What We Talk About When We Talk About the Wedge Pressure
2017; Lippincott Williams & Wilkins; Volume: 10; Issue: 9 Linguagem: Inglês
10.1161/circheartfailure.117.004450
ISSN1941-3297
AutoresBrian A. Houston, Ryan J. Tedford,
Tópico(s)Congenital Heart Disease Studies
ResumoHomeCirculation: Heart FailureVol. 10, No. 9What We Talk About When We Talk About the Wedge Pressure Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBWhat We Talk About When We Talk About the Wedge Pressure Brian A. Houston, MD and Ryan J. Tedford, MD Brian A. HoustonBrian A. Houston From the Division of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston. and Ryan J. TedfordRyan J. Tedford From the Division of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston. Originally published14 Sep 2017https://doi.org/10.1161/CIRCHEARTFAILURE.117.004450Circulation: Heart Failure. 2017;10:e004450See Articles by Wright et al and Naeije et alThere is a joke that goes something like this: A mathematician, a statistician, and an economist all apply for the same job. The interviewer asks them all the same question: "What is two plus two?" The mathematician, without much thought, answers, "Four." When the interviewer says, "Four exactly?" the mathematician, with a touch of incredulity replies, "Of course." The statistician says, "Four, plus or minus ten percent. But on average, four." When asked "What is two plus two?" the economist stands up, locks the door, closes the shades, and says "What do you want it to be?" As highlighted in a careful study by Wright et al,1 in this issue of Circulation: Heart Failure, we need to decide what we want the pulmonary arterial wedge pressure (PAWP) to be, or more precisely, how we want it to be measured and what we want it to tell us.The current study takes a novel approach to investigate the controversial parameter of diastolic pressure difference, in particular focusing on how variations in measurement techniques affect hemodynamic assessment and disease classification.1 The diastolic pressure difference, more commonly referred to as the diastolic pulmonary gradient (DPG), has risen to prominence as a marker of pulmonary vascular disease in the setting of left heart failure through sound physiological reasoning. As first suggested by Naeije et al2 in 2013, the more traditional markers of pulmonary vascular disease "out-of-proportion" to left heart disease (transpulmonary gradient [TPG] and pulmonary vascular resistance) are fraught with physiological concerns. The TPG, defined as mean pulmonary artery pressure minus the PAWP, does not account for flow state or the impact of left heart failure on pulmonary vascular compliance. The latter impacts pulmonary vascular resistance in a similar manner given TPG is in the numerator of its calculation. Thus, these traditional parameters may provide an inaccurate (or at least incomplete) picture of the pulmonary vasculature. By assessing only diastolic pressures, the DPG interrogates the pulmonary vasculature in the setting of cardiac diastasis—thus obviating contributions of flow and the arterial Windkessel function. Indeed, in an initial study, a DPG of >7 mm Hg predicted a worse median survival in patients with postcapillary pulmonary hypertension and a TPG >12 mm Hg.3 However, several other studies thereafter have reported an absence of DPG's prognostic power, including some which report that nearly 50% of patients had a seemingly physiologically implausible negative DPG.4–6 It has been recently argued that variations in how the PAWP is reported, as well as intrinsic difficulties in its measurement, are responsible for this discrepancy.7 As the authors note, "the practice of PAWP measurement is variable." In the calculations of a hemodynamic parameter typically represented by a small number (such as DPG), small variations in measurement technique will inevitably make a large difference.Wright et al1 sought to investigate a more precise measurement technique for PAWP and thereby improve the accuracy of the DPG calculation. In 141 advanced heart failure patients undergoing right heart catheterization, the authors calculated PAWP in 2 ways. First, during a brief breath hold at end-expiration, automated digital pressure measurements were acquired using a commercial system (designated usual practice PAWP). Next, the authors measured PAWP at the onset of the electric QRS and used that as the PAWP (designated as the QRS-gated PAWP). Each PAWP measurement was then used to calculate DPG.As in keeping with other studies, the authors found that a high proportion of the calculated usual practice DPG's were negative (43%).4–6 Using the QRS-gated PAWP, fewer patients (26%) had a negative DPG. Overall, 72 patients had pulmonary hypertension because of left heart disease (PAWP >15 mm Hg). Based on the usual practice PAWP and DPG, only 6 of these patients were classified as having combined post- and precapillary pulmonary hypertension (CpcPH) defined by DPG >7 mm Hg. Using the QRS-gated PAWP and recalculated DPG, 11 more patients were found to have CpcPH. The frequency of negative DPG values also decreased, and the group-average DPG was higher. The presence of a high PAWP (by usual methods) and larger V waves was associated with an increasing likelihood of a negative DPG value. This was not noted when using the QRS-gated PAWP. The reclassified patients had a higher TPG than those who remained in the isolated postcapillary pulmonary hypertension group. It is unclear if the usual practice PAWP or QRS-gated PAWP was used in calculating TPG, but because the QRS-gated PAWP was usually lower, if anything, the study may have underestimated the number of patients reclassified from isolated postcapillary pulmonary hypertension to CpcPH. Mortality was not different during 1-year follow-up based on the reclassification categories; though given the relative small numbers, power was likely insufficient to detect a difference.The authors' approach to standardize temporal measurement of the PAWP such that it provides a true representation of diastolic pressure is to be lauded, though one point of debate should be considered. Because of the phase delay between the left atrial pressure and PAWP (70+15 ms) and known electromechanical delay between depolarization and contraction (≈90 ms), the representation of end-diastolic pressure on the PAWP should occur 130 to 200 ms after the onset of the QRS.8,9 Thus, by using the onset-of-QRS PAWP, the study is potentially comparing end-diastolic pulmonary arterial pressures to non-end-diastolic PAWP (or merely near-end-diastolic PAWP). Using the graphical representation of ECG, pulmonary pressure, and PAWP from the study, one can appreciate how using the PAWP at QRS initiation may underestimate PAWP (and could overestimate DPG; Figure). To address this concern, in the supplemental materials, the authors report that they measured PAWP in 42 patients manually using the A-wave peak, which occurred 129 ms after the QRS duration on average. This method led to a higher PAWP than when measuring at the beginning of the QRS. One might suggest, however, that capturing the mean A wave (which correlates to the pre–C wave and end diastole) would be the most temporally appropriate measure—though this is not always a straightforward task. The temporal phase delay may vary from patient to patient, and there are concerns that alterations in atrial compliance or atrial arrhythmias may change the ability to estimate pre–C wave pressure using the mean A wave. By measuring at the beginning of the QRS, the authors have at least assured that they are reliably capturing a near-end-diastolic PAWP and thereby avoiding the effects of V waves, which are systolic phenomena.Download figureDownload PowerPointFigure. The pulmonary artery wedge pressure (PAWP) is phase delayed by 130 to 200 ms from the ECG. Thus, end-diastolic PAWP (pre C-wave pressure; represented by the green arrow) occurs later than the QRS-gated PAWP used (blue arrow). By subtracting diastolic pulmonary arterial pressure (red arrow and red dotted line) from the QRS-gated value (yellow dotted line), it is possible that one overestimates the true diastolic pulmonary gradient (difference between red dotted line and blue dotted line). Adapted from Wright et al1 with permission. Copyright ©2017, American Heart Association.Before describing this novel method of measuring the PAWP as more accurate, we must inquire as to what we are asking the PAWP to accurately represent. Just like the economist in the joke, we need to ask ourselves what we want the PAWP to tell us. If we require an accurate depiction of left ventricular end-diastolic pressure, then care should be taken to use true end-diastolic PAWP pressure (or as close to end diastole as we can reliably obtain). We agree with the authors that this is likely the method that should be used to define DPG. If we require the PAWP to represent the sum total of passive pressure to which the pulmonary vasculature is exposed, then using the automated mean across the cardiac cycle may be more appropriate, though we should not be surprised when this method of measurement leads to odd arithmetically obtained parameters (such as negative DPGs or highly discrepant left ventricular end-diastolic pressure and PAWPs). The uncomfortable truth is that the PAWP has been measured and reported in many different ways in the literature, and it is equally variably obtained in clinical practice. Even heart failure and pulmonary hypertension guidelines have failed to recommend a standardized approach.10,11 This issue would matter little if small discrepancies in measurement were clinically unimportant. However, differentiation between diseases with disparate prognoses and treatment courses (eg, pulmonary arterial hypertension and pulmonary hypertension because of left heart disease) often hinge on differences in PAWP measurement of 1 to 2 mm Hg. By using an easily standardized way of ensuring diastolic PAWP measurement, the authors here have taken a step forward in a necessary direction—the standardization of how we measure and report PAWP—and shown that this small step makes a large difference.Perhaps just as relevant as the attention paid to PAWP measurement techniques is the supplemental analysis of the diastolic pulmonary artery pressure, which compares manual measurements, attempting to correct for waveform artifacts, versus usual practice (automatic interpretation). The authors demonstrate a bias of +1.7 mm Hg with wide 95% limits of agreement (−3.2 to +6.7 mm Hg), but no overall slope to the bias. These data would confirm that some of the negative or inaccurate DPG values encountered in clinical practice are not only related to practices of PAWP measurement but are also compounded by limits of diastolic pulmonary artery pressure interpretation and fidelity.Accompanying the Wright study in this issue is a comprehensive review by Naeije et al, which details our current and ever-changing understanding of pulmonary hypertension because of left heart disease.12 In support of Wright et al's endeavor to isolate PAWP measurement in diastole, there is acknowledgment of the role that improper incorporation of V waves can have on PAWP measurement. In addition to the well-described debate surrounding prognostic value of various precapillary parameters, the review also focuses appropriate attention on the importance of right ventricular function and adaptation—noting that it is likely not the pulmonary vascular pressure profile itself that worsens prognosis, but the upstream effect that the pulmonary pressure (or more precisely, right heart afterload) enacts, which leads to a poor prognosis. Finally, the review also highlights the emerging evidence of a pulmonary vascular disease–specific genotype13 and phenotype14 in CpcPH. Although these studies do not provide definitive evidence of the superiority of one definition over another, this deep disease typing in conjunction with targeted randomized therapeutic trials may ultimately prove a superior tactic to define this condition.As Naeije et al suggest, CpcPH and isolated postcapillary pulmonary hypertension may indeed be separate disease entities with divergent physiologies and prognoses. But, unless we all know what each other is talking about when we talk (or write) about the hemodynamic criteria that define these diseases (such as PAWP, diastolic pulmonary artery pressure, pulmonary vascular resistance, and DPG), then our progress will be stymied in developing therapies targeted to each disease. Wright et al have suggested a measurement technique so that when anyone asks, "what is the wedge?", we do not have to lock the door and close the shades. By using this standard and easily replicable technique, we can all know what we are talking about when we talk about the wedge.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Circ Heart Fail is available at http://circheartfailure.ahajournals.org.Correspondence to: Ryan J. Tedford, MD, Medical University of South Carolina (MUSC), Strom Thurmond Gazes Bldg, Room 215, 114 Doughty St/MSC592, Charleston, SC 29425. E-mail [email protected]References1. Wright SP, Moayedi Y, Foroutan F, Agarwal S, Paradero G, Alba AC, Baumwol J, Mak S. Diastolic pressure difference to classify pulmonary hypertension in the assessment of heart transplant candidates.Circ Heart Fail. 2017; 10:e004077. doi: 10.1161/CIRCHEARTFAILURE.117.004077.LinkGoogle Scholar2. Naeije R, Vachiery JL, Yerly P, Vanderpool R. The transpulmonary pressure gradient for the diagnosis of pulmonary vascular disease.Eur Respir J. 2013; 41:217–223. doi: 10.1183/09031936.00074312.CrossrefMedlineGoogle Scholar3. Gerges C, Gerges M, Lang MB, Zhang Y, Jakowitsch J, Probst P, Maurer G, Lang IM. Diastolic pulmonary vascular pressure gradient: a predictor of prognosis in "out-of-proportion" pulmonary hypertension.Chest. 2013; 143:758–766. doi: 10.1378/chest.12-1653.CrossrefMedlineGoogle Scholar4. Tampakakis E, Leary PJ, Selby VN, De Marco T, Cappola TP, Felker GM, Russell SD, Kasper EK, Tedford RJ. The diastolic pulmonary gradient does not predict survival in patients with pulmonary hypertension due to left heart disease.JACC Heart Fail. 2015; 3:9–16. doi: 10.1016/j.jchf.2014.07.010.CrossrefMedlineGoogle Scholar5. Tedford RJ, Beaty CA, Mathai SC, Kolb TM, Damico R, Hassoun PM, Leary PJ, Kass DA, Shah AS. Prognostic value of the pre-transplant diastolic pulmonary artery pressure-to-pulmonary capillary wedge pressure gradient in cardiac transplant recipients with pulmonary hypertension.J Heart Lung Transplant. 2014; 33:289–297. doi: 10.1016/j.healun.2013.11.008.CrossrefMedlineGoogle Scholar6. Nagy AI, Venkateshvaran A, Merkely B, Lund LH, Manouras A. Determinants and prognostic implications of the negative diastolic pulmonary pressure gradient in patients with pulmonary hypertension due to left heart disease.Eur J Heart Fail. 2017; 19:88–97. doi: 10.1002/ejhf.675.CrossrefMedlineGoogle Scholar7. Tampakakis E, Tedford RJ. Balancing the positives and negatives of the diastolic pulmonary gradient.Eur J Heart Fail. 2017; 19:98–100. doi: 10.1002/ejhf.704.CrossrefMedlineGoogle Scholar8. Pinsky MR, Payen D. Functional Hemodynamic Monitoring. NewYork, NY: Springer Science & Business Media; 2006.Google Scholar9. Ragosta MTextbook of Clinical Hemodynamics. Philadelphia, PA: Saunders; 2008.Google Scholar10. Galiè N, Humbert M, Vachiery JL, Gibbs S, Lang I, Torbicki A, Simonneau G, Peacock A, Vonk Noordegraaf A, Beghetti M, Ghofrani A, Gomez Sanchez MA, Hansmann G, Klepetko W, Lancellotti P, Matucci M, McDonagh T, Pierard LA, Trindade PT, Zompatori M, Hoeper M, Aboyans V, Vaz Carneiro A, Achenbach S, Agewall S, Allanore Y, Asteggiano R, Paolo Badano L, Albert Barberà J, Bouvaist H, Bueno H, Byrne RA, Carerj S, Castro G, Erol Ç, Falk V, Funck-Brentano C, Gorenflo M, Granton J, Iung B, Kiely DG, Kirchhof P, Kjellstrom B, Landmesser U, Lekakis J, Lionis C, Lip GY, Orfanos SE, Park MH, Piepoli MF, Ponikowski P, Revel MP, Rigau D, Rosenkranz S, Völler H, Luis Zamorano J. 2015 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension: The Joint Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS): Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC), International Society for Heart and Lung Transplantation (ISHLT).Eur Heart J. 2016; 37:67–119. doi: 10.1093/eurheartj/ehv317.CrossrefMedlineGoogle Scholar11. McLaughlin VV, Archer SL, Badesch DB, Barst RJ, Farber HW, Lindner JR, Mathier MA, McGoon MD, Park MH, Rosenson RS, Rubin LJ, Tapson VF, Varga J; American College of Cardiology Foundation Task Force on Expert Consensus Documents; American Heart Association; American College of Chest Physicians; American Thoracic Society, Inc; Pulmonary Hypertension Association. ACCF/AHA 2009 expert consensus document on pulmonary hypertension a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents and the American Heart Association developed in collaboration with the American College of Chest Physicians; American Thoracic Society, Inc.; and the Pulmonary Hypertension Association.J Am Coll Cardiol. 2009; 53:1573–1619. doi: 10.1016/j.jacc.2009.01.004.CrossrefMedlineGoogle Scholar12. Naeije R, Gerges M, Vachiery J-L, Caravita S, Gerges C, Lang IM. Hemodynamic phenotyping of pulmonary hypertension in left heart failure.Circ Heart Fail. 2017; 10:e004082. doi: 10.1161/CIRCHEARTFAILURE.117.004082.LinkGoogle Scholar13. Assad TR, Hemnes AR, Larkin EK, Glazer AM, Xu M, Wells QS, Farber-Eger EH, Sheng Q, Shyr Y, Harrell FE, Newman JH, Brittain EL. Clinical and biological insights into combined post- and pre-capillary pulmonary hypertension.J Am Coll Cardiol. 2016; 68:2525–2536. doi: 10.1016/j.jacc.2016.09.942.CrossrefMedlineGoogle Scholar14. Caravita S, Faini A, Deboeck G, Bondue A, Naeije R, Parati G, Vachiery JL. Pulmonary hypertension and ventilation during exercise: role of the pre-capillary component.J Heart Lung Transplant. 2017; 36:754–762. doi: 10.1016/j.healun.2016.12.011.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByBundgaard H, Axelsson Raja A, Iversen K, Valeur N, Tønder N, Schou M, Christensen A, Bruun N, Søholm H, Ghanizada M, Fry N, Hamilton E, Boesgaard S, Møller M, Wolsk E, Rossing K, Køber L, Rasmussen H and Vissing C (2022) Hemodynamic Effects of Cyclic Guanosine Monophosphate-Dependent Signaling Through β3 Adrenoceptor Stimulation in Patients With Advanced Heart Failure: A Randomized Invasive Clinical Trial, Circulation: Heart Failure, 15:7, (e009120), Online publication date: 1-Jul-2022. Baratto C, Caravita S, Soranna D, Dewachter C, Bondue A, Zambon A, Badano L, Parati G and Vachiéry J (2022) Exercise haemodynamics in heart failure with preserved ejection fraction: a systematic review and meta‐analysis, ESC Heart Failure, 10.1002/ehf2.13979 Vachiéry J and Caravita S (2022) Group 2 Pulmonary Hypertension: Clinical Features and Treatment Encyclopedia of Respiratory Medicine, 10.1016/B978-0-08-102723-3.00076-7, (665-677), . Maeder M, Weber L, Seidl S, Weilenmann D, Hochholzer D, Joerg L, Chronis J, Rigger J, Haager P and Rickli H (2021) Wedge Pressure vs Left Ventricular End-Diastolic Pressure for Pulmonary Hypertension Classification and Prognostication in Severe Aortic Stenosis, CJC Open, 10.1016/j.cjco.2021.07.004, 3:12, (1428-1437), Online publication date: 1-Dec-2021. Petit T, Claessen G, Claeys M, La Gerche A, Claus P, Ghysels S, Delcroix M, Ciarka A, Droogne W, Van Cleemput J, Willems R, Voigt J, Bogaert J and Janssens S (2021) Right ventricular and cyclic guanosine monophosphate signalling abnormalities in stages B and C of heart failure with preserved ejection fraction, ESC Heart Failure, 10.1002/ehf2.13514, 8:6, (4661-4673), Online publication date: 1-Dec-2021. Weber L, Rickli H, Haager P, Joerg L, Weilenmann D, Chronis J, Rigger J, Buser M, Ehl N and Maeder M (2021) Hemodynamics Prior to Valve Replacement for Severe Aortic Stenosis and Pulmonary Hypertension during Long-Term Follow-Up, Journal of Clinical Medicine, 10.3390/jcm10173878, 10:17, (3878) Baratto C, Caravita S, Soranna D, Faini A, Dewachter C, Zambon A, Perego G, Bondue A, Senni M, Badano L, Parati G and Vachiéry J (2021) Current Limitations of Invasive Exercise Hemodynamics for the Diagnosis of Heart Failure With Preserved Ejection Fraction, Circulation: Heart Failure, 14:5, Online publication date: 1-May-2021. Birati E and Mazurek J (2021) Changes in Pulmonary Vascular Resistance after Left Ventricular Assist Device Implantation: "The Post-VAD Residual", Journal of Cardiac Failure, 10.1016/j.cardfail.2021.03.001, 27:5, (618-619), Online publication date: 1-May-2021. Wright S, Dawkins T, Eves N, Shave R, Tedford R and Mak S (2021) Hemodynamic function of the right ventricular-pulmonary vascular-left atrial unit: normal responses to exercise in healthy adults, American Journal of Physiology-Heart and Circulatory Physiology, 10.1152/ajpheart.00720.2020, 320:3, (H923-H941), Online publication date: 1-Mar-2021. Leuchte H, Halank M, Held M, Borst M, Ewert R, Klose H, Lange T, Meyer F, Skowasch D, Wilkens H and Seyfarth H (2021) Differenzialdiagnostik der pulmonalen Hypertonie am Beispiel der Kollagenose assoziierten PAH im Kontext chronischer Lungen- und Linksherzerkrankungen, Pneumologie, 10.1055/a-1204-3248, 75:02, (122-137), Online publication date: 1-Feb-2021. Ponz I, Nuche J, Sanchez Sanchez V, Sanchez-Gonzalez J, Blazquez-Bermejo Z, Caravaca Perez P, Garcia-Cosio Carmena M, de Juan Baguda J, Rodríguez Chaverri A, Sarnago Cebada F, Arribas Ynsaurriaga F, Ibañez B and Delgado Jiménez J (2021) Non-Invasive Assessment of Pulmonary Vasculopathy, Hearts, 10.3390/hearts2010002, 2:1, (5-14) Maurides S, Blankinship D, Panneerselvam K, Jackson G, Ghio S, Tedford R and Houston B (2020) Pulmonary Artery Wedge Pressure Respiratory Variation Increases With Sodium Nitroprusside Vasodilator Challenge, Journal of Cardiac Failure, 10.1016/j.cardfail.2020.09.476, 26:12, (1096-1099), Online publication date: 1-Dec-2020. Manouras A, Lund L, Gellér L, Nagy A and Johnson J (2020) Critical appraisal of the instantaneous end‐diastolic pulmonary arterial wedge pressures, ESC Heart Failure, 10.1002/ehf2.13057, 7:6, (4247-4255), Online publication date: 1-Dec-2020. Manouras A, Johnson J, Lund L and Nagy A (2020) Optimizing diastolic pressure gradient assessment, Clinical Research in Cardiology, 10.1007/s00392-020-01641-w, 109:11, (1411-1422), Online publication date: 1-Nov-2020. Bonno E, Viray M, Jackson G, Houston B and Tedford R (2020) Modern Right Heart Catheterization: Beyond Simple Hemodynamics, Advances in Pulmonary Hypertension, 10.21693/1933-088X-19.1.6, 19:1, (6-15), Online publication date: 1-Jan-2020. Dragu R, Hardak E, Ohanyan A, Adir Y and Aronson D (2019) Prognostic value and diagnostic properties of the diastolic pulmonary pressure gradient in patients with pulmonary hypertension and left heart disease, International Journal of Cardiology, 10.1016/j.ijcard.2019.05.016, 290, (138-143), Online publication date: 1-Sep-2019. Blankinship D, Katz M, Lozonschi L, Tedford R and Houston B (2018) Pulmonary artery wedge pressure respiratory variation is correlated with haemodynamic improvement with increased left ventricular assist system speed, European Journal of Heart Failure, 10.1002/ejhf.1355, 21:2, (251-253), Online publication date: 1-Feb-2019. Vachiéry J, Tedford R, Rosenkranz S, Palazzini M, Lang I, Guazzi M, Coghlan G, Chazova I and De Marco T (2019) Pulmonary hypertension due to left heart disease, European Respiratory Journal, 10.1183/13993003.01897-2018, 53:1, (1801897), Online publication date: 1-Jan-2019. Domingo E, Grignola J, Trujillo P, Aguilar R and Roman A (2018) Proximal pulmonary arterial wall disease in patients with persistent pulmonary hypertension after successful left‐sided valve replacement according to the hemodynamic phenotype, Pulmonary Circulation, 10.1177/2045894018816972, 9:1, (1-10), Online publication date: 1-Jan-2019. Hemnes A, Opotowsky A, Assad T, Xu M, Doss L, Farber-Eger E, Wells Q and Brittain E (2018) Features Associated With Discordance Between Pulmonary Arterial Wedge Pressure and Left Ventricular End Diastolic Pressure in Clinical Practice, Chest, 10.1016/j.chest.2018.08.1033, 154:5, (1099-1107), Online publication date: 1-Nov-2018. Caravita S, Mariani D, Blengino S, Branzi G, Crotti L and Parati G (2018) Pulmonary hypertension due to a stiff left atrium: Speckle tracking equivalents of large V-waves, Echocardiography, 10.1111/echo.14117, 35:9, (1464-1466), Online publication date: 1-Sep-2018. Menachem J, Birati E, Zamani P, Owens A, Atluri P, Bermudez C, Drajpuch D, Fuller S, Kim Y, Mascio C, Palanivel V, Rame J, Wald J, Acker M and Mazurek J (2018) Pulmonary hypertension: Barrier or just a bump in the road in transplanting adults with congenital heart disease, Congenital Heart Disease, 10.1111/chd.12606, 13:4, (492-498), Online publication date: 1-Jul-2018. Caravita S, Faini A, Carolino D'Araujo S, Dewachter C, Chomette L, Bondue A, Naeije R, Parati G, Vachiéry J and Lionetti V (2018) Clinical phenotypes and outcomes of pulmonary hypertension due to left heart disease: Role of the pre-capillary component, PLOS ONE, 10.1371/journal.pone.0199164, 13:6, (e0199164) Caravita S, Dewachter C, Soranna D, D'Araujo S, Khaldi A, Zambon A, Parati G, Bondue A and Vachiéry J (2018) Haemodynamics to predict outcome in pulmonary hypertension due to left heart disease: a meta-analysis, European Respiratory Journal, 10.1183/13993003.02427-2017, 51:4, (1702427), Online publication date: 1-Apr-2018. Ramu B, Houston B and Tedford R (2018) Pulmonary Vascular Disease: Hemodynamic Assessment and Treatment Selection—Focus on Group II Pulmonary Hypertension, Current Heart Failure Reports, 10.1007/s11897-018-0377-9, 15:2, (81-93), Online publication date: 1-Apr-2018. Sweitzer N (2017) Editor's Perspective, Circulation: Heart Failure, 10:9, Online publication date: 1-Sep-2017. September 2017Vol 10, Issue 9 Advertisement Article InformationMetrics © 2017 American Heart Association, Inc.https://doi.org/10.1161/CIRCHEARTFAILURE.117.004450PMID: 28912264 Originally publishedSeptember 14, 2017 Keywordsprognosispulmonary hypertensionEditorialsheart failurevascular diseasespulmonary wedge pressurehemodynamicsPDF download Advertisement SubjectsPulmonary Hypertension
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