PMID- 38132665
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231224
IS  - 2308-3425 (Electronic)
IS  - 2308-3425 (Linking)
VI  - 10
IP  - 12
DP  - 2023 Dec 16
TI  - Pulmonary Vasodilator Therapy in Severe Pulmonary Hypertension Due to Chronic 
      Obstructive Pulmonary Disease (Severe PH-COPD): A Systematic Review and 
      Meta-Analysis.
LID - 10.3390/jcdd10120498 [doi]
LID - 498
AB  - Background: Chronic obstructive pulmonary disease-associated pulmonary 
      hypertension (PH-COPD) results in a significant impact on symptoms, quality of 
      life, and survival. There is scant and conflicting evidence about the use of 
      pulmonary hypertension (PH) specific therapy in patients with PH-COPD. Study 
      Design and Methods: PubMed, OVID, CINAHL, Cochrane, Embase, and Web of Science 
      were searched using various MESH terms to identify randomized controlled trials 
      (RCTs) or observational studies investigating PH-specific therapies in patients 
      with severe PH-COPD, defined by mean pulmonary artery pressure (mPAP) of more 
      than 35 mm Hg or pulmonary vascular resistance (PVR) of more than 5 woods units 
      on right heart catheterization. The primary outcome was a change in mPAP and PVR. 
      Secondary outcomes were changes in six-minute walk distance (6MWD), changes in 
      the brain-natriuretic peptide (BNP), New York Heart Association (NYHA) functional 
      class, oxygenation, and survival. Results: Thirteen studies satisfied the 
      inclusion criteria, including a total of 328 patients with severe PH-COPD. Out of 
      these, 308 patients received some type of specific therapy for PH. There was a 
      significant reduction in mPAP (mean difference (MD) -3.68, 95% CI [-2.03, -5.32], 
      p < 0.0001) and PVR (MD -1.40 Wood units, 95% CI [-1.97, -0.82], p < 0.00001). 
      There was a significant increase in the cardiac index as well (MD 0.26 
      L/min/m(2), 95% CI [0.14, 0.39], p < 0.0001). There were fewer patients who had 
      NYHA class III/lV symptoms, with an odds ratio of 0.55 (95% CI [0.30, 1.01], p = 
      0.05). There was no significant difference in the 6MWD (12.62 m, 95% CI [-8.55, 
      33.79], p = 0.24), PaO(2) (MD -2.20 mm Hg, 95% CI [-4.62, 0.22], p = 0.08), or 
      BNP or NT-proBNP therapy (MD -0.15, 95% CI [-0.46, 0.17], p = 0.36). Conclusion: 
      The use of PH-specific therapies in severe PH-COPD resulted in a significant 
      reduction in mPAP and PVR and increased CI, with fewer patients remaining in NYHA 
      functional class III/IV. However, no significant difference in the 6MWD, 
      biomarkers of right ventricular dysfunction, or oxygenation was identified, 
      demonstrating a lack of hypoxemia worsening with treatment. Further studies are 
      needed to investigate the use of PH medications in patients with severe PH-COPD.
FAU - Elkhapery, Ahmed
AU  - Elkhapery A
AUID- ORCID: 0000-0003-0705-1137
AD  - Department of Internal Medicine, Rochester General Hospital, Rochester, NY 14621, 
      USA.
FAU - Hammami, M Bakri
AU  - Hammami MB
AUID- ORCID: 0000-0003-3422-5163
AD  - Department of Internal Medicine, Jacobi Medical Center-Albert Einstein College of 
      Medicine, New York, NY 10461, USA.
FAU - Sulica, Roxana
AU  - Sulica R
AD  - Division of Pulmonary, Sleep and Critical Care Medicine, Department of Medicine, 
      New York University Grossman School of Medicine and NYU Langone Health, New York, 
      NY 10016, USA.
FAU - Boppana, Hemanth
AU  - Boppana H
AD  - Department of Internal Medicine, Rochester General Hospital, Rochester, NY 14621, 
      USA.
FAU - Abdalla, Zeinab
AU  - Abdalla Z
AD  - Rochester General Hospital Research Institute, Rochester, NY 14621, USA.
FAU - Iyer, Charoo
AU  - Iyer C
AD  - Department of Internal Medicine, Rochester General Hospital, Rochester, NY 14621, 
      USA.
FAU - Taifour, Hazem
AU  - Taifour H
AD  - Department of Internal Medicine, Unity Hospital, Rochester, NY 14626, USA.
FAU - Niu, Chengu
AU  - Niu C
AD  - Department of Internal Medicine, Rochester General Hospital, Rochester, NY 14621, 
      USA.
FAU - Deshwal, Himanshu
AU  - Deshwal H
AUID- ORCID: 0000-0003-2086-1281
AD  - Division of Pulmonary, Sleep and Critical Care Medicine, Department of Medicine, 
      West Virginia University School of Medicine, Morgantown, WV 26505, USA.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20231216
PL  - Switzerland
TA  - J Cardiovasc Dev Dis
JT  - Journal of cardiovascular development and disease
JID - 101651414
PMC - PMC10743410
OTO - NOTNLM
OT  - COPD
OT  - endothelin receptor antagonists
OT  - phosphodiesterase 5 inhibitors
OT  - prostacyclin analogs
OT  - pulmonary hypertension
OT  - severe PH-COPD
COIS- A.E., M.B.H., H.B., Z.A., C.I., H.T., C.N. and H.D. have no financial disclosures 
      or conflict of interest related to this study. R.S. (Sulica) has received 
      research support from Bayer, United Therapeutics, Acceleron, Bellerophon, 
      Gossamer, Enzyvant, Aerovate, and Merck and served on advisory boards for 
      Actelion, Janssen, Enzyvant, Merck, Bayer, Gossamer, and United Therapeutics.
EDAT- 2023/12/22 12:42
MHDA- 2023/12/22 12:43
PMCR- 2023/12/16
CRDT- 2023/12/22 09:11
PHST- 2023/11/02 00:00 [received]
PHST- 2023/11/29 00:00 [revised]
PHST- 2023/12/13 00:00 [accepted]
PHST- 2023/12/22 12:43 [medline]
PHST- 2023/12/22 12:42 [pubmed]
PHST- 2023/12/22 09:11 [entrez]
PHST- 2023/12/16 00:00 [pmc-release]
AID - jcdd10120498 [pii]
AID - jcdd-10-00498 [pii]
AID - 10.3390/jcdd10120498 [doi]
PST - epublish
SO  - J Cardiovasc Dev Dis. 2023 Dec 16;10(12):498. doi: 10.3390/jcdd10120498.