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Cardiomyopathy II: Dilated Cardiomyopathy

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Related Experiment Video

Updated: Jun 13, 2026

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
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Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

Published on: July 5, 2021

Chronic mountain sickness and the heart.

Fabiola León-Velarde1, Francisco C Villafuerte, Jean-Paul Richalet

  • 1Departamento de Ciencias Biológicas y Fisiológicas, Facultad de Ciencias y Filosofia, Universidad Peruana Cayetano Heredia, Lima 31, Perú. fabiola.leon-velarde@upch.pe <fabiola.leon-velarde@upch.pe>

Progress in Cardiovascular Diseases
|April 27, 2010
PubMed
Summary

Chronic Mountain Sickness (CMS) causes high-altitude pulmonary hypertension and right ventricular enlargement. Acetazolamide shows promise in reducing pulmonary vascular resistance in CMS patients.

Related Experiment Videos

Last Updated: Jun 13, 2026

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
09:20

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice

Published on: July 5, 2021

Area of Science:

  • Cardiopulmonary physiology
  • High-altitude medicine
  • Pathophysiology of Chronic Mountain Sickness

Background:

  • Chronic Mountain Sickness (CMS) is a significant high-altitude pathology characterized by excessive erythrocytosis.
  • Severe CMS can lead to high-altitude pulmonary hypertension (HAPH), pulmonary arteriole remodeling, and right ventricular enlargement.
  • Cardiopulmonary changes in CMS are influenced by altitude, hypoxemia, and pulmonary vascular resistance.

Purpose of the Study:

  • To summarize clinical and pathophysiological features of the cardiopulmonary system in CMS.
  • To review research findings on CMS, particularly from the Andes.
  • To highlight recent therapeutic strategies for CMS.

Main Methods:

  • Review of existing literature on cardiopulmonary aspects of CMS.
  • Analysis of cardiac output, pulmonary acceleration time, and pulmonary vascular resistance in CMS patients.
  • Examination of systemic blood pressure control and orthostatic stress tolerance.

Main Results:

  • Cardiac output is lower in CMS patients compared to sea-level dwellers.
  • Mean pulmonary acceleration time is reduced, and pulmonary vascular resistance index is elevated in CMS.
  • CMS individuals exhibit a less effective vasoconstrictor reflex but similar orthostatic tolerance due to larger blood volume.

Conclusions:

  • CMS involves significant cardiopulmonary alterations, including pulmonary hypertension and altered vascular resistance.
  • Acetazolamide treatment effectively improved pulmonary acceleration time and reduced pulmonary vascular resistance in CMS patients.
  • Further research is directed towards developing pharmacological interventions for CMS treatment.