STENOSIS AND INSUFFICIENCY 



657 



ml, witli the average at 125 ml. The left \entriclc was, 

 in the cases with mitral stenosis, of normal or small 

 size and emptied almost completely at maximum 

 systole. The thickness of the left ventricular wall lay 

 between 7 and 10 mm, with the average at 8 mm. In 

 mitral incompetence in sinus rhythm the left ventricu- 

 lar volume was increased in diastole, and the systolic 

 residual blood was also increased. The left ventricular 

 wall thickness lay between 8 and 1 3 mm, averaging 

 10 mm. When atrial fibrillation had occurred, the 

 left ventricle had a greatly increased diastolic volume 

 and residual blood volume. The left ventricular wall 

 was between 10 and 15 mm thick. 



Grant el al. (gi) studied volume changes of the 

 left atrium by angiocardiography and related them to 

 pressures and flow. Increase in left atrial \oliime be- 

 yond 500 ml tended to be associated with mitral 

 insufficiency. In six patients the left atrial \olume 

 exceeded i liter. Soloff et al. (187) used a similar 

 technique but made no attempt to calculate the left 

 atrial volume more accurately. They found the left 

 atrial \olume in patients with mitral stenosis to be 2 

 to 12 times the normal (estimated in four patients). 

 The increase in volume was not related to age or 

 duration of the rheumatic state. There was no con- 

 stant relationship among various parts of intracardiac 

 circulation time, left atrial size, and degree of mitral 

 stenosis, as reported by the surgeon. 



LEFT HE.\RT LESIONS 



Aortic Stenosis 



The acute hemodynamic consequences of aortic 

 stenosis have been studied in isolated heart prepara- 

 tions or in more or less intact, open-chest animals. 

 Considerable difficulties hamper the reproduction of 

 the human lesion, consisting of stenosis in the valve 

 opening itself or in subaortic stenosis — where the 

 resistance to flow is localized below the valve. In both 

 these lesions the flow to the coronary ostia is reduced. 

 In studies in circulatory models, Porje ft al. (162, 163) 

 actually have demonstrated the low or even negative 

 lateral pressures existing in the sinus of Valsalva dur- 

 ing the ejection of blood through a stenosed aortic 

 orifice. In contrast, most animal experiments have 

 had to rely upon stenosis induced above the sinus of 

 Valsah'a, where the stenosis is caused by constriction 

 of the aorta. This may give valid results for the study 

 of acute lesions or for the study of the myocardial 

 response to acute overload, but may not give exact 



information about the dynamics of the human lesion 

 with its slowly developed stenosis, where the myo- 

 cardium reacts with hypertrophy concomitant with 

 decreased coronary flow. Katz and co-workers (iio) 

 in 1927 studied the cardiodynamic consequences of 

 acute experimental stenosis of the aorta, which was 

 produced with a ligature placed about i cm above the 

 aortic valve (the coronary arteries thus had adequate 

 or even higher systolic filling pressure in contrast to 

 human aortic stenosis). 



The contour of the left ventricular pressure curve 

 was altered, with increased height and more peaked 

 summit. The change in the ventricular pressure curve 

 was partly the result of the constriction itself, which 

 decreases the conversion of the potential mechanical 

 energy to kinetic energy of flow, and partly the result 

 of the increase in the diastolic stretch of the ventricle. 

 The normal parallelism in the fundamental contour 

 of the aortic and left ventricular curves during the 

 ejection period disappeared when stenosis was pro- 

 duced. The amplitude of the curves, as well as the 

 gradient of ascent, changed in opposite directions, and 

 the peaks no longer coincided in time. The aortic 

 pressure pulse changed in the following manner: the 

 pulse amplitude decreased, the general pressure level 

 was lowered, the ejection period was prolonged, the 

 gradient of ascent was diminished, the curve was 

 superimposed by systolic and early diastolic vibra- 

 tions, and a sharp vibration occurred low down on the 

 ascent of the curve. The authors suggested that this 

 vibration was created by the suction action of the 

 suddenly produced swift axial stream beyond the 

 constriction. 



Mo.scovitz & Wilder (153), who studied the arterial 

 and ventricular pressure pulses, produced aortic 

 stenosis in dogs by constricting the aorta at a level 

 just above the valve cusps. They also attempted to 

 evaluate the influence of combinations of stenosis and 

 incompetence on these pressures. 



The effect of superimposing stenosis on the normal 

 and insufficient aortic pulses was in both instances to 

 narrow the pulse pressure, delay the systolic peak, and 

 produce a prominent anacrotic notch in a lowered 

 position on the ascending limb. The contour charac- 

 teristic of aortic insufficiency was dominated and 

 masked by the superimposed stenosis, although the 

 maintenance of a low diastolic pressure indicated that 

 insufficiency was present. 



In aortic stenosis the anacrotic notch retained its 

 low position on the ascending limb, although its 

 characteristics became less clear as the central pulse 

 moved peripherally. When aortic stenosis was pro- 



