The prognosis of atrial after mitral valvotomy
fibrillation
P. B. Halmos, M.D., M.R.C.P.I.* Bevast, Northern Ireland
I
t has been estimated that 20 to 50 per cent of patients who undergo mitral valvotomy will develop atria1 fibrillation l-5 The persistence of this postoperatively. arrhythmia is of significance since it has a deleterious effect on the circulation and is associated with a high incidence of systemic embolization. The present study, based on a review of 1,000 mitral valvotomies, was undertaken to assess the prognosis of postoperative atria1 ftbrillation and study the effect of various factors on its production and abolition. Material
One thousand mitral valvotomies were performed between 1950 and 1964, in Wards 5 and 6 of the Royal Victoria Hospital, Belfast. During the first part of this period, the finger or knife was used to divide the mitral valve, whereas later a transventricular dilator was used. The surgical technique otherwise remained unchangecl. The cardiac rhythm of 855 patients who survived for a week after their first valvotomy was studied. The rhythm was confirmed by electrocardiogram before and usually more than once after operation. All patients were on digitalis preoperatively. None was given prophylactic quinidine. When quinidine conversion was Received for publication *Royal Victori+ Hospital,
30
Oct. 11, 1965. Grosvenor Rd.,
Belfast
required, it was attempted on the twelfth postoperative day by giving quinidine sulfate in a dose of 3, 6, 9, and 12 grains at 2-hour intervals until conversion was achieved. If required, this regimen was repeated on the second and third days. When sinus rhythm was established, the patient was started on a maintenance dose of quinidine, 3 grains four times a day. Results
Patients in s&s rhythm preoperatively. Of the 855 patients studied, sinus rhythm was present in 620 (72.5 per cent). One hundred and thirty-seven (22 per cent) developed atria1 fibrillation after the mitral valvotomy. It was found that development of atria1 fibrillation was more likely in patients over 40 years of age (p < O.OOl), in those with a history of paroxysmal attacks of severe palpitations (p < O.OOl), and in those in whom no or only slight division of commissures was achieved at valvotomy (0.02 < p < 0.05). Sex, right ventricular hypertrophy, preoperative mitral regurgitation, and the surgeon’s estimate of postoperative reflux had no influence on the results. The onset of atria1 fibrillation usually occurred in the first postoperative week and was maximal in the second 24 hours after operation (Fig. 1). The incidence of spontaneous reversion ~-as 13.6 per cent 12, Northern
Ireland.
Prognosis
1 ,
+
1 2 3 L1 5 6 Postoperative
Fig. 1. Time of onset mitral valvotomy.
7 8 9 10 11 12 13 1L, IL+ days of atria1
fibrillation
after
when atria1 fibrillation appeared during the first postoperative week, and 18.1 per cent when it appeared later. Spontaneous reversion to sinus rhythm occurred in a total of 18 patients (13.1 per cent). Quinidine conversion was attempted in the other 119 patients and was successful in 84 (70.5 per cent). The attempt at conversion had to be abandoned because of severe gastrointestinal disturbance in 3 patients. Signs of mild toxicity, not requiring discontinuation of therapy, however, were seen in 15 patients. Age, sex, right ventricular hypertrophy, and cardiothoracic ratio did not influence spontaneous or quinidine conversion. Quinidine conversion was successful in 53. 3 per cent of patients who had mitral regurgitation preoperatively, and in 75 per cent when the patients showed no evidence of an incompetent mitral valve. Sinus rhythm was established in 42.8 per cent of patients in whom only poor division of commissures was achieved. The percentage of conversion rose to 74.1 per cent in the group in which mitral obstruction was satisfactorily relieved. The above-mentioned differences just failed to reach statistical significance at the 0.05 level. Patients in atria1 Jib&la/ion preoperatively. There were 235 patients (27.5 per cent) in this group. After mitral valvotomy, quinidine conversion was attempted in 15 patients. Sinus rhythm was established in 6 (40 per cent). There was one case of spontaneous conversion among the 235
of atria1 fibrillation
after mitral vulvotomy
31
patients. Reversion to sinus rhythm occurred in this patient 3 weeks after valvotomy, although she has had atria1 fibrillation for over 3 years. Follow-up of patients. Of the 18 spontaneous conversions, there were 7 reversions to atria1 fibrillation after an interval of 1 to 10 years of sinus rhythm, The average duration was 4.7 years. Sinus rhythm persisted up to the present time in 11 patients, with an average duration of 3.6 >.ears (Table I j. Follow-up data were available in 80 of the 84 patients in whom sinus rhythm was successfully re-established with quinidine. Reversion to atria1 fibrillation occurred in 60 patients after an interval of 1 month to 9 years. The average duration was 2.8 years. ‘Twenty of them are still in sinus rhythm. In these it has been present for 1
Table I. Follow-,up results in 18 patients whose postoperative atria1 Jibrillation converted to sinus rhythm spontaneously (100 per cent follow-up) Sinus rhythm persists Number
of patients
Longest
follow-up
Average duration sinus rhythm
(yr.) of (yr.)
Reversion atria1 jihrilla;ion
11
7
5
10
3.6
4.7
to
Table 11. Follow-up resubts in 80 patients whose postoperative atrial jibrillation was converted to sinus rhythm with quinidine Sinus rhythm persists Number Longest
of patients follow-up
Average duration sinus rhythm
(yr.) of (yr.)
Reversion atria1 jihrillation
20
60
7
9
3.4
2.8
to
,-im. Iicart
Hcllmos
32
Jaly,
I.
1966
Table 11.1. Three-year follow-up of patients with spontaneousand quinidine conversion Length
of follow-up
(yr.)
--__ Number
of
patients
Rhythm
1
2
i
1
3
conversion
1.5
SR AF
1-l 1
13 2
12 3
Quinidint conversion (postoperative :\F)
47
SR AF
34 13
25 22
17 30
Quinidine conversion (preoperative AI;)
6
SR At;
1 5
0 6
0 6
Spontanexls
SK:
Sinus
rhythm.
.lF:
Atria1
fibrillation.
to 7 years, with an average duration of 3.4 years (Table II). In all 6 patients in whom long-standing atria1 fibrillation had been abolished postoperatively, reversion to atria1 fibrillation occurred within 1 year, within 6 months in 5 of them. When all of the patients who had been followed for at least 3 years were examined, the superior prognosis of spontaneous conversion was clearly demonstrated (Table I II). In view of the good long-term results in the latter group it was compared with the group of patients who maintained sinus rhythm throughout the postoperative period. The corresponding figures in these two groups for patients in sinus rhythm at 1, 2 and 3 years of follow-up were 94, X7, 80 and 95, 93, 90 per cent, respectively. Discussion
The incidence of postoperative atria1 fibrillation depends, to some extent, on preoperative preparation. Kittle and Crockett6 found that, although the over-all incidence of postoperative atria1 fibrillation was 26 per cent, in patients who received cluinidine and digoxin preoperatively it was only 16 per cent: 30 to 35 per cent of their patients who were given either drug or none at all developed atria1 fibrillation. The younger the patient the less likely is the development of atria1 fibrillation.
Patients over 40 who undergo valvotomy are particularly susceptible to the development of atria1 fibrillation, and this is the group in which every attempt should be made to prevent this complication by the use of prophylactic drug therapy. A history of previous episodes of severe palpitations is also a good indication for prophylactic therapy. It has been suggested7 that it is more difficult to establish sinus rhythm in patients who had significant mitral obstruction. It seems to be probable that the increased left atria1 pressure due to the narrowed valve orifice not only militates ag,ainst the successof conversion but predisposes to postoperative changes in rhythm. This was confirmed by the finding that patients whose significant mitral obstruction was unrelieved at operation were more likely to develop postoperative fibrillation. There have been varying reports of the importance of mitral incompetence in the occurrence of postoperative atria1 fibrillation. Kittle and Crockett” stated that only 1 of their 41 patients who fibrillated after operation had predominant mitral regurgitation. Others*~8~gfound positive correlation between the presence of mitral incompetence and postoperative fibrillation. The results in this study did not support the latter findings. I’ostoperative fibrillation was present in 21.7 per cent of patients without, and in 27.6 per
Prognosis
mitral insufficiency. Severity cent with, of reflux as estimated by the surgeon did not bear a positive correlation with the appearance of atria1 fibrillation. The onset of atria1 fibrillation appears most commonly during the first postoperative week. Attention has been drawn to the higher incidence of spontaneous conversion when atria1 fibrillation occurred during this period.2J0 Among our patients, those developing atria1 fibrillation during the second week had a higher rate of spontaneous conversion. The small numbers did not allow statistical analysis. If conversion to sinus rhythm takes place spontaneously, the prognosis is good. Eighty per cent of our patients have remained in sinus rhythm for up to 3 years. The over-all percentage of spontaneous conversion was smaller in the present series than in most other series reported in the literature. A possible reason for this discrepancy is that all patients with recent atria1 fibrillation were given quinidine sulfate on the fourteenth postoperative to establish sinus day, in an attempt rhythm. In the absence of quinidine therapy in some of these patients, spontaneous conversion might have occurred at a liter date. Quinidine conversion was successful in 72.4 per cent. A success rate of 40 per cent \jras achieved with chronic atria1 fibrillation. This compares with figures of 70 to 95 per cent reported in postoperative cases,2s6,8 and with 58.5 per cent reported by Eismeyer” in 1,058 cases of chronic atria1 fibrillation. There were no embolic episodes during conversion. It is undoubted that this risk exists, but its likelihood has been assessed to be not more than 1.5 per cent in the 48 hours after conversion,‘” and is likely to be even smaller in postoperative patients in whom the left atrium has been flushed free of clots, and the atria1 appendage removed. This inherent danger of conversion is more than balanced by the strong evidence for the deleterious effects of continued atria1 fibrillationgJ3 and for t.he circulatory improvement that follows establishment of sinus rhythm.14.‘j The relapse rate among patients requiring quinidine for conversion was disappointingly high. Our results indicate
of atrid jifibrillution
ufter mitral vdvotomy
33
that it is not worth while to attempt conversion in patients who fibrillated prior since reversion to atria1 to operation, fibrillation occurred in 83 per cent of them Tvithin 6 months. I’atients who require quinidine for postoperative atria1 fibrillation will eventually suffer a recurrence of this arrhythmia. However, 50 per cent of them were in sinus rhythm after 2 years, and 30 per cent after 3 years. Since it is impossible to predict the prognosis of the individual case, conversion in every patient seems to be justified. Bloomlo reported one patient with preoperative atria1 fibrillation in whom spontaneous conversion to sinus rhythm occurred after valvotomy. He could find no other documented cases in the literature. We have encountered one such case out of 235 patients. We can only assume that in our case the onset of a&al fibrillation was not caused by severe rheumatic involvement of the myocardium, but was initiated and maintained by the high left atria1 pressure, stretching of the atria1 lvall, and the abnormal hemodynamic situation caused by the tight mitral stenosis. Once these factors were relieved, sinus rhythm returned. Summary
The prognosis of atria1 fibrillation occurring after mitral valvotomy has been reviewed. Six hundred and twenty patients were in sinus rhythm preoperatively. Atria1 fibrillation developed in 137 (22 per cent). In 18 (13.1 per cent) of these, conversion to sinus rhythm occurred spontaneously; quinidine was successfully used with the same end result in 84 (72.4 per cent). Conversion of long-standing atria1 fibrillation n-as successful in only 40 per cent of cases. Once sinus rhythm was established, those in whom conversion had occurred spontaneously had the best prognosis. I wish to thank Dr. J. F. Pantridge for his permission to study these patients who were all under his care. REFERENCES 1. Wood, P.: An appreciation of mitral stenosis, Brit. M. J. 1:lOSl and 1113, 1954. 2. Heinz, I~., and Hultgren, H.: Atria1 fibrillations
34
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Am. Heart 1. July, 1966
Hulmos
following mitral valvotomy, Arch. Int. Med. 99:896, 1957. Ellis, L. B., Harken, D. E., and Black, H.: A clin.cal study of 1,000 consecutive cases of mitral stenosis two to nine years after mitral valvuloplasty, Circulation 19:803, 1959. Black, H., Lown, B., and Bartholomay, A. F.: The value of quinidine in the prevention of atri.xl fibrillation after mitral valvuloplasty, Circulation 23:519, 1961. Lowther, C. P., and Turner, R. W. D.: Deterioration after mitral valvotomy, Brit. M. J. 1:1027 and 1102, 1962. Kittle, C. F., and Crockett, J. E.: The etiology and prevention of atria1 fibrillation after mitral valvotomy, J. Thorac. & Cardiovas. Surg. 38:X3, 19.59. Sokolow, M.: The present status of therapy of the cardiac arrhythmias with quinidine, AM. HEP.KT J. 42:771, 1951. Fraser, H. R. L., and Turner, R. W. D.: Auricular fibrillation, with special reference to rheumatic heart disease, Brit. M. J. 2:1414, 195s. Otto, J. F., Jr., Hutcheson, J. M., Jr., Abelmarn, W. H., Harkness, D. E., Gray, J. E.,
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and Ellis, L. B.: Clinical observations before and after mitral valvuloplasty. Physical, radiologic and electrocardiographic changes, New England J. Med. 253:995, 1955. Bloom, V. R.: The prognosis of atria1 fibrillation following mitral valvotomy, Brit. Heart J. 25:595, 1963. Eismayer, G.: Die Behandlung unregelm&ssiger Herztstigkeit mit Chinidin, Deutsches Arch. klin. Med. 156:182, 1927. Goldman, M. J.: The management of chronic atria1 fibrillation, indications for and methods of conversion to sinus rhythm, Prog. Cardiovas. Dis. 2:465, 1960. Phillips, E., and Levine, S. A.: Auricular fibrillation without other evidence of heart disease. A cause of reversible heart failure, Am. J. Med. 7:478, 1949. Kory, R. C., and Meneely, G. R.: Cardiac output in auricular fibrillation, with observations on the effect of conversion to normal sinus rhythm, J. Clin. Invest. 30:653. 1951. Halmos, P. B., and Patterson, G. C.: The effect of atria1 fibrillation on the cardiac output, Brit. Heart J. 27:719, 1965.