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The correlation between hemodynamics and degree of pulmonary vascular obstruction (PVO) is known to be poor in chronic thromboembolic pulmonary hypertension (CTEPH), which makes the selection of patients eligible for pulmonary endarterectomy (PEA) challenging. It can be postulated that patients with similar PVO but different hemodynamic severity have different postoperative hemodynamics and exercise capacity. Therefore, we aimed to assess the effects of PEA on hemodynamics and exercise physiology in mild and severe CTEPH patients. We retrospectively studied 18 CTEPH patients with a mild hemodynamic profile (mean pulmonary arterial pressure [mPAP] between 25 and 30 mmHg at rest) and CTEPH patients with a more severe hemodynamic profile (mPAP > 30 mmHg), matched by age, gender, and PVO. Cardiopulmonary exercise testing parameters were evaluated at baseline and 18 months following PEA. At baseline, exercise capacity, defined as oxygen uptake, was less severely impaired in the mild CTEPH group compared to the severe CTEPH group. After PEA, in the mild CTEPH group, ventilatory efficiency and oxygen pulse improved significantly (p < 0.05), however, the change in ventilatory efficiency and oxygen pulse was smaller compared to the severe CTEPH group. Only in the severe CTEPH group exercise capacity improved significantly (p < 0.001). Hence, in the present study, postoperative hemodynamic outcome and the CPET‐determined recovery of exercise capacity in mild CTEPH patients did not differ from a matched group of severe CTEPH patients. [ABSTRACT FROM AUTHOR]

Background: Pulmonary arterial hypertension (PAH) increases right ventricular (RV) workload and decreases myocardial oxygen reserve, eventually leading to poor cardiac output. This study created and assessed a novel model of RV work output based on RV hemodynamics and oxygen supply, allowing new insight into causal mechanisms of RV dysfunction. Methods: The RV function model was built upon an earlier, left ventricular model and further adjusted for more accurate clinical use. The model assumes that RV total power output (1) is the sum of isovolumic and stroke power and (2) is linearly related to its right coronary artery oxygen supply. Thus, when right coronary artery flow is limited or isovolumic power is elevated, less energy is available for producing cardiac output. The original and adjusted models were validated via data from patients with idiopathic PAH (n = 14) and large animals (n = 6) that underwent acute pulmonary banding with or without hypoxia. Results: Both models demonstrated strong, significant correlations between RV oxygen consumption rate and RV total power output for PAH patients (original model, R2 = 0.66; adjusted model, R2 = 0.78) and sheep (original, R2 = 0.85; adjusted, R2 = 0.86). Furthermore, the models demonstrate a significant inverse relationship between required oxygen consumption and RV efficiency (stroke power/total power) (p < 0.001). Lastly, higher NYHA class was indicative of lower RV efficiency and higher oxygen consumption (p = 0.013). Conclusion: Right ventricular total power output can be accurately estimated directly from pulmonary hemodynamics and right coronary perfusion during PAH. This model highlights the increased vulnerability of PAH patients with compromised right coronary flow coupled with high afterload. [ABSTRACT FROM AUTHOR]

Background and objective: Patients with coronavirus disease 2019 (COVID‐19) pneumonia present with typical findings on chest computed tomography (CT), but the underlying histopathological patterns are unknown. Through direct regional correlation of imaging findings to histopathological patterns, this study aimed to explain typical COVID‐19 CT patterns at tissue level. Methods: Eight autopsy cases were prospectively selected of patients with PCR‐proven COVID‐19 pneumonia with varying clinical manifestations and causes of death. All had been subjected to chest CT imaging 24–72 h prior to death. Twenty‐seven lung areas with typical COVID‐19 patterns and two radiologically unaffected pulmonary areas were correlated to histopathological findings in the same lung regions. Results: Two dominant radiological patterns were observed: ground‐glass opacity (GGO) (n = 11) and consolidation (n = 16). In seven of 11 sampled areas of GGO, diffuse alveolar damage (DAD) was observed. In four areas of GGO, the histological pattern was vascular damage and thrombosis, with (n = 2) or without DAD (n = 2). DAD was also observed in five of 16 samples derived from areas of radiological consolidation. Seven areas of consolidation were based on a combination of DAD, vascular damage and thrombosis. In four areas of consolidation, bronchopneumonia was found. Unexpectedly, in samples from radiologically unaffected lung parenchyma, evidence was found of vascular damage and thrombosis. Conclusion: In COVID‐19, radiological findings of GGO and consolidation are mostly explained by DAD or a combination of DAD and vascular damage plus thrombosis. However, the different typical CT patterns in COVID‐19 are not related to specific histopathological patterns. Microvascular damage and thrombosis are even encountered in the radiologically normal lung. [ABSTRACT FROM AUTHOR]

Pulmonary hypertension ( PH) resulting from left heart failure is an increasingly recognized clinical entity. To distinguish isolated postcapillary PH from combined post- and precapillary PH, the use of a diastolic pressure gradient ( DPG = diastolic Pulmonary Artery Pressure − Pulmonary Arterial Wedge Pressure, dPAP − PAWP) has been advocated over the transpulmonary pressure gradient ( TPG = mean Pulmonary Artery Pressure − PAWP, mPAP − PAWP) since DPG was suggested to be independent of cardiac output ( CO) and only slightly related to PAWP, while TPG depends on both. We quantitatively derived and compared the DPG and TPG. Using right heart catheterization data ( n = 1054), we determined systolic pulmonary artery pressure ( sPAP), dPAP and mPAP, PAWP, and CO. From this data, we derived TPG and DPG and tested their dependence on PAWP and CO. We found that dPAP and sPAP are proportional with mPAP over a wide range of PAWP (1-31 mmHg), with dPAP = 0.62m PAP and sPAP = 1.61m PAP. As a consequence, TPG and DPG are equally dependent on PAWP: TPG = mPAP − PAWP, and DPG = 0.62m PAP − PAWP. Furthermore, we showed that both TPG and DPG depend on CO. The absolute increase in DPG with CO is 62% of the TPG increase with CO, but the relative dependence is the same. Both TPG and DPG depend on PAWP and CO. Thus, in principle, there are no major advantages for using DPG to distinguish postcapillary pulmonary hypertension from combined post- and precapillary pulmonary hypertension. [ABSTRACT FROM AUTHOR]

Aims Increased afterload in idiopathic pulmonary arterial hypertension (IPAH) causes right ventricular (RV) hypertrophy and failure. Since RV remodelling occurs with alterations in RV oxygen metabolism, increasing our understanding in the factors determining RV O2 consumption in IPAH is necessary. In the left ventricle, it is known that heart rate and systolic blood pressure are the main determinants of myocardial O2 consumption (MVO2). However, the normal right heart has lower oxygen extraction and perfusion than the left myocardium, and RV energy metabolism is changed in hypertrophy. Therefore, it is not obvious that the relationsships of pressure and heart rate to MVO2 hold for the overloaded human right heart. We hypothesize that systolic pulmonary artery pressure (PAP) and heart rate (HR) are the major determinants of RV MVO2 in IPAH. Methods and results In 18 IPAH patients (New York Heart Association class II and III), RV MVO2 was determined using positron emission tomography and 15O tracers. PAP and HR were measured during right heart catheterization. RV MVO2 was found to be related to systolic PAP (R2 = 0.54, P < 0.001), and inversely to stroke volume (R2 = 0.32, P = 0.015) and HR (R2 = 0.32, P = 0.014). Relationships of MVO2 to the rate pressure product (RPP), i.e. systolic pressure × HR, and wall stress were R2 = 0.55, P < 0.001, and R2 = 0.30, P = 0.020, respectively. Multiple regression of MVO2 on HR and systolic PAP gave R2 = 0.59, P = 0.001. Conclusion Systolic PAP and HR are the major determinants of RV MVO2 in IPAH. A further increase of HR and PAP with IPAH progression suggests a compromised RV myocardial oxygen availability. [ABSTRACT FROM AUTHOR]

Aims: In pulmonary arterial hypertension (PAH), the exercise-induced increase in stroke volume (SV) is limited by the increase in pulmonary artery pressure. In left heart failure (LHF), systemic arterial pressure increases little during exercise, and the SV increase is limited by the left ventricle itself. These differences might be reflected by a dissimilar SV and heart rate (HR) response to exercise, which could have important therapeutic implications, for example in beta-blocker therapy. Therefore, we tested the hypothesis that SV and HR responses during exercise are different between PAH and LHF patients. [ABSTRACT FROM PUBLISHER]

Purpose To investigate whether an existing method for correction of phase offset errors in phase-contrast velocity quantification is applicable for assessment of main pulmonary artery flow with an MR scanner equipped with a high-power gradient system. Materials and Methods The correction method consists of fitting a surface through the time average of stationary pixels of velocity-encoded phase images, and subtracting this surface from the velocity images. Pixels are regarded as stationary if their time standard deviation falls into the lowest percentile. Flow was measured in the main pulmonary artery of 15 subjects. Each measurement was repeated on a stationary phantom. The phase offset error in the phantom was used as a reference. Correction was applied with varying polynomial surface orders (0-5) and stationarity percentiles (5-50%). The optimal surface order and stationarity percentile were determined by comparing the fitted surface with the phantom. Results Using a first-order surface and a (noncritical) 25% percentile, the correction method significantly reduced the phase offset error from 1.1 to 0.35 cm/second (RMS), which is equivalent to a reduction from 11% to 3.3% of mean volume flow. Phase error correction strongly affected stroke volume (range -11 to 26%). Conclusion The method significantly reduces phase offset errors in pulmonary artery flow. J. Magn. Reson. Imaging 2005;22:73-79. © 2005 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Purpose To assess the accuracy of several noninvasive MRI-based estimators of pulmonary artery pressure by comparing them with invasive pressure measurement. Materials and Methods We compared five MRI methods with invasive pressure measurement by catheterization, in one group of pulmonary hypertension (PH) patients. Doppler echocardiography was included as a reference method. Main inclusion criterion was a mean pulmonary artery pressure above 25 mmHg at catheterization. MRI velocity quantification was used to obtain pulmonary flow acceleration and ejection times, and pulse wave velocity. The ventricular mass index was also assessed on MRI. Two commercially available 1.5-T systems were used for this study. Results Data from 44 patients were analyzed. Correlation of acceleration time with mean pressure was: r = -0.21, P = 0.21, correlation of the acceleration/ejection time ratio with systolic pressure was: r = -0.26, P = 0.01. The ventricular mass index showed the best correlation with mean pressure, with r = 0.56, P < 0.001. Using the pulse wave velocity and the cross-sectional area of the pulmonary artery, the mean pressure could not be estimated accurately. Conclusion Accurate estimation of pulmonary artery pressure in PH patients was not feasible by the MRI estimators studied. These noninvasive methods cannot replace right heart catheterization at this moment. J. Magn. Reson. Imaging 2005;22:67-72. © 2005 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Background Appropriate treatment of pulmonary hypertension (PH) is critically dependent on accurate discrimination between pre- and postcapillary PH. However, clinical discrimination is challenging and frequently requires a right heart catheterization. Existing risk scores to detect postcapillary PH have suboptimal discriminatory strength. We have previously shown that platelet-derived RNA profiles may have diagnostic value for PH detection. Here, we hypothesize that platelet-derived RNAs can be employed to select unique biomarker panels for the discrimination between pre- and postcapillary PH. Methods and Results Blood platelet RNA from whole blood was isolated and sequenced from 50 patients with precapillary PH (with different PH subtypes) as well as 50 patients with postcapillary PH. RNA panels were calculated by ANOVA statistics, and classifications were performed using a support vector machine algorithm, supported by particle swarm optimization. We identified in total 4279 different RNAs in blood platelets from patients with pre- and postcapillary PH. A particle swarm optimization-selected RNA panel of 1618 distinctive RNAs with differential levels together with a trained support vector machine algorithm accurately discriminated patients with precapillary PH from patients with postcapillary PH with 100% sensitivity, 60% specificity, 80% accuracy, and 0.95 (95% CI, 0.86-1.00) area under the curve in the independent validation series (n=20). Conclusions This proof-of-concept study demonstrates that particle swarm optimization/support vector machine-enhanced classification of platelet RNA panels may be able to discriminate precapillary PH from postcapillary PH. This research provides a foundation for the development of a blood test with a high negative predictive value that would improve early diagnosis of precapillary PH and prevents unnecessary invasive testing in patients with postcapillary PH.

Background Pulmonary endarterectomy (PEA) for chronic thromboembolic pulmonary hypertension improves resting hemodynamics and right ventricular (RV) function. Because exercise tolerance frequently remains impaired, RV function may not have completely normalized after PEA. Therefore, we performed a detailed invasive hemodynamic study to investigate the effect of PEA on RV function during exercise. Methods and Results In this prospective study, all consenting patients with chronic thromboembolic pulmonary hypertension eligible for surgery and able to perform cycle ergometry underwent cardiac magnetic resonance imaging, a maximal cardiopulmonary exercise test, and a submaximal invasive cardiopulmonary exercise test before and 6 months after PEA. Hemodynamic assessment and analysis of RV pressure curves using the single-beat method was used to determine load-independent RV contractility (end systolic elastance), RV afterload (arterial elastance), RV-arterial coupling (end systolic elastance-arterial elastance), and stroke volume both at rest and during exercise. RV rest-to-exercise responses were compared before and after PEA using 2-way repeated-measures analysis of variance with Bonferroni post hoc correction. A total of 19 patients with chronic thromboembolic pulmonary hypertension completed the entire study protocol. Resting hemodynamics improved significantly after PEA. The RV exertional stroke volume response improved 6 months after PEA (79±32 at rest versus 102±28 mL during exercise; P <0.01). Although RV afterload (arterial elastance) increased during exercise, RV contractility (end systolic elastance) did not change during exercise either before (0.43 [0.32-0.58] mm Hg/mL versus 0.45 [0.22-0.65] mm Hg/mL; P =0.6) or after PEA (0.32 [0.23-0.40] mm Hg/mL versus 0.28 [0.19-0.44] mm Hg/mL; P =0.7). In addition, mean pulmonary artery pressure-cardiac output and end systolic elastance-arterial elastance slopes remained unchanged after PEA. Conclusions The exertional RV stroke volume response improves significantly after PEA for chronic thromboembolic pulmonary hypertension despite a persistently abnormal afterload and absence of an RV contractile reserve. This may suggest that at mildly elevated pulmonary pressures, stroke volume is less dependent on RV contractility and afterload and is primarily determined by venous return and conduit function.

Background Recognition of precapillary pulmonary hypertension (PH) has significant implications for patient management. However, the low a priori chance to find this rare condition in community hospitals may create a barrier against performing a right heart catheterization (RHC). This could result in misclassification of PH and delayed diagnosis/treatment of precapillary PH. Therefore, we investigated patient characteristics and echocardiographic parameters associated with the decision whether to perform an RHC in patients with incident PH in 12 Dutch community hospitals. Methods and Results In total, 275 patients were included from the OPTICS (Optimizing PH Diagnostic Network in Community Hospitals) registry, a prospective cohort study with patients with incident PH; 157 patients were diagnosed with RHC (34 chronic thromboembolic PH, 38 pulmonary arterial hypertension, 81 postcapillary PH, 4 miscellaneous PH), while 118 patients were labeled as probable postcapillary PH without hemodynamic confirmation. Multivariable analysis showed that older age (>60 years), left ventricular diastolic dysfunction grade 2-3, left atrial dilatation were independently associated with the decision to not perform an RHC, while presence of prior venous thromboembolic events or pulmonary arterial hypertension-associated conditions, right atrial dilatation, and tricuspid regurgitation velocity ≥3.7 m/s favor an RHC performance. Conclusions Older age and echocardiographic parameters of left heart disease were independently associated with the decision to not perform an RHC, while presence of prior venous thromboembolic events or pulmonary arterial hypertension-associated conditions, right atrial dilation, and severe PH on echocardiography favored an RHC performance. As such, especially elderly patients may be at an increased risk of diagnostic delays and missed diagnoses of treatable precapillary PH, which could lead to a worse prognosis.

Background Although most newly presenting patients with pulmonary hypertension (PH) have elevated pulmonary artery wedge pressure, identification of so-called postcapillary PH can be challenging. A noninvasive tool predicting elevated pulmonary artery wedge pressure in patients with incident PH may help avoid unnecessary invasive diagnostic procedures. Methods and Results A combination of clinical data, ECG, and echocardiographic parameters was used to refine a previously developed left heart failure risk score in a retrospective cohort of pre- and postcapillary PH patients. This updated score (renamed the OPTICS risk score) was externally validated in a prospective cohort of patients from 12 Dutch nonreferral centers the OPTICS network. Using the updated OPTICS risk score, the presence of postcapillary PH could be predicted on the basis of body mass index ≥30, diabetes mellitus, atrial fibrillation, dyslipidemia, history of valvular surgery, sum of SV1 (deflection in V1 in millimeters) and RV6 (deflection in V6 in millimeters) on ECG, and left atrial dilation. The external validation cohort included 81 postcapillary PH patients and 66 precapillary PH patients. Using a predefined cutoff of >104, the OPTICS score had 100% specificity for postcapillary PH (sensitivity, 22%). In addition, we investigated whether a high probability of heart failure with preserved ejection fraction, assessed by the H 2 FPEF score (obesity, atrial fibrillation, age >60 yrs, ≥2 antihypertensives, E/e' >9, and pulmonary artery systolic pressure by echo >35 mmHg), similarly predicted the presence of elevated pulmonary artery wedge pressure. High probability of heart failure with preserved ejection fraction (H 2 FPEF score ≥6) was less specific for postcapillary PH. Conclusions In a community setting, the OPTICS risk score can predict elevated pulmonary artery wedge pressure in PH patients without clear signs of left-sided heart disease. The OPTICS risk score may be used to tailor the decision to perform invasive diagnostic testing.