PMID- 20417348
OWN - NLM
STAT- MEDLINE
DCOM- 20100513
LR  - 20161125
IS  - 1873-1740 (Electronic)
IS  - 0033-0620 (Linking)
VI  - 52
IP  - 6
DP  - 2010 May-Jun
TI  - Chronic mountain sickness and the heart.
PG  - 540-9
LID - 10.1016/j.pcad.2010.02.012 [doi]
AB  - 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.
FAU - Leon-Velarde, Fabiola
AU  - Leon-Velarde F
AD  - Departamento de Ciencias Biologicas y Fisiologicas, Facultad de Ciencias y 
      Filosofia, Universidad Peruana Cayetano Heredia, Lima 31, Peru. 
      fabiola.leon-velarde@upch.pe <fabiola.leon-velarde@upch.pe>
FAU - Villafuerte, Francisco C
AU  - Villafuerte FC
FAU - Richalet, Jean-Paul
AU  - Richalet JP
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Prog Cardiovasc Dis
JT  - Progress in cardiovascular diseases
JID - 0376442
SB  - IM
MH  - Altitude
MH  - Altitude Sickness/blood/drug therapy/*physiopathology
MH  - Blood Pressure
MH  - *Cardiac Output
MH  - Cardiovascular System/*physiopathology
MH  - *Chemoreceptor Cells
MH  - Chronic Disease
MH  - Clinical Trials as Topic
MH  - Hematocrit
MH  - Humans
MH  - Hypertension, Pulmonary/*physiopathology
MH  - Hypertrophy, Right Ventricular/physiopathology
MH  - Hypoxia/*physiopathology
MH  - Polycythemia/physiopathology
MH  - Pulmonary Artery/physiopathology
MH  - Randomized Controlled Trials as Topic
MH  - Respiratory System/*physiopathology
MH  - Vascular Resistance
RF  - 76
EDAT- 2010/04/27 06:00
MHDA- 2010/05/14 06:00
CRDT- 2010/04/27 06:00
PHST- 2010/04/27 06:00 [entrez]
PHST- 2010/04/27 06:00 [pubmed]
PHST- 2010/05/14 06:00 [medline]
AID - S0033-0620(10)00041-1 [pii]
AID - 10.1016/j.pcad.2010.02.012 [doi]
PST - ppublish
SO  - Prog Cardiovasc Dis. 2010 May-Jun;52(6):540-9. doi: 10.1016/j.pcad.2010.02.012.