STENOSIS AND INSUFFICIENCY 



671 



The patho-anatomical changes observed can be 

 graded from mild to severe, and seem to be correlated 

 with the extent of impediment to the circulation in 

 the left heart. Mild changes consist of dilatation of the 

 capillaries to the extent that their width can accomo- 

 date five or six red blood cells. The number of capil- 

 laries seems to have increased and there is herniation 

 of the capillaries into the alveolar spaces with slight 

 thickening of the capillary basement membrane. 

 Severe lesions are characterized by a further increase 

 in interstitial connective tissue and further thickening 

 of the capillary basement membrane. Interstitial 

 collagen may separate the capillaries from the alveo- 

 lar space. The capillary endothelium may change 

 to a cuboidal form. The capillary lumen appears to 

 be narrow within these thickened walls and may be 

 difficult to discern. Intimal thickening of arteries and 

 hyperplastic arteriolosclerosis tend to become in- 

 creasingly marked with a greater degree of change 

 in the alveolar walls. These changes are not uniform 

 through the whole \'ascular bed in any given lung 

 and tend to be more marked in the basal parts. In 

 advanced cases the main pulmonary artery becomes 

 more or less dilated with a thickened wall, which 

 may show advanced sclerosis. 



In several cases of mitral insufficiency pathological 

 changes of the pulmonary vascular bed have been 

 described that are essentially identical with those 

 found earlier in mitral stenosis. Ross et al. (173) thus 

 described medial hypertrophy sclerosis and intimal 

 thickening of the pulmonary vessels in 4 of 23 pa- 

 tients with mitral incompetence where lung biopsies 

 or post-mortem lung sections were available for 

 microscopic study. Similarly, Becker et al. (14) and 

 Smith and collaborators (186) described advanced 

 changes of the pulmonary blood vessels in patients, 

 with aortic stenosis or systemic hypertension, dying 

 after long-standing chronic left ventricular failure. 

 The most pronounced change here also was media 

 hypertrophy. 



The great resistance to flow through the small pul- 

 monary arterial vessels found in mitral stenosis and 

 other advanced left heart lesions is thus associated 

 with medial hypertrophy of the small arteries. The 

 specific mechanism by which this arterial response 

 is brought about is not known [see (131)]. Most prob- 

 ably it is related to the increased pulmonary venous 

 pressure resulting from the failing ventricle or the 

 mitral block. The mechanism would then be identical 

 in mitral stenosis, mitral incompetence, and left 

 ventricular failure. Rheumatic vasculitis or other 



rheumatic changes in the lungs would not then have 

 to be postulated. 



Increase in left atrial pressure in isolated dog lungs 

 or lung segments causes a decrease of pulmonary 

 vascular resistance, presumably through the disten- 

 tion of the vascular bed (25). The same observation 

 has been made in intact animals when mitral stenosis 

 was acutely created (95). Common to these observa- 

 tions is the acute and short-lasting nature of the pres- 

 sure elevations. In man, when the narrowing of the 

 mitral valve occurs over a time space of several years 

 or even decades, the elevation of the left atrial pres- 

 sure is almost always followed by an increased vascular 

 resistance. In some patients with marked and long- 

 standing mitral stenosis the pulmonary arterial pres- 

 sure may be so high as to exceed even the systemic 

 arterial pressure. In these cases the pulmonary vascu- 

 lar resistance is markedly elevated, and the left atrial 

 pressure is usually not excessively high and may even 

 be lower than in other similar cases with lower resist- 

 ance. To what extent this is due to the anatomical 

 changes described above with chronic edema and 

 fibrosis, or to active \'ascular constriction, is still un- 

 known. It has been suggested that this increase in 

 resistance serves the purpose of protecting the pul- 

 monary capillaries from a high intravascular pressure 

 which otherwise would cause fatal pulmonary edema 

 ("protective pulmonary hypertension") (208). The 

 increased pulmonary venous pressure would pre- 

 sumably goxern the extent of vasoconstriction via 

 some hypothetic pressure receptor in the venous bed 

 or left atrium. Such an active increase in vascular 

 tone could then give rise to the medial hypertrophy 

 and other patho-anatomical changes that, according 

 to this view, would be secondary to the functional 

 protective hypertension. 



Reports have been published coinparing the find- 

 ings from lung biopsies with the preoperatively deter- 

 mined pulmonary arteriolar resistance and showing a 

 lack of correlation between the calculated resistance 

 and the extent of vascular changes in the lung biopsies 

 (32, 55, 82). From this it has been concluded that 

 vasoconstriction within the lung is an important factor 

 in producing pulmonary hypertension in mitral 

 stenosis. As the lung biopsy usually was taken from 

 the anterior border of the left upper lobe, a part of 

 the lung that cannot be thought to be representative 

 for the whole vascular bed, this conclusion does not 

 seem to be justified. 



Studies on the effect of a constant infusion of acet\l- 

 choline in the pulmonary artery of patients with 

 mitral stenosis and pulmonary hypertension demon- 



