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Background: The current classification of pulmonary hypertension (PH) distinguishes between pre-capillary (PAWP ≤ 15 mmHg) and post-capillary (PAWP > 15 mmHg) forms, with left heart disease, especially heart failure with preserved ejection fraction (HFpEF), being a common cause of PH. We investigated the suitability of an HFpEF diagnosis instead of PAWP in diagnosing PH associated with HFpEF. Methods: In a retrospective, single-center analysis, we reviewed diagnoses from our database, focusing on patients initially diagnosed with idiopathic pulmonary arterial hypertension (IPAH) or PH associated with HFpEF (PH-HFpEF) based on their PAWP. These patients were reclassified, distinguishing between HFpEF and non-HFpEF cases. Patients with PH-HFpEF were further stratified by PAWP (≤15 mmHg or >15 mmHg). Results: The study included 350 patients: 214 (61.1%) with PAWP ≤ 15 mmHg and 136 (38.9%) with PAWP > 15 mmHg. Replacing the PAWP criterion with the HFpEF criterion resulted in the reclassification of 121 of 350 (34.6%) patients (115 of 214 [53.7%] from IPAH to PH-HFpEF and 6 of 136 [4.4%] from PH-HFpEF to IPAH). The final disposition was IPAH (n = 105, 30%), PH-HFpEF with PAWP ≤ 15 mmHg (n = 115, 32.9%), and PH-HFpEF with PAWP > 15 mmHg (n = 130, 37.1%). Characteristics such as age distribution, functional impairment, co-morbidities, echocardiographic indices of HFpEF, pulmonary vascular resistance, response to PH medications, and unadjusted survival were comparable between the two HFpEF cohorts but differed substantially from those with IPAH. Conclusions: PH-HFpEF patients with PAWP ≤ 15 mmHg resemble those with PAWP > 15 mmHg but differ from IPAH cases. Incorporating non-invasive HFpEF criteria could refine PH diagnostic classification. [ABSTRACT FROM AUTHOR]

Introduction: Doppler‐derived pulmonary pulse transit time (pPTT) is an auspicious hemodynamic marker in chronic pulmonary diseases. The aim is to compare four distinct pPTT measurements and its relation to right cardiac and pulmonary function. Methods: Prospectively, 25 chronic obstructive pulmonary disease (COPD) patients (four patients excluded) and 32 healthy subjects underwent repeated distinct pPTT measurements, standard echocardiography, and pulmonary function testing on the same day. pPTT was defined as the interval from the R or Q‐wave in the electrocardiogram to the corresponding pulse wave Doppler peak late systolic (S) 2 or diastolic (D) pulmonary vein flow velocity (pPTT R‐S, Q‐S, R‐D, Q‐D). Reproducibility was assessed using Bland–Altman analysis, coefficient of variation (COV), intraclass correlation coefficient (ICC), and power calculations. Associations with right ventricular RV tissue and pulse wave Doppler velocities (RV E', RV S', RV A', RV E, RV A, RV E/E', RV E/A), TAPSE, right ventricular fractional area change, left ventricular systolic and diastolic function (LV ejection fraction, E, A, E/A, E/E', septal E', lateral E'), LA diameters, as well as forced expiratory volume in 1 s, forced vital capacity (FVC) predicted (%), and in liters were analyzed. Results: There was no significant difference and no bias between pPTT measures (p range:.1–.9). COV was in COPD 1.2%–2.3%, in healthy subjects 1.0%–3.1%. ICC ranged from.92 (COPD) to.96 (healthy subjects). In COPD significant correlations were found for pPTT R‐S, Q‐S and R‐D with RV E', (all > ρ:.49, < p =.0364), pPTT R‐S, Q‐S with RV E/E' (both > ρ:.49, < p =.0291), pPTT Q‐S with RV S´ (ρ:.58, p =.0134), RV A (ρ:.59, p =.0339) and heart rate > ρ: −.39, < p =.0297). pPTT R‐S, R‐D showed significant correlations with FVC predicted (%) (ρ:.48 p =.0224) and FVC (l) (ρ:.47 p =.0347). Conclusions: All pPTT measures exhibited high reproducibility. In COPD patients pPTT measures correlate with diastolic right ventricular function. Defining Q as starting point seems clinically advantageous considering electromechanical desynchrony in patients with conduction disorders. [ABSTRACT FROM AUTHOR]

Objectives: Recent studies suggest the existence of an idiopathic pulmonary arterial hypertension (IPAH) phenotype affecting mostly patients with a smoking history, characterised by low diffusion capacity for carbon monoxide (DLCO) without clinically significant emphysema. This study’s objective was to test the hypothesis of a loss of pulmonary capillaries as an underlying mechanism by comparison to other patient groups with and without pulmonary hypertension (PH).Between March 2019 and June 2023, patients of four groups were recruited for this observational study: IPAH with preserved (1) and low DLCO (2), combined pulmonary fibrosis and emphysema with PH (3), and emphysema without PH (4). Patients underwent clinical CT and 129Xe MRI including dissolved-phase imaging yielding the ratio of 129Xe in red blood cells and membrane tissues (RBC-M), chemical shift saturation recovery for determining RBC fraction η and diffusion-weighted imaging yielding surface-volume ratio. Kruskal–Wallis tests were used for statistical analysis.Twenty-nine participants were recruited, of which 22 (age 64 ± 10, 11 male, 5/5/7/5 for the individual groups) could be included in the analysis. RBC-M and η were reduced in IPAH with low versus preserved DLCO and emphysema groups (p ≤ 0.01). CT low-attenuation area percentage was not increased in IPAH with low DLCO compared to any group. 129Xe MRI-derived surface-volume ratio was reduced in IPAH with low versus preserved DLCO (p = 0.04).Results are consistent with a loss of pulmonary capillaries in patients with IPAH and low DLCO along with destruction of alveolar tissue, likely due to early diffuse emphysema.QuestionA loss of pulmonary capillaries has been suggested in patients with IPAH and low diffusion capacity without clinically significant emphysema on CT.Findings129Xe uptake in red blood cells and lung surface-volume ratio were reduced in IPAH patients with low compared to preserved diffusion capacity.Clinical relevanceThis study furthers the understanding of the underlying pathological mechanisms in IPAH with low diffusion capacity, providing evidence that loss of pulmonary capillaries is accompanied by alveolar tissue destruction despite near-normal CT.Materials and methods: Recent studies suggest the existence of an idiopathic pulmonary arterial hypertension (IPAH) phenotype affecting mostly patients with a smoking history, characterised by low diffusion capacity for carbon monoxide (DLCO) without clinically significant emphysema. This study’s objective was to test the hypothesis of a loss of pulmonary capillaries as an underlying mechanism by comparison to other patient groups with and without pulmonary hypertension (PH).Between March 2019 and June 2023, patients of four groups were recruited for this observational study: IPAH with preserved (1) and low DLCO (2), combined pulmonary fibrosis and emphysema with PH (3), and emphysema without PH (4). Patients underwent clinical CT and 129Xe MRI including dissolved-phase imaging yielding the ratio of 129Xe in red blood cells and membrane tissues (RBC-M), chemical shift saturation recovery for determining RBC fraction η and diffusion-weighted imaging yielding surface-volume ratio. Kruskal–Wallis tests were used for statistical analysis.Twenty-nine participants were recruited, of which 22 (age 64 ± 10, 11 male, 5/5/7/5 for the individual groups) could be included in the analysis. RBC-M and η were reduced in IPAH with low versus preserved DLCO and emphysema groups (p ≤ 0.01). CT low-attenuation area percentage was not increased in IPAH with low DLCO compared to any group. 129Xe MRI-derived surface-volume ratio was reduced in IPAH with low versus preserved DLCO (p = 0.04).Results are consistent with a loss of pulmonary capillaries in patients with IPAH and low DLCO along with destruction of alveolar tissue, likely due to early diffuse emphysema.QuestionA loss of pulmonary capillaries has been suggested in patients with IPAH and low diffusion capacity without clinically significant emphysema on CT.Findings129Xe uptake in red blood cells and lung surface-volume ratio were reduced in IPAH patients with low compared to preserved diffusion capacity.Clinical relevanceThis study furthers the understanding of the underlying pathological mechanisms in IPAH with low diffusion capacity, providing evidence that loss of pulmonary capillaries is accompanied by alveolar tissue destruction despite near-normal CT.Results: Recent studies suggest the existence of an idiopathic pulmonary arterial hypertension (IPAH) phenotype affecting mostly patients with a smoking history, characterised by low diffusion capacity for carbon monoxide (DLCO) without clinically significant emphysema. This study’s objective was to test the hypothesis of a loss of pulmonary capillaries as an underlying mechanism by comparison to other patient groups with and without pulmonary hypertension (PH).Between March 2019 and June 2023, patients of four groups were recruited for this observational study: IPAH with preserved (1) and low DLCO (2), combined pulmonary fibrosis and emphysema with PH (3), and emphysema without PH (4). Patients underwent clinical CT and 129Xe MRI including dissolved-phase imaging yielding the ratio of 129Xe in red blood cells and membrane tissues (RBC-M), chemical shift saturation recovery for determining RBC fraction η and diffusion-weighted imaging yielding surface-volume ratio. Kruskal–Wallis tests were used for statistical analysis.Twenty-nine participants were recruited, of which 22 (age 64 ± 10, 11 male, 5/5/7/5 for the individual groups) could be included in the analysis. RBC-M and η were reduced in IPAH with low versus preserved DLCO and emphysema groups (p ≤ 0.01). CT low-attenuation area percentage was not increased in IPAH with low DLCO compared to any group. 129Xe MRI-derived surface-volume ratio was reduced in IPAH with low versus preserved DLCO (p = 0.04).Results are consistent with a loss of pulmonary capillaries in patients with IPAH and low DLCO along with destruction of alveolar tissue, likely due to early diffuse emphysema.QuestionA loss of pulmonary capillaries has been suggested in patients with IPAH and low diffusion capacity without clinically significant emphysema on CT.Findings129Xe uptake in red blood cells and lung surface-volume ratio were reduced in IPAH patients with low compared to preserved diffusion capacity.Clinical relevanceThis study furthers the understanding of the underlying pathological mechanisms in IPAH with low diffusion capacity, providing evidence that loss of pulmonary capillaries is accompanied by alveolar tissue destruction despite near-normal CT.Conclusion: Recent studies suggest the existence of an idiopathic pulmonary arterial hypertension (IPAH) phenotype affecting mostly patients with a smoking history, characterised by low diffusion capacity for carbon monoxide (DLCO) without clinically significant emphysema. This study’s objective was to test the hypothesis of a loss of pulmonary capillaries as an underlying mechanism by comparison to other patient groups with and without pulmonary hypertension (PH).Between March 2019 and June 2023, patients of four groups were recruited for this observational study: IPAH with preserved (1) and low DLCO (2), combined pulmonary fibrosis and emphysema with PH (3), and emphysema without PH (4). Patients underwent clinical CT and 129Xe MRI including dissolved-phase imaging yielding the ratio of 129Xe in red blood cells and membrane tissues (RBC-M), chemical shift saturation recovery for determining RBC fraction η and diffusion-weighted imaging yielding surface-volume ratio. Kruskal–Wallis tests were used for statistical analysis.Twenty-nine participants were recruited, of which 22 (age 64 ± 10, 11 male, 5/5/7/5 for the individual groups) could be included in the analysis. RBC-M and η were reduced in IPAH with low versus preserved DLCO and emphysema groups (p ≤ 0.01). CT low-attenuation area percentage was not increased in IPAH with low DLCO compared to any group. 129Xe MRI-derived surface-volume ratio was reduced in IPAH with low versus preserved DLCO (p = 0.04).Results are consistent with a loss of pulmonary capillaries in patients with IPAH and low DLCO along with destruction of alveolar tissue, likely due to early diffuse emphysema.QuestionA loss of pulmonary capillaries has been suggested in patients with IPAH and low diffusion capacity without clinically significant emphysema on CT.Findings129Xe uptake in red blood cells and lung surface-volume ratio were reduced in IPAH patients with low compared to preserved diffusion capacity.Clinical relevanceThis study furthers the understanding of the underlying pathological mechanisms in IPAH with low diffusion capacity, providing evidence that loss of pulmonary capillaries is accompanied by alveolar tissue destruction despite near-normal CT.Key Points: Recent studies suggest the existence of an idiopathic pulmonary arterial hypertension (IPAH) phenotype affecting mostly patients with a smoking history, characterised by low diffusion capacity for carbon monoxide (DLCO) without clinically significant emphysema. This study’s objective was to test the hypothesis of a loss of pulmonary capillaries as an underlying mechanism by comparison to other patient groups with and without pulmonary hypertension (PH).Between March 2019 and June 2023, patients of four groups were recruited for this observational study: IPAH with preserved (1) and low DLCO (2), combined pulmonary fibrosis and emphysema with PH (3), and emphysema without PH (4). Patients underwent clinical CT and 129Xe MRI including dissolved-phase imaging yielding the ratio of 129Xe in red blood cells and membrane tissues (RBC-M), chemical shift saturation recovery for determining RBC fraction η and diffusion-weighted imaging yielding surface-volume ratio. Kruskal–Wallis tests were used for statistical analysis.Twenty-nine participants were recruited, of which 22 (age 64 ± 10, 11 male, 5/5/7/5 for the individual groups) could be included in the analysis. RBC-M and η were reduced in IPAH with low versus preserved DLCO and emphysema groups (p ≤ 0.01). CT low-attenuation area percentage was not increased in IPAH with low DLCO compared to any group. 129Xe MRI-derived surface-volume ratio was reduced in IPAH with low versus preserved DLCO (p = 0.04).Results are consistent with a loss of pulmonary capillaries in patients with IPAH and low DLCO along with destruction of alveolar tissue, likely due to early diffuse emphysema.QuestionA loss of pulmonary capillaries has been suggested in patients with IPAH and low diffusion capacity without clinically significant emphysema on CT.Findings129Xe uptake in red blood cells and lung surface-volume ratio were reduced in IPAH patients with low compared to preserved diffusion capacity.Clinical relevanceThis study furthers the understanding of the underlying pathological mechanisms in IPAH with low diffusion capacity, providing evidence that loss of pulmonary capillaries is accompanied by alveolar tissue destruction despite near-normal CT. [ABSTRACT FROM AUTHOR]