IN THE presence of structural obstruction to the free flow of blood from the lungs to the left ventricle, such as in classic mitral stenosis, proliferative thickening of the walls of the small arteries and arterioles occurs.1 It has been conjectural whether such changes are coincidental findings related to high pressures in the left atrium and pulmonary artery or whether, in some unique way, they cause pulmonary hypertension in excess of the obstruction to venous outflow and at times protect the pulmonary capillaries against excessive pressures. The absence of correlation between increased pulmonary arterial pressures and clinical evidence of pulmonary congestion in patients having mitral stenosis led Borden and associates2 to conclude that, in addition to the reflected high pressures in the left atrium, an anatomic obstructive factor existed in the pulmonary vascular tree. The absence of increased volume of pulmonary blood among patients with mitral stenosis, as
EDWARDS JE, BURCHELL HB. MULTILOBAR PULMONARY VENOUS OBSTRUCTION WITH PULMONARY HYPERTENSION: "Protective" Arterial Lesions in the Involved Lobes. AMA Arch Intern Med. 1951;87(3):372–378. doi:10.1001/archinte.1951.03810030045004
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