Nimish Mehta, PhD, MBA, CCMEP1; Tara Herrmann, PhD1; Chad Williamson, MS, MBA2; Steven D. Nathan, MD3

1Medscape, LLC, New York, NY, USA; 2CE Outcomes, LLC, Birmingham, AL, USA; 3Inova Fairfax Hospital, Falls Church, VA, USA

Success of Educational Interventions on Pulmonary Arterial Hypertension Management Success of Educational Interventions on Pulmonary Arterial Hypertension Management

purpose

Pulmonary arterial hypertension (PAH) -- a progressive and fatal disorder— is underrecognized and inadequately treated based on current evidence-based guideline recommendations. Delays in diagnosis of more than 2 years and inadequate treatment have been identified from the REVEAL registry.1,2 A study was conducted to determine if online educational interventions could improve competence and performance of pulmonologists and cardiologists with respect to PAH management.

methods

• A cohort of practicing pulmonologists and cardiologists in the United States was identified prior to the launch of a series of 4 educational interventions designed to address gaps in the care of patients with PAH.3-6

• The outcomes survey method to measure performance included knowledge- and case-based multiple-choice questions derived from current evidence-based recommendations. The domains assessed included diagnosis, pathophysiology, evidence-based treatment strategies, and monitoring.

• Confidentiality of survey respondents was maintained and responses were de-identified and aggregated prior to analysis.

• Non-practicing clinicians and clinicians not involved in the care of patients with PAH were excluded from the study.

• Responses to questions associated with the clinical cases and aligned to individual interventions were collected and compared with baseline data (collected prior to participation in educational interventions) in order to assess the effect of education on the practice patterns of participants.

• Chi-square tests were conducted to detect differences between the baseline and the post-education assessment responses among pulmonologists and cardiologists.

A total of 455 participants – including 277 pulmonologists and 178 cardiologists – were assessed in this study. Compared with the baseline assessment, significant improvements were found as a result of participation in the educational interventions, specifically:

• More cardiologists selected right heart catheterization to diagnose PAH (73% post-education vs 53% baseline, P = .01) and identified the correct hemodynamics for a patient at high risk (91% post-education vs 75% baseline, P = .01)

• More pulmonologists correctly identified a positive vasodilator test as a decrease in mean pulmonary arterial pressure (mPAP) by at least 10 mm Hg to ≤ 40 mm Hg (85% post-education vs 71% baseline, P = .02)

• 13% more pulmonologists (P = .04) correctly identified 25 mm Hg as the cut-off mPAP value to diagnose PAH

• 20% more pulmonologists and 19% more cardiologists recognized the action of phosphodiesterase type 5 (PDE-5) inhibitors in relation to PAH pathogenesis (Figure 1)

• Pulmonologists (P = .004) and cardiologists (P = .04) were more likely to recognize the goals of combination therapy (Figure 2)

• 22% more cardiologists would consider dual or trial therapy for PAH in a patient with persistent World Health Organization (WHO) functional class 3 or 4 symptoms (76% before and 88% after; P = .04)

• Pulmonologists (P = .01) and cardiologists (P = .01) were more likely to recognize the mechanism of action of PAH therapies (Figure 3)

results

Conclusions and Clinical Implications

This study demonstrated the success of well-designed, targeted, online educational interventions in improving the practice patterns of pulmonologists and cardiologists in the assessment and management of patients with PAH. Statistically significant improvements in several domains of PAH management may result in improvements in patient care and outcomes.

References 1. Brown LM, Chen H, Halpern S, et al. Delay in recognition of pulmonary arterial hypertension: factors identified from the

REVEAL Registry. Chest. 2011;140(1):19-26.

2. Gillman J, BS, Farber HW, Miller DP, Meltzer LA, McGoon M. Pulmonary arterial hypertension (PAH)-specific therapy at time of worsening to functional class IV in patients from The REVEAL Registry. Paper presented at: American Thoracic Society Meeting; May 18-23, 2012; San Francisco, CA.

3. Waxman AB. Guided by rationale: therapeutic strategies in PAH. Medscape Education Pulmonology. March 15, 2012. http://www.medscape.org/viewarticle/759084. Accessed October 10, 2013.

4. Nathan SD, Farber HW. Live on PAH: breathing life into patient with PAH. Medscape Education Pulmonology. April 12, 2012. http://www.medscape.org/viewarticle/761723. Accessed October 10, 2013.

5. Gomberg-Maitland M, Champion HC, Preston IR, Torres F. What would you do? Expert perspectives on challenging scenarios in pulmonary arterial hypertension. Medscape Education Pulmonology. June 15, 2012. http://www.medscape.org/viewarticle/765339. Accessed October 10, 2013.

6. Nathan SD, Shlobin OA. Taking steps to improve patient outcomes in PAH. Medscape Education Pulmonology. July 13, 2012. http://www.medscape.org/viewarticle/767051. Accessed October 10, 2013.

Acknowledgements

The educational interventions and outcomes measurement were funded through an independent educational grant from Gilead Sciences, Inc. Poster layout was provided by Christopher Clarke and Irina Kogan of Medscape, LLC.

For more information, contact Nimish Mehta, PhD, MBA, CCMEP, Senior Director, Educational Strategy, Medscape, LLC, nmehta@medscape.net.

figure 1 Improved recognition of pathogenesis of PAH.

Prostacyclin and thromboxane are unaffected in the

pulmonary circulation but can be altered in the liver

and spleen

Nitric oxide (NO) is a potent vasoconstrictor, and high

levels have been shown in the pulmonary circulation

Endothelin-1 is a potent vasodilator, and levels in the lungs are known to be

extremely low in the plasma of patients with PAH

Phosphodiesterase type 5 (PDE-5) inhibition prevents the breakdown of cyclic guanosine

monophosphate (cGMP), thereby augmenting the action of NO*

Cardiologists baseline (n=48)Cardiologists post-education (n=56)

Pulmonologists baseline (n=108)Pulmonologists post-education (n=73)

Which of the following statements best describes the pathogenesis of PAH?

100%

80%

60%

40%

20%

0%

6%2%

27%

65%

5% 4%7%

84%

6% 5%

21%

68%

0% 0%

12%

88%

Card P =.02*Pulm P =.002*

figure 2 Role of combination therapy in patients with PAH.

The goal of combination therapy is to maximize efficacy, minimize toxicity, and allow for

targeting of more than 1 pathologic pathway*

Multiple, large-scale, randomized trials have shown efficacy for

combination therapy in exercise improvement and long-term

survival

Combination therapy is no more effective than single

agent therapy and should be avoided due to the potential for

increased risk of toxicity

Combination therapy is only effective in lower risk patients

(WHO functional class 1 and 2)

Cardiologists baseline (n=47)Cardiologists post-education (n=56)

Pulmonologists baseline (n=108)Pulmonologists post-education (n=73)

Which of the following statements is true regarding combination therapy for PAH?100%

80%

60%

40%

20%

0%

77%

19%

0%4%

91%

7%2% 0%

77%

19%

5%0%

93%

4% 3%0%

Card P =.04*Pulm P =.004*

figure 3 Appropriate selection of PAH therapy based on mechanism of action.

Treprostinil Bosentan Sildenafil Ambrisentan*

Cardiologists baseline (n=48)Cardiologists post-education (n=56)

Pulmonologists baseline (n=107)Pulmonologists post-education (n=72)

Which of the following is an orally active, selective endothelin receptor antagonist (ie, targeted toward endothelin receptor type A only)?

100%

80%

60%

40%

20%

0%

12%

38% 17%33%

14%

25%

0%

61%

11%

25%

7%

57%

7%

14%

4%

75%

Card P =.01*Pulm P =.01*