STENOSIS AND INSUFFICIENCY 



667 



phase. Tiiis should be compared to the findings of 

 Braunwald, Sarnoff and Stainsby who, in isolated 

 dog hearts, did not find any shortening of the ejection 

 time in mitral incompetence, if the forward cardiac 

 output was held constant. 



The elevation of left atrial pressure is transmitted 

 backward and, as in mitral stenosis or other conditions 

 with chronic elevation of the pulmonary venous 

 pressure, the pulmonary artery pressure increases. 

 Usually the increase of pulmonary vascular resistance 

 is small, especially in early cases or cases with only a 

 minor degree of regurgitation. In long standing lesions 

 of marked degree the pulmonary vascular resistance 

 may increase considerably, leading to right ventricular 

 hypertension, right ventricular hypertrophy and, 

 ultimately, right-sided congestive failure. 



The cardiac output may be normal in cases with 

 mitral incompetence. As long as the regurgitated 

 amount is fairly small, the load on the myocardium 

 is negligible and no difficulty seems to exist in keeping 

 a normal forward output both at rest and during 

 exercise. Only in cases with marked regurgitation, 

 where the element of myocardial strain and failure 

 has been added, does the cardiac output decrease 

 below normal values (and below the needs of the 

 body). An immediate increase in forward cardiac 

 output usually follows the successful surgical correc- 

 tion of mitral regurgitation. 



In the light of dog experiments by Braunwald 

 et al. (29), the train of events in clinical mitral in- 

 competence may be explained as follows: Large 

 regurgitant flows may exist without striking eleva- 

 tions of left ventricular end-diastolic pressure or left 

 atrial mean pressure if the myocardial contractility 

 is unimpaired. However, ventricular function may 

 be compromised by processes such as rheumatic 

 carditis, by altered structure of contractile proteins 

 accompanying an increased myocardial burden, or 

 by the existence of arterial hypertension or aortic 

 valve disease [see (115)]. (To this, acute or chronic 

 hypervolemia may be added.) In these circumstances 

 adequate forward cardiac output can be maintained 

 only by elevation of ventricular end-diastolic pres- 

 sure. The large regurgitant flow then results in further 

 elevation of left atrial mean pressure; this in turn 

 may be responsible for the development of increased 

 pulmonary vascular resistance and anatomic changes 

 in the pulmonary vascular bed. Right ventricular 

 hypertrophy and ultimately failure then occurs as 

 a consequence of the increased pressure load against 

 which the ventricle has to work. 



Because the presence or absence of myocardial 



FIG. 7. Moving picture record of an incompetent mitral 

 valve made on the pulse duplicator. Frames numbered i, 2, 

 and 3 arc during ventricular systole. The cycle actually lasts 

 through 14 frames, but for illustrative purposes alternate 

 frames have been deleted. Note that the valve orifice is larger 

 early in systole (frame i) . . . . the valve does not "snap" to a 

 closed position, rather it "floats" tovi'ard that position. This 

 serves to illustrate the variation of valvular regurgitant orifice 

 resistance. [From Davila (43).] 



damage leads to important difTfercnce in clinical 

 reaction to the cardiac lesions of mitral incompetence, 

 several clinicians maintain that clinical symptoms of 

 mitral incompetence do not appear until left ven- 

 tricular failure has started. The findings in the acute 

 experiments of Braunwald and as,sociates strongly 

 emphasize this possibility, at least that clinical symp- 

 toms do not appear until .something else is added to 

 the regurgitation, be this increased peripheral resist- 

 ance, hypervolemia, or myocardial failure. 



RIGHT HEART LESIONS 



Valvular lesions of the right heart are less common 

 than those of the left, and have consequently attracted 

 less interest. The easy access to the great veins, the 

 right atrium, and the diff"erent ostia of the right heart 

 has, however, permitted a rapid increase in knowl- 

 edge during the last decade, especially about the 

 right-sided lesions occurring in clinical work. Ex- 

 perimental procedures have also been designed in 

 increasing numbers for the creation and study of 

 right heart lesions in animals. 



