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About This Activity

Activity Description and Learning Objectives

In this activity, experts in cardiology, pulmonary vascular disorder and respiratory specialists discuss the biological and pathophysiological mechanisms of CTEPH and how they impact on treatment decisions relating to the use of medical therapies in daily clinical practice.

This activity has been jointly provided by Oakstone and touchIME. Oakstone Publishing is accredited by the ACCME to provide continuing medical education to physicians.

After watching this activity, participants should be better able to:

Target Audience

This activity is designed to meet the educational needs of pulmonologists, cardiologists, cardiopulmonary surgeons, rheumatologists and other HCPs involved in the care of patients with CTEPH globally.

Disclosures – Faculty

Oakstone Publishing has assessed conflict of interest with its faculty, authors, editors, and any individuals who were in a position to control the content of this CME activity. Any identified relevant conflicts of interest were resolved for fair balance and scientific objectivity of studies utilized in this activity. Oakstone Publishing’s planners, content reviewers, and editorial staff disclose no relevant commercial interests.

PROF. IRENE LANG discloses: Grants/research support: Actelion, AOPOrphan, Consultant/Advisory Boards: Actelion, AOPOrphan, Medtronic, Ferrer

PROF. MARC HUMBERT discloses: Grants/research support: Bayer, GSK, Actelion, Consultant/Advisory Boards: Actelion, Bayer, GSK, Merck, United Therapeutics, Acceleron

DR. MARK TOSHNER discloses: Consultant/Advisory Boards: Morphogen-IX

Content Reviewer

Walter Murray Yarbrough, MD has no financial interests/relationships or affiliations in relation to this activity.

Touch Medical Writer

Paul Taylor has no financial interests/relationships or affiliations in relation to this activity.

Requirement for Successful Completion

This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of Oakstone Publishing and touchIME. Oakstone Publishing is accredited by the ACCME to provide continuing medical education for physicians.

Oakstone Publishing designates this enduring material for a maximum of 0.5 AMA PRA Category 1 Credit™️. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

In order to receive credit for this activity, participants must review and complete the post-test and evaluation form. A score of 70% or higher is needed to obtain CME credit. Statements of credit are awarded upon successful completion of the post-test and evaluation form.

Date of original release: April 21, 2020. Date credits expire: April 21, 2021.

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CME Post-test

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Q1. Which of the following factors would be assessed as being a poor prognostic indicator when determining operability in patients with CTEPH?

  1. A. Inaccessible vascular obstruction
  2. B. PAP out of proportion to morphological lesions
  3. C. Significant prohibitive comorbidities
  4. D. All of the above

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An international registry reported that despite similarities in clinical presentation, operable and non-operable patients with CTEPH may have distinct associated medical conditions.1 Approximately 40% of the patients in the registry were considered inoperable due to concern for inaccessible vascular obstruction, PAP out of proportion to morphological lesions and significant prohibitive comorbidities.2
CTEPH, chronic thromboembolic pulmonary hypertension; DVT, deep vein thrombosis; PAP, pulmonary artery pressure; PE, pulmonary embolism.

Reference

1. Pepke-Zaba J, et al. Circulation 2011;124:1973-1981.
2. Kim NH, et al. Chronic thromboembolic pulmonary hypertension. Eur Respir J 2019;53:1801915.

Q2. How do clinical agents used to treat CTEPH target the NO–sGC–cGMP pathway?

  1. A. Increase NO levels to inhibit the growth of smooth muscle cells
  2. B. Activate NO binding to sGC to inhibit cGMP synthesis
  3. C. Stabilize NO-sGC binding to increase cGMP synthesis
  4. D. Indirectly stimulate sGC to inhibit platelet aggregation

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Recent evidence suggests the involvement of the NO–sGC–cGMP pathway in the pathophysiology of CTEPH. NO produced by vascular endothelium inhibits platelet aggregation and growth of smooth muscle cells. NO also activates sGC to synthesise cGMP, a second messenger with many actions including smooth muscle relaxation.

cGMP, cyclic guanosine monophosphate; CTEPH, chronic thromboembolic pulmonary hypertension; NO, nitric oxide; sGC, soluble guanylate cyclase.

Reference

Tonelli AR, et al. Pulm Circ 2013;3:20–30.

Q3. Which of the following statements best describes the clinical outcomes reported for CHEST-1 study?

  1. A. Pulmonary vascular resistance decreased in the riociguat group and increased in the placebo group
  2. B. Riociguat was also associated with no change in WHO functional class
  3. C. No serious adverse events were reported in the riociguat group
  4. D. There was no difference in the 6-minute walk distance in the riociguat group compared with the placebo group

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By week 16, the 6-minute walk distance had increased by a mean of 39 m in the riociguat group, as compared with a mean decrease of 6 m in the placebo group (least-squares mean difference, 46 m; 95% confidence interval [CI], 25 to 67; P<0.001). Pulmonary vascular resistance decreased by 226 dyn·sec·cm–5 in the riociguat group and increased by 23 dyn·sec·cm–5 in the placebo group (least-squares mean difference, –246 dyn·sec·cm–5; 95% CI, –303 to –190; P<0.001). Riociguat was also associated with significant improvements in the NT-proBNP level (P<0.001) and WHO functional class (P=0.003). The most common serious adverse events were right ventricular failure (in 3% of patients in each group) and syncope (in 2% of the riociguat group and in 3% of the placebo group). WHO, World Health Organization. Reference

Ghofrani HG, et al. N Engl J Med 2013;369:319-329.

Q4. Your patient with CTEPH has recently undergone successful PEA. What would be your recommendations for anticoagulation therapy in this patient based on current guidelines?

  1. A. Lifelong oral anticoagulation with VKAs
  2. B. Anticoagulation therapy is not recommended following successful PEA or BPA
  3. C. NOACs should be considered as first-choice
  4. D. Oral anticoagulation should only be considered for low-risk patients

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The European Society of Cardiology guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society recommend lifelong anticoagulation for inoperable patients and those who have undergone successful PEA or BPA.
BPA, balloon pulmonary angioplasty; PEA, pulmonary endarterectomy.

References

Konstantinides SV, et al. Eur Respir J 2019;54:1901647.

Konstantinides SV, et al. Eur Heart J 2020;41:543–603.

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touchEXPERT OPINIONS

Medical therapy for CTEPH: From biology
to new treatment options

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Introduction

Watch leading experts involved in the care of patients with CTEPH discuss the latest issues and controversies in the medical management of CTEPH and related comorbidities, including the evolving data supporting the use of oral therapy, the application of oral therapies in clinical practice and how the underlying biology impacts on treatment decisions.

This activity is intended for pulmonologists, cardiologists, cardiopulmonary surgeons, rheumatologists and other HCPs involved in the care of patients with CTEPH globally.

Learning Objectives

After watching this touchEXPERT OPINIONS, you should be able to:

  • Describe the biological and pathophysiological mechanisms of CTEPH
  • Summarize the evolving data supporting the use of oral therapies
  • Explain how new developments in medical therapy for the treatment of CTEPH will change daily practice