most all patients. The results suggest that the onset of symptomatic supraventricular tachyarrhythmias have a nonuniform diurnal distribution that follows a detinite circadian pattern. In contrast to previous investigations3 we found that AF and paroxysmal SVT have signifi- cantly different diurnal distributions. Paroxysmal SVT occurs mainly during the daytime, whereas AF has a statistically significant peak during the night. The mech- anisms responsible for this difference are not known. Variations of autonomic tone have been hypothesized to have a role in the pathogenesis of supraventricular ar- rhythmias.7 Experimentally, AF can be induced by ad- ministration of acetylcholine.8 Moreover, in patients with frequent paroxysmal AF, the onset of the arrhyth- mia is often associated with an increased vagal drive.9 In this series, the time of onset of AF had 2 distinct peaks, the first between midnight and 2 A.M., and the latter after lunch. Both these periods were characterized by predominance of vagal tone.‘O Diurnal distribution of the onset of AF was similar in patients without de- tectable heart disease and in those with “secondary” AF. Furthermore, the pattern did not differ even in pa- tients (approximately 9%) in whom the onset of AF was associated with angina1 crisis. These findings suggest that circadian variability of AF is independent from its etiology and in particular is not significantly influenced by myocardial ischemia. The incidence of paroxysmal reentry SVT, in accordance with previous inves- tigations2,” was greater in the diurnal hours during which adrenergic prevalence may induce electrophysio- logic changes in the atrioventricular node.” Moreover, catecholamines enhance ectopic activity, increasing the likelihood of starting the reentrant mechanism. The abo- lition of the morning peak induced by B-adrenergic blockers is consistent with this hypothesis2

The onset of symptomatic AF and paroxysmal SVT is characterized by different diurnal distributions that are not influenced by etiology. Although our findings may be useful for timing antiarrhythmic treatment, we should acknowledge that the observed diurnal distribu- tion may not be applicable to all supraventricular ar- rhythmias, because some do occur in the absence of symptoms.

REFERENCES 1. Muller JE, Tofler GH, Stone PH. Circadian variation and triggers of onset of acute ctvdiovaxular disease. Circularion 198979733-743. 2. Irwin JM, McCarthy EA, Wilkinson WE, Ptitchett ELC. Circadian occurrence of symptomatic paroxysmal supravenbicular tachycardia in untreated patients. Cir- cd&m 1988;77:298-300. 3. Kupary M, Koskinen P, L.&none” H. Double-peaking circadian variation in the occurrence of sustained supravenhicula~ tachyarrhythmias. Am Heart J 1990, 120:136&1369. 4. Rostagno C, Paladini B, Pini C, Taddei T, Russo L, Giglioli C, Margheri M, Bettini G. Feasibility of out of hospital treatment of supraventricular tachycaxlias. Am J Cardiol 1991;68:119-122. 5. Bar FW, Brugada P, Dassner WRM, Wellens HJ. Differential diagnosis of tachy- cardias with mmow QRS complex (short max 0.12 set). Am J Cardiol 1984, 54:5.55-560. 6. Brigham C. Arbogart B, Guillaume GC, Lee JK, Halberg F. Inferential statisti- cal methods for estimating and comparing cosinor parameters. Chronohiolo~y 1982; 9:397439. 7. Waxman MB, Wald RW, Cameron D. Interactions between the autonomic ner- vous system and tachycardia in man. Cardiol C/in 1983; 1: 143-150. 13. Nahum LH, Hoff HE. Production of auticolar fibrillation by application of acetyl- beta-methyl choline chloride to localized region of the auricolar surface. Am J Phys- id 1940; 129:428436. 9. Coumel P, Leclercq JF, Attuel P. Paroxysmal atrial fibrillation. In: Kulkrtos HE, Olsson SB, Schlepper M. eds. Atria1 Fibrillation. Molndal: AB Hassle, 1982: 158-178. 10. Nademanee K, Christenson PD, Robertson HA, Intarachot V, Hanuood BJ, Feild DQ. Role of parasympathetic activity in the diurnal variation of heart rate in man: heart rate sptxhum analysis of Holter monitoring (abstr). Circulation 1988; 78(wppl II):ll-610. 11. Turton MB, Deegan T. Circadian variations of plasma catecholamine, cortisol and immunoreactive insulin concentrations in supine subjects. Clin Chim Acta 1974; 55:389-397.

Morphologic Patterns in Patients Undergoing Reoperation After Repair of Rheumatic Mitral Regurgitation Edward Turner, MD, Thomas Wisenbaugh, MD, Vania Sinovich, MB BCh, Stephanus Cronje, MB BCh, MMed, and Pinhas Sareli, MD

I n young patients with rheumatic mitral regurgitation (MB), valve repair is more desirable than prosthetic

valve replacement. This is particularly true in develop- ing countries where anticoagulation with warfarin is dif- ficult to monitor, and also in women of childbearing po- tential in whom warfarin is relatively contraindicated. The durability of repair in rheumatic MR may not be as good as in myxomatous disease.14 The explanation for the less satisfactory results of repair in rheumatic than degenerative disease has not been clearly defined, but could be due to either a worse initial outcome owing to extensive valvular disease, or to ongoing rheumatic ac- tivity that damages an initially good result. This study examines retrospectively the morphologic patterns pres-

From the Department of Cardiothoracic Surgery, Johannesburg Hospi- tal, Johannesburg, South Africa, and Cardiology Department, Barag- wanath Hospital, P.O. Bertsham 2013, Johannesburg, South Africa. Manuscript received June 12, 1992; revised manuscript received and accepted July 30, 1992.

ent in patients undergoing mitral valve repair and sub- sequent reoperation for recurrent or ongoing valve dys- function.

Chart reviews were per$ormed in 350 patients re- ferred by the Cardiology Department at Baragwanath Hospital for repair of mitral incompetence during the years 1981 to 1988. All valves had been assessed at the time of surgery with regard to function and were judged to be purely or predominantly incompetent. Of these pa- tients, 63 who underwent reoperation between the years 1981 and 1990 because of ongoing or recurrent mitral valve dysfunction were ident$ed. Mitral dysfunction was determined by clinical and echocardiographic ex- amination, and few patients underwent invasive evalu- ation. All patients with a nonrheumatic etiology (n = 3), and those in whom operative reports were incomplete or unavailable (n = 9) were excludedfrom analysis. The operative reports of the remaining 51 patients who un- derwent reoperation are the basis for this review.

BRIEF REPORTS 455

TABLE I Surgical Techniques (n = 51)

No. (%)

Carpentier-Edwards ring used Ring size

28 30 32 34 36

Chordal shortening Chordal resection Commissural splitting Posterior leaftlet mobilization

47 (92)

4 (8) 6 (12)

19 (27) 16 (31)

2 (4) 49 196) 36 (71) 19 (37) 34 (67)

TABLE II Patient Characteristics at Reoperation

Group 1 Group 2 p Value

Age at reoperation (year) 14 r 5 26 f 10 < 0.0001 Interval to reoperation (mo) 23 2 30 42 k 31 <O.Ol Activity

Active 12 (57%) 2 (7%) <0.05 Chronic 9 (43%) 28 (93%)

Mitral lesion Pure MR 18 (86%) 23 (76%) MR+MS 3 (14%) 5 (17%) Pure MS 0 2 (6%)

Technical factors 9 (43%) 7 (19%)

MR = mitral regurgitation; MS = mitral stenosis. I

I- TABLE Ill Morphologic Findings at Time of Initial Repair

Finding

Group 1 (n = 21) No. (%)

Annular dilatation 20 (95) AML prolapse 21 (100)

Chordal elongation 21 (100) Chordal rupture 0 (0)

PML retraction 12 (57) Prolapse 0 (0)

Leaflet thickening 17 (81) Subvalvular disease 6 (29) Commissural fusion 6 (29)

Group 2 (n = 30) No. (%I

27 (90) 28 (93) 28 (93)

3 (10) 13 (43)

2 (7) 21 (70)

8 (27) 13 (43)

No statistically slgnlficant differences between groups by Fisher’s exact test. AML = anterot mitral leaflet; PML = posterior mitral leaflet.

Repairs were performed using techniques developed by Carpentier,j discussed at length elsewhere,3 by the same 2 surgeons who were experienced in these tech- niques of repair. Table I lists the techniques used. Valve competency after repair was tested by injecting saline solution at high pressure through a cannula inserted in the apex of the left ventricle.

At the time of reoperation, other morphologic fea- tures noted were the surgeon’s subjective estimation of annular dilation, commissural fusion, leaflet retraction and prolapse, chordal elongation, fusion and rupture, and the presence of any ring dehiscence. All valves were determined to be rheumatically diseased at the time of original surgery, because of the presence of these anatomic abnormalities and the absence of myx- omatous changes with extensive billowing. Patients were divided into 2 groups according to the presence (group 1) or absence (group 2) of macroscopic evidence of rheumatic activity at the time of valve repair. Surgi-

TABLE IV Mitral Lesion at Reoperation

Group 1 (n = 21) No. (%)

Group 2 (n = 30) No. (%)

MR 18 (86) 23 (77) MR+MS 3 (14) 5 (17) MS 0 (0) 2 (7) IE 2 (10)

IE = infective endocarditis; other abbreviations as in Table Il.

1 (3)

TABLE V Morphologic Findings at Reoperation

Group 1 Group 2 (n = 21) (n = 30) No. (%I No. (%)

Ring dehiscence Mild 3 (15) 6 (20) Severe 0 (0) 2 (7)

Annular dilatation 2 (10) 1 (3) AMLflail 2 (10) 2 (7)

Prolapse 9 (43) 12 (40) Retracted 5 (24) 14 (47F Chordal elongation 8 (38) 11 (36) Chordal rupture 6 (29) 6 (20)

PML prolapsed 1 (5) 0 (0) Retracted 8 (38) 19 (63)

Leaflet thickening 13 (62) 21 (70) Commissural fusion 3 (14) 5 (16) Subvalvular disease 5 (24) 9 (30) Infective endocarditis 2 (10) 1 (3)

*No statistically significant differences between groups, although anterior leaflet retraction tended to be more frequent (p = 0.07) in chronic group.

Abbreviations as in Table Ill.

cal evidence suggestive of active rheumatic injlamma- tion was as previously described6: pericarditis, edema- tous thickening of the leaflets, erythema and hemor- rhage within the leaflet tissue, and pinhead vegetations of the free edge of the mitral leaflets in the absence of infective endocarditis. Although the results of serology were not available in all patients, each patient judged by the surgeon to have active rheumatic inflammation had been referred with a clinical diagnosis of active rheumatic carditis, as established by previously pub- lished criteria.6 In the previous study,6 94% of patients with clinical and serologic evidence of active carditis also had macroscopic evidence at the time of surgery.

Statistics were obtained using Mann-Whitney U test for continuous variables and Fisher’s exact test for categoric variables.

The mitral lesion was assessed surgically to be pure MR in I6 patients (76%) of group 1 and in 16 (53%) of group 2, and mixed mitral disease in 5 (24%) of group 1 and in 14 (4770) of group 2 (p = NS for both). Sixteen patients (74%) in group 1 were female com- pared with 25 (83%) in group 2 (p = NS). Patients who had active valve inflammation at the time of the origi- nal repair were younger (12 f 4 vs 22 f 9 years; p <O.OOOl) than were those with inactive disease, as were those with active inflammation at the time of reopera- tion (13 + 5 vs 24 f 10 years; p <O.OOl). Furthermore, the interval to reoperation was shorter when there was active inflammation at the initial repair (Table II) or re- operation (10 f 13 vs 44 f 32 months; p <O.OOOl).

456 THE AMERICANJOURNALOFCARDIOLOGY VOLUME 71 FEBRUARY15,1993

Table III lists the morphologicJindings at the initial repair. Annular dilatation and either chordal rupture or elongation resulting in anterior leaflet prolapse were the most frequent, important surgical findings in both groups. Posterior leaflet retraction was also frequently found; anterior leaflet retraction was considered a con- traindication to repair and was therefore not a feature of these patients.

Table IV shows functional pathology at the time of reoperation. All but 2 patients who had isolated mitral stenosis had MR as the indication for reoperation.

Table V lists morphologic findings at reoperation. Although some degree of ring dehiscence was found in I1 patients, it was not thought to be responsible for the MR by the surgeon in 9 of these, because the annulus was not dilated and dehiscence was not severe. The main feature of recurrent mitral dysfunction was ante- rior leaflet prolapse with elongated chordae, although anterior leaflet retraction also appeared to be a fre- quent finding in group 2.

Technical factors responsible for ongoing mitral valve dysfunction were present in 1.5 patients (29%) of the total group. These factors included dtjiculty in posi- tioning sutures due to friable tissues, dehiscent sutures, inability to restore leaflet coaptation, and chordal rup- ture due to excessive tension. In all 15 patients, the sur- geon had expressed concern about the quality of the re- pair. All I.5 patients had to undergo reoperation within I year of the repair (mean interval 3.4 months in group I, and 3.2 months in group 2); 9 of these patients were in group I. Annular dilatation was found in 2 patients in whom a ring had not been used and in I in whom the ring had become severely detached. Although re- current anterior leaflet prolapse was frequently a fac- tor in ongoing mitral valve dysfunction, the incidence of chordal rupture was much higher than in patients in whom technical complications were not present (6 of 9 in group 1 and 3 of 6 in group 2 vs 0 of 39).

The present study comprised a group of patients found almost exclusively in the “developing world,” where rheumatic disease continues to be endemic. Sev- eral characteristics distinguish this group from those of other studies: First, the mean age of the 51 patients was 17 years. Second, there was a high incidence of acute carditis (42%), in which the predominant functional pathology was previously shown to be IvX6 Although the absence of chronic fibrosis and stenosis should ren- der these valves more repairable, the potential for re- current active in&mmation in very young subjects may undermine the results of repair7 Chauvaud et al8 ana- lyzed the long-term results of mitral valve repair in chil- dren, but only 4 of 84 were in the acute phase. How- ever, 12 patients (14%) in that study had to undergo re- operation for recurrent or ongoing valve dysfunction, most within 2 years of repair. Duran et al9 also analyzed repair for rheumatic dysfunction and reported that 17 pa- tients (12%) had to undergo reoperation within 2 years of valve repair; mean age in those reoperated was 17 years, 6 of whom had evidence of active carditis. Our

group of patients with active carditis was even younger (mean age 12 years) and had an average interval to re- operation of almost 2 years, albeit with a wide variation. In this group, the incidence of technical complications (i.e., poor initial result) was higher than in patients pre- senting in a chronic phase. This has been attributed by Antunes et al3 to tissue edema compromising the stabil- ity of sutures.

The morphologic pattern of recurrence of valve dys- function is similar in some respects to the original valve pathology, whether active or chronic; prolapse of the an- terior leaflet and elongated chordae are 2 important and constant features. In contrast, annular dilatation, fre- quently found at the initial repair, is prevented by the implantation of an annuloplasty ring and is therefore not a feature of recurrent valve dysfunction in our series, where rings were usually part of the repair. Anterior leaflet retraction appeared to be a frequent finding in group 2 at reoperation and is surely a consequence of the chronic it&mmatory process. Even a perfect initial result may be undermined by ongoing inflammatory activity, often subtle or subclinical,10 despite prophylac- tic penicillin, which was used in all our patients. This aspect is critical to the long-term stability of valve re- pair for a disease that is essentially a chronic inflamma- tion.

Another factor that has a role in recurrent or ongo- ing valve dysfunction may be the learning curve8 asso- ciated with this technically complex procedure. This may have been responsible for the need to reoperate in 29% of our cases owing to technical factors, usually for severe MR detected in the early postoperative period.

The results suggest that either new techniques of re- pair will be needed or mitral valve replacement should be substituted in many “third world” situations (such as ours) where rheumatic activity is endemic.

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1988;78:1087-1098. 5. Carpentier A. Cardiac valve surgery-the “French correction.” J Thorac Car- diovasc Surg 1983;86:323-337. 6. Marcus RH, Sareli P, Pocock WA, Meyer TE, Magalbaes MP, Grieve T, Anhmes MJ, Barlow JB. Functional anatomy of severe mitral regurgitation in active rheumat- ic carditis. Am J Cardiol 1989;63:577-584. 7. Olson L, Subramanian S, Ackermann D, Orszulac T, Edwards W. Surgical patbol- ogy of the mitral valve: a study of 7 12 cases spanning 2 1 years. Mayo Clin Proc 1987:62:22-34. 8. Chauvaud S, Per& P, Touati G, Relland, Kara S, Benomar M, Carpentier A. Long term results of valve repair in children with acquired mitml incompetence. Cimdarion 1986;74(suppl 1):1-104-I-109. 9. Dumn C, Gometza B, Balasnndaram S, Al Halees Z. A feasibility study of valve repair in rheumatic mitral regurgitation. Eur Heart J 1991: 12(suppl B):34-38. 10. Edwards W, Peterson K, Edwards J. Active valwlitis associated with rheu- matic valvular diseaw and active myccarditis. Circulation 1978:57:181-l 85.

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