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Review
. 2020 Dec 1;76(22):2671-2681.
doi: 10.1016/j.jacc.2020.10.007.

Cardiopulmonary Hemodynamics in Pulmonary Hypertension and Heart Failure: JACC Review Topic of the Week

Affiliations
Review

Cardiopulmonary Hemodynamics in Pulmonary Hypertension and Heart Failure: JACC Review Topic of the Week

Bradley A Maron et al. J Am Coll Cardiol. .

Abstract

Pulmonary hypertension (PH) is an independent risk factor for adverse clinical outcome, particularly in left heart disease (LHD) patients. Recent advances have clarified the mean pulmonary artery pressure (mPAP) range that is above normal and is associated with clinical events, including mortality. This progress has for the first time resulted in a new clinical definition of PH that is evidenced-based, is inclusive of mPAP >20 mm Hg, and emphasizes early diagnosis. Additionally, pulmonary vascular resistance (PVR) 2.2 to 3.0 WU, considered previously to be normal, appears to associate with elevated clinical risk. A revised approach to classifying PH patients as pre-capillary, isolated post-capillary, or combined pre-/post-capillary PH now guides point-of-care diagnosis, risk stratification, and treatment. Exercise hemodynamic or confrontational fluid challenge studies may also aid decision-making for patients with PH-LHD or otherwise unexplained dyspnea. This collective progress in pulmonary vascular and heart failure medicine reinforces the critical importance of accurate hemodynamic assessment.

Keywords: heart failure; hemodynamics; pulmonary hypertension.

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Conflict of interest statement

Author Disclosures Dr. Maron is supported by grants R01HL139613-01, R01HL1535-02, U54HL119145, and R21HL145420, the Cardiovascular Medical Research Education Foundation, and McKenzie Family Charitable Trust, Boston Biomedical Innovations Center; has served as a consultant for Actelion; and is coinventor of patents or patent applications that are related to pulmonary hypertension (U.S. Patent #9,605,047; PCT/US2015/029672; Provisional ID: #62475955; Provisional ID: #24624; Provisional ID: #24622). Dr. Kovacs has received personal fees and nonfinancial support from Actelion, Bayer, GlaxoSmithKline, Merck Sharp and Dohme, Boehringer Ingelheim, Novartis, Chiesi, Vitalaire, Ferrer, and AOP outside the submitted work. Dr. Tedford has consulting relationships with Medtronic, Aria CV Inc., Arena Pharmaceuticals, and United Therapeutics; has served on a steering committee for Abbott, Acceleron, and Medtronic; has served on a research Advisory Board for Abiomed; and has performed hemodynamic core lab work for Actelion and Merck. Dr. Vaidya has served as a consultant for Bayer, United Therapeutics, Liquidia, and Actelion; and has served on the nonpromotional Speakers Bureau for Bayer, Actelion, and United Therapeutics. Dr. Bhatt has served on the Advisory Board of Cardax, CellProthera, Cereno Scientific, Elsevier Practice Update Cardiology, Level Ex, Medscape Cardiology, PhaseBio, PLx Pharma, and Regado Biosciences; has served on the Board of Directors of Boston VA Research Institute, Society of Cardiovascular Patient Care, and TobeSoft; has served as Chair of the American Heart Association Quality Oversight Committee, NCDR-ACTION Registry Steering Committee, and VA CART Research and Publications Committee; has served on data monitoring committees for Baim Institute for Clinical Research (formerly Harvard Clinical Research Institute, for the PORTICO trial, funded by St. Jude Medical, now Abbott), Cleveland Clinic (including for the ExCEED trial, funded by Edwards), Contego Medical (Chair, PERFORMANCE 2), Canadian Medical and Surgical Knowledge Translation Research Group (clinical trial steering committees), Duke Clinical Research Institute, Mayo Clinic, Mount Sinai School of Medicine (for the ENVISAGE trial, funded by Daiichi-Sankyo), and Population Health Research Institute; has received honoraria from the American College of Cardiology (Senior Associate Editor, Clinical Trials and News, ACC.org; Vice-Chair, ACC Accreditation Committee), Baim Institute for Clinical Research (formerly Harvard Clinical Research Institute; RE-DUAL PCI clinical trial steering committee funded by Boehringer Ingelheim; AEGIS-II executive committee funded by CSL Behring), Belvoir Publications (Editor-in-Chief, Harvard Heart Letter), Duke Clinical Research Institute (clinical trial steering committees, including for the PRONOUNCE trial, funded by Ferring Pharmaceuticals), HMP Global (Editor-in-Chief, Journal of Invasive Cardiology), Journal of the American College of Cardiology (Guest Editor; Associate Editor), K2P (Co-Chair, interdisciplinary curriculum), Level Ex, Medtelligence/ReachMD (CME steering committees), MJH Life Sciences, Population Health Research Institute (for the COMPASS operations committee, publications committee, steering committee, and USA national co-leader, funded by Bayer), Slack Publications (Chief Medical Editor, Cardiology Today’s Intervention), Society of Cardiovascular Patient Care (Secretary/Treasurer), and WebMD (CME steering committees); has served as Deputy Editor of Clinical Cardiology; has received research funding from Abbott, Afimmune, Amarin, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Cardax, Chiesi, CSL Behring, Eisai, Ethicon, Ferring Pharmaceuticals, Forest Laboratories, Fractyl, Idorsia, Ironwood, Ischemix, Lexicon, Lilly, Medtronic, Pfizer, PhaseBio, PLx Pharma, Regeneron, Roche, Sanofi, Synaptic, and The Medicines Company; has received royalties from Elsevier (Editor, Cardiovascular Intervention: A Companion to Braunwald’s Heart Disease); has served as site co-investigator for Biotronik, Boston Scientific, CSI, St. Jude Medical (now Abbott), and Svelte; has served as a Trustee of the American College of Cardiology; and has performed unfunded research for FlowCo, Merck, Novo Nordisk, and Takeda. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Figures

Figure 1.
Figure 1.. The continuum of clinical risk between pulmonary vascular resistance and mortality in patients with pulmonary hypertension.
(A) The PVR continuum of all-cause mortality risk in patients with elevated mPAP (defined in the dataset shown here as ≥19 mmHg) begins at ~2.2 WU and increases through 6 WU. However, the slope of this relationship hinges substantially on the absence or presence of pulmonary venous hypertension at the time of right heart catheterization, depicted in (B) and (C) after stratifying the population by low and high pulmonary artery wedge pressure (PAWP), respectively. WU, Wood unit. The grey line inset is the kernel density estimate, representing the relative density of patients across PVR values. Reproduced with permission from Ref. .
Figure 2.
Figure 2.. Integrating the cardiopulmonary hemodynamic and clinical profile of patients with pulmonary hypertension (PH).
Diagnosing PH is achieved by right heart catheterization, and requires a mean pulmonary artery pressure (mPAP) >20 mmHg. Patients are then classified by hemodynamic category, which together with the clinical profile and other supporting data (e.g., chest imaging, serology, genetic testing) is used to determine the PH clinical group. Certain clinical groups are incompatible with hemodynamic classifications; for example, pulmonary arterial hypertension (PAH) cannot be diagnosed in patients with isolated post-capillary or combined pre-/post-capillary PH hemodynamics. Treatment is based on clinical group, as reviewed in Refs. and .Overall, pulmonary vasodilator therapies are not indicated in PH due to left heart disease (LHD), regardless of PVR. PVR, pulmonary vascular resistance; PAWP, pulmonary artery wedge pressure; PVOD, pulmonary veno-occlusive disease; CTEPH, chronic thromboembolic PH.
Figure 3.
Figure 3.. Indications for right heart catheterization (RHC).
(Left) In the traditional approach to RHC, hemodynamic assessment is performed in patients with a clinical indication following clinical optimization including diuresis. PAH, pulmonary arterial hypertension. (Right) A future direction for RHC approach considers patients with a traditional indication for RHC as well as patients with clinical parameters suggestive of early or unexplained pulmonary hypertension (PH). In this scenario, RHC prior to diuresis may be considered to clarify the PH hemodynamic classification of patients (particularly post-capillary PH vs. combined pre- and post-capillary PH). In select patients, repeat RHC may be indicated to monitor therapy response or reassess PH hemodynamic classification. Unexplained dyspnea is dyspnea without a clear etiology based on results from standard non-invasive testing (e.g., echocardiography, cardiopulmonary exercise testing, others); eRVSP, estimated right ventricular systolic pressure by echocardiography; LHD, left heart disease.
Figure 4.
Figure 4.. Pulmonary Artery Pressure Waveforms.
(A)Over-dampening. Note that characteristic dichrotic notch is not seen. Over-dampening occurs when air is introduced into the catheter or tubing and may result in reduction of the overall amplitude of the pressure tracing (mean pressure is usually not affected). This can be addressed by flushing the catheter or tubing. (B) Under-dampening. Also called catheter ringing and occurs when the frequency of the transmitted waveform (heart rate) approximates the natural resonance frequency of the transducer system. This falsely increases the amplitude of the waveform. Similar to over-dampening, mean pressure is usually not affected. Ringing artifact may be reduced by introducing a small amount of a denser fluid, such as blood or contrast, into the catheter, with careful attention not to overdamp the signal (C) Example of an optimal pulmonary artery pressure waveform with preserved dichroic notch but minimal systolic and diastolic ringing artifact.
Figure 5.
Figure 5.. Pulmonary Artery Wedge Pressure (PAWP) Waveforms.
(A)Typical PAWP tracing. A-wave, c-wave, and v-wave as noted in red. End-diastole occurs just prior to the c-wave, and thus, pressure at this point correlates best with left ventricular end-diastolic pressure. When the c-wave is not well seen, averaging the peak and trough of the a-wave is recommended. In this example, the v-wave is normal amplitude. Mean PAWP (black horizontal line), which an average pressure over the entire cardiac cycle, is essentially equal to end-diastolic PAWP. (B) A-wave, and v-wave as noted in red (c-wave not appreciated).Very large amplitude V waves are present. Here, mean PAWP (black horizontal line) is significantly greater than end-diastolic PAWP.
Central illustration.
Central illustration.. Contemporary model of pulmonary hypertension assessment in left heart disease.
(Left) The classical approach to pulmonary hypertension (PH) assessment in left heart disease (LHD) emphasized data from right heart catheterization (RHC) to delineate patients with mean pulmonary artery pressure (mPAP) ≥25 mmHg and a post-capillary component (PAWP >15 mmHg). An elevated PVR ≥3.0 WU associated with advanced heart failure (HF) clinically. Overall, data collection emphasized end-stage disease. (Right) The contemporary approach to PH-LHD focuses on early RHC, which is based on (A) data demonstrating that the hemodynamic continuum of clinical risk relative to mortality and heart failure hospitalization includes mPAP >20 mmHg and PVR ≥2.2 WU. (B) Data from RHC is also used to classify patients into one of three established PH hemodynamic subtypes. RV, right ventricle. Table: Adapted from Ref. .

References

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