Debate on valvular heart disease. Con: early surgical intervention in valvular heart disease.

Debate on Valvular Heart Disease

15 16 17 17 18 19

216

pulmonary hypertension following cardiac surgery. Circulation 33/34: supp!. 1, pp. 107-114 (1966). ROSKY, L. and RODMAN, T.: Medical aspects of open-heart surgery. New Eng!. J. Med.274: 833-886 (1966). Ross, J. and BRAUNWALD, E.: Aortic stenosis. Circulation 37: supp!. 3, pp. 61-67 (1968). SELZER, A. and CoHN, K.: Natural history of mitral stenosis: a review. Circulation 45: 878-890 (1972). SELZER, A. and COHN, K.: The 'myocardial factor' in valvular heart diseases, pp. 178-189 (Davis, Philadelphia 1973). SZEKELY, P.: Systemic embolism and anticoagulant prophylaxis in rheumatic heart disease. Br. med. J. 9: 1209-1212 (1964).

K. COHN, MD, FACC Co-Director, Division of Cardiology, Vice-Chairman, Department of Medicine, Presbyterian Hospital, Pacific Medical Center, San Francisco, Calif. (USA)

Con: Early Surgical Intervention in Valvular Heart Disease l NICHOLAS

T.

KOUCHOUKOS

This research was supported in part by Program Project Grant HL 11,310, National Heart and Lung Institute, Bethesda, Md.

Downloaded by: Weizmann Inst. of Science 132.77.150.148 - 2/13/2018 9:55:31 AM

The decision to recommend valvular repair or replacement in patients with valvular heart disease is based primarily on knowledge of the natural history of the valvular lesion without operation, on the risk of operation, on the performance of the valvular prosthesis employed, and on the functional reserve of the ventricular myocardium. Recently, because of declining operative mortality rates and improved prosthetic valves, valve replacement has been recommended for patients who are not severely symptomatic but who have evidence for impaired myocardial function, in the hope of preventing further deterioration of cardiac function and thereby improving long-term survival [1-5]. For the purposes of this discussion, we shall focus primarily on aortic and mitral valvular incompetence, since patients with these lesions often have slow progression of their symptoms even in the presence of significant hemodynamic abnormalities. The decision to recommend valve replacement in such patients is often a difficult one, and operation has generally been reserved for those patients who are significantly disabled (New York Heart Association functional class III or IV), when their exercise tolerance has become severely lim-

217


ited, overt symptoms of cardiac failure have appeared, and medical therapy has become ineffective. Valve replacement in many of these patients then becomes palliative rather than curative, and the severity of myocardial dysfunction present postoperatively adversely affects the long-term results.

Problems Related to Selection of Patients for Operation

As noted above, knowledge of the natural history of the specific valvular lesion is desirable in order to compare the results of operative and nonoperative therapy. A prospective study of the life history of patients with rheumatic aortic incompetence has been reported by SPAGNUOLO et al. [6]. Patients with moderate or marked left ventricular enlargement, systolic blood pressure above 140 mm Hg or diastolic pressure below 40 mm Hg, and electrocardiographic evidence (voltage) of left ventricular hypertrophy with either ST segment depression or T-wave inversion were considered to be in the 'cumulative high risk' category. 78% of these patients were alive 3 years after entering this category, and 70% 6 years afterwards. Of interest

20

10

Jt J

J A1~

1 2 3 4 5 ~ ~ ~ 1~ YEARS OF FOLLOY"",,P FROM THE TIME

EACH PATIENT .JOINED HIS GROUP

run~~~~ro~~~U~~7G4

Fig. 1. Survival rates in patients with aortic incompetence but without congestive failure (CHF) or angina pectoris in selected groups (low risk and high risk). 0 = Cumulative low risk; • = cumulative high risk. Reprinted with permission from SPAGNUOLO et al. [6].


ClR311913 8 G 4 220 000 0 0 0

218

was the fact that even the patients in this group who were initially asymptomatic had a relatively poor prognosis, since only 34% were alive and without congestive failure or angina 3 years later, and 13% 6 years later (fig. 1). These authors stated that the development of angina and congestive failure was evidence of the beginning of a progressive downhill course. GOLDSCHLAGER et al. [7] have shown that the hemodynamic abnormalities associated with chronic aortic incompetence often precede the development of clinical disability and that by the time the symptoms become severe, irreversible myocardial damage may be present. Comparable data on the natural history of mitral incompetence, particularly of the chronic type, are not readily available. The multiple causes of mitral incompetence (rheumatic valvulitis, bacterial endocarditis, connective tissue disorders, coronary artery disease with papillary muscle rupture or dysfunction, primarily myocardial disorders), and the problems encountered in accurately diagnosing the precise etiology before death partially account for the lack of data of this type. As with aortic incompetence, there is often slow progression of symptoms. By the time the symptoms become severe enough to consider valve replacement, there may be severe impairment of cardiac function. Table I shows that the early mortality following mitral valve replacement is clearly affected by the severity of preoperative cardiac disability. Recent studies have emphasized the importance of coexisting myocardial abnormalities in patients with valvular heart disease and the effects of valve replacement on myocardial function. Of a series of 71 patients undergoing valve replacement (mitral, aortic, or combined mitral and aortic) who were functional class III or IV reported by HILDNER et al. [11], 55% had ventricular angiographic evidence of myocardial dysfunction preoperatively. Postoperatively, although 86% of the patients improved clinically by at least one functional class, 56% had angiographic evidence of myocardial dysfunction. Ofthe 14 patients in this group having aortic valve replacement for stenosis and/or incompetence, nine (64%) had improved contractility following operation, while two (14%) were unchanged and three (22%) had decreased contractility. Of the 47 patients with mitral valve disease (stenosis, incompetence or mixed lesions), ventricular contractility improved postoperatively in only seven patients (15%), whereas 24 patients (51 %) had no change, and 16 (34%) had a decrease in contractility. It is noteworthy that five of six patients (83%) with mitral incompetence had worse myocardial contractility postoperatively than preoperatively, while only five of 16 patients (31 %) with mitral stenosis had such deterioration.



219


TabTe 1. Effect of functional class (New York Heart Association classification) on early mortality following mitral valve replacement

Authors

III IV III IV III IV III IV

LITWAK et aT. [8] FISHMAN et aT. [9] MULLIN et aT. [10] ALLEN et aT. [5]

Number of patients

73 37 95 36 37 12 109 24

Early deaths

%

n

3 11

7 9 7 5 3 4

4 30 7 25 19 42 3 17

Hemodynamic studies by GAULT et al. [12] in five patients following aortic valve replacement for severe aortic valvular incompetence indicated that the preoperative depression of myocardial contractility and abnormal left ventricular pressure-volume relationships present in four patients persisted after valve replacement, even though all were symptomatically improved and left ventricular end-diastolic pressure and cardiac index at rest returned toward normal. BAILEY et al. [13] from our institution observed differing survival rates following valve replacement for aortic incompetence when the patients were classified according to the preoperative ejection fraction. In eleven patients with an ejection fraction greater than 45%, the cumulative survival rates at 1, 3 and 5 years were 100, 91 and 81 %, respectively, whereas in 17 patients with ejection fractions less than 45% these ~urvival rates were 71, 46, and 37%. ECKBERG et al. [14] studied the mechanics ofleft ventricular contraction in eleven patients with chronic severe mitral regurgitation. Two of these patients were functional class II and nine were functional class III. Compared with normal patients, these patients had significantly larger left ventricular end-diastolic circumferences and volumes and higher total left ventricular stroke volumes. Although the ejection fraction and extent of fiber shortening were normal in all but two patients, depressed shortening velocities, suggesting depressed left ventricular myocardial contractility, were present in most. They concluded that favorable unloading conditions early during systole in patients with mitral regurgitation appeared to mask the effects of a depressed inotropic state on the pumping function of the heart. VOKONAS et al. [15] recently reported hemodynamic studies in 25 patients with isolated mitral regurgitation of varying severity. These patients were subdivided ac-


Functional class


220

cording to whether or not the left ventricular ejection fraction was normal. Those with normal ejection fractions (70 ±2%) were termed 'compensated' and those with decreased ejection fractions (34 ± 3%) were termed 'decompensated'. In eight of the 15 patients with compensated mitral regurgitation, corrective surgery was carried out because of clinical symptoms of congestive heart failure. The surgery was uncomplicated in all and clinical improvement was observed uniformly following operation. The seven less symptomatic patients received no treatment or medical therapy alone and remained symptomatically unchanged during a mean follow-up period of approximately 2 years. In contrast, six of the ten patients with decompensated mitral valve regurgitation underwent valve replacement, and clinical improvement was noted in only three. Two patients exhibited progressive deterioration and died 8 and 41 months after operation. The deterioration in these patients was attributed to either a progression of underlying secondary myocardial failure, or to the los

~

'"

~ 70

~

.~ u

60

ll!

50

40

t

f,HOSPITAL MORTALITY

o

I

2

3

-4

5

Fig. 3. Actuarial survival after operation of alI patients (n=267) and of patients having single and double valve replacement during 1963-1966 (n=116) and 1967-1970 (n= 118). Data corrected for survival up to October 31, 1972.• = Single or double valve replacement (1967-1970),70% alive (estimated); 0 = alI patients (1963-1970), 60% alive; .... = single or double valve replacement (1963-1966), 47% alive. Reprinted with permission from CAREY et al. [3].


YEARS AFTER OPERATION


224

of cardiac lesions is performed too late in the course of the disease to significantly influence rehabilitation in most patients. Thromboembolism remains one of the most serious and most frequently encountered complications following valve replacement, particularly of the mitral valve. The introduction of the Starr-Edwards cloth-covered, composite-seat, metallic ball prosthesis (models 6310-6320) has significantly reduced the incidence of thromboembolic complications as compared with the earlier Starr-Edwards ball valves. Ten (7%) of our own series of 139 patients having mitral valve replacement with this prosthesis have had thromboembolic episodes, and these were fatal in three patients [5]. Similarly low thromboembolic rates have been reported by others with this prosthesis [4, 18] and with the Bjork-Shiley prosthesis [22] and the Beall-Surgitool prosthesis [23], which are disc valves. Low thromboembolic rates without anticoagulant therapy have been observed with stent-mounted preserved aortic xenografts [24] and fresh aortic allografts [25], although the longterm function of these valves is uncertain. Infective endocarditis, periprosthetic valvular leaks and mechanical malfunction can occur with all types of prosthetic valves. They are relatively minor causes of postoperative mortality and morbidity, however, when compared to myocardial failure and thromboembolism. Significant hemolysis requiring transfusions or replacement of the prosthesis has occurred in a small percentage of patients, particularly when periprosthetic valvular regurgitation has been present. The hazards of long-term anticoagulation with warfarin derivatives constitute another major problem following valve replacement, and represent a major cause of postoperative morbidity and mortality [5, 18]. Hopefully, durable prosthetic devices will be developed in the near future which will not require anticoagulant therapy.

Patients with valvular heart disease, particularly aortic and mitral incompetence, may have significant derangement of myocardial function, often in the absence of significant symptoms, which directly affects early and late survival and functional status following valve replacement. With declining hospital mortality rates and improved valvular prostheses, consideration must be given to valve replacement in patients of this type in order to preserve myocardial function. This should improve long-term survival and the functional results following valve replacement. Attention should be directed to identifying and closely observing patients of this type, perhaps with noninvasive techniques, and proceeding with valve replacement before irreversible myocardial damage has occurred.


Summary


225

2 2 3

4

5

6

7

8

9

10

11

12

13

14

15

KIRKLIN, J.W.: Replacement of the mitral valve for mitral incompetence. Surgery, St Louis 72: 827-836 (1972). KOUCHOUKOS, N.T.: Problems with mitral valve replacement; in KIRKLIN Advances in cardiovascular surgery, chap. 16, pp. 205-216 (Grune & Stratton, New York 1973). CAREY, J.S.; HUGHES, R.K.; PLESTED, W.G.; NELSON, C.B.; SACKS, E., and SALVAY, H.: Functional rehabilitation after cardiac valve surgery. Ann. thorac. Surg. 16: 492-504 (1973). BONCHEK, L.I.; ANDERSON, R.P., and STARR, A.: Mitral valve replacement with cloth-covered composite-seat prostheses: the case for early operation. J. thorac. cardiovasc. Surg. 67: 93-109 (1974). ALLEN, W.B.; KARP, R.B., and KoucHoUKos, N.T.: Mitral valve replacement: Starr-Edwards cloth-covered composite-seat prosthesis. Archs Surg., Chicago 109: 642-647 (1974). SPAGNUOW, M.; KLOTH, H.; T ARANTA, A; DOYLE, E., and PASTERNACK, B.: Natural history of rheumatic aortic regurgitation: criteria predictive of death, congestive heart failure, and angina in young patients. Circulation 44: 368-380 (1971). GOLDSCHLAGER, N.; PFEIFER, J.; COHN, K.; POPPER, R., and SELZER, A: The natural history of aortic regurgitation: a clinical and hemodynamic study. Am. J. Med. 54: 577-588 (1973). LITWAK, R.S.; SILVAY,J.; GADBOYS,H.L.; LUKBAN, S. B.; SAKURAI,H.,and CASTROBLANCO, J.: Factors associated with operative risk in mitral valve replacement. Am. J. Cardio!. 23: 335-348 (1969). FISHMAN, N.H.; EDMUNDS, L.H.; HUTCHINSON, J.C., and ROE, B.B.: Five-year experience with the Smeloff-Cutter mitral prosthesis. J. thorac. cardiovasc. Surg. 62: 345-356 (1971). MULLIN, E.M.,jr.; GLANCY, D.L.; HIGGS, L.M.; EpSTEIN, S.E., and MORROW, AG.: Current results of operation for mitral stenosis: clinical and hemodynamic assessments in 124 consecutive patients treated by closed commissurotomy, open commissurotomy or valve replacement. Circulation 46: 298-308 (1972). HILDNER, F.J.; JAVIER, R.P.; COHEN, L.S.; SAMET, P.; NATHAN, M.J.; YAHR, W.Z., and GREENBERG, J.J.: Myocardial dysfunction associated with valvular heart disease. Am. J. Cardio!. 30: 319-326 (1972). GAULT, J.H.; COVELL, J.W.; BRAUNWALD, E., and Ross, J., jr.: Left ventricular performance following correction of free aortic regurgitation. Circulation 42: 773-780 (1970). BAILEY, M.T.; FEILD, B.J., and BAXLEY, W.A: Left ventricular function prior to surgery for aortic valve incompetence: prognostic implications. Abstract. Circulation 49/50: supp!. 3, p.41 (1974). ECKBERG, D.L.; GAULT, J.H.; BOUCHARD, R.L.; KARLINER, J.S., and Ross, J., jr.: Mechanics of left ventricular contraction in chronic severe mitral regurgitation. Circulation 47: 1252-1259 (1973). VOKONAS, P.S.; GORLIN, R.; COHN, P.F.; HERMAN, M.V., and SONNENBLICK, E.H.: Dynamic geometry of the left ventricle in mitral regurgitation. Circulation 48: 786-796 (1973).


References

Debate on Valvular Heart Disease 16

17

18

19

20 21 22

23

24

25

226

RANKIN, J.S.; NICHOLAS, L.M., and KOUCHOUKOS, N.T.: Experimental mitral regurgitation. Effects on left ventricular function before and after elimination of chronic regurgitation in the dog. J. thorac. cardiovasc. Surg. 70: 478-488 (1975). KARP, R.B.; KmKLIN, J.W.; KOUCHOUKOS, N.T., and PACIFICO, A.D.: Comparison of three devices to replace the aortic valve. Circulation 49/50: suppl. 2, pp. 163-169 (1974). lSOM, O.W.; WILLIAMS, C.D.; FALK, E.A.- GLASSMAN, E., and SPENCER, F.C.: Longterm evaluation of cloth-covered metallic ball prostheses. J. thorac. cardiovasc. Surg. 64: 354-367 (1972). DUVOISIN, G.E.; WALLACE, R.B.; ELLIS, F.H.,jr.; ANDERSON, M.W., and MCGooN, D.C.: Late results of cardiac-valve replacement. Circulation 37/38 suppl. 2, p.75 (1968). STARR, A.; HERR, R.H., and WOOD, J.A.: Mitral replacement: review of six years' experience. J. thorac. cardiovasc. Surg. 54: 333-358 (1967). REES, J.R.; HOLSWADE, G.R., and LILLEHEI, C.W.: Patient status five or more years after mitral valve replacement. Ann. thorac. Surg. 14: 30-37 (1972). ARIS, A.; FAST, A.J.; TECTOR, A.J.; FLEMMA, R.J., and LEPLEY, D.: A comparative study of ball and disc prostheses in mitral valve replacement. J. thorac. cardiovasc. Surg. 68: 335-343 (1974). BEALL, A.c., jr.; BRICKER, D.L., and MESSMER, B.J.: Results of mitral valve replacement with Dacron-velour-covered Teflon-disc prosthesis. Ann. thorac. Surg. 9: 195-202 (1970). KOUCHOUKOS, N.T.; KERR, A.R.; SHEPPARD, L.C.; CEBALLOS, R.C., and KIRKLIN, J. W.: Heterograft replacement of the mitral valve: clinical, hemodynamic and pathological features. Circulation 41/42: suppl. 2, p. 20 (1970). GRAHAM, A.F.; SHROEDER, J.S.; DAILY, P.O., and HARRISON, D.C.: Clinical and hemodynamic studies in patients with homograft mitral valve replacement. Circulation 44: 334--342 (1971).

Prof. N.T. KOUCHOUKOS, MD, Department of Surgery, University of Alabama Medical Center, University Station, Birmingham, AL 35294 (USA)

VOGEL: From what I have heard, I have the feeling that no one will be recommending surgery for the person with moderate or tight mitral stenosis if they are asymptomatic. However, I believe that many doctors would think seriously about operating on such a patient. I would like to hear both speakers comment on this. KOUCHOUKOS: The discussion today was directed at valve replacement. I think, we would feel strongly that any patient with pure mitral stenosis who could tolerate a mitral commissurotomy should have it. I think, clearly the operative risk is very low in that group of patients. Valve replacement is a different problem and, I think, one has to think a little more carefully about recommending valve replacement for the reasons we pointed out today. But that is not a large problem in our experience.


Discussion

227

COHN: I think, I more or less have already stated my point of view that there is little indication for operating on the asymptomatic patient. The chance of running into serious problems is almost negligible except for thromboembolism, which is not prevented by surgery. I personally would not recommend commissurotomy on the patient who is asymptomatic and who has mitral stenosis. We seldom perform commissurotomies in people over 40 years of age because our experience has been so bad, in that the stiff valve just does not open well and they tend to either get restenosis or never are adequately treated in the first place. PATON: Do you hold the view that there is no evidence that commissurotomy prevents further thromboembolism? COHN: No. I hold the view that the evidence is not convincing. There is evidence for everything in medicine. PATON: That is true, but there was a paper a good many years ago by ELLIS and HARKEN on roughly 1,500 cases of commissurotomy in which they had 17% thromboembolic incidents before commissurotomy and 1.7% after. COHN: Yes, there are at least two or three other papers that have compared the incidence of thromboembolic complications in patients with mitral stenosis before and after surgery, and little difference has been shown in those patients which were operated on versus those which have been treated medically. There are no good control studies. There are no studies, that I am aware of, where they have segregated out those people that had severe stenosis from those that had more mild stenosis. Of course, it is possible that the patient who is asymptomatic with tight mitral stenosis might be at greater risk than the patient with moderate stenosis. KELEMEN: I would like to ask Dr. COHN what he feels is the usefulness of exercise testing in aortic valve disease, specifically in aortic stenosis, its safety, and in aortic insufficiency; also, whether it is helpful in the serial evaluation of patients. COHN: I have to give you somewhat of a gut reaction because we have not looked into this systematically. Our impression is that exercise testing, although it is not nearly as dangerous as people would have you believe in aortic stenosis, has not been particularly useful to us in evaluating patients with aortic valve disease. The length of time they go on the treadmill does not tend to correlate with anything as far as we have been able to tell. Whether or not the patient develops ST depression is not too useful, because we have already mentioned that left ventricular hypertrophy per se may produce either true or false positive exercise tests, although we would not hesitate to perform an exercise test in a patient with aortic insufficiency or in a patient with aortic stenosis, if the patient is not having exercise-induced syncope. Given a reasonable indication for performing it, we would do so, but I doubt that it would be particularly helpful. With regard to that, I have to agree with NICK that the use of noninvasive techniques to follow these patients who have strains on their left ventricle is very important, and I personally believe that using the echocardiogram is one of the most important ways of following aortic insufficiency. We can follow serial changes in ejection fraction, left ventricular end-diastolic dimensions and left ventricular end-systolic dimensions. I believe that changes in these parameters in aortic insufficiency, and less commonly in mitral insufficiency, probably are useful in selecting patients for surgery. Our experience with aortic insufficiency and Initral insufficiency is a little bit different from that mentioned by Dr. KOUCHOUKOS. We seldom see patients with chronic mitral insufficiency that develop severe impairment


Discussion


228

in their ejection fraction. That is to say, because of the very small impedance to ejection, the ventricle is not really stressed very much in mitral insufficiency, as the blood can escape into the left atrium. So mitral insufficiency tends to be a lesion which is extremely well tolerated and most of the patients that we have studied with mitral regurgitation tend to have a normal ejection fraction. Even the patients with flagrant heart failure due to ruptured chordae have normal ejection fractions. Their ventricles are working like gangbusters. The problem is that they are ejecting all the blood backward, so that if I found the ejection fraction wasdropping, and was 20 to 25%, I might begin worrying about operating on him. We just do not find that as a common Problem. Similarly, our experience is totally different from STAGNOLU'S. I mention this because there are not a lot of natural history studies in aortic insufficiency. STAGNOLU'S group made a big point of the presence of angina. Yet we almost never find angina in the absence of coronary disease in the presence of aortic insufficiency. We would agree that once chronic congestive heart failure occurs in aortic insufficiency it is probably too late, but the vast majority of patients do not have chronic congestive failure, and if one follows them for a number of years, they often do not get it.

KOUCHOUKOS: Dr. COHN mentioned the ejection fraction in patients with mitral regurgitation and I certainly would not argue with what he says. I think there are patients who present with very low ejection fractions and by the time they develop low ejection fractions, there is significant trouble ahead, whether they are treated medically or surgically. I would think that a normal ejection fraction in a patient with severe mitral regurgitation probably implies some impairment of ventricular function and I would not use that as a reason to say that he does not need to be operated on at present and could be watched. Obviously we need more sophisticated methods or parameters than the ejection fraction, but this certainly correlates with difficulty early postoperatively. The problem of the left ventricle, which has been exposed for a chronic period of time to mitral regurgitation, is in the elimination of the mitral regurgitation, because if the ventricle, particularly the one that is large and dilated, now is rendered competent, the afterload on this ventricle is significantly increased, and this is the problem we encounter early postoperatively with low cardiac output and markedly elevated left ventricular end-diastolic pressure. In many cases there is a progressive downhill course despite all therapeutic interventions that are available and the patient succumbs. With regard to where the myocardial damage occurs after an open-heart operation, is it there before the operation, does it occur during the operation or does it occur in the postoperative period? I think injury to the myocardium occurs during all of these periods. But, we would submit that the ventricle that is at greatest risk for sustaining an intraoperative or postoperative myocardial injury is one that is severely diseased preoperatively. This has been our experience. For example, the massively hypertrophied left ventricle in aortic stenosis is at the greatest risk for the socalled stone heart syndrome or for the development of severe endocardial hemorrhagic necrosis. ROSE: Dr. KOUCHOUKOS, our big problem has been what is meant by doing the cases earlier. If I may, I would like to present a case and ask both you and Dr. COHN what you would do. A 25-year-old man presented with aortic insufficiency and mild exercise intolerance. He had cardiomegaly on chest film and LVH with ST-T wave changes on his


PATON: Would you also like to comment about ventricular function immediately after mitral valve replacement?

229

EKG. Cardiac catheterization revealed an ejection fraction of 40% and a LV end-diastolic pressure of 22. Would you, gentlemen, tell me how you would approach this problem? COHN: I think, everybody immediately notices that the discussion always falls back on aortic insufficiency, because nobody knows what to do with aortic insufficiency. I missed a couple of those numbers, but what I would do with the asymptomatic patient with aortic insufficiency is to routinely do hemodynamic studies and noninvasive studies including echo, and then follow the patient longitudinally. If at the first study he has severe impairment in hemodynamic function, including significant resting abnormalities, this may constitute an indication for surgery. If he does not, I would probably follow the patient, and with an enlarging heart size by Xray, enlarging heart size by echo, diminishing ejection fraction or the appearance of symptoms, I would go ahead. If all of these remain stable and the patient functions normally and does not have resting hemodynamic abnormalities to begin with, I would probably leave the patient alone. I may catheterize him again in 5 years or so. We have not arrived at the point where we are doing that yet only because our interest in aortic insufficiency had not gelled 5 years ago to the extent that we had enough sense to do that. KOUCHOUKOS: I would agree. There is not a lot of information available. I would probably advise operation in this man. I think that the slide I showed you of our own data, where we have looked at the ejection fraction in a number of patients, showed that his prognosis even with surgery would not be spectacular. The data of Dr. SPAGNOLLI, whether you choose to believe it or not, show that once the patient develops angina, symptoms of failure, or left ventricular enlargement, he is on a progressive downhill slide. and therefore he probably ought to be operated upon before the ejection fraction falls lower and the risk of surgery goes up. With an ejection fraction of less than 0.45, his prognosis is already severely limited even if he has a good surgical result. CONTI: I am somewhat fuzzy about SPAGNOLLI'S data and maybe I was taking a nap here while you were talking. I apologize to you for that. But, were these groups highrisk and low-risk groups? Were these patients asymptomatic at the time that they were being evaluated? KOUCHOUKOS: Maybe somebody from his group is here and could discuss the data better, but I think his group of patients who showed the progressive deterioration were asymptomatic at the time they were entered into the study. They became symptomatic. They either developed angina or symptoms of congestive heart failure. CONTI: Was there any difference in the age of the high- and low-risk group? That is one question. And do we know anything about the subsequent medical management of this so-called high-risk patient? KOUCHOUKOS: No, I cannot comment on that. Maybe KEITH can from his own series. CONTI: KEITH made the point about not sending people to the backwoods and making sure they are treated properly medically, and I wonder whether we know anything about the details of the medical management of the high-risk patients. COHN: I do not think there is any evidence, incidentally, that medical management per se changes the natural history. It may act as a narcotic to eliminate some of the symptoms and lull the physician into a false sense of security. So, we do not push hard with digitalis or diuretics if a patient has AI or MR and is beginning to develop symptoms. CONTI: Even with a big heart? With an enlarging heart?


Discussion


230

HOFFMAN: I would like to make some comments on the pathophysiology of aortic incompetence. Exercise is not very helpful in the asymptomatic patient, as this is probably the only lesion which gets better with exercise, because with exercise the regurgitant fraction decreases. You might recall an excellent study by JUDGE in which he took patients with aortic incompetence in severe congestive heart failure and paced them, with striking improvement. There was a drop in end-diastolic pressure, an increase in forward cardiac output and improvement in ejection fraction. So in the asymptomatic patient, I think, exercise is not very helpful. You might recall the paper by HARVEY and HUFNAGEL pointing out that the angina in aortic incompetence is frequently atypical in that it occurs at night. One of the things that happens at night is that the pulse rate goes down. The studies that Dr. BUCKBURG and I have done with animal models of aortic incompetence show that as you produce a severe fall of diastolic aortic pressure, what you do is decrease the diastolic area available for perfusion, the systolic area either remains the same or increases and, in fact, one can produce subendocardial ischemia in animals. I wonder whether measuring these areas, which can be done quite simply at catheterization, might give us some information in patients as to how deranged the coronary perfusion might be. COHN: Just a brief comment. I agree with JULIEN completely. Actually, exercise is not quite so benign in aortic insufficiency as is pacing, in that pacing improves function, whereas with exercise left ventricular filling pressure rises and cardiac output may not rise sufficiently. I agree that patients with severe aortic insufficiency and huge hearts can be put on a treadmill and walk forever. The point about angina is a good one. Our experience is that, although we acknowledge the presence of this very atypical form of angina, it probably occurs in less than 1% of the overall aortic insufficiency population. SHERMAN: Dr. COHN'S comments about mitral stenosis are different than those in our institution where Dr. LEONARD has popularized the use of exercise testing in the hemodynamic laboratory for evaluation of patients. I think this is because the so-called asymptomatic patient with mitral stenosis may really not be asymptomatic. In our experience, mitral stenosis in young males and females is very difficult to judge from a symptom point of view. Because these patients desire to be active, and because they gradually limit themselves unknowingly, exercise testing in the hemodynamic laboratory, looking for induced pulmonary hypertension, is very valuable. Similarly the middle-aged female of 40, who slows down because she thinks this is natural for her age and does not tell a physician that she is really symptomatic, may go unnoticed for many years. We thought many of these patients probably had symptoms from age 40, but did not appear to be symptomatic until age 55. Therefore, we routinely exercise patients in our laboratory. As a consequence, we have operated on many patients that Dr. COHN perhaps would not have operated on. However, we believe that commissurotomy can be done early and safely and is a benefit to these patients in the long term. We are now seeing many of these patients 10 years after their first commissurotomy and it is very encouraging to see the life-style that they have led over this time. I think it is better than the natural history of the disease. COHN: The main thing I would take exception to is that you called 40 middle-aged. Aside from that, when I was a Fellow I became interested in the hemodynamics in mitral stenosis, although I never published this data because it probably was not publishable.


COHN: Yes. I might mention that, contrary to popular belief, there are little data to indicate that digitalis significantly benefits myocardial function in the presence of aortic insufficiency.

231

We looked at all the mitrals that we had done. We had done resting and exercise hemodynamic evaluations and I was interested to learn that every mitral stenotic patient has abnormalities in hemodynamics; even in mild mitrals their wedge pressure with exercise goes up to 20-25 mm Hg almost invariably, except for this middle-aged woman syndrome, if you will, where the cardiac output does not change. But I have had a difficult time in finding a single case of mitral stenosis, no matter how mild, moderate or severe, that does not have significant hemodynamic impairment. BORGENHAGEN: I would like to ask a question to either one of the speakers about the means by which you establish trends in individual patients who are late class II or early class III and in whom the question of surgery is being considered. We used to obtain serial chest Xrays and we still do, at frequencies of once each month, every 6 months or every year, depending upon the patient. We now have a procedure which is noninvasive, possibly more expensive, but which can be obtained at equal frequencies, namely the echocardiogram. I would like you to comment on how frequently you obtain echocardiograms in patients in whom surgery is being considered, so that you can establish trends in individual patients. PATON: If I could add to that question; what is the availability in your institution of multi crystal echocardiography and do you think that that is going to significantly help us, as opposed to the single crystal? CoHN: First of all, nobody knows the answer to your question. I think that the frequency with which one evaluates a case depends upon an early assessment of the trends and the early assessment of the hemodynamics. If thinks look marginal to begin with, you might want to obtain serial data every 3 months, which is what I do, and then if things look stable, maybe every 6 or 9 months or a year. But nobody really knows. In mitral insufficiency, I think that this is less likely to be a malignant disease, so I would not be as anxious to study patients under a year period of time. As to the question of the multicrystal, there are many techniques now, or at least there are two principal techniques besides the single crystal. One is the multicrystal and the other is the gadget that rocks in some way and gives one the same sort of picture that was so beautifully demonstrated in the earlier sessions. We do not have either of these. All of these techniques are very infantile and extremely expensive today. I believe the Duke apparatus runs in the hundreds of thousands of dollars. But personally I believe that this is the direction for the future. My own belief is that the rocking single transducer is going to supplant the multicrystal as far as getting better resolution. We all hope for an inexpensive tool which will give us echos of the entire heart rather than one section. PATON: NICK, do you have multiple crystal availability? Those pictures fascinated me. How exensive is it, MIKE? JOHNSON: In regard to cost, our machine costs a hundred thousand or more to build, but that is because of the developmental design, etc. Production of a machine like this is not going to run into the hundreds of thousands of dollars. PATON: Do you think 50,000 dollars, or what are we talking about? JOHNSON: The present equipment is 50,000 dollars, you know. That is a very reasonable price, I think. That limits it from a private practitioner's office. I want to make a comment about the use of single probe echo in patients with valvular disease. I think, this in itself is a very useful technique in a patient without coronary artery disease in whom vou are looking at a normally contracting ventricle or poorly contracting ventricle


Discussion


232


which is not asynergistic. We follow patients serially and I think it is helpful to look at left ventricular dimensions, their serial change in dimensions, and how fast the posterior and septal walls move. I think, the single probe echo is going to be useful for many years to come. Eventually, once the price comes down, multiprobe echos are going to be used. But until that time, we can stilI use the single probe very nicely in patients with valvular disease. PATON: I know the surgical group at Stanford is trying to develop a multicrystal unit that could be used to provide on-line digital information on cardiac output in postoperative patients. And if ever we can get to the point where one can strap something to a person's chest and get an immediate accurate readout of their cardiac output, it would be marvelous. KOUCHOUKOS: We have had a little experience with the single crystal echo postoperatively in trying to assess these parameters. It is very difficult from the technical standpoint because of all the gadgetry. And it has not been very successful so far. Perhaps, the multicrystal will. COHN: Not just because of the gadgetry, but because of bleeding and the intrathoracic problems. We have a very difficult time in getting an echo of excellent quality in the postoperative period when we need it most. JOHNSON: In the postoperative period following prosthetic valve replacement, another major problem is that the septum is abnormal. Whether that is due to TI or secondary to surgery, one cannot estimate cardiac output by single echo in a prosthetic valve replacement. One other technique is being developed and that is looking at the prosthetic valve itself. By looking at the velocity with which the valve opens, the duration of diastole, and knowing the valve area, one can calculate the cardiac output. PATON: Do vou two gentlemen wish to take a final thrust at each other? I think it has been a very good discussion and I would like to announce that we have an approval from the American College of Cardiology for another program next year. One of the nice things about this conference is to be able to greet friends here year after year. Many of you very faithfully come from long distances. We hope to see you all again next year, the same place, same time, same seats, same snow, same climate. Thank you very much.

Debate on valvular heart disease. Pro: patients with valvular disease should have significant exercise intolerance beofre surgical intervention.

Surgical treatment of valvular heart disease.

Virus valvular heart disease.

Valvular heart disease in pregnancy.

Echocardiography in valvular heart disease.

Genetics of valvular heart disease.

Implications of third heart sounds in patients with valvular heart disease. The Veterans Affairs Cooperative Study on Valvular Heart Disease.

Pathophysiology of valvular heart disease.

Decade in review--valvular disease: Current perspectives on treatment of valvular heart disease.

The year in valvular heart disease.

Antithrombotic therapy in valvular heart disease.

Coronary atherosclerosis in valvular heart disease.

Cytotoxic serum factor in valvular heart disease.

Neurologic complications of valvular heart disease.

Valvular heart disease: the technologic dilemma.

Third heart sounds in patients with valvular heart disease.

Incomplete Kawasaki disease: early findings consist of congestive heart failure due to valvular heart disease.

Epidemiology of acquired valvular heart disease.

HLA antigens and acquired valvular heart disease.

Debate on congenital heart disease. Con: early total repair is not always preferable to palliative surgery in congenital heart disease.

Antithrombotic therapy for coronary artery disease and valvular heart disease.

[Valvular heart disease in hospitals in Lome (Togo)].

Recent advances in echocardiography for valvular heart disease.

Exercise testing and stress imaging in valvular heart disease.