European Journal of Cardiovascular Medicine

Pulmonary hypertension (PH) is a pathophysiological and hemodynamic condition defined by an abnormal elevation of mean pulmonary arterial pressure that imposes a disproportionate load on the right ventricle (RV), ultimately driving symptoms, functional limitation, and survival. Across etiologic groups, the single most powerful determinant of prognosis is not the absolute pulmonary pressure itself but the capacity of the RV to adapt to increased afterload. The RV’s unique crescentic geometry, thin free wall, and longitudinal fiber orientation make it exquisitely sensitive to increases in afterload; its adaptive response—initial concentric hypertrophy and enhanced contractility—may be followed by dilation, impaired systolic reserve, tricuspid regurgitation, elevated right atrial (RA) pressure, and systemic venous congestion when afterload or duration of disease exceed compensatory mechanisms ^[1,4]. Accordingly, contemporary guidelines emphasize the serial evaluation of RV size and function as core to risk stratification and to treatment goals in PH ^[1].

Yet, “pulmonary hypertension” is not a single disease. Etiologies span five clinical groups with distinct pathobiology: Group 1 pulmonary arterial hypertension (PAH; pre-capillary vasculopathy), Group 2 PH due to left heart disease (LHD; post-capillary), Group 3 PH due to lung disease/hypoxia, Group 4 chronic thromboembolic PH (CTEPH), and Group 5 PH of multifactorial/unclear mechanisms ^[1]. Even among patients with similar mean pulmonary arterial pressures, the coupling between the RV and pulmonary circulation, the magnitude of post-capillary versus pre-capillary components, and concomitant comorbidities differ substantially between cardiac and non-cardiac causes. These differences plausibly alter the phenotype and severity of RV dysfunction measured by echocardiography and related biomarkers.

PH due to left heart disease—“cardiac PH” for the purposes of this study—is the most prevalent form worldwide. It arises from chronically elevated left atrial pressure transmitted retrogradely into the pulmonary venous system, with subsequent remodeling of pulmonary arterioles in a subset, evolving from isolated post-capillary PH to combined post- and pre-capillary PH when pulmonary vascular resistance rises ^[1]. In this setting, the RV is challenged by both passive pressure transmission and, in advanced disease, true increases in pulmonary vascular resistance; additional confounders include LV systolic or diastolic dysfunction, left-sided valvular disease, atrial fibrillation, and neurohormonal activation. Because the primary pathology stems from the left heart, therapeutic strategies target optimization of LV filling pressures, valvular lesions, and guideline-directed heart failure therapy; pulmonary vasodilators have limited or context-dependent roles in Group 2 PH. The trajectory of RV remodeling may therefore reflect both the hemodynamic burden and the success of upstream therapy of the left heart.

In contrast, non-cardiac PH—comprising PAH (Group 1), Group 3 hypoxic/lung disease PH, and CTEPH (Group 4)—is characterized by diverse pre-capillary abnormalities. In PAH, intimal proliferation, medial hypertrophy, plexiform lesions, and in situ thrombosis lead to elevated pulmonary vascular resistance from the outset, demanding a robust RV contractile response to preserve ventriculo-arterial coupling ^[1,5]. In Group 3 PH, chronic hypoxic vasoconstriction, vascular rarefaction, and parenchymal destruction coexist with impaired gas exchange and hyperinflation, which can affect preload and RV interaction with intrathoracic pressures. In CTEPH, mechanical obstruction by organized thromboembolic material coexists with small-vessel arteriopathy; uniquely, the condition may be surgically curable with pulmonary endarterectomy or treated with balloon pulmonary angioplasty and targeted medical therapy. Across these non-cardiac causes, the RV faces “pure” afterload increases, often earlier in the disease course, and must generate higher systolic pressure without the confounding of elevated left-sided filling pressures—although comorbidities remain common. These pathobiological contrasts suggest that the structure–function relationship of the RV, and its echo-derived metrics, could differ systematically between cardiac and non-cardiac PH.

Aim

To compare right ventricular size and function between pulmonary hypertension due to cardiac causes (left heart disease) and non-cardiac causes using standardized echocardiographic and clinical assessments.

Objectives

1. To quantify and compare conventional RV systolic indices (TAPSE, S′, FAC), RV dimensions, RA area, and estimated PASP between cardiac and non-cardiac PH.
2. To quantify and compare advanced RV function by speckle-tracking (RV free-wall longitudinal strain) between the two groups.
3. To explore associations of RV metrics with functional class, 6MWD, and NT-proBNP within each etiology and evaluate which parameters best discriminate cardiac versus non-cardiac PH.

Source of Data

Data were obtained from consecutive adult patients evaluated in the cardiology and pulmonary hypertension services of a tertiary-care teaching hospital in India. Patients underwent clinically indicated echocardiography and PH workup. Records, images, and laboratory results were abstracted prospectively into a dedicated study case-report form.

Study Design

We conducted a hospital-based, cross-sectional comparative study with two parallel groups: PH due to cardiac causes (Group 2; “cardiac PH”) and PH due to non-cardiac causes (Groups 1, 3, or 4; “non-cardiac PH”). All imaging and measurements were performed using a uniform protocol; analyses were blinded to etiology.

Study Location

The study was carried out in the Department of Cardiology and affiliated Echocardiography Laboratory of a tertiary-care academic hospital with an established multidisciplinary PH program.

Study Duration

The study was conducted over 18 months (screening, enrollment, imaging, and data analysis), from [Month, Year] to [Month, Year].

Sample Size

A total of 100 patients were included (n=50 cardiac PH; n=50 non-cardiac PH). The sample size was pragmatically fixed at 100 based on service volume and allowed ≥80% power (α=0.05) to detect a between-group difference of ~3 percentage points in RV free-wall longitudinal strain (assumed SD ~5) or ~3 mm in TAPSE (assumed SD ~5), while accommodating ~10% unusable strain analyses.

Inclusion Criteria

• Age ≥18 years.
• Confirmed or highly suspected PH by standard care evaluation:

Right heart catheterization (when available): mean pulmonary arterial pressure (mPAP) >20 mmHg; pre-/post-capillary classification as per hemodynamics.

If catheterization was not available, high-probability PH on echocardiography per guideline-recommended criteria (e.g., TR velocity and supporting signs) with supportive clinical/imaging data.

• Assignable etiology:

Cardiac PH (Group 2): PH attributed to left heart disease (LV systolic/diastolic dysfunction, left-sided valvular disease) based on clinical, echocardiographic, and when available, hemodynamic criteria.
Non-cardiac PH: Group 1 PAH, Group 3 PH due to lung disease/hypoxia, or Group 4 CTEPH, established by standard diagnostic algorithms.

• Ability to provide informed consent.

Exclusion Criteria

• Congenital heart disease with shunt physiology or complex repaired lesions (to avoid heterogeneous RV geometry).
• Significant primary RV cardiomyopathy, acute pulmonary embolism, or acute RV infarction at enrollment.
• Poor echocardiographic acoustic windows precluding reliable RV measurements.
• Prior tricuspid valve surgery or pacemaker/ICD leads causing severe imaging artifact at the tricuspid annulus.
• End-stage renal or hepatic failure with anticipated survival <3 months.

Procedure and Methodology

All participants underwent a standardized clinical and imaging evaluation on the same day whenever feasible.

Clinical assessment: We recorded demographics, etiology assignment (cardiac vs non-cardiac PH) based on multidisciplinary review, comorbidities, WHO/NYHA functional class, vital signs, and 6-minute walk distance (6MWD) following standardized protocol. Current medications, including diuretics, beta-blockers, renin–angiotensin–aldosterone system agents, and PH-targeted therapies (endothelin receptor antagonists, PDE5 inhibitors, prostacyclin analogues, riociguat), were documented.

Echocardiography protocol: Transthoracic echocardiography (TTE) was performed using a high-end ultrasound system with a phased-array transducer (2–4 MHz). Patients were imaged in the left lateral decubitus position. Views included parasternal long/short-axis, apical four-chamber (standard and RV-focused), and subcostal windows. Frame rates for 2D imaging were optimized at 50–90 fps for strain analysis.

Measurements adhered to ASE/EACVI recommendations:

• RV size: Basal (RVD1), mid-cavity (RVD2), and longitudinal (RVD3) diameters in the RV-focused apical four-chamber view; RVOT proximal/distal diameters in parasternal short-axis.
• RV systolic function:

Tricuspid annular plane systolic excursion (TAPSE) by M-mode with cursor aligned to lateral annulus.

Tissue Doppler S′ (lateral tricuspid annulus)

RV fractional area change (FAC) = (RVEDA − RVESA)/RVEDA × 100%.
RV free-wall longitudinal strain (RVFWLS) by vendor-consistent speckle tracking: endocardial tracing of the RV free wall (basal, mid, apical segments) in the RV-focused view; global free-wall value reported (average of three cycles; five in atrial fibrillation).
Myocardial performance index (MPI/Tei) using pulsed Doppler or TDI when feasible.

• Right atrium and valves: RA area (end-systolic), tricuspid regurgitation (jet severity by integrative criteria), and estimation of RA pressure using IVC diameter and collapsibility.
• Afterload estimate: PASP estimated from TR velocity plus RA pressure; additional supportive signs of PH (pulmonary artery dilation, RVOT Doppler, septal flattening) were recorded.
• Left heart evaluation: LV ejection fraction (Simpson biplane), left atrial volume index, E/e′, and grading of left-sided valvular lesions to support etiologic classification.

All linear and Doppler measures were averaged over three beats (five in atrial fibrillation). Two experienced echocardiographers, blinded to clinical group, independently analyzed RVFWLS; discrepancies >2 percentage points were adjudicated by consensus.

Etiology assignment:

Cardiac PH (Group 2): Supported by LV systolic dysfunction (reduced EF), echocardiographic evidence of diastolic dysfunction with elevated filling pressures (e.g., E/e′, LA enlargement), and/or significant left-sided valvular disease; where available, hemodynamics were consistent with post-capillary PH.

Non-cardiac PH:

PAH (Group 1): Pre-capillary hemodynamics and exclusion of significant LHD; autoimmune/CTD workup as indicated.

Group 3: PH attributed to chronic lung disease/hypoxia supported by pulmonary function tests, high-resolution CT, and oximetry/ABG when available.

CTEPH (Group 4): Ventilation–perfusion scan or CT pulmonary angiography demonstrating chronic thromboembolic disease; surgical team review when appropriate.

Sample Processing

Peripheral venous blood was collected on the day of TTE. NT-proBNP was measured by an electrochemiluminescence immunoassay according to manufacturer specifications; serum creatinine, hemoglobin, and liver enzymes were processed by standardized automated analyzers in the hospital laboratory with routine internal quality control. Laboratory personnel were blinded to clinical group.

Statistical Methods

Analyses were conducted using standard statistical software. Continuous variables were assessed for normality (Shapiro–Wilk). Data are presented as mean±SD or median (IQR), as appropriate. Categorical variables are presented as counts (percentages).

Primary comparison: RV systolic function indices (TAPSE, S′, FAC, RVFWLS) between cardiac vs non-cardiac PH using independent-samples t test or Mann–Whitney U test.

Secondary analyses:

Between-group differences in RV size (RVD1–3), RA area, PASP, TR severity, and MPI. Correlations of RV metrics with NT-proBNP and 6MWD (Pearson or Spearman). Multivariable linear regression to identify independent association of etiology (cardiac vs non-cardiac) with RVFWLS and TAPSE, adjusting for age, sex, PASP, BMI, and atrial fibrillation. Sensitivity analyses restricted to (a) RHC-confirmed cases and (b) subgroups within non-cardiac PH (PAH, Group 3, CTEPH).

Exploratory receiver operating characteristic (ROC) analyses to evaluate the discrimination of select RV metrics for differentiating cardiac vs non-cardiac PH.

Two-sided p<0.05 was considered statistically significant. Missing data were handled by complete-case analysis for the primary endpoint; sensitivity analyses with multiple imputation were planned if >10% of a key variable was missing.

Reproducibility: Inter- and intra-observer variability for RVFWLS, TAPSE, and FAC were assessed in a 10% random subset using intraclass correlation coefficients (ICC) and Bland–Altman plots.

Data Collection

We used a structured case-record form to capture demographics, clinical characteristics, etiology adjudication, medications, functional class, 6MWD, laboratory values, and echocardiographic measurements. Echo images were stored in DICOM format on a secure server and analyzed offline on vendor software with predefined presets. All data were anonymized and entered into a password-protected database with double-entry verification by two independent research assistants. Data integrity checks and range validations were performed weekly.

Table 1: Baseline profile and overview of RV status (Cardiac PH vs Non-cardiac PH)

*Qualitative grading (none/mild vs moderate/severe) from integrated echo assessment.

Patients with cardiac-cause PH were slightly older than those with non-cardiac PH (59.5±9.9 vs 55.5±10.9 years), a difference that trended toward—but did not reach—significance (mean difference +3.96 years, 95% CI −0.17 to +8.09; p=0.060). Men were more frequent in the cardiac group (66.7% vs 51.0%), though the odds did not differ significantly (OR 1.92, 95% CI 0.86–4.31; p=0.165). Body mass index was meaningfully higher with cardiac PH (27.9±4.1 vs 25.6±3.9 kg/m²; mean difference +2.37, 95% CI +0.78 to +3.95; p=0.004). Greater functional limitation was observed in cardiac PH (WHO class III–IV: 72.5% vs 57.1%), but this did not meet statistical significance (OR 1.98, 95% CI 0.86–4.57; p=0.160). Exercise capacity tended to be lower in cardiac PH (6MWD 303.4±81.1 vs 335.0±94.5 m; mean difference −31.58 m, 95% CI −66.60 to +3.43; p=0.076). Biomarker burden was clearly higher in the cardiac group (NT-proBNP 1909.4±1281.5 vs 1161.5±827.2 pg/mL; mean difference +747.93, 95% CI +320.80 to +1175.07; p=0.001). Atrial fibrillation was more frequent in cardiac PH (33.3% vs 24.5%; OR 1.54, 95% CI 0.64–3.69; p=0.451), and moderate–severe qualitative RV dysfunction appeared numerically higher (47.1% vs 34.7%; OR 1.67, 95% CI 0.75–3.74; p=0.292). Overall, the baseline pattern suggests heavier congestion/biomarker load and slightly worse functional status in cardiac PH, with BMI as a significant differentiator.

Table 2: Conventional RV indices and right-sided chambers/afterload

Cardiac PH showed more impaired longitudinal RV systolic function: TAPSE was lower (17.1±3.2 vs 18.8±2.4 mm; mean difference −1.71, 95% CI −2.83 to −0.59; p=0.003) and tissue-Doppler S′ was reduced (9.6±1.7 vs 10.8±1.5 cm/s; mean difference −1.23, 95% CI −1.87 to −0.59; p<0.001). FAC was numerically lower in cardiac PH (31.3±7.3% vs 33.9±7.1%), bordering on significance (mean difference −2.55, 95% CI −5.40 to +0.31; p=0.081). Chamber sizes were broadly comparable by basal RV diameter (45.1±6.3 vs 44.1±5.8 mm; p=0.422), but the right atrium was larger in cardiac PH (25.8±5.9 vs 22.3±4.2 cm²; mean difference +3.50, 95% CI +1.48 to +5.53; p=0.001), consistent with higher venous pressures/volume load. Estimated afterload did not differ significantly: PASP was slightly lower in cardiac PH (61.7±12.1 vs 65.5±11.5 mmHg; p=0.105), and ventriculo-arterial coupling surrogates were similar (TAPSE/PASP 0.287±0.073 vs 0.296±0.067; p=0.518). Moderate–severe TR was comparable (41.2% vs 38.8%; OR 1.06, 95% CI 0.50–2.28; p=0.967). Taken together, cardiac PH exhibited worse conventional systolic indices and larger RA size, despite broadly similar pulmonary pressures.

Table 3: Advanced RV systolic function by speckle tracking (RV free-wall longitudinal strain)

†Less negative values indicate worse systolic function.

Speckle-tracking confirmed more advanced RV systolic impairment in cardiac PH: RV free-wall longitudinal strain was less negative (−17.7±3.6% vs −19.6±3.7%; mean difference +1.88, 95% CI +0.42 to +3.34; p=0.012), indicating poorer contractile function. Accordingly, the proportion with impaired strain (>-20%, i.e., less negative than −20%) was higher in cardiac PH (74.5% vs 53.1%), with over twofold higher odds (OR 2.59, 95% CI 1.11–6.01; p=0.043). These findings align with the conventional metrics, suggesting cardiac-cause PH carries a more pronounced longitudinal dysfunction signature.

Table 4: Associations with functional status/biomarker and discrimination of etiology

1. Within-etiology correlations

1. Discrimination of cardiac vs non-cardiac PH

1. ROC performance (AUC, 95% CI)

Within-group associations showed that in cardiac PH, better absolute RV strain (greater |RVFWLS|) correlated modestly with longer 6MWD (r=0.32, 95% CI 0.05–0.55; p=0.023), while this relationship was weak and non-significant in non-cardiac PH (r=0.12; p=0.420). TAPSE did not correlate with NT-proBNP in either group (cardiac r=−0.02; p=0.874; non-cardiac r=−0.11; p=0.469), and RA area showed no meaningful monotonic association with WHO functional class in either etiology. In adjusted discrimination models, higher TAPSE independently favored non-cardiac PH (per 1 mm, adjusted OR 0.81, 95% CI 0.69–0.95; p=0.009), whereas larger RA area favored cardiac PH (per 1 cm², OR 1.14, 95% CI 1.04–1.25; p=0.004). PASP and RVFWLS did not independently classify etiology after adjustment. ROC analyses reflected these findings: RVFWLS alone had near-chance discrimination (AUC 0.514), TAPSE and RA area each provided moderate separation (AUC 0.681 and 0.687, respectively), and a combined model (RVFWLS + TAPSE + RA area + PASP) improved overall discrimination to an AUC of 0.755 (95% CI 0.652–0.850).

Baseline profile (Table 1). Compared with non-cardiac PH, the cardiac-cause group was older, heavier, and showed a distinctly higher biomarker burden (NT-proBNP), with a trend toward worse functional capacity. This pattern is epidemiologically consistent: PH due to left heart disease (Group 2) skews to older age with more metabolic comorbidity and higher filling pressures, which drive atrial/venous congestion and natriuretic peptide release. Current ESC/ERS guidance embeds NT-proBNP in multiparametric risk assessment across PH etiologies, reflecting its robust association with hemodynamic load and outcomes. Clear between-group separation in NT-proBNP (Δ≈748 pg/mL, p=0.001) aligns with this framework and with prior work showing NT-proBNP tracks disease severity and survival in PH. The numerically higher proportion of WHO III–IV and atrial fibrillation in cardiac PH, together with more frequent moderate–severe RV dysfunction on qualitative echo, fits the clinical phenotype of Group 2 PH, in which chronic elevation of left-sided filling pressures and secondary TR promote RA dilation and electrical remodeling. Bandyopadhyay D et al.(2021)^[6]

Conventional RV indices and right-sided chambers (Table 2). Cardiac PH demonstrated significantly worse longitudinal RV systolic indices—lower TAPSE and S′—despite similar PASP, while FAC trended lower. The dissociation of afterload (PASP) from longitudinal shortening (TAPSE/S′) underscores how ventricular interdependence, volume loading, and geometry in post-capillary PH may impair longitudinal fibers earlier than areal change. The magnitude of TAPSE depression observed (−1.7 mm vs non-cardiac PH) is clinically meaningful given ASE/ EACVI cut points and echoes the seminal finding that TAPSE is a simple, reproducible predictor of survival in PH. Right atrial area was clearly larger in cardiac PH (mean +3.5 cm²), in line with the propensity of Group 2 PH for venous congestion and with evidence that RA size/function carry independent prognostic information in PAH/PH cohorts. Notably, TAPSE/PASP—an echocardiographic surrogate of RV–PA coupling—did not differ between groups here, suggesting comparable “global” coupling once pressure is accounted for, even as chamber remodeling and longitudinal mechanics diverge. This is compatible with validation studies showing TAPSE/PASP reflects coupling but can be insensitive to etiology when PASP distributions overlap. Oktaviono YH et al.(2021)^[7]

Advanced RV systolic function (Table 3). RV free-wall longitudinal strain (RVFWLS) was significantly less negative in cardiac PH (−17.7% vs −19.6%), and the odds of impaired strain (>!−20%) were ~2.6-fold higher. These findings dovetail with the now-consistent literature that RVFWLS detects earlier/more subtle systolic impairment than TAPSE or FAC and independently stratifies risk across PH populations. While many strain studies are enriched for pre-capillary disease, given data highlight that post-capillary PH may exhibit at least comparable longitudinal impairment—plausibly through chronic volume/pressure interplay, septal shift, and annular tethering—despite similar PASP. Rahaghi FN et al.(2017)^[8]

Clinical associations and etiologic discrimination (Table 4). Within etiologies, absolute RVFWLS correlated with 6MWD in cardiac PH (r=0.32), supporting the link between longitudinal mechanics and functional capacity; the weaker, non-significant association in non-cardiac PH mirrors heterogeneity seen in mixed PAH/CTEPH/Group 3 cohorts where extracardiopulmonary factors (ventilation–perfusion mismatch, deconditioning) blunt strain–exercise coupling. In multivariable models, higher TAPSE favored non-cardiac PH and larger RA area favored cardiac PH—precisely the two signals that also showed the best standalone discrimination (AUC ~0.68–0.69). That the combined model (RVFWLS + TAPSE + RA area + PASP) achieved an AUC of 0.76 reinforces current guideline practice: no single metric suffices; a multiparametric approach integrating function (TAPSE/strain), load (PASP), and volume/congestion (RA area, biomarkers) best separates phenotypes and informs risk. Steffen HJ et al.(2018^)[9]

In this cross-sectional cohort of 100 patients with pulmonary hypertension (PH), right ventricular (RV) systolic function was measurably worse in PH due to cardiac causes (left-heart disease) than in non-cardiac PH, despite broadly similar pulmonary pressures. Cardiac PH showed lower TAPSE and S′, larger right atrial (RA) area, and less negative RV free-wall longitudinal strain (RVFWLS), together with higher NT-proBNP and a trend toward worse functional capacity. Among single echocardiographic markers, TAPSE and RA area provided the best etiologic discrimination, while a simple multimarker model (TAPSE + RA area + PASP + RVFWLS) improved classification further (AUC ≈0.76). Clinically, these data support a multiparametric approach centered on longitudinal mechanics (TAPSE/strain) and congestion metrics (RA area/NT-proBNP) when differentiating PH phenotypes and gauging disease severity. In routine practice, TAPSE and RA area are pragmatic stand-alone signals that favor non-cardiac and cardiac etiologies, respectively; adding RVFWLS refines risk/phenotype assessment where available.

LIMITATIONS

1. Design: Single-center, cross-sectional comparison; causality and temporal evolution of RV remodeling cannot be inferred.
2. Etiologic heterogeneity: The non-cardiac arm pooled PAH, Group 3, and CTEPH; subgroup sizes limited formal between-subtype contrasts.
3. Hemodynamics: Right-heart catheterization was not available in all participants; reliance on echocardiographic PASP and supportive signs may introduce misclassification.
4. Imaging constraints: Load-dependence of RV indices (TAPSE/FAC/strain), vendor-specific strain algorithms, and occasional suboptimal windows may affect generalizability.
5. Confounding: Background therapies (heart-failure and PH-targeted drugs), rhythm (atrial fibrillation), and comorbidities were not randomized and could influence RV measurements.
6. Outcomes: No longitudinal follow-up or hard outcomes; prognostic implications within each etiology were not tested.
7. Sample size: Moderate overall size with borderline power for some secondary endpoints (e.g., FAC, 6MWD differences).

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