Chronic Mountain Sickness-Phobrang Type

Nath, C S; Kashyap, Samir; Subramanian, Anandaraja

doi:10.14429/dsj.34.6088

Cited by 3 publications

(2 citation statements)

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“…Similar confusion exists between the terms "Monge9s disease" and "CMS". The term "CMS" is used to describe both highaltitude excessive erythrocythosis in South Americans and congestive failure of the right heart without excessive polycythaemia in the Himalayas [12][13][14]. Recently, GE and HELUN [13] proposed to change the term "CMS" to "highaltitude heart disease" for congestive right heart failure without excessive polycythaemia in the Himalayas [13].…”

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High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

Maggiorini¹,

León‐Velarde²

2003

European Respiratory Journal

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High-altitude pulmonary hypertension: a pathophysiological entity to different diseases. M. Maggiorini, F. Léon-Velarde. #ERS Journals Ltd 2003. ABSTRACT: Pulmonary hypertension is a hallmark of high-altitude pulmonary oedema (HAPE) and of congestive right heart failure in subacute mountain sickness (SMS) and chronic mountain sickness (CMS) in the Himalayas and in the end-stage of CMS (Monge9s disease) in the Andes.There are studies to suggest that transmission of excessively elevated pulmonary artery pressure and/or flow to the pulmonary capillaries leading to alveolar haemorrhage is the pathophysiological mechanism of HAPE.In the Himalayas, HAPE was successfully prevented by extending the acclimatisation period from a few days to 5 weeks, however, this did not prevent the occurrence of congestive right heart failure after several weeks of stay at 6,000 m. This leads to the concept that rapid remodelling of the small precapillary arteries prevents HAPE but not the development of right heart failure in SMS and CMS.Unresponsiveness of pulmonary hypertension to oxygen at high altitude and its complete resolution only after weeks of stay at low altitude suggest that structural rather than functional changes are its pathophysiological mechanism. Since pulmonary hypertension at high altitude is the driving force leading to high-altitude pulmonary oedema and "high-altitude right heart failure" in newcomers and residents of high altitude, the authors propose to adjust current terminology accordingly. The physiological response of the pulmonary circulation to hypobaric and normobaric hypoxia is to increase pulmonary arteriolar resistance. The magnitude of hypoxic pulmonary vasoconstriction is highly variable between humans, probably based on genetics and adaptive mechanisms. Sites of hypoxic pulmonary vasoconstriction are small pulmonary arterioles and veins of a diameter of v900 mm, the veins accounting for y20% of the total increase in pulmonary vascular resistance caused by hypoxia [1,2]. The structural changes in small pulmonary arteries and veins appear to reflect this genetically based and adaptive process [3][4][5] in humans and animals. Excessive hypoxic pulmonary vasoconstriction, and thus susceptibility to develop a right heart failure within weeks at high altitude, was first described in Colorado cattle [6]. Indian soldiers stationed at an altitude between 5,800-6,700 m [7] and Han infants in Lhasa [8] develop severe congestive right heart failure within weeks or months after arrival at high altitude. An excessively elevated pulmonary artery pressure (PAP) has not only been reported to cause high altitude cor pulmonale within weeks, months, or years in newcomers, but also in high-altitude residents of the Andes and nonacclimatised climbers prone to high-altitude pulmonary oedema (HAPE) [9]. The results of these studies suggest that an excessive rise in PAP is a common denominator in HAPE [9], the syndrome described by SUI et al. [8] in infants and by ANAND et al. [7] in adults at 6,700 m and termed "subacute...

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High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

Maggiorini¹,

León‐Velarde²

2003

European Respiratory Journal

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“…Despite the vast amount of material on HA available .in Western literature, it is worth noting that the largest series on high altitude pulmonary oe› dema (HAPO) [3,4] and acute mountain sick› ness (AMS) [5] as well as the new entity of 'adult subacute mountain sickness' (SAMS) [6) have been described from India. Other works by our medical officers and specialists include the entity of high altitude pulmonary hypertension [7,8), one of the earliest descrip› tions of high altitude cerebral oedema (HACO) [9), and the detection of chronic mountain sickness [10]. These important early observations are due to dedicated indi› viduals WOl'kingunder difficult and primitive conditions.…”

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confidence: 99%