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{{Pulmonary hypertension}}
{{Pulmonary hypertension}}
{{CMG}}; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]
{{CMG}}; '''Assistant Editor(s)-in-Chief:''' [[User:Ralph Matar|Ralph Matar]]; {{Jose}}


==Overview==
==Overview==
Several laboratory tests are required in the evaluation of a patient for pulmonary hypertension. Laboratory tests help either in the exclusion of other differential diagnosis or in the determination of any medical condition that might be the cause of the pulmonary hypertension. [[Biochemistry]], [[hematology]] and [[thyroid function tests]] are required in all patients with pulmonary hypertension.They are important for the diagnosis of [[chronic hemolytic anemia]], [[myeloproliferative disorder]]s, thyroid disorders and [[chronic renal failure]] on [[dialysis]].
There are no specific [[diagnostic]] [[Laboratory|lab]] findings associated with [[pulmonary hypertension]]. Despite that, several [[laboratory]] tests are required in the evaluation of a [[patient]] for pulmonary hypertension to assess its severity or possible associated causes. [[Biochemistry]], [[hematology]] and [[thyroid function tests]] are required in all [[patients]] with pulmonary hypertension. They are important for the [[diagnosis]] of [[chronic hemolytic anemia]], [[myeloproliferative disorder]]s, [[thyroid disorders]] and [[chronic renal failure]] on [[dialysis]].


==Laboratory Findings==
==Laboratory Findings==
*[[Biochemistry]], [[hematology]] and [[thyroid function tests]] are required in all patients with pulmonary hypertension.They are important for the diagnosis of [[chronic hemolytic anemia]], [[myeloproliferative disorder]]s, thyroid disorders and [[chronic renal failure]] on [[dialysis]].
* Serologic testing to detect connective tissue diseases ([[systemic sclerosis]]), [[HIV]], and hepatitis.
**[[Systemic sclerosis]] is very important to exclude in pulmonary hypertension because this systemic disease his risk factor for the development of pulmonary arterial hypertension. Anti-Scl-70, [[Anti-centromere antibodies|anti-centromere]], and U3-RNP are typically positive.
*Liver function tests should be done to exclude [[portal hypertension]].


==Other Biomarkers==
*[[Biochemistry]], [[hematology]] and [[thyroid function tests]] are required in all [[patients]] with pulmonary hypertension. They are important for the [[diagnosis]] of [[chronic hemolytic anemia]], [[myeloproliferative disorder]]s, [[thyroid disorders]], and [[chronic renal failure]] on [[dialysis]].
*[[Serologic]] testing to detect [[connective tissue diseases]] ([[systemic sclerosis]]), [[HIV]], and [[hepatitis]].
**[[Systemic sclerosis]] is an important [[disease]] to exclude in pulmonary hypertension because this systemic disease is a [[risk factor]] for the development of pulmonary arterial hypertension. Anti-Scl-70, [[Anti-centromere antibodies|anti-centromere]], and U3-RNP markers are typically positive.
*[[Liver function tests]] should be done to exclude [[portal hypertension]].
 
===Other Biomarkers===


===Brain natriuretic peptide (BNP) and N-terminal fragment of BNP (NT-proBNP)===
===Brain natriuretic peptide (BNP) and N-terminal fragment of BNP (NT-proBNP)===
* [[Brain natriuretic peptide]] (BNP) is elevated in pulmonary hypertension of various classes:
** 1.1. Idiopathic PAH (IPAH)
** 1.4.1 PAH associated with [[connective tissue disease]]
** 1.4.4 [[Congenital heart diseases]] (with systemic-to-pulmonary shunts)
** 3.1 Pulmonary hypertension due to [[chronic obstructive pulmonary disease]]
** 3.2 Pulmonary hypertension due to [[interstitial lung disease]]
** 4. Chronic thromboembolic pulmonary hypertension (CTEPH)
** 5.3 Pulmonary hypertension with metabolic disorders such as [[Gaucher disease]]


* BNP levels correlate with hemodynamic parameters, exercise capacity, and [[New york heart association functional classification|NYHA functional class]] and bear prognostic significance in IPAH, in pulmonary hypertension due to lung diseases, and in chronic [[thromboembolic]] pulmonary hypertension.<ref name="Nagaya-2000">{{Cite journal  | last1 = Nagaya | first1 = N. | last2 = Nishikimi | first2 = T. | last3 = Uematsu | first3 = M. | last4 = Satoh | first4 = T. | last5 = Kyotani | first5 = S. | last6 = Sakamaki | first6 = F. | last7 = Kakishita | first7 = M. | last8 = Fukushima | first8 = K. | last9 = Okano | first9 = Y. | title = Plasma brain natriuretic peptide as a prognostic indicator in patients with primary pulmonary hypertension. | journal = Circulation | volume = 102 | issue = 8 | pages = 865-70 | month = Aug | year = 2000 | doi =  | PMID = 10952954 }}</ref><ref name="Kucher-2003">{{Cite journal  | last1 = Kucher | first1 = N. | last2 = Printzen | first2 = G. | last3 = Goldhaber | first3 = SZ. | title = Prognostic role of brain natriuretic peptide in acute pulmonary embolism. | journal = Circulation | volume = 107 | issue = 20 | pages = 2545-7 | month = May | year = 2003 | doi = 10.1161/01.CIR.0000074039.45523.BE | PMID = 12742987 }}</ref><ref name="ten Wolde-2003">{{Cite journal  | last1 = ten Wolde | first1 = M. | last2 = Tulevski | first2 = II. | last3 = Mulder | first3 = JW. | last4 = Söhne | first4 = M. | last5 = Boomsma | first5 = F. | last6 = Mulder | first6 = BJ. | last7 = Büller | first7 = HR. | title = Brain natriuretic peptide as a predictor of adverse outcome in patients with pulmonary embolism. | journal = Circulation | volume = 107 | issue = 16 | pages = 2082-4 | month = Apr | year = 2003 | doi = 10.1161/01.CIR.0000070020.79932.DB | PMID = 12707233 }}</ref><ref name="Leuchte-2006">{{Cite journal  | last1 = Leuchte | first1 = HH. | last2 = Baumgartner | first2 = RA. | last3 = Nounou | first3 = ME. | last4 = Vogeser | first4 = M. | last5 = Neurohr | first5 = C. | last6 = Trautnitz | first6 = M. | last7 = Behr | first7 = J. | title = Brain natriuretic peptide is a prognostic parameter in chronic lung disease. | journal = Am J Respir Crit Care Med | volume = 173 | issue = 7 | pages = 744-50 | month = Apr | year = 2006 | doi = 10.1164/rccm.200510-1545OC | PMID = 16415273 }}</ref>  
*[[Brain natriuretic peptide]] (BNP) is elevated in pulmonary hypertension of various classes:
* N-terminal fragment of BNP (NT-proBNP) has been studied as an alternative biomarker to BNP in various classes of pulmonary hypertension.
**1.1. Idiopathic PAH (IPAH)
* Higher NT-proBNP and peak oxygen uptake were shown to be independent predictors of mortality and a supramedian NT-proBNP level indicated a significantly lower survival.<ref name="Andreassen-2006">{{Cite journal  | last1 = Andreassen | first1 = AK. | last2 = Wergeland | first2 = R. | last3 = Simonsen | first3 = S. | last4 = Geiran | first4 = O. | last5 = Guevara | first5 = C. | last6 = Ueland | first6 = T. | title = N-terminal pro-B-type natriuretic peptide as an indicator of disease severity in a heterogeneous group of patients with chronic precapillary pulmonary hypertension. | journal = Am J Cardiol | volume = 98 | issue = 4 | pages = 525-9 | month = Aug | year = 2006 | doi = 10.1016/j.amjcard.2006.02.061 | PMID = 16893710 }}</ref><ref name="Fijalkowska-2006">{{Cite journal  | last1 = Fijalkowska | first1 = A. | last2 = Kurzyna | first2 = M. | last3 = Torbicki | first3 = A. | last4 = Szewczyk | first4 = G. | last5 = Florczyk | first5 = M. | last6 = Pruszczyk | first6 = P. | last7 = Szturmowicz | first7 = M. | title = Serum N-terminal brain natriuretic peptide as a prognostic parameter in patients with pulmonary hypertension. | journal = Chest | volume = 129 | issue = 5 | pages = 1313-21 | month = May | year = 2006 | doi = 10.1378/chest.129.5.1313 | PMID = 16685024 }}</ref>
**1.4.1 PAH associated with [[connective tissue disease]]
**1.4.4 [[Congenital heart diseases]] (with systemic-to-pulmonary shunts)
**3.1 Pulmonary hypertension due to [[chronic obstructive pulmonary disease]]
**3.2 Pulmonary hypertension due to [[interstitial lung disease]]
**4. Chronic thromboembolic pulmonary hypertension (CTEPH)
**5.3 Pulmonary hypertension with metabolic disorders such as [[Gaucher disease]]
 
*BNP levels correlate with hemodynamic parameters, exercise capacity, and [[New York heart association functional classification|NYHA functional class]] and bear [[prognostic]] significance in IPAH, in pulmonary hypertension due to lung diseases, and in chronic [[thromboembolic]] pulmonary hypertension.<ref name="Nagaya-2000">{{Cite journal  | last1 = Nagaya | first1 = N. | last2 = Nishikimi | first2 = T. | last3 = Uematsu | first3 = M. | last4 = Satoh | first4 = T. | last5 = Kyotani | first5 = S. | last6 = Sakamaki | first6 = F. | last7 = Kakishita | first7 = M. | last8 = Fukushima | first8 = K. | last9 = Okano | first9 = Y. | title = Plasma brain natriuretic peptide as a prognostic indicator in patients with primary pulmonary hypertension. | journal = Circulation | volume = 102 | issue = 8 | pages = 865-70 | month = Aug | year = 2000 | doi =  | PMID = 10952954 }}</ref><ref name="Kucher-2003">{{Cite journal  | last1 = Kucher | first1 = N. | last2 = Printzen | first2 = G. | last3 = Goldhaber | first3 = SZ. | title = Prognostic role of brain natriuretic peptide in acute pulmonary embolism. | journal = Circulation | volume = 107 | issue = 20 | pages = 2545-7 | month = May | year = 2003 | doi = 10.1161/01.CIR.0000074039.45523.BE | PMID = 12742987 }}</ref><ref name="ten Wolde-2003">{{Cite journal  | last1 = ten Wolde | first1 = M. | last2 = Tulevski | first2 = II. | last3 = Mulder | first3 = JW. | last4 = Söhne | first4 = M. | last5 = Boomsma | first5 = F. | last6 = Mulder | first6 = BJ. | last7 = Büller | first7 = HR. | title = Brain natriuretic peptide as a predictor of adverse outcome in patients with pulmonary embolism. | journal = Circulation | volume = 107 | issue = 16 | pages = 2082-4 | month = Apr | year = 2003 | doi = 10.1161/01.CIR.0000070020.79932.DB | PMID = 12707233 }}</ref><ref name="Leuchte-2006">{{Cite journal  | last1 = Leuchte | first1 = HH. | last2 = Baumgartner | first2 = RA. | last3 = Nounou | first3 = ME. | last4 = Vogeser | first4 = M. | last5 = Neurohr | first5 = C. | last6 = Trautnitz | first6 = M. | last7 = Behr | first7 = J. | title = Brain natriuretic peptide is a prognostic parameter in chronic lung disease. | journal = Am J Respir Crit Care Med | volume = 173 | issue = 7 | pages = 744-50 | month = Apr | year = 2006 | doi = 10.1164/rccm.200510-1545OC | PMID = 16415273 }}</ref>
*N-terminal fragment of BNP (NT-proBNP) has been studied as an alternative [[biomarker]] to BNP in various classes of pulmonary hypertension.
*Higher NT-proBNP and peak oxygen uptake were shown to be independent predictors of mortality and a supramedian NT-proBNP level indicated a significantly lower survival.<ref name="Andreassen-2006">{{Cite journal  | last1 = Andreassen | first1 = AK. | last2 = Wergeland | first2 = R. | last3 = Simonsen | first3 = S. | last4 = Geiran | first4 = O. | last5 = Guevara | first5 = C. | last6 = Ueland | first6 = T. | title = N-terminal pro-B-type natriuretic peptide as an indicator of disease severity in a heterogeneous group of patients with chronic precapillary pulmonary hypertension. | journal = Am J Cardiol | volume = 98 | issue = 4 | pages = 525-9 | month = Aug | year = 2006 | doi = 10.1016/j.amjcard.2006.02.061 | PMID = 16893710 }}</ref><ref name="Fijalkowska-2006">{{Cite journal  | last1 = Fijalkowska | first1 = A. | last2 = Kurzyna | first2 = M. | last3 = Torbicki | first3 = A. | last4 = Szewczyk | first4 = G. | last5 = Florczyk | first5 = M. | last6 = Pruszczyk | first6 = P. | last7 = Szturmowicz | first7 = M. | title = Serum N-terminal brain natriuretic peptide as a prognostic parameter in patients with pulmonary hypertension. | journal = Chest | volume = 129 | issue = 5 | pages = 1313-21 | month = May | year = 2006 | doi = 10.1378/chest.129.5.1313 | PMID = 16685024 }}</ref>


===Cyclic guanosine monophosphate (cGMP)===
===Cyclic guanosine monophosphate (cGMP)===
* [[Cyclic guanosine monophosphate]] (cGMP) is produced by the activation of guanylate cyclase and can be viewed as an indirect marker of nitric oxide production.
 
* Plasma cGMP levels are higher in patients with pulmonary hypertension and decrease after inhalation of [[iloprost]].<ref name="Wiedemann-2001">{{Cite journal  | last1 = Wiedemann | first1 = R. | last2 = Ghofrani | first2 = HA. | last3 = Weissmann | first3 = N. | last4 = Schermuly | first4 = R. | last5 = Quanz | first5 = K. | last6 = Grimminger | first6 = F. | last7 = Seeger | first7 = W. | last8 = Olschewski | first8 = H. | title = Atrial natriuretic peptide in severe primary and nonprimary pulmonary hypertension: response to iloprost inhalation. | journal = J Am Coll Cardiol | volume = 38 | issue = 4 | pages = 1130-6 | month = Oct | year = 2001 | doi =  | PMID = 11583893 }}</ref>  
*[[Cyclic guanosine monophosphate]] ([[cGMP]]) is produced by the activation of guanylate cyclase and can be viewed as an indirect marker of [[nitric oxide]] production.
* A significant correlation between baseline plasma cGMP and severity of pulmonary arterial hypertension has also been reported.
*Plasma [[cGMP]] levels are higher in [[patients]] with pulmonary hypertension and decrease after inhalation of [[iloprost]].<ref name="Wiedemann-2001">{{Cite journal  | last1 = Wiedemann | first1 = R. | last2 = Ghofrani | first2 = HA. | last3 = Weissmann | first3 = N. | last4 = Schermuly | first4 = R. | last5 = Quanz | first5 = K. | last6 = Grimminger | first6 = F. | last7 = Seeger | first7 = W. | last8 = Olschewski | first8 = H. | title = Atrial natriuretic peptide in severe primary and nonprimary pulmonary hypertension: response to iloprost inhalation. | journal = J Am Coll Cardiol | volume = 38 | issue = 4 | pages = 1130-6 | month = Oct | year = 2001 | doi =  | PMID = 11583893 }}</ref>
* Nitric oxide inhalation provoked a prompt increase in cGMP production, however, the magnitude of cGMP release is not linked with a decrease in pulmonary vascular resistance.<ref name="Ghofrani-2002">{{Cite journal  | last1 = Ghofrani | first1 = HA. | last2 = Wiedemann | first2 = R. | last3 = Rose | first3 = F. | last4 = Weissmann | first4 = N. | last5 = Schermuly | first5 = RT. | last6 = Quanz | first6 = K. | last7 = Grimminger | first7 = F. | last8 = Seeger | first8 = W. | last9 = Olschewski | first9 = H. | title = Lung cGMP release subsequent to NO inhalation in pulmonary hypertension: responders versus nonresponders. | journal = Eur Respir J | volume = 19 | issue = 4 | pages = 664-71 | month = Apr | year = 2002 | doi =  | PMID = 11998996 }}</ref>
*A significant correlation between baseline plasma [[cGMP]] and severity of pulmonary arterial hypertension has also been reported.
*[[Nitric oxide]] inhalation provoked a prompt increase in [[cGMP]] production, however, the magnitude of [[cGMP]] release is not linked with a decrease in pulmonary [[vascular resistance]].<ref name="Ghofrani-2002">{{Cite journal  | last1 = Ghofrani | first1 = HA. | last2 = Wiedemann | first2 = R. | last3 = Rose | first3 = F. | last4 = Weissmann | first4 = N. | last5 = Schermuly | first5 = RT. | last6 = Quanz | first6 = K. | last7 = Grimminger | first7 = F. | last8 = Seeger | first8 = W. | last9 = Olschewski | first9 = H. | title = Lung cGMP release subsequent to NO inhalation in pulmonary hypertension: responders versus nonresponders. | journal = Eur Respir J | volume = 19 | issue = 4 | pages = 664-71 | month = Apr | year = 2002 | doi =  | PMID = 11998996 }}</ref>


===D-dimer===
===D-dimer===
* D-dimer is a degradation product of cross-linked fibrin and may represent microvascular thrombosis which is implicated in the pathogenesis of pulmonary hypertension.
 
* D-dimer has been shown to be increased and correlates with disease severity as measured by [[NYHA classification|NYHA class]], resting [[oxygen saturation]], and mean pulmonary artery pressure.
*[[D-dimer]] is a degradation product of cross-linked fibrin and may represent microvascular [[thrombosis]] which is implicated in the pathogenesis of pulmonary hypertension.
* There was also an inverse correlation between [[d-dimer]] levels and one-year survival in patients with primary pulmonary hypertension.<ref name="Shitrit-2002">{{Cite journal  | last1 = Shitrit | first1 = D. | last2 = Bendayan | first2 = D. | last3 = Rudensky | first3 = B. | last4 = Izbicki | first4 = G. | last5 = Huerta | first5 = M. | last6 = Fink | first6 = G. | last7 = Kramer | first7 = MR. | title = Elevation of ELISA d-dimer levels in patients with primary pulmonary hypertension. | journal = Respiration | volume = 69 | issue = 4 | pages = 327-9 | month =  | year = 2002 | doi = 63270 | PMID = 12169745 }}</ref><ref name="Shitrit-2002-02">{{Cite journal  | last1 = Shitrit | first1 = D. | last2 = Bendayan | first2 = D. | last3 = Bar-Gil-Shitrit | first3 = A. | last4 = Huerta | first4 = M. | last5 = Rudensky | first5 = B. | last6 = Fink | first6 = G. | last7 = Kramer | first7 = MR. | title = Significance of a plasma D-dimer test in patients with primary pulmonary hypertension. | journal = Chest | volume = 122 | issue = 5 | pages = 1674-8 | month = Nov | year = 2002 | doi =  | PMID = 12426270 }}</ref>
*[[D-dimer]] has been shown to be increased and correlates with disease severity as measured by [[NYHA classification|NYHA class]], resting [[oxygen saturation]], and mean pulmonary artery pressure.
*There was also an inverse correlation between [[d-dimer]] levels and one-year survival in [[patients]] with primary pulmonary hypertension.<ref name="Shitrit-2002">{{Cite journal  | last1 = Shitrit | first1 = D. | last2 = Bendayan | first2 = D. | last3 = Rudensky | first3 = B. | last4 = Izbicki | first4 = G. | last5 = Huerta | first5 = M. | last6 = Fink | first6 = G. | last7 = Kramer | first7 = MR. | title = Elevation of ELISA d-dimer levels in patients with primary pulmonary hypertension. | journal = Respiration | volume = 69 | issue = 4 | pages = 327-9 | month =  | year = 2002 | doi = 63270 | PMID = 12169745 }}</ref><ref name="Shitrit-2002-02">{{Cite journal  | last1 = Shitrit | first1 = D. | last2 = Bendayan | first2 = D. | last3 = Bar-Gil-Shitrit | first3 = A. | last4 = Huerta | first4 = M. | last5 = Rudensky | first5 = B. | last6 = Fink | first6 = G. | last7 = Kramer | first7 = MR. | title = Significance of a plasma D-dimer test in patients with primary pulmonary hypertension. | journal = Chest | volume = 122 | issue = 5 | pages = 1674-8 | month = Nov | year = 2002 | doi =  | PMID = 12426270 }}</ref>


==References==
==References==
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Latest revision as of 14:19, 9 June 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editor(s)-in-Chief: Ralph Matar; José Eduardo Riceto Loyola Junior, M.D.[2]

Overview

There are no specific diagnostic lab findings associated with pulmonary hypertension. Despite that, several laboratory tests are required in the evaluation of a patient for pulmonary hypertension to assess its severity or possible associated causes. Biochemistry, hematology and thyroid function tests are required in all patients with pulmonary hypertension. They are important for the diagnosis of chronic hemolytic anemia, myeloproliferative disorders, thyroid disorders and chronic renal failure on dialysis.

Laboratory Findings

Other Biomarkers

Brain natriuretic peptide (BNP) and N-terminal fragment of BNP (NT-proBNP)

  • BNP levels correlate with hemodynamic parameters, exercise capacity, and NYHA functional class and bear prognostic significance in IPAH, in pulmonary hypertension due to lung diseases, and in chronic thromboembolic pulmonary hypertension.[1][2][3][4]
  • N-terminal fragment of BNP (NT-proBNP) has been studied as an alternative biomarker to BNP in various classes of pulmonary hypertension.
  • Higher NT-proBNP and peak oxygen uptake were shown to be independent predictors of mortality and a supramedian NT-proBNP level indicated a significantly lower survival.[5][6]

Cyclic guanosine monophosphate (cGMP)

  • Cyclic guanosine monophosphate (cGMP) is produced by the activation of guanylate cyclase and can be viewed as an indirect marker of nitric oxide production.
  • Plasma cGMP levels are higher in patients with pulmonary hypertension and decrease after inhalation of iloprost.[7]
  • A significant correlation between baseline plasma cGMP and severity of pulmonary arterial hypertension has also been reported.
  • Nitric oxide inhalation provoked a prompt increase in cGMP production, however, the magnitude of cGMP release is not linked with a decrease in pulmonary vascular resistance.[8]

D-dimer

  • D-dimer is a degradation product of cross-linked fibrin and may represent microvascular thrombosis which is implicated in the pathogenesis of pulmonary hypertension.
  • D-dimer has been shown to be increased and correlates with disease severity as measured by NYHA class, resting oxygen saturation, and mean pulmonary artery pressure.
  • There was also an inverse correlation between d-dimer levels and one-year survival in patients with primary pulmonary hypertension.[9][10]

References

  1. ↑ Nagaya, N.; Nishikimi, T.; Uematsu, M.; Satoh, T.; Kyotani, S.; Sakamaki, F.; Kakishita, M.; Fukushima, K.; Okano, Y. (2000). "Plasma brain natriuretic peptide as a prognostic indicator in patients with primary pulmonary hypertension". Circulation. 102 (8): 865–70. PMID 10952954. Unknown parameter |month= ignored (help)
  2. ↑ Kucher, N.; Printzen, G.; Goldhaber, SZ. (2003). "Prognostic role of brain natriuretic peptide in acute pulmonary embolism". Circulation. 107 (20): 2545–7. doi:10.1161/01.CIR.0000074039.45523.BE. PMID 12742987. Unknown parameter |month= ignored (help)
  3. ↑ ten Wolde, M.; Tulevski, II.; Mulder, JW.; Söhne, M.; Boomsma, F.; Mulder, BJ.; Büller, HR. (2003). "Brain natriuretic peptide as a predictor of adverse outcome in patients with pulmonary embolism". Circulation. 107 (16): 2082–4. doi:10.1161/01.CIR.0000070020.79932.DB. PMID 12707233. Unknown parameter |month= ignored (help)
  4. ↑ Leuchte, HH.; Baumgartner, RA.; Nounou, ME.; Vogeser, M.; Neurohr, C.; Trautnitz, M.; Behr, J. (2006). "Brain natriuretic peptide is a prognostic parameter in chronic lung disease". Am J Respir Crit Care Med. 173 (7): 744–50. doi:10.1164/rccm.200510-1545OC. PMID 16415273. Unknown parameter |month= ignored (help)
  5. ↑ Andreassen, AK.; Wergeland, R.; Simonsen, S.; Geiran, O.; Guevara, C.; Ueland, T. (2006). "N-terminal pro-B-type natriuretic peptide as an indicator of disease severity in a heterogeneous group of patients with chronic precapillary pulmonary hypertension". Am J Cardiol. 98 (4): 525–9. doi:10.1016/j.amjcard.2006.02.061. PMID 16893710. Unknown parameter |month= ignored (help)
  6. ↑ Fijalkowska, A.; Kurzyna, M.; Torbicki, A.; Szewczyk, G.; Florczyk, M.; Pruszczyk, P.; Szturmowicz, M. (2006). "Serum N-terminal brain natriuretic peptide as a prognostic parameter in patients with pulmonary hypertension". Chest. 129 (5): 1313–21. doi:10.1378/chest.129.5.1313. PMID 16685024. Unknown parameter |month= ignored (help)
  7. ↑ Wiedemann, R.; Ghofrani, HA.; Weissmann, N.; Schermuly, R.; Quanz, K.; Grimminger, F.; Seeger, W.; Olschewski, H. (2001). "Atrial natriuretic peptide in severe primary and nonprimary pulmonary hypertension: response to iloprost inhalation". J Am Coll Cardiol. 38 (4): 1130–6. PMID 11583893. Unknown parameter |month= ignored (help)
  8. ↑ Ghofrani, HA.; Wiedemann, R.; Rose, F.; Weissmann, N.; Schermuly, RT.; Quanz, K.; Grimminger, F.; Seeger, W.; Olschewski, H. (2002). "Lung cGMP release subsequent to NO inhalation in pulmonary hypertension: responders versus nonresponders". Eur Respir J. 19 (4): 664–71. PMID 11998996. Unknown parameter |month= ignored (help)
  9. ↑ Shitrit, D.; Bendayan, D.; Rudensky, B.; Izbicki, G.; Huerta, M.; Fink, G.; Kramer, MR. (2002). "Elevation of ELISA d-dimer levels in patients with primary pulmonary hypertension". Respiration. 69 (4): 327–9. doi:63270 Check |doi= value (help). PMID 12169745.
  10. ↑ Shitrit, D.; Bendayan, D.; Bar-Gil-Shitrit, A.; Huerta, M.; Rudensky, B.; Fink, G.; Kramer, MR. (2002). "Significance of a plasma D-dimer test in patients with primary pulmonary hypertension". Chest. 122 (5): 1674–8. PMID 12426270. Unknown parameter |month= ignored (help)
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