Review Article

Valvular Heart Disease in Heart Failure with Preserved Ejection Fraction

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Abstract

Heart failure with preserved ejection fraction (HFpEF) is associated with reduced functional capacity and quality of life, as well as with high rates of heart failure hospitalisation and mortality. Valvular heart disease (VHD) is frequently encountered in patients with HFpEF, and both conditions share common risk factors, such as age, hypertension, diabetes and coronary artery disease, which may contribute to their shared pathogenesis and progression. With recent advances in percutaneous therapies for VHD and an improved understanding of HFpEF, there is a growing interest in the relationship between VHD and HFpEF. In this review, we provide an overview of the pathophysiology, epidemiology and management strategies of tricuspid regurgitation, mitral regurgitation, aortic stenosis and aortic regurgitation in the setting of HFpEF.

Keywords

HFpEF, mitral regurgitation, tricuspid regurgitation, aortic stenosis, aortic regurgitation, epidemiology,

Received:

Accepted:

Published online:

DOI: https://doi.org/10.15420/cfr.2025.13

Disclosure: AA has received travel support from the Swedish Heart Lung Foundation. AW has received travel support from the Swedish Society of Cardiology and Swedish Heart Lung Foundation. GS has received grants from CSL Vifor Pharma, Boehringer Ingelheim, AstraZeneca, Merck, Cytokinetics, Servier, Novartis, Boston Scientific, Pharmacosmos, Bayer and Medtronic; consulting fees from TEVA, AstraZeneca, Medical Education Global Solutions, Atheneum, Genesis, CSL Vifor, Servier and Translational Medicine Academy Foundation; honoraria from Novartis, Roche, Cytokinetics, Hikma, Medtronic, Pharmacosmos, AstraZeneca, Menarini, CSL Vifor Pharma, Intas and Getz; travel support from Boehringer Ingelheim and Servier; and serves on advisory boards for AstraZeneca, Bayer, Uppsala Clinical Research Center, Servier, Abbott, Edwards Lifesciences, CSL Vifor and Cytokinetics. RTH has received speaker fees from Abbott Structural, Baylis Medical, Edwards Lifesciences and Philips Healthcare; has institutional consulting contracts for which she receives no direct compensation with Abbott Structural, Boston Scientific, Edwards Lifesciences, Medtronic and Novartis; and is Chief Scientific Officer for the Echocardiography Core Laboratory at the Cardiovascular Research Foundation for multiple industry-sponsored trials, for which she receives no direct industry compensation. LHL has received consulting fees (all payments to the author’s institution) from AstraZeneca, Vifor Pharma, Bayer, Pharmacosmos, Boehringer Ingelheim, Edwards Lifesciences, Biopeutics, Alleviant and Owkin and honoraria from AstraZeneca, Novartis, Boehringer Ingelheim, Bayer, Pharmacosmos, Vifor Pharma, Amgen and Novo Nordisk; holds a patent for AnaCardio and owns stock in AnaCardio. BS serves on an advisory board for Cardiovalve. GS and LHL are on the Cardiac Failure Review editorial board; this did not influence peer review. All other authors have no conflicts of interest to declare.

Funding: AA is supported by the Swedish Heart and Lung Foundation (20251411). AW reports funding from the Swedish Heart and Lung Foundation (20251166) and the Swedish Medical Society (SLS-1001488). BS is supported by Stockholm County Council (FoUI-988371), the Swedish Heart-Lung Foundation (20230578; 20250207), the Swedish Research Council (2022-01472), the Swedish Society for Medical Research (SSMF; SG-23-0142-B), the Swedish Society of Medicine (SLS; 987010) and Karolinska Institutet (2-116/2023).

Correspondence: Bahira Shahim, Division of Cardiology, Department of Medicine, Solna, Karolinska Institutet, 171 76 Stockholm, Sweden. E: bahira.shahim@ki.se

Copyright:

© The Author(s). This work is open access and is licensed under CC-BY-NC 4.0. Users may copy, redistribute and make derivative works for non-commercial purposes, provided the original work is cited correctly.

Heart failure with preserved ejection fraction (HFpEF) accounts for approximately half of all cases of heart failure (HF).1–3 Although HFpEF has a similarly poor survival rate to that of HF with reduced ejection fraction (HFrEF), the proportion of cardiovascular deaths is lower in HFpEF than HFrEF.4 HFpEF is characterised by alterations in myocardial structure, function and metabolism leading to left ventricular (LV) diastolic dysfunction, elevated LV filling pressures and pulmonary congestion. Any factors that exacerbate diastolic load can worsen the clinical trajectory and prognosis of HFpEF. Valvular heart disease (VHD) is frequently encountered in patients with HFpEF and shares common risk factors for disease development and progression, including age, hypertension, obesity, metabolic dysfunction, chronic kidney disease and AF.1–3,5 VHD may contribute to HFpEF as a primary cause leading to altered haemodynamics or it may develop as a consequence of HFpEF.6 However, primary valve diseases that directly affect the valve leaflets are not included in the definition of HFpEF.7 Notably, VHD is reported as the primary aetiology for HFpEF in approximately 20% of patients.8

In a report of 714,368 patients with median age of 68 years who underwent echocardiography at 35 community and academic cardiology programmes, tricuspid regurgitation (TR) was the most common VHD (7.1%), followed by mitral regurgitation (MR; 6.5%), aortic stenosis (AS; 4.1%) and aortic regurgitation (AR; 2.3%).9

In a report from the European Society of Cardiology (ESC) Heart Failure Long-Term Registry on moderate to severe VHD across the HF phenotypes, the most common VHDs in HFpEF patients were isolated TR (10%), followed by isolated MR (9%), combined TR/MR (8%), AS (8%), AR (6%) and combined AS/AR (3%).10 Compared with patients with HFrEF, those with HFpEF had a twofold higher risk of having isolated TR. One-year mortality rates in HFpEF were highest among those with combined TR/MR or isolated TR, followed by isolated MR. Patients with HFpEF and TR also experienced higher rates of non-cardiovascular mortality. In addition, patients with TR and HFpEF tend to respond less effectively to neurohormonal modulation therapies than those with MR. This may be due to the distinct pathophysiology of TR, which often occurs in the context of right-sided HF, pulmonary hypertension and biatrial myopathy, making it challenging to manage with therapies initially developed to target left-sided HF mechanisms.3,11 Although percutaneous valvular interventions have become the standard of care for patients with severe AS and are increasingly offered to patients with moderate to severe MR, they are only beginning to emerge for patients with TR and AR.

This review aims to provide a concise overview of the pathophysiology and management strategies of VHD (TR, MR, AS and AR) in patients with HFpEF.

Pathophysiology of HFpEF

In a healthy heart, ventricular contraction is isovolumetric. During exercise, the heart adapts by increasing both end-diastolic volume (EDV) and end-systolic volume (ESV), resulting in a rise in stroke volume (SV), while LV end-diastolic pressure (LVEDP) remains constant. However, in HFpEF, the LV becomes stiffer and, as EDV and ESV increase, LVEDP also increases. A reduced contractile reserve and impaired chronotropic regulation lead to an insufficient increase in SV. In more advanced stages of HFpEF, LVEDP remains elevated even at rest.12 Despite preserved LV ejection fraction (LVEF), which is a key criterion for diagnosis, LV long-axis systolic function is often impaired in HFpEF.7 The left atrium (LA) also plays an important role in LV haemodynamics, serving as reservoir for venous blood during systole and maintaining mitral valve competency.13

The exact mechanisms leading to HFpEF are not fully understood.11,14 Myocardial fibrosis and myocyte hypertrophy have been observed in cardiac biopsies, but moderate to severe fibrosis is found in fewer than 30% of patients, a rate similar to that in patients with HFrEF.15 It has been suggested that abnormal phosphorylation of sarcomeres may contribute to myocardial stiffness.16 Another potential mechanism involves impaired nitric oxide/cGMP/protein kinase G signalling, which normally has antifibrotic and antihypertrophic effects.11 Inflammation and oxidative stress can reduce nitric oxide levels, downregulating this protective pathway.

A plausible unifying hypothesis for HFpEF is comorbidity-driven systemic inflammation, leading to microvascular (including coronary) endothelial dysfunction and secondary changes in cardiac interstitium and cardiomyocytes.17,18 The presence of elevated levels of inflammatory markers in HFpEF patients, coupled with observations of reduced coronary flow reserve and a high prevalence of obesity, suggests that systemic inflammation may contribute to epicardial tissue dysfunction.19–21 In HFpEF patients with obesity, increased plasma volumes and right ventricular (RV) dilatation may further affect LV function through the shared interventricular septum.22 In addition, systemic inflammatory diseases, such as rheumatic conditions, have been linked to HFpEF.11,23

Although HFpEF is a chronic condition, it can present with acute decompensation due to various triggers. VHD is a more common primary cause of acute HF in patients with HFpEF than in those with HFrEF because the stiff, non-compliant LV is highly sensitive to sudden increases in pressure or volume.24

Management of HFpEF

Unlike HFrEF, for which a combination of guideline-directed medical therapies is proven to reduce mortality, limited agents have proven benefit in the HFpEF population. Sodium–glucose cotransporter 2 (SGLT2) inhibitors have been shown to reduce the rates of HF hospitalisations in HFpEF. Therefore, they are strongly recommended in both European and US HF guidelines.25,26 A recent meta-analysis of randomised controlled trials suggests that SGLT2 inhibitors may reduce the risk of mortality in patients with HFpEF.27 Mineralocorticoid receptor antagonists may improve diastolic function in HFpEF patients and are likely beneficial.28,29 Recently, finerenone, a newer mineralocorticoid receptor antagonist, has been shown to reduce cardiovascular death and hospitalisation compared with placebo in HFpEF patients.30 In contrast, angiotensin receptor–neprilysin inhibitors have not been proven to be beneficial in patients with HFpEF. However, they have been approved for an expanded indication in the US for HFpEF patients at the lower end of the ejection fraction spectrum.25 Angiotensin II receptor blockers are sometimes used as alternatives to angiotensin receptor–neprilysin inhibitors, whereas angiotensin-converting enzyme inhibitors have not been shown to improve outcomes in HFpEF.25 Women may experience a greater therapeutic response to angiotensin receptor–neprilysin inhibitors and mineralocorticoid receptor antagonists than men.30,31 This may be explained by smaller LV size in women, which can result in a higher LVEF. Consequently, women presenting with LVEF in the range 50–55% may have more impaired LV function than men, potentially deriving greater benefit from these therapies.25 Diuretics are recommended to manage signs and symptoms of congestion, while achieving blood pressure targets and managing other comorbidities are crucial to prevent morbidity.32

Mitral Regurgitation

Pathophysiology

MR disrupts the haemodynamics of the heart by causing blood to flow backwards into the LA during systole (Figure 1), prolonging the ejection phase and maintaining the ejection fraction while reducing the forward SV.33 MR is categorised as either primary due to degenerative conditions or secondary due to atrial or ventricular dysfunction. Secondary MR, also called functional MR (FMR), is the category most commonly encountered in HFpEF.

Figure 1: Mitral Regurgitation in Heart Failure with Preserved Ejection Fraction

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In patients with HFpEF and FMR, there is a complex interplay between the LA and LV. The main aetiology of LA myopathy in HFpEF is diastolic dysfunction, which leads to elevated LVEDP and places stress on the LA. As the LA struggles against this increased afterload, it undergoes remodelling with annular dilatation (even in the absence of LV dilatation) and reduced contraction, which can result in atrial FMR (AFMR).13,33 The degree of LV diastolic dysfunction is directly correlated with the severity of LA dysfunction. Physical exercise further exacerbates the development of FMR by increasing LV filling pressures.

Inflammation resulting from common HFpEF comorbidities, such as hypertension, diabetes, chronic kidney disease and advanced age, can precipitate the development of LA dysfunction.34 This inflammation may cause atrial fibrosis, which leads to altered LA pressure, dilation and the further development of AFMR.13 AF is present in 30–60% of patients with HFpEF and leads to LA enlargement and worsened MR. This MR can, in turn, promote AF, thereby creating a vicious cycle.13 Patients with HFpEF and MR generally have worse outcomes, even if the MR is mild.35–37 However, it remains unclear whether MR is simply a marker of disease severity and LA involvement or whether it actively contributes to worsening of LA function.33

Management Strategies

The updated 2025 ESC/European Association for Cardio-Thoracic Surgery guidelines on the management of valvular heart disease advocate the importance of distinguishing the underlying mechanism of functional MR (atrial versus ventricular), which represents a significant upgrade from the 2021 guidelines.38,39

In theory, treating MR should improve outcomes in HFpEF patients because their haemodynamics are more sensitive to MR than those of patients with HFrEF.34

Medical management of MR primarily focuses on reducing LV pressure. Angiotensin II receptor blockers may mitigate profibrotic changes and SGLT2 inhibitors show potential in improving LA remodelling.13 Volume status optimisation with diuretics has been shown to reduce LA pressure more than LV pressure.40 This disproportionate reduction in pressure augments the closing forces of the mitral valve and reduces regurgitant volume.34 In patients with HFpEF and AF, early rhythm control with antiarrhythmic drugs or catheter ablation is crucial to interrupt the viscious cycle of LA remodelling and LV dysfunction. Meta-analyses suggest that rhythm control in AF reduces mortality in HFpEF, although MR severity was not specifically analysed in these studies.41,42

For patients with FMR and HFpEF, percutaneous mitral valve transcatheter edge-to-edge repair (M-TEER) is an option. However, major trials such as MITRA-FR, COAPT and RESHAPE-HF2 focused on patients with HFrEF with LVEF in the range of 15–40% (MITRA-FR) and 20–50% (COAPT and RESHAPE-HF2).43–45 Notably, a subgroup analysis from the COAPT trial showed that TEER for secondary MR was consistently effective in reducing mortality and improving quality of life and functional capacity in patients with HFpEF, defined as LVEF >40%, and in those with severe (LVEF ≤30%) versus moderate (LVEF >30%) LV dysfunction.46 A recent study also indicated that patients with AFMR experienced fewer HF hospitalisations during the 6 months after M-TEER.47

The EVEREST II study included patients with LVEF up to 60%, but subanalyses for HFpEF were not performed.48 Surgical mitral annuloplasty may be effective for reducing FMR, although the evidence is limited to smaller studies.13 Although surgical options for symptomatic FMR may not increase survival rates, they have been shown to improve symptoms and quality of life.49

Guidelines recommend treating MR with medical therapy and considering valve interventions if symptoms persist.39,50 However, isolated MR surgery is generally not recommended unless a patient requires concomitant cardiac surgery for another indication.39 In a German trial of patients with FMR, M-TEER was non-inferior to surgical repair or replacement.50 However, that trial was small and did not allow assessment of any potential interaction between LVEF and the type of intervention. For AFMR patients, mitral ring annuloplasty is suggested as an alternative, although more evidence is needed to support this recommendation. The US guidelines specify that patients with preserved LVEF and symptomatic MR should be considered for mitral valve surgery following optimisation of HF therapies.32

Tricuspid Regurgitation

Pathophysiology

Studies have reported a stronger association between HFpEF and TR compared to HFrEF, which may be due to shared epidemiological and mechanistic factors.51 Up to 40% of HFpEF patients are thought to have TR.4 The tricuspid valve is the largest valve, typically thinner than the mitral valve, and usually consists of three leaflets, although variations with additional leaflets are common. The anatomy of the tricuspid valve makes the annulus particularly prone to dilatation and flattening. Primary TR is an intrinsic abnormality of the valve itself, whereas secondary TR is the result of atrial or ventricular mechanisms. Secondary TR is the most common form in patients with significant TR. TR is graded as mild, moderate, severe, massive and torrential, combining echocardiographic qualitative measures, such as colour Doppler, and quantitative measures, such as effective regurgitant orifice area and proximal isovelocity surface area.52,53

Mild TR can be observed in healthy individuals without any physiological impact.49 However, when the tricuspid annulus dilates more than 40%, TR often becomes clinically significant. Significant or worsening TR is associated with a poor prognosis.49 Isolated TR is associated with worse outcomes in HFpEF patients than in their counterparts without VHD and carries the same risk as combined MR and TR.5,10

Elevated left-sided filling pressures and postcapillary pulmonary hypertension in HFpEF contribute to ventricular functional TR, whereas right atrial myopathy in HFpEF, with or without AF, leads to annular dilatation and atrial functional TR (Figure 2). Notably, TR in HFpEF does not necessarily occur in the presence of RV dysfunction. However, RV remodelling is a strong factor for progressive TR in HFpEF patients because it can lead to leaflet tethering and annular dilation, thereby worsening TR.3,51

Figure 2: Tricuspid Regurgitation in Heart Failure With Preserved Ejection Fraction

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In HFpEF patients with latent pulmonary disease, an increase in pulmonary vascular resistance with exercise increases right-sided filling pressures and reveals underlying TR. Furthermore, severe TR can also cause HFpEF, because RV dilation resulting from TR can lead to septal bowing into the LV, impairing LV diastolic function.3 In the setting of HFpEF, TR contributes to reduced SV, reduced RV contractility and abnormal interaction between the ventricles.3

Management Strategies

Optimal treatment for TR, especially in patients with HFpEF, remains an area with significant evidence gaps. Patients with symptomatic TR typically present with signs of right-sided HF, including peripheral oedema, ascites, jugular venous distension, hepatomegaly and fatigue.54 Therapeutic strategies for TR should focus on reducing volume load and right ventricular afterload.49,54 Loop diuretics and mineralocorticoid antagonists have shown particular benefit.1 In addition, maintaining both rate and rhythm may help reduce tricuspid annular dilatation, and active restoration to sinus rhythm may reduce both RV and LV volumes.54,55 Although research on patients with HFpEF and TR is limited, one longitudinal study identified AF as a common and significant risk factor for worsening TR in this population.56

Surgical options for isolated TR carry high in-hospital mortality rates (8.8%), with valve replacement posing a greater risk than repair.57 In contrast, recent studies on TEER in TR (T-TEER) have shown low complications rates.58 Although T-TEER has yet to meet primary endpoints beyond symptom relief and quality of life, a 2-year follow-up study demonstrated a sustained reduction in TR severity and a lower annualised rate of recurrent HF hospitalisations compared with medical therapy alone (Supplementary Table 1).59,60

However, a major limitation of transcatheter tricuspid valve intervention trials is the lack of sham controls and double blinding, a particularly critical issue when patient-reported outcomes are a key endpoint. Future studies could address this by verifying patient-reported outcomes with objective data, such as activity monitors, and by including surrogate endpoints like biomarkers. Longer-term follow-up is also necessary.61 Furthermore, existing trials exhibit significant heterogeneity in their study populations and should be refined to focus on specific patient phenotypes, such as those with HFpEF. Standardising medical therapy before and after intervention and including contemporary treatments, such as SGLT2 inhibitors, will also be crucial for future research.

Despite these challenges, the current International Alliance to Improve Disease Outcomes global guidelines recommend T-TEER in select patients with TR to improve quality of life and reduce hospitalisations for HF.62

Both US (American Heart Association [AHA]/American College of Cardiology [ACC]) and European (ESC) guidelines suggest that valve surgery should be considered in patients with severe TR if they are undergoing left-sided valve surgery.39,49 The AHA/ACC guidelines recommend that isolated TR surgery should be considered in patients with severe primary TR with right-sided HF symptoms.49 The ESC guidelines advise against isolated TR surgery in the presence of severe RV dysfunction.39

Aortic Stenosis

Pathophysiology

AS is the most prevalent valvular disease in Western countries.63 Many patients with AS and preserved LVEF share the same risk factors and phenotype as those with HFpEF. There is evidence suggesting that common factors, such as systemic inflammation, female sex and obesity, may drive the development of both conditions.5,63 As a result, many HFpEF patients with AS may not be explicitly diagnosed with HFpEF, because AS is often viewed as the primary cause of symptoms, making it an ‘HFpEF-mimicker’ in the clinical setting.63 Within the severe AS population, approximately 40% of patients appear to have HFpEF.64 However, this prevalence may be underestimated, because a larger proportion of AS patients likely have coexisting HFpEF, in addition to a symptomatic AS, as supported by follow-up data from patients undergoing transcatheter aortic valve implantation (TAVI).65,66

Severe AS increases afterload, leading to concentric LV hypertrophy as a compensatory response over time (Figure 3). The LV hypertrophy impairs diastolic relaxation due to elevated wall tension in the LV, which, in turn, raises LA pressures. When HFpEF coexists with AS, a vicious cycle may ensue, with AS exacerbating diastolic dysfunction in an already compromised ventricle.67

Figure 3: Aortic Stenosis in Heart Failure with Preserved Ejection Fraction

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The HFpEF phenotype has been associated with an increased presence of paradoxical low-flow, low-gradient severe AS, which may be due to intrinsic myocardial disease. In AS, the HFpEF phenotype has also been associated with earlier symptom onset at lower gradients, more severe symptoms and greater residual symptoms after TAVI.68,69 It has been postulated that cardiac dysfunction, rather than AS itself, is the primary driver of symptomatology and adverse haemodynamics in this population.69

Management Strategies

Definitive management for AS remains limited to valve replacement due to gaps in understanding the pathophysiology of aortic valve calcification. Although there are no specific management guidelines for patients with combined AS and HFpEF, it is crucial to address both conditions. These patients may also benefit from a different approach with regard to the timing of interventions.

Current guidelines recommend management of hypertension in AS patients, which also overlaps with HFpEF management strategies.49 However, there is an ongoing debate about optimal blood pressure targets in AS, because evidence to support specific goals is lacking. Statins are recommended for primary and secondary prevention in AS patients, although they have not been shown to slow AS progression.70 HFpEF patients who undergo TAVI may benefit from renin–angiotensin system inhibitors and SGLT2 inhibitors.71 One study found that patients with preserved LVEF after TAVI who received renin–angiotensin system inhibitor therapy had lower mortality rates than those who did not, a benefit not observed in patients with reduced LVEF.72 In a recent trial of HF patients with severe AS undergoing TAVI, the majority of whom had HFpEF, SGLT2 inhibitor use was associated with a lower incidence of death or worsening HF.73

There is strong evidence that aortic valve replacement (AVR) lowers mortality and improves symptoms and LVEF among patients with severe AS (Supplementary Table 2).74–77 Guidelines from both European and US societies recommend AVR for select patients with AS, with the choice between TAVI and surgery often based on a heart team’s assessment of individual patient factors.39,49 For patients under 70 years of age with severe, high-gradient, symptomatic AS and low surgical risk, AVR is recommended regardless of LVEF. AVR is also recommended for asymptomatic patients undergoing other cardiac surgeries. For patients with preserved LVEF, AVR is advised if AS is the likely cause of symptoms, especially if symptoms are induced by exercise testing. Despite the growing body of evidence on TAVI, a dedicated meta-analysis of randomised controlled trials specifically examining outcomes in patients with HFpEF is currently lacking.

Aortic Regurgitation

Pathophysiology

AR occurs due to malcoaptation of the aortic valve leaflets, leading to backflow of blood into the LV during diastole. This can be caused by intrinsic valve pathology, such as congenital bicuspid valves, endocarditis or rheumatic disease, or by secondary causes related to dilation of the aortic root or ascending aorta.

The subsequent regurgitant flow increases LV end-diastolic volume, triggering compensatory eccentric hypertrophy and dilatation (Figure 4).78 This chronic volume overload increases LV wall stress and progressively impairs LV diastolic function, leading to elevated LVEDP and subsequent LA pressure elevation and dilation. Over time, this chronic stress promotes myocardial fibrosis, which further exacerbates diastolic dysfunction.74 In patients with HFpEF, the volume and pressure overload from AR are believed to worsen the underlying condition, because AR is an independent marker for worsened outcomes in HFpEF patients.79

Figure 4: Aortic Regurgitation in Heart Failure with Preserved Ejection Fraction

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Management Strategies

Management of AR includes treatment of HF and hypertension because patients with AR often present with these conditions.80 Medications that lower afterload, such as vasodilators, may provide some physiological relief, although they do not replace the need for surgical intervention if AR becomes severe. β-blockers prolong diastole and may increase regurgitant volume and should therefore be used with caution. Surgical intervention remains the primary treatment option for AR, with similar recommendations by the ACC/AHA and ESC for timing and patient selection.39,49

In asymptomatic patients, surgery is generally recommended if LVEF is ≤55% without other causes for LV dysfunction. However, the ESC guidelines recommend a lower threshold for LVEF of ≤50% if surgical risk is low. For patients undergoing cardiac surgery for other reasons, the ACC/AHA guidelines recommend concomitant AVR in the presence of moderate AR, although this is not explicitly recommended by the ESC guidelines. There are no specific recommendations for patients with HFpEF, but because HFpEF patients are more sensitive to LV volume overload, symptoms likely occur earlier than in patients without HFpEF.

Although TAVI is commonly used for AS, it has limitations for AR due to the lack of aortic valve calcification, which in AS creates a landing zone for the TAVI device.80 Without this calcified structure, TAVI placement can be more challenging in AR, increasing the risk of valve misalignment and paravalvular leak. Nevertheless, advances in TAVI technology have improved outcomes, with newer-generation valves showing reduced paravalvular leak and better positioning.81 In the updated ESC guidelines, TAVI may be considered for selected patients with severe AR who are ineligible for surgery.39

Conclusion

VHD is frequently encountered in patients with HFpEF, confounds interpretation of symptoms and severity and shares common risk factors for disease development and progression, including age, hypertension, obesity, metabolic dysfunction, chronic kidney disease and AF.1,2,82 VHD may either contribute to HFpEF as a primary cause due to altered haemodynamics or be a secondary consequence of HFpEF. Due to their higher sensitivity to volume and pressure overload, patients with HFpEF are more likely to experience exacerbated symptoms from VHDs compared to patients in other HF categories. Currently, there are no HFpEF-specific guidelines for managing VHD. However, given their distinct pathophysiology and higher symptom burden, patients with HFpEF may benefit from tailored recommendations, particularly regarding the timing and selection of valvular interventions. Although percutaneous valvular interventions have become the standard of care for patients with severe AS and are increasingly offered to patients with moderate to severe MR, they are also beginning to emerge for patients with TR and AR.

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