**13. Conclusions**

Pulmonary hypertension in chronic lung disease and/or hypoxia is a relatively common complication caused by complex pathophysiologic processes. Alveolar hypoxia, either sus‐ tained or repetitively intermittent, triggers the development of PH, although other mecha‐ nisms are also important. Development of PH is associated with worsening dyspnoea with the long-term prognosis dependant on the underlying disease process. Treatment of PH is largely defined by the underlying lung pathology. Therefore, etiological diagnosis and assessment of PH byWHOfunctional class is criticalformanagement.Different classes ofdrug therapieshave beendevelopedasaresultofourcurrentunderstandingofthepathophysiologyofPH.Although the treatments have had some impact on the progression of PH, further research is required to more fully understand the condition and develop better therapeutic approaches.

[3] Cottin, V, Nunes, H, Brillet, P. Y, Delaval, P, Devouassoux, G, Tillie-leblond, I, et al. Combined pulmonary fibrosis and emphysema: a distinct underrecognised entity.

Pulmonary Hypertension in Chronic Lung Diseases and/or Hypoxia

http://dx.doi.org/10.5772/55681

35

[4] Fraser, K. L, Tullis, D. E, Sasson, Z, Hyland, R. H, Thornley, K. S, & Hanly, P. J. Pul‐ monary hypertension and cardiac function in adult cystic fibrosis: role of hypoxemia.

[5] Orr, R, Smith, L. J, & Cuttica, M. J. Pulmonary hypertension in advanced chronic ob‐

[6] Cuttica, M. J, Kalhan, R, Shlobin, O. A, Ahmad, S, Gladwin, M, Machado, R. F, et al. Categorization and impact of pulmonary hypertension in patients with advanced

[7] Scharf, S. M, Iqbal, M, Keller, C, Criner, G, Lee, S, & Fessler, H. E. Hemodynamic characteristics of patients with severe emphysema. Am J Respir Crit Care Med

[8] Tonnelli, A. R, Fernandez-bussy, S, Lodhi, S, Akindipe, O. A, Carrie, R. D, Hamilton, K, et al. Prevalence of pulmonary hypertension in end-stage cystic fibrosis and corre‐

[9] Xu, X-Q, & Jing, Z-C. High-altitude pulmonary hypertension. Eur Respir Rev (2009). ,

[10] Leon-velarde, F, Maggiorini, M, Reeves, J. T, Aldashev, A, Asmus, I, Bernardi, L, et al. Consensus statement on chronic and subacute high altitude diseases. High Alt

[11] Aldashev, A. A, Sarybaev, A. S, Sydykov, A. S, Kalmyrzaev, B. B, Kim, E. V, Mama‐ nova, L. B, et al. Characterization of high-altitude pulmonary hypertension in the Kyrgyz: association with angiotensin-converting enzyme genotype. Am J Respir Crit

[12] Wu, T. Y, & Ge, R. L. An investigation on high-altitude heart disease. Natl Med J Chi‐

[13] Leon-velarde, F, & Mejia, O. Gene expression in chronic high altitude diseases. High

[14] Sajkov, D, Cowie, R. J, Thornton, A. T, Espinoza, H. A, & Mcevoy, R. D. Pulmonary hypertension and hypoxemia in obstructive sleep apnea syndrome. Am J Respir Crit

[15] Sajkov, D, Wang, T, Saunders, N. A, Bune, A. J, & Neill, A. M. Douglas McEvoy RD. Daytime pulmonary hemodynamics in patients with obstructive sleep apnea patients

without lung disease. Am J Respir Crit Care Med (1999). , 159, 1518-1526.

lation with survival. J Heart Lung Transplant (2010). , 29(8), 865-872.

structive pulmonary disease. Curr Opin Pulm Med (2012). , 18(2), 138-143.

Eur Respir J (2005). , 26, 586-593.

Chest (1999). , 115(5), 1321-1328.

(2002). , 166, 314-322.

18(111), 13-17.

Med Biol (2005). , 6, 147-157.

na (1983). , 63, 90-92.

Care Med (2002). , 166(10), 1396-1402.

Alt med Biol (2008). , 9, 130-139.

Care Med (1994). , 144, 416-422.

COPD. Respir Med (2010). , 104, 1877-1882.
