Emergency department initiation of guideline-directed cardiovascular pharmacotherapy: an under-recognized opportunity

To the Editor, The emergency department (ED) represents a pivotal interface between acute cardiovascular events and long-term disease management. Despite major advances in acute stabilization and reperfusion strategies, the initiation of guideline-directed medical therapy (GDMT) frequently remains deferred to inpatient teams or outpatient follow-up. Yet, because many patients with acute cardiovascular disease first present to the ED, this setting may represent an under-recognized opportunity for the earlier initiation of evidence-based pharmacotherapy and improved continuity of care. In heart failure (HF), sodium–glucose cotransporter 2 inhibitors (SGLT2i) have demonstrated consistent reductions in cardiovascular death and hospitalization across a broad spectrum of ejection fractions. In the dapagliflozin and prevention of adverse-outcomes in heart failure trial, dapagliflozin significantly reduced worsening HF or cardiovascular death among patients with reduced ejection fraction, independent of diabetes status[1]. Similarly, EMPEROR-Reduced and EMPEROR-Preserved confirmed benefits across HF phenotypes[2,3]. Despite these data, real-world analyses continue to show suboptimal prescription rates at discharge, particularly among older adults and women[4]. Because acute decompensated HF commonly presents through the ED, this setting may help identify eligible patients and facilitate early evidence-based therapy or a clear pathway for rapid initiation. At the same time, most of the supporting evidence for early GDMT initiation derives from hospitalized rather than ED-specific populations, highlighting an important translational gap between trial evidence and emergency care practice. Antithrombotic therapy represents another domain where ED-based optimization may improve outcomes. In atrial fibrillation, direct oral anticoagulants (DOACs) reduce stroke and systemic embolism compared with warfarin while maintaining favorable bleeding profiles[5]. Yet, anticoagulation initiation during ED encounters for new-onset atrial fibrillation remains inconsistent, despite guideline recommendations favoring early risk stratification and anticoagulation in eligible patients[6]. Similarly, in acute coronary syndromes (ACS), early implementation of high-intensity statins and dual antiplatelet therapy (DAPT) is associated with improved outcomes, including a reduction in recurrent ischemic events[7]. Given that many patients with suspected ACS initially present to the ED, timely initiation of evidence-based pharmacotherapy at this stage may help reduce gaps in secondary prevention. Evidence supporting early initiation of disease-modifying therapy is well established in hospitalized populations. In the PIONEER-HF trial, initiation of sacubitril/valsartan during hospitalization for acute decompensated HF led to a greater reduction in N-terminal pro-B-typr natriuretic peptide without excess adverse events compared with enalapril[8]. Additional evidence supporting early intensification of therapy comes from the STRONG-HF trial, which demonstrated that rapid up-titration of guideline-directed HF therapy following acute hospitalization significantly improved clinical outcomes compared with usual care[9]. These findings suggest that early pharmacologic optimization is not only feasible but may confer incremental benefit. However, it is important to recognize that most trials evaluating early GDMT initiation have been conducted in inpatient settings rather than in EDs specifically, underscoring the need for further ED-focused implementation studies. From a systems perspective, structured transition-of-care programs, standardized discharge pathways, and multidisciplinary medication reviews have been associated with improved adherence and reduced readmissions following cardiovascular hospitalization[10]. Barriers to ED initiation are multifactorial and include time constraints, uncertainty regarding outpatient follow-up, and concerns about hemodynamic stability during evaluation. Additional structural challenges may also influence prescribing decisions, including medicolegal concerns associated with initiating long-term therapies in the ED, institutional formulary restrictions, diagnostic uncertainty during early assessment, and variability in access to reliable outpatient follow-up. Patient heterogeneity, particularly in individuals with multiple comorbidities or fluctuating clinical status, may further contribute to clinician hesitancy when considering immediate pharmacotherapy initiation. However, many contemporary agents, including SGLT2 inhibitors and DOACs, have favorable safety profiles and require minimal titration. With appropriate patient selection and clinical judgment, early initiation may therefore be feasible for selected individuals. Incorporating protocolized risk stratification and multidisciplinary discharge planning may mitigate implementation challenges while aligning acute care with chronic disease modification. As cardiovascular pharmacotherapy continues to evolve, the ED should not function solely as a stabilization arena but as a therapeutic inflection point. Embedding GDMT initiation into acute care workflows may narrow the gap between guideline recommendations and real-world practice. Prospective implementation studies examining ED-based initiation strategies, patient adherence, and long-term outcomes are warranted to define the optimal integration of pharmacologic innovation into emergency cardiovascular care. In conclusion, the ED represents a pivotal yet underutilized setting for the early initiation of guideline-directed cardiovascular pharmacotherapy. Bridging acute management with longitudinal therapy optimization may provide a pragmatic opportunity to improve cardiovascular outcomes at a population level.