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• W4210693669 abstract "This article refers to ‘Effect of sacubitril/valsartan on investigator-reported ventricular arrhythmias in PARADIGM-HF’ by J.P. Curtain et al., published in this issue on pages 551–561. A multidisciplinary ‘Heart Team’ approach has been formalized and integrated into the clinical management of many cardiovascular conditions including multivessel coronary artery disease,1 valvular heart disease,2 peripheral artery disease, pulmonary embolism, and cardiogenic shock. Indeed, Heart Team evaluation has been guideline-recommended in select scenarios to facilitate complex clinical decision-making informed by diverse stakeholder input. In heart failure with reduced ejection fraction (HFrEF), recent years have seen continued expansion of available medical and device-based therapies, leading to challenging decisions around the relative appropriateness and timing of interventions. Should a ‘Heart Team’ approach be routinely applied to aid primary prevention implantable cardioverter-defibrillator (ICD) decision-making in HFrEF to identify appropriate candidates, ensure complete guideline-directed medical therapy (GDMT) optimization, and individualize timelines for device implantation? The PARADIGM-HF (Prospective Comparison of ARNI With ACEI to Determine Impact on Global Mortality and Morbidity in Heart Failure) trial established the benefits of sacubitril/valsartan over enalapril in reducing all-cause mortality, including its major components (death from worsening heart failure [HF] and sudden cardiac death [SCD]), in patients with HFrEF.3 However, SCD remains a major cause of death in patients with chronic HFrEF, and can be attributed to electrical (including ventricular arrhythmias [VA] and bradyarrhythmias) or other causes (e.g. acute coronary syndrome, electrolyte imbalances).4 Guidelines currently recommend optimal HFrEF pharmacotherapy and ICD implantation to reduce SCD risk in select patients with HFrEF.5, 6 In this issue of the Journal, Curtain et al.7 evaluated whether sacubitril/valsartan reduced the incidence of VA, ICD discharges, or resuscitated cardiac arrest compared with enalapril in a post hoc analysis of PARADIGM-HF. Participants had HFrEF with left ventricular ejection fraction (LVEF) ≤40%, New York Heart Association (NYHA) functional class II–IV, and HF hospitalization within the previous year and/or elevated natriuretic peptide levels. All investigator-reported adverse events were screened for report of VA (including ventricular tachycardia, ventricular fibrillation, ventricular flutter, and torsades de pointes) or ICD discharge. Among 8399 patients analysed, 4.0% experienced and 4.4% experienced the composite of VA, ICD shock, or resuscitated cardiac arrest. Patients who experienced VA had greater illness severity reflected by medical comorbidities but did not have differences in NYHA class or Kansas City Cardiomyopathy Questionnaire clinical summary scores compared with those who did not have VA. Patients with VA were also significantly more likely to have a prior ICD or cardiac resynchronization therapy defibrillator (CRT-D). Sacubitril/valsartan reduced the risk of VA (hazard ratio [HR] 0.76; 95% confidence interval [CI] 0.62–0.95) and of the composite of VA, ICD shock, or resuscitated cardiac arrest (HR 0.79; 95% CI 0.65–0.97) compared with enalapril. These findings were consistent in sensitivity analyses that only included VA events reported as serious adverse events or with all-cause mortality as a competing risk. Notably, when patients were categorized by HFrEF aetiology, those with non-ischaemic HF had a substantially lower risk of VA with sacubitril/valsartan compared with enalapril (HR 0.53; 95% CI 0.37–0.78), while those with ischaemic HF did not (HR 0.93; 95% CI 0.71–1.21) (pinteraction = 0.02). However, when patients were categorized by presence of prior ICD or CRT-D, consistent reductions in VA risk were observed with sacubitril/valsartan compared with enalapril (pinteraction = 0.95). These and prior analyses of PARADIGM-HF8 suggest that sacubitril/valsartan may preferentially reduce SCD risk in patients with non-ischaemic HF compared with ischaemic HF. The possibility of misclassification of HF aetiology must be considered when interpreting these results. However, the enhanced reverse remodelling effects of sacubitril/valsartan in patients with non-ischaemic cardiomyopathy compared with ischaemic cardiomyopathy and the fact that LVEF improvement is more closely linked to a reduction in adverse outcomes in patients with non-ischaemic cardiomyopathy may account for these findings.9 The primary limitations of this study lie in its post hoc, non-prespecified nature. Additionally, given that outcomes were based on investigator-reported adverse events without adjudication or electrocardiographic, device interrogation, or ambulatory rhythm monitoring data, the overall burden of VA events may be underestimated. Importantly, each component of contemporary HFrEF GDMT appears to reduce the risk of the two major modes of death in patients with HFrEF – worsening HF and SCD (Figure 1). Randomized clinical trials have shown that β-blockers (by 31%),10 angiotensin receptor blockers (ARB) (by 15% in the CHARM programme11), and mineralocorticoid receptor antagonists (by 23%12) consistently lower risk of sudden death. Recent analyses from DAPA-HF (Dapagliflozin and Prevention of Adverse Outcomes in Heart Failure) have shown that the sodium–glucose cotransporter-2 inhibitor dapagliflozin reduces the risk of serious VA, resuscitated cardiac arrest, or sudden death by 21%.13 Evidence of benefit of angiotensin-converting enzyme inhibitors (ACEi) on sudden death risk is less certain.14 Taken together with the relatively low risk of serious VA over a 3-month period, the results of this analysis support current guidelines recommending ICD implantation for primary prevention of SCD only if LVEF remains ≤35% after a minimum of 3 months of use of combination therapy with Class I recommended drugs for HFrEF.5 Moreover, these results emphasize the importance of continued optimization of GDMT in eligible patients with HFrEF who have already undergone ICD or CRT-D implantation, as these subjects experienced lower risk for VA with sacubitril/valsartan. These and other considerations highlight the multidisciplinary nature of care for patients with HFrEF, especially between HF and electrophysiology specialists. However, in clinical practice this care is often siloed, which may contribute to suboptimal treatment and patient outcomes. Indeed, large real-world registry data demonstrate that pharmacotherapy is infrequently optimized prior to primary prevention ICD placement in patients with HFrEF, even when considering limited therapy with β-blocker and ACEi/ARB.15 Furthermore, patients in this experience who did not have some degree of GDMT optimization prior to ICD implantation had higher 1-year mortality. Given the complex interplay between the optimal dosing, timing, and combinations of drug and device therapies for patients with HFrEF and the need to carefully consider clinical patient characteristics and values, procedural risks, and prognosis, a Heart Team approach has the potential to improve patient outcomes. In the context of patients with HFrEF who may be candidates for ICD and/or CRT-D therapy, concurrent evaluation by electrophysiology and HF clinicians could provide opportunities to review patients' overall care trajectory and facilitate GDMT optimization, with subsequent re-assessment for device candidacy. In patients who have already undergone device implantation, continued collaborative evaluation could allow for device parameter and drug therapy review, and potentially earlier referral for advanced therapies in patients who experience a heightened burden of VA events. Early single centre collaborative experiences have been suggestive of effective synergy between specialties, but these clinical programmes need to be structured, formalized, and standardized to facilitate scalability across systems of care. These data also push us to reexamine existing issues around sudden death prevention in HFrEF. First, the pathways by which components of GDMT influence VA risk may extend beyond remodelling alone, and these mechanisms require further elucidation. Second, as landmark clinical trials that established the benefits of ICDs were conducted on the background of medical therapy that is no longer considered contemporary, newer trials may be needed to better define their role in current care. Finally, investigations that define the appropriate duration of contemporary pharmacotherapy prior to committing to device therapies should be conducted. More specifically, comprehensive strategies of combining drug and device therapy in patients with HFrEF may need to be tailored based on phenotypic characteristics. For instance, patients who exhibit early intolerance of pharmacotherapies may benefit from earlier device therapy such as CRT, which could in turn improve haemodynamic status and ventricular remodelling. Robust clinical trial evidence has supported the central role of comprehensive medical therapy in reducing risks of sudden death in HFrEF. The traditional ‘waiting period’ prior to device implantation must be reshaped into an active treatment optimization period that may ultimately render many individuals at low enough risk of sudden death to defer primary prevention ICD implantation. With accelerated progress in scientific discovery and drug and device development in the management of HFrEF, we believe a Heart Team approach will best operationalize these advances to improve the health of our patients. Conflict of interest: A.S.V. serves on an advisory board for Broadview Ventures, has received consulting fees from Buoy Health Inc, and has received support from the National Heart, Lung, and Blood Institute T32 postdoctoral training grant T32HL007604 and the Daniel Pierce Family Fellowship in Advanced Heart Disease. J.P.S. has received consulting fees/honoraria from Abbott, Biotronik, Boston Scientific, Cardiologs, CVRx, Cardiac Rhythm Group, EBR, Impulse Dynamics, Implicity, Medtronic, Medscape, Microport, New Century Health, Nopras, Orchestra BioMed, Octagos Health, and Sanofi. M.V. has received research grant support or served on advisory boards for American Regent, Amgen, AstraZeneca, Bayer AG, Baxter Healthcare, Boehringer Ingelheim, Cytokinetics, Lexicon Pharmaceuticals, Novartis, Pharmacosmos, Relypsa, Roche Diagnostics, and Sanofi; speaker engagements with Novartis and Roche Diagnostics; and participates in clinical trial committees for studies sponsored by Galmed, Impulse Dynamics, Novartis, and Occlutech." @default.
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• W4210693669 date "2022-02-13" @default.
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• W4210693669 title "A Heart Team approach to contemporary device decision‐making in heart failure" @default.
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• W4210693669 doi "https://doi.org/10.1002/ejhf.2445" @default.
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