From snapshot to trajectory: A multimodality right-heart monitoring framework across the heart failure spectrum

Abstract

Right ventricular (RV) dysfunction, pulmonary vascular load, tricuspid regurgitation, and venous congestion are important determinants of symptoms and outcomes across the heart failure spectrum, yet longitudinal follow-up remains predominantly left ventricle-centered. This narrative review summarizes the physiological and multimodality imaging basis for serial right-heart assessment across HFrEF, HFmrEF, and HFpEF, using SGLT2 inhibition and dapagliflozin as a contemporary mechanistic example rather than the basis for a drug-specific monitoring algorithm.

We propose a pragmatic, therapy-agnostic trajectory framework integrating clinical status, biomarkers, echocardiography, cardiac magnetic resonance, and selective invasive hemodynamics. The approach distinguishes RV dysfunction from overt right-heart failure, incorporates loading conditions, rhythm and tricuspid regurgitation phenotype, and prioritizes serial direction of change over isolated measurements. Emerging SGLT2 inhibitor data provide signals of favorable hemodynamic and RV–pulmonary arterial interaction in selected populations, although dedicated RV-focused randomized evidence remains limited. Suggested reassessment windows are illustrative rather than validated and should be individualized. This framework is intended to complement conventional heart failure assessment and support selective advanced imaging or hemodynamic clarification when clinical and right-heart trajectories are discordant.

1. Introduction

Contemporary heart failure care increasingly emphasizes early implementation of guideline-directed disease-modifying therapy and longitudinal assessment of treatment response across the ejection-fraction spectrum [1], [2]. However, follow-up remains predominantly focused on symptoms, congestion, biomarkers, and left ventricular indices. This may incompletely characterize patients in whom pulmonary vascular load, TR, venous congestion, and RV reserve substantially influence functional limitation, treatment response, and prognosis [3], [4].

RV dysfunction is relevant across HFrEF, HFmrEF, and HFpEF, although its mechanisms and loading conditions differ across phenotypes [3], [5]. Pulmonary venous hypertension, pulmonary vascular remodeling, ventricular interdependence, secondary TR, rhythm disturbance, and advanced biventricular disease may all contribute to the observed right-heart phenotype [3], [5], [6].

Serial assessment should therefore move beyond a single RV measurement and integrate RV performance, pulmonary pressure, RV–PA interaction, congestion, rhythm, and left-heart context. Echocardiography provides the practical first-line platform, while advanced imaging and invasive haemodynamics provide complementary clarification when non-invasive findings are uncertain or management-changing [4], [6].

Importantly, this principle is not specific to a single HF therapy. Changes in loading conditions and clinical trajectory may occur following initiation or intensification of multiple components of guideline-directed therapy [1], [2]. SGLT2 inhibitors—and dapagliflozin in particular—provide a useful contemporary case study because mechanistic, haemodynamic, and exercise-physiology data have begun to explore their effects on the RV–pulmonary vascular unit. Accordingly, this review proposes a therapy-agnostic trajectory-first framework, while critically examining SGLT2 inhibitor evidence as an illustrative example rather than as justification for a drug-specific monitoring protocol.

2. Why the right heart matters across the heart failure spectrum

The rationale for monitoring the right heart during HF treatment is both physiological and clinical. The RV is highly afterload-sensitive, and relatively modest changes in pulmonary vascular load may result in substantial changes in RV performance, functional capacity, and prognosis [3], [5], [6]. The relevance of RV dysfunction is not confined to HFpEF; impaired RV performance is associated with adverse physiology and outcomes across HF phenotypes [3], [5].

Interpretation of RV change requires particular attention to loading conditions and TR. TR may result from primary leaflet disease, pulmonary hypertension and RV remodeling with ventricular annular dilation, or predominantly atrial/annular remodeling, particularly in atrial fibrillation [4], [7], [8]. These phenotypes can materially influence RV systolic indices and estimation of pulmonary pressure. Left-sided filling pressures, diastolic function, chamber geometry, and concomitant valvular disease should therefore remain part of the physiological context in which the right heart is interpreted [9], [10].

Serial echocardiographic comparison should use standardized acquisition and measurement techniques. Contemporary right-heart guidance supports a multiparametric assessment rather than reliance on a single RV measurement [4], while standardized chamber quantification and deformation-imaging methodology remain important for reproducible longitudinal comparisons [10], [11].

This is particularly relevant in HFpEF, where resting haemodynamics may underestimate exertional filling pressures, pulmonary vascular load, and impairment of RV reserve [12], [13]. The objective is therefore not to identify one universally “normal” number, but to determine whether the patient's right-heart phenotype is moving in a favorable, stable, or adverse direction.

3. Physiological and methodological foundations: loading conditions, TR phenotype, and RV–PA coupling

A useful conceptual anchor for longitudinal right-heart follow-up is RV–PA coupling, which reflects how effectively RV contractile performance adapts to pulmonary arterial load [3], [5]. Although invasive pressure–volume-derived coupling is physiologically more complete, it is not practical for routine serial care. TAPSE/sPAP remains a pragmatic non-invasive surrogate with prognostic value in HF, but it should be interpreted alongside its individual components and the clinical context rather than as an isolated treatment threshold [4], [5].

Serial interpretation must explicitly account for preload, afterload, rhythm, and TR mechanism and severity [4], [7], [8]. In severe TR, changes in TAPSE, RV fractional area change, strain, and Doppler-derived sPAP may not reliably represent true improvement or deterioration in RV–PA interaction. Similarly, changes in left-sided filling pressure and volume status can alter pulmonary load without representing structural RV remodeling [6], [9].

RV dysfunction and right-heart failure should not be used interchangeably. RV dysfunction describes impaired RV mechanical performance, whereas right-heart failure is a clinical syndrome characterized by inadequate forward flow and/or systemic venous congestion. RV dysfunction may therefore exist without overt right-heart failure, while improvement in edema or congestion after treatment does not necessarily establish structural RV reverse remodeling [3].

Two practical principles follow. First, rhythm, heart rate, blood pressure, volume status, TR severity, and image quality should be documented at each meaningful serial assessment [4], [7], [10], [11]. Second, directional trajectories should be favored over interpretation of small isolated changes, particularly when values lie close to measurement variability. The framework therefore begins with a reproducible baseline anchor followed by clinically appropriate reassessment. Suggested time windows described below are pragmatic examples rather than prospectively validated or mandatory intervals.

3.1. SGLT2 inhibition as an illustrative case study: what the right-heart evidence does—and does not—show

Large outcome trials establish the clinical benefit of dapagliflozin across HFrEF and HFmrEF/HFpEF [14], [15], with pooled patient-level data supporting benefit across the range of ejection fraction [16]. However, these studies were not designed to demonstrate RV reverse remodeling, and their clinical outcome benefits should not be interpreted as direct evidence of a right-heart-specific treatment effect.

More focused mechanistic studies provide a stronger physiological signal. PRESERVED-HF demonstrated early improvement in symptoms and functional limitation in HFpEF [17], while CAMEO-DAPA demonstrated favorable changes in filling pressures and exercise haemodynamics [18]. More directly relevant to the present framework, Reddy et al. reported improved exercise RV–pulmonary vascular interaction following dapagliflozin in HFpEF [19]. Remote PA-pressure monitoring has also demonstrated reductions in pulmonary artery pressure following dapagliflozin initiation, providing a complementary longitudinal haemodynamic signal [20].

Evidence outside conventional acquired LV-dominant HF further illustrates both potential benefit and the limitations of extrapolation. In the prospective DAPA-SRV study of symptomatic patients with a systemic RV, dapagliflozin was associated with improvements in functional capacity, quality of life, fractional area change, and systemic RV longitudinal strain at 6 months, although the study was small, single-center, and non-randomized [21]. Conversely, a CMR analysis from EMPA-HEART CardioLink-6 found no significant effect of empagliflozin on RV mass, RV volumes, or RVEF over 6 months in patients with type 2 diabetes and coronary disease [22]. These neutral findings are important and argue against assuming uniform RV reverse remodeling as a class effect.

Taken together, current evidence supports biological plausibility and provides selected signals of favorable haemodynamic or RV–PA effects, but it does not validate a dapagliflozin-specific RV monitoring algorithm, imaging threshold, or reassessment interval. Evidence from empagliflozin or other SGLT2 inhibitors should be used to inform class-level biological context rather than presented as direct dapagliflozin-specific evidence. The proposed framework is therefore therapy-agnostic and is not intended to guide dapagliflozin dose titration.

A concise synthesis of the principal mechanistic and clinical signals relevant to RV–PA monitoring is provided in Table 2.

Table 2.

Selected SGLT2 inhibitor evidence relevant to right-heart and pulmonary vascular physiology.

Study	Population	Right-heart/PA signal	Important limitation	Interpretation
DAPA-HF [14]	HFrEF	Reduced HF events	RV remodeling not a primary endpoint	Supports clinical efficacy, not direct RV remodeling
DELIVER [15]/pooled DAPA-HF–DELIVER [16]	HFmrEF/HFpEF and broad EF spectrum	Consistent clinical benefit	No dedicated RV endpoint	Supports therapy across EF spectrum
PRESERVED-HF [17]	HFpEF	Improved symptoms/function	Not an RV-remodeling trial	Supports early clinical response
CAMEO-DAPA [18]	HFpEF	Improved filling pressures/exercise haemodynamics	Small mechanistic study	Supports haemodynamic plausibility
Reddy et al. [19]	HFpEF	Improved exertional RV–PA interaction	Secondary analysis; selected population	Most direct acquired-HF RV–PA signal
Mullens et al. [20]	HF with implantable PA sensor	Reduction in PA pressure	Small observational cohort	Continuous pulmonary-load signal
DAPA-SRV [21]	Symptomatic systemic RV dysfunction	Improved FAC and RV strain	Small, single-center, non-randomized	Supportive but not generalizable to acquired HF
Sarak et al. [22]	T2DM + CAD	No significant change in RV mass, volumes or RVEF	Post-hoc CMR analysis; normal baseline RV	Important neutral evidence

Abbreviations: CKD, chronic kidney disease; EF, ejection fraction; HF, heart failure; HFmrEF, heart failure with mildly reduced ejection fraction; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; PA, pulmonary artery; RV, right ventricle.

3.2. A practical therapy-agnostic trajectory framework

The proposed therapy-agnostic, trajectory-first approach is summarized in Fig. 1. The purpose of this framework is not to prescribe a drug-specific imaging schedule, but to standardize how right-heart and pulmonary vascular signals may be incorporated into comprehensive HF follow-up after clinically meaningful treatment initiation or intensification. Baseline assessment should establish the HF phenotype, loading conditions, and a reproducible right-heart profile incorporating TAPSE, RV fractional area change, RV free-wall strain when feasible, sPAP, and TAPSE/sPAP, together with TR severity, RA/IVC findings, rhythm, heart rate, blood pressure, and volume status [4], [5], [7], [10], [11]. A practical minimum serial reporting set is outlined in Table 1.

Fig. 1.

Proposed therapy-agnostic trajectory-first framework for serial right-heart assessment in heart failure. Suggested reassessment timing is illustrative and should be individualized according to clinical status and phenotype.

Table 1.

Minimum multidomain dataset for trajectory-based heart failure monitoring.

Domain	Core variables (minimum set)	Why it matters	Serial reporting recommendation	Key caveats
Left-heart context	LVEF; LV volumes when relevant; E/e′; LAVI; MR severity	Defines HF phenotype and left-sided contribution to pulmonary/RV loading	Interpret alongside right-heart assessment when clinically relevant	Not every variable requires repetition at every visit
RV systolic performance	TAPSE; RV FAC; S′; RV free-wall longitudinal strain (RVfwLS), if feasible	Captures complementary longitudinal and global RV systolic function	Report absolute values and directional change from baseline	Load-dependent; image quality and strain methodology affect reproducibility
Pulmonary vascular load	sPAP derived from TR jet; TR velocity when reliable	Provides a practical non-invasive estimate of RV afterload	Report with TR signal quality and clinical/loading context	May be unreliable with poor TR envelope, severe TR, or changing volume status
RV–PA coupling	TAPSE/sPAP; optional RVfwLS/sPAP in experienced laboratories	Integrates RV performance relative to pulmonary load	Report absolute value and change from baseline	Error in either component may propagate into the ratio; not a treatment threshold
Right-heart failure/congestion	RA area/volume; IVC size/collapsibility; JVP; peripheral edema; ascites; weight; diuretic requirement	Distinguishes isolated RV dysfunction from clinically overt right-heart failure and systemic congestion	Document together with symptoms and biomarkers at meaningful reassessments	Highly preload-dependent; improvement in congestion does not necessarily indicate RV reverse remodeling
Tricuspid valve context	TR severity and, where feasible, mechanism/phenotype	TR materially affects RV loading, RV measurements, and sPAP interpretation	Grade TR at each serial echocardiographic reassessment	Primary, ventricular-functional, and atrial-functional TR should not be considered equivalent
Rhythm and haemodynamic context	Sinus rhythm/AF; heart rate; blood pressure	Provides essential context for comparison between studies	Document at every imaging timepoint	Rhythm or rate changes may substantially alter apparent trajectory
Biomarker/renal context	NT-proBNP; creatinine/eGFR; ± hs-cTn when clinically relevant	Helps contextualize congestion, cardiorenal interaction, and apparent imaging change	Align laboratory assessment with major clinical/imaging reassessments when available	Biomarkers are non-specific and should not be interpreted in isolation
Clinical trajectory	NYHA class; dyspnea/exercise tolerance; recurrent HF events; volume status	Anchors imaging changes to patient-level clinical response	Record at baseline and each meaningful reassessment	Clinical and imaging trajectories may be discordant

The proposed dataset is intended to support structured longitudinal assessment rather than mandate repetition of every variable at every visit. Selection and timing should be individualized according to HF phenotype, clinical stability, treatment changes, image quality, and whether the result is expected to influence management. CMR or invasive haemodynamics should be reserved for selective clarification of uncertain or discordant trajectories rather than routine serial assessment.

Abbreviations: AF, atrial fibrillation; FAC, fractional area change; hs-cTn, high-sensitivity cardiac troponin; IVC, inferior vena cava; NT-proBNP, N-terminal pro-B-type natriuretic peptide; PA, pulmonary artery; RA, right atrium; RV, right ventricle; RVfwLS, right ventricular free-wall longitudinal strain; sPAP, systolic pulmonary artery pressure; TAPSE, tricuspid annular plane systolic excursion; TR, tricuspid regurgitation.

In clinically stable outpatients, an early reassessment at approximately 8–12 weeks may represent a pragmatic illustrative window for evaluating directional change following major treatment initiation or intensification. This timing is not prospectively validated and should not be considered mandatory. Early symptomatic and haemodynamic effects have been observed within weeks to months in mechanistic SGLT2 inhibitor studies [17], [18], [19], [20], but the appropriate timing of imaging should be individualized according to phenotype, clinical stability, congestion, treatment changes, and local practice.

A later reassessment around 6 months may help determine whether an initially favorable or discordant signal persists; again, this represents an illustrative rather than validated interval. Six-month imaging has been used in mechanistic RV studies [21], [22], but patients with clinical deterioration, recurrent congestion, suspected pulmonary hypertension progression, or acute right-heart failure should be reassessed substantially earlier as clinically indicated. A streamlined implementation dataset for longitudinal audit and pathway governance is summarized in Table 3.

Table 3.

Illustrative reassessment windows and escalation triggers for trajectory-based monitoring.

Time point	Primary aim	Minimum reassessment components	Favorable trajectory — example	Escalation/action triggers
Baseline (T0)	Establish phenotype, loading context, and anchor values	Clinical status; BP/HR; renal function; NT-proBNP if available; echocardiographic minimum dataset (Table 1)	Not applicable — anchor assessment	Poor echo quality; uncertain phenotype; suspected clinically significant/disproportionate PH; consider advanced testing if results would change management
Early reassessment — illustrative window (∼8–12 weeks in clinically stable patients)	Detect directional change after major treatment initiation or intensification	Symptoms/functional status; congestion markers; NT-proBNP if available; repeat echo minimum dataset using the same methodology	Concordant improvement in symptoms/congestion with stable or improving RV performance and/or RV–PA coupling	Worsening symptoms; recurrent congestion; deterioration in RV performance/coupling; major clinical–imaging discordance
Later reassessment — illustrative window (∼6 months)	Assess persistence of trajectory and refine subsequent follow-up	Repeat clinical, biomarker, and echocardiographic assessment; review trajectory from baseline	Sustained favorable clinical and RV trajectory; stable/improving loading conditions; no recurrent decompensation	Persistent limitation despite apparent euvolaemia; worsening RV trajectory; uncertain pulmonary vascular phenotype; recurrent HF admissions
Ongoing individualized follow-up	Maintain surveillance and detect trajectory drift	Reassessment frequency individualized according to HF phenotype, clinical trajectory, risk, and prior findings (clinical ± biomarkers ± echocardiography)	Stable symptoms and serial physiological/imaging measures	New symptoms; rising natriuretic peptides; recurrent congestion; worsening TR; declining RV function; unexplained clinical deterioration
Escalation pathway — when triggered	Improve diagnostic certainty and align treatment with mechanism	CMR for RV volumes/RVEF when clarification is needed; invasive haemodynamics ± exercise when PH mechanism or filling pressures remain uncertain; CPET in selected patients	Clarification of mechanism allowing targeted management	Reserve advanced testing for situations in which results are expected to clarify mechanism or change management

The proposed intervals are pragmatic examples and are not prospectively validated or mandatory. Reassessment timing should be individualized according to HF phenotype, clinical stability, treatment changes, congestion, and risk. Earlier assessment is appropriate with clinical deterioration, recurrent congestion, suspected PH progression, acute right-heart failure, or major clinical–imaging discordance.

Abbreviations: BP, blood pressure; CMR, cardiac magnetic resonance; CPET, cardiopulmonary exercise testing; HR, heart rate; NT-proBNP, N-terminal pro-B-type natriuretic peptide; PH, pulmonary hypertension; RV, right ventricle; RVEF, right ventricular ejection fraction; TR, tricuspid regurgitation.

3.3. Interpreting trajectories and integrating biomarkers, imaging, and context

A multidomain interpretation framework integrating left-heart context, RV performance, pulmonary vascular load, RV–PA coupling, congestion/TR, and biomarker/renal status is shown in Fig. 2. The purpose of this overlay is to reduce over-reading of small echo shifts and to support clinically coherent decision-making when imaging and symptoms diverge. In routine practice, minor changes in right-heart indices are common and often reflect altered loading conditions rather than true structural or functional remodeling. Integrating biomarker context (e.g., NT-proBNP and, where appropriate, hs-cTn), symptom evolution, and volume status improves the likelihood that observed imaging changes are interpreted correctly.

Fig. 2.

Multidomain heart failure trajectory dashboard integrating left-heart phenotype, RV performance, RV–PA coupling, congestion/TR, and clinical/biomarker context. CMR and invasive haemodynamics are reserved for selective confirmation when clinically relevant.

This approach is particularly useful in patients with fluctuating congestion, atrial fibrillation, obesity, chronic kidney disease, or complex pulmonary comorbidity, where single-domain interpretation is often misleading. A trajectory-first model therefore prioritizes consistency of acquisition, context-rich reporting, and repeated assessments under reasonably comparable conditions rather than rigid dependence on one variable or threshold. In this sense, the framework is designed to support clinical judgement, not replace it. Right-heart trajectories should never be interpreted in isolation from the left heart. Serial assessment should incorporate the underlying HF phenotype and, where clinically relevant, LVEF, LV volumes, diastolic indices, left atrial size, mitral regurgitation, natriuretic peptides, renal function, blood pressure, rhythm, and volume status [1], [2], [9], [10]. The framework therefore adds a structured right-heart dimension to comprehensive HF follow-up rather than creating a parallel RV-only pathway.

3.4. When to escalate beyond echocardiography

Escalation beyond echocardiography should be considered when persistent limitation coexists with discordant trajectories, when coupling-oriented indices worsen despite apparent euvolaemia, when pulmonary hypertension phenotype remains uncertain, or when echocardiographic quality is insufficient for confident serial interpretation (e.g., severe tricuspid regurgitation, obesity, poor acoustic windows, or inadequate TR jet for sPAP estimation). Illustrative examples of favorable, discordant, and progressive trajectories and their implications are shown in Fig. 3.

Fig. 3.

Hypothetical examples illustrating favorable, discordant, and progressive right-heart trajectories. Numerical values are illustrative and are not proposed treatment thresholds.

CMR is particularly useful when precise RV volumes, RVEF, or flow quantification are required, when echocardiographic measurements are internally inconsistent, or when confirmation of RV remodeling would materially influence management [23], [24]. Serial CMR should use standardized acquisition and analysis approaches to preserve longitudinal comparability.

Interpretation of coupling-oriented echocardiographic surrogates also requires caution in severe tricuspid regurgitation or unstable loading states, where apparent changes may misrepresent true RV–PA interaction if regurgitation severity and preload/afterload context are not integrated into the report [7], [8]. In such settings, escalation is often less about obtaining “more data” and more about obtaining data with greater interpretive reliability.

When the pulmonary hypertension phenotype is uncertain, hemodynamic classification should follow contemporary definitions and guideline frameworks [6], [25]. Standardized assessment of TR and LV diastolic function is essential because both materially influence interpretation of RV loading and Doppler-derived pulmonary pressure estimates [7], [9]. When symptoms remain disproportionate to resting findings, cardiopulmonary exercise testing may help define the dominant limitation mechanism and guide further investigation [26]. Where HFpEF itself remains diagnostically uncertain, established diagnostic algorithms can support phenotyping and determine whether exercise or invasive hemodynamic assessment is appropriate [27].

4. Future directions and implementation challenges

The next phase of work in this field should focus on making right-heart monitoring both physiologically grounded and scalable. RV biology and RV failure mechanisms continue to support a coupling-focused monitoring philosophy, but they also underscore the need for reproducible, clinically deployable metrics that perform well outside expert laboratories [28], [29]. In parallel, HFpEF is increasingly recognized as a systemic, comorbidity-driven syndrome with heterogeneous substrates and phenogroups, and this heterogeneity argues against a one-size-fits-all monitoring strategy based solely on ejection fraction labels [30], [31], [32]. Monitoring targets are more likely to be clinically useful when they are aligned with the dominant mechanism in an individual patient (e.g., pulmonary vascular load, congestion vulnerability, chronotropic limitation, renal congestion, or mixed cardiopulmonary drivers).

Implementation science is equally important. Trajectory-based monitoring should align with modern heart failure definitions and auditable care pathways, including consistent phenotype labels, standardized reassessment windows, and clear escalation logic that can be applied across care settings rather than only in specialist centers [33]. This is particularly relevant if right-heart monitoring is to move from a niche expert practice to a reproducible component of mainstream heart failure follow-up.

Finally, when disproportionate pulmonary arterial hypertension is suspected—especially in congenital heart disease-associated PAH—or when follow-up risk stratification directly influences therapy intensity, referral to specialist pathways remains essential. In these contexts, validated PAH risk frameworks and disease-specific expertise should guide decisions beyond the scope of a general heart failure monitoring pathway [34], [35].

5. Limitations

Several limitations should be emphasized. First, the proposed trajectory framework is conceptual and has not been prospectively validated as a treatment-response or escalation algorithm. Second, evidence linking specific HF therapies to serial RV remodeling remains heterogeneous; for SGLT2 inhibitors, direct RV-focused evidence is considerably smaller than the evidence supporting their overall clinical benefit [14], [15], [16], [17], [18], [19], [20], [21], [22]. Third, echocardiographic RV and RV–PA coupling indices remain load- and technique-dependent and should not be interpreted independently of TR, rhythm, pulmonary pressure estimation, and volume status [4], [5], [7], [8]. Fourth, access to CMR and invasive haemodynamics varies across centers. Finally, the suggested reassessment windows are pragmatic examples rather than evidence-based mandatory intervals. Prospective studies should determine whether structured right-heart trajectory monitoring improves clinical decision-making or outcomes beyond contemporary guideline-based HF follow-up.

6. Conclusion

Right-heart assessment in heart failure should evolve from isolated measurements toward structured longitudinal interpretation. A trajectory-first framework integrating RV performance, pulmonary vascular load, RV–PA coupling, TR, congestion, biomarkers, and left-heart context may improve phenotypic characterization across the HF spectrum. Emerging SGLT2 inhibitor data provide an important contemporary example of this concept but do not currently justify a drug-specific monitoring algorithm. Echocardiography should remain the practical first-line tool, with CMR and invasive haemodynamics reserved for selected patients with uncertain or discordant trajectories. Prospective validation is needed to determine whether this approach improves clinical decision-making and outcomes.

CRediT authorship contribution statement

Arif Albulushi: Writing – original draft, Supervision, Conceptualization. Mohammed Al Habsi: Visualization, Methodology. Amira Al-Kharusi: Validation, Formal analysis.

Consent

All information discussed is derived from previously published literature. Ethical approval and informed consent were therefore not applicable.

Ethical approval and consent to participate

This manuscript is a narrative review based exclusively on previously published studies and publicly available data. No new human participants were recruited, and no individual patient-level data were collected or analyzed by the authors. Therefore, institutional review board or ethics committee approval and informed consent were not required for this work.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Data availability

This review did not involve direct patient contact, new data collection, or access to identifiable personal data.