Increased pulmonary pressures and myocardial wall stress in children with severe malaria

Jacqueline J Janka1, Ousmane A Koita, Broulaye Traoré

  • 1Clinical Center (Critical Care Medicine Department) and Pulmonary and Vascular Medicine and Translational Medicine Branches, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.

Insights

Severe malaria in children causes nitric oxide (NO) depletion and increased pulmonary pressures, similar to sickle cell disease. This suggests intravascular hemolysis activates a harmful cascade affecting the cardiopulmonary system.

Area of Science:

  • Hematology
  • Cardiovascular Medicine
  • Infectious Diseases

Background:

  • Chronic intravascular hemolysis is linked to nitric oxide (NO) depletion and pulmonary hypertension in sickle cell disease.
  • The study investigates if similar pathophysiology occurs in children with severe malaria.

Purpose of the Study:

  • To determine if severe malaria in children leads to nitric oxide depletion and associated cardiopulmonary complications.
  • To compare pathophysiological markers in children with severe malaria against healthy controls.

Main Methods:

  • Assessed hemolysis severity via plasma hemoglobin and arginase-1 levels.
  • Measured nitric oxide (NO) metabolism using whole-blood nitrite and plasma NO consumption.
  • Evaluated cardiovascular effects using echocardiography, NT-proBNP, and soluble vascular cell adhesion molecule-1.

Main Results:

  • Children with severe malaria exhibited higher hemolysis markers and increased NO consumption.
  • Reduced whole-blood nitrite levels were observed in severe malaria cases.
  • Elevated pulmonary arterial pressures, NT-proBNP, and soluble vascular cell adhesion molecule-1 confirmed cardiopulmonary stress.

Conclusions:

  • Severe malaria in children is associated with increased pulmonary pressures and myocardial wall stress.
  • These findings suggest nitric oxide (NO) depletion due to intravascular hemolysis is activated in severe malaria.
  • The study indicates a shared pathophysiological pathway involving intravascular hemolysis and NO depletion in both malaria and sickle cell disease.
Abstract

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