2% received 2 current recommended drugs, β‐blockers were prescribed in 93.4%, while a renin‐angiotensin system inhibitor or an angiotensin receptor–neprilysin inhibitor was prescribed in 68.2%. A mineralocorticoid receptor antagonist was prescribed in 32.5%, although none of the patients showed contraindications to mineralocorticoid receptor antagonist prescription. A sodium‐glucose cotransporter 2 inhibitor could be prescribed in 71.1% of patients. On the basis of current recommendations, 46.2% could receive the 4 foundational drugs at discharge. Renal dysfunction was associated with <2 foundational drugs prescribed. After adjusting for age and renal function, use of ≥2 drugs was associated with lower risk of rehospitalization during the 30 days after discharge. Conclusions: A quadruple therapy could be directly implementable at discharge, potentially providing prognostic advantages. Renal dysfunction was the main prevalent condition limiting this approach.

Aims: Coronary artery disease (CAD) is a common cause of heart failure (HF). Whether coronary revascularization improves outcomes in patients with HF receiving guideline-recommended pharmacological therapy (GRPT) remains uncertain; therefore, we conducted a systematic review and meta-analysis of relevant randomized controlled trials (RCTs). Methods and results: We searched in public databases for RCTs published between 1 January 2001 and 22 November 2022, investigating the effects of coronary revascularization on morbidity and mortality in patients with chronic HF due to CAD. All-cause mortality was the primary outcome. We included five RCTs that enrolled, altogether, 2842 patients (most aged <65 years; 85% men; 67% with left ventricular ejection fraction ≤35%). Overall, compared to medical therapy alone, coronary revascularization was associated with a lower risk of all-cause mortality (hazard ratio [HR] 0.88, 95% confidence interval [CI] 0.79–0.99; p = 0.0278) and cardiovascular mortality (HR 0.80, 95% CI 0.70–0.93; p = 0.0024) but not the composite of hospitalization for HF or all-cause mortality (HR 0.87, 95% CI 0.74–1.01; p = 0.0728). There were insufficient data to show whether the effects of coronary artery bypass graft surgery or percutaneous coronary intervention were similar or differed. Conclusions: For patients with chronic HF and CAD enrolled in RCTs, the effect of coronary revascularization on all-cause mortality was statistically significant but neither substantial (HR 0.88) nor robust (upper 95% CI close to 1.0). RCTs were not blinded, which may bias reporting of the cause-specific reasons for hospitalization and mortality. Further trials are required to determine which patients with HF and CAD obtain a substantial benefit from coronary revascularization by either coronary artery bypass graft surgery or percutaneous coronary intervention.

Atherothrombosis, the primary driver of acute cardiovascular (CV) events, is characterized by the activation of three key pathophysiological pathways: platelets, coagulation, and inflammation. Dual antiplatelet therapy (DAPT) is the current standard of care for patients with acute coronary syndrome, providing significant reductions in cardiovascular (CV) events, albeit with an associated increased risk of bleeding. However, the high residual risk of recurrent events among these patients highlights the need for alternative strategies to treat and prevent atherothrombosis. To this extent, several approaches aimed at targeting atherothrombosis have been proposed. Among these, a strategy of dual-pathway inhibition simultaneously targeting platelets, using single or DAPT, and coagulation, using a low-dose anticoagulant such as rivaroxaban 2.5 mg twice daily, has shown to reduce CV events but at the expense of increased bleeding. Targeting inflammatory pathways has the potential to be a highly effective strategy to tackle atherothrombosis without increasing bleeding risk. Several anti-inflammatory agents have been tested in patients with coronary artery disease, but to date only colchicine is approved for secondary prevention on top of standard care, including antiplatelet therapy. However, many aspects of colchicine’s mechanism of action, including its antiplatelet effects and how it synergizes with antiplatelet therapy, remain unclear. In this review, we summarize the available clinical and pre-clinical evidence on the antiplatelet effects of colchicine and its synergistic interactions with antiplatelet therapy, highlighting their potential role in addressing atherothrombosis.

Water and salt retention, in other words congestion, are fundamental to the pathophysiology of heart failure and are important therapeutic targets. Echocardiography is the key tool with which to assess cardiac structure and function in the initial diagnostic workup of patients with suspected heart failure and is essential for guiding treatment and stratifying risk. Ultrasound can also be used to identify and quantify congestion in the great veins, kidneys and lungs. More advanced imaging methods might further clarify the aetiology of heart failure and its consequences for the heart and periphery, thereby improving the efficiency and quality of care tailored with greater precision to individual patient need.

Background and Aims: Many patients with cancer develop heart failure (HF), and many patients with HF develop cancer. Inter-relationships between their natural histories are rarely reported. Methods: Health records were obtained for a Scottish region. People aged >50 years were classified by the presence or absence of HF, loop diuretics (a pharmacological marker of congestion), and cancer. Incident cancer, mortality, and cause of death were recorded. Results: Of 317 178 people aged >50 years, 11 268 (3.6%) had HF of whom 6276 were prescribed loop diuretics; a further 19 044 (6.0%) received loop diuretics. Thus, 30 312 (9.6%) people met an expanded definition of heart failure (HFexp). Annual cancer incidence was slightly higher for those with HFexp (incidence rate ratio 1.10; P < .001), varying amongst cancer types. For people with neither cancer nor HFexp, mortality was <3% annually; most deaths were cardiovascular. For those with cancer but not HFexp, annual mortality was 6.3% for women and 9.0% for men; most died of cancer. For those with HFexp but not cancer, annual mortality ranged from 6.6% to 18.4% depending on sex and HFexp criteria applied; most deaths were cardiovascular. For those with both cancer and HFexp, annual mortality ranged from 14.5% to 28.4%; cardiovascular and cancer mortality rates were similar. Few patients died at home (∼20%). Conclusions: Patients with HFexp have a slightly higher risk of cancer overall, but this may vary according to cancer type. Patients with both cancer and HFexp have a poor prognosis with a similar proportion of deaths attributed to cancer and cardiovascular disease.