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Prog Cardiovasc Dis. 2010 May-Jun;52(6):540-9. doi: 10.1016/j.pcad.2010.02.012.

Chronic mountain sickness and the heart.

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Departamento de Ciencias Biológicas y Fisiológicas, Facultad de Ciencias y Filosofia, Universidad Peruana Cayetano Heredia, Lima 31, Perú. <>


Chronic Mountain Sickness (CMS) is an important high-altitude (HA) pathology in most mountainous regions of the world. Although its most characteristic sign is excessive erytrocytosis (EE), in the more severe stages of the disease, high-altitude pulmonary hypertension (HAPH), with remodeling of pulmonary arterioles and right ventricular enlargement is commonly found. The degree of ventricular hypertrophy depends on the vasoconstrictor pulmonary response, the intensity of vascular resistance and the level of altitude, and therefore on the degree of hypoxemia. This chapter briefly summarizes the existing data regarding the clinical and pathophysiological features of the cardiopulmonary system in CMS, with emphasis in findings from research in the Andes. The literature shows variability in cardiac output values in CMS, which might be related to the degree of EE. Recent findings have shown that cardiac output (l/min) is lower in CMS when compared with sea-level (SL) dwellers. Mean pulmonary acceleration time (ms) is significantly lower in CMS subjects than in SL and HA natives, and pulmonary vascular resistance index (Wood units) is higher in CMS and HA natives when compared with SL dwellers. Systemic blood pressure has similar values in CMS patients and healthy HA natives, but some differences arise in its control mechanisms. Although CMS individuals have a less effective vasoconstrictor reflex, their tolerance to orthostatic stress is similar to that of healthy HA natives which might be explained in terms of the larger blood volume present in CMS subjects. At present research is directed to design strategies on pharmacological intervention for CMS treatment. Recently, a clinical trial with acetazolamide, in patients with CMS has proven to be effective in increasing mean pulmonary acceleration time and decreasing pulmonary vascular resistance index, which might be indirectly due the reduction of hematocrit.

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