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Eur J Cardiothorac Surg 2004;25:807-811
© 2004 Elsevier Science NL
a Department for Cardiac Surgery, University Hospital Schleswig-Holstein, Luebeck, Germany
b Herzzentrum, Segeberger Kliniken GmbH, Bad Segeberg, Germany
c Klinik fuer Kardiologie, Helios Kliniken Schwerin, Schwerin, Germany
Received 18 September 2003; received in revised form 18 December 2003; accepted 9 January 2004.
* Corresponding author. Address: Klinik für Herzchirurgie, Universitaetsklinikum, Ratzeburger Allee 160, D-23538 Luebeck, Germany. Tel.: +49-451-500-2108; fax: +49-451-500-2051
e-mail: sievers{at}medinf.mu-luebeck.de
| Abstract |
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Key Words: Surgery Ventricles Aneurysm Sudden death Follow-up studies
| 1. Introduction |
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LV-aneurysm repair (LVAR) reduces LV-size [8,9] and may thus also reduce the incidence of late arrhythmias because myocardial stretching is thought to contribute to the development of arrhythmias [10]. However, a recent review concluded that it is not known whether LVAR without concomitant anti-arrhythmic surgical procedures is sufficient for prevention of late arrhythmias or sudden death [11]. Heart failure and thus surgery for heart failure is expected to increase in frequency, therefore, the incidence of arrhythmias after LVAR with and without concomitant anti-arrhythmic surgery is of interest with regard to the optimal treatment for patients with LV-aneurysms.
For many years, we have performed LVAR without additional arrhythmia ablation procedures. We therefore reviewed our own results after LVAR only, obtained follow-up information in order to determine the incidence of sudden death and investigated its predictors.
| 2. Material and methods |
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2.3. Analysis of the LV-angiograms
The 30° right anterior oblique (RAO) view of the preoperative LV cineangiograms was analyzed using a software (QCA-CMS; Medis; Leiden, Netherlands) that allows manual tracing of the LV outlines. To derive data on regional left ventricular function, the centerline method was applied to the endsystolic and enddiastolic LV outlines. LV-aneurysms were classified according to the predominating regional wall motion abnormality with the following definitions: dyskinetic if absolute motion of contiguous chords was less than zero (80%) and akinetic (20%) if equal to zero. The extent of non-contracting muscle or asynergy was calculated as the percent length of LV-perimeter showing fractional shortening below two SDs from mean normal values; the percent length of the LV-perimeter that showed akinesia and dyskinesia, respectively, was also recorded. To obtain absolute ventricular volumes, the Area Length method and a regression equation according to Kennedy (to correct for differences between an ellipsoid model and the actual LV shape) was applied to the ventricular outlines of the RAO view [13,14]. Because of the different methodology (a monoplane as compared to a biplane method in most other studies), ventricular volumes are not directly comparable to other studies. Ventricular volumes were then normalized for body-surface area. LV-ejection fraction and stroke volume were calculated from enddiastolic and endsystolic volumes. Table 2 summarizes the laevocardiographic results.
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2.5. Definition of sudden death
Sudden death was defined as death within 1 h after the onset of symptoms or death after a witnessed cardiac arrest or abrupt collapse that was not preceded by symptoms lasting more than 1 h [15]. If there were any symptoms prior to death, only those deaths were classified as sudden in which the symptoms prior to death were not typical of myocardial infarction.
2.6. Statistical methods
Ordinal variables are presented as absolute numbers and relative frequencies. Continuous data are presented as mean±SD, except where otherwise stated. Univariate analysis for continuous data was performed using the MannWhitney U-test. A survival curve was constructed using the KaplanMeier method. Univariate analysis of all variables given in the text or tables in order to assess their relation with late mortality was performed by the log-rank test or the Cox proportional hazards method. Multivariable analysis excluding factors with large P-values in univariate tests was performed by Cox proportional hazards. The proportional hazards assumption was assessed by checking that there was no significant evidence of the need to include cross-product terms involving covariates and the logarithm of survival time. P<0.05 was chosen to indicate statistical significance. For analyses, SAS, release 6.12 (SAS institute, Cary, NC), or Minitab, release 12 (Minitab Inc., State College, PA), were used.
| 3. Results |
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3.2. Perioperative results
Six patients (4.1%) died perioperatively, four from ongoing low-output syndrome and two after multiorgan failure had developed. Thirty-six patients experienced ventricular tachyarrhythmias necessitating treatment in the first postoperative days. In five patients, defibrillation for ventricular fibrillation was needed.
3.3. Follow-up period
At follow-up, the patients had significantly less symptoms (median: NYHA II, minimummaximum: NYHA IIIV, P<0.001). During follow-up, 19 patients died (linearized mortality rate including surgery 5.4%/year). The KaplanMeier estimate of 5-year survival was 78% (Fig. 1)
. The majority of deaths during follow-up were cardiac-related (84%). Most cardiac deaths were sudden (n=7). Other causes of late cardiac death were worsening CHF (n=5), and documented acute myocardial infarction (n=4).
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Multivariate analysis did not provide additional information. No incidence of near-missed death could be elucidated. During follow-up, one patient received implantation of an automated cardioverter/defibrillator (ICD).
| 4. Discussion |
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LV-aneurysm resection for therapy of ventricular arrhythmias was first published in 1959 [16], and several subsequent reports suggested that LV-aneurysmectomy may be a reliable treatment for refractory malignant ventricular arrhythmias [17,18]. This finding can probably be explained by the reduction of LV-size created by LVAR resulting in decreased wall tension and oxygen demand. This theory fits experimental data that suggest that increased wall tension may play an essential part in arrhythmia pathogenesis [10].
However, we observed a high incidence of sudden death late after LVAR and a significant association between late sudden death and ventricular tachyarrhythmias early postoperatively. Our finding indicates that arrhythmogenic foci may be present after LVAR in the freshly decompressed heart. This is supported by reports that identified silent ventricular tachycardias in patients who had undergone aneurysmectomy for treatment of ventricular tachycardias [19] or showed that recurrent ventricular arrhythmias involved an anatomic substrate, usually within the border zone of the infarction [20]. Therefore, many groups today combine LVAR with endocardial resection and/or cryoablation in patients with clinical and/or inducible ventricular arrhythmias [9,21] with documented success [22,23]. The etiology of late death, however, is explicitly addressed in only two current large studies on LVAR. In both studies, LVAR had been extensively combined with arrhythmia ablation (in 40 [21] and 50% [22] of the patients). In these reports, the frequency of sudden deaths appears to be lower than in our study: Mickleborough [21] found the majority of deaths to be due to CHF (19/31) and only four (13%) deaths to be either sudden or due to documented ventricular arrhythmias. Di Donato [22] reports on 48 late deaths, nine (19%) of which were sudden. This preventive approach, however, may add to the complexity and risk of the operation.
The perioperative mortality rate in our study is quite low when compared to other groups [8,9,22]. Contrary to other studies, we operated upon a series of patients with a high prevalence of classic dyskinetic LV-aneurysms (80% in our study vs. 33% in the RESTORE-group [8]). However, the size of the LV-aneurysm (as expressed by the extent of non-functioning myocardium or asynergy) appears to be comparable to other studies. In our study, the mean extent of asynergy was 51% as compared with 4260% in other studies [21,24]. On the other hand, the ejection fraction was slightly higher than in other studies [8,9,21] reflecting a considerable preservation of the contractile function of remote myocardium. We believe that this was crucial for obtaining the low in-hospital mortality and has also contributed to the low prevalence of significant concomitant mitral valve regurgitation. Theoretically, however, the less invasive surgical approach (by omitting concomitant anti-arrhythmic surgery) may also have contributed to the results.
There is another option besides prevention, i.e. treatment of late arrhythmias using an ICD. This approach is very attractive because arrhythmias developing after LVAR may not have been inducible preoperatively [22]. In addition, the MADIT-II trial demonstrated that postinfarction patients had a significantly improved prognosis after implantation of an ICD [7]. Patients in the MADIT-II trial had severely reduced LV-function and therefore most likely overlap with patients who undergo LVAR. Nevertheless, the results of the MADIT-II study cannot be easily applied to patients who had undergone LVAR because MADIT-II excluded all patients who had undergone coronary revascularization (almost always concomitant to LVAR) within 3 months before enrollment and patients with NYHA class IV (23% of the patients in our study). So far, it has not been tested which approach (concomitant arrhythmia ablation procedure vs. prophylatic ICD) to patients undergoing LVAR is more efficacious, but such studies are strongly encouraged.
A strange and unexplained finding of our study is the fact that patients who received a bypass graft to the RCA had an increased chance of dying suddenly. All patients who died suddenly and who received a venous graft to the RCA had either a right dominant or balanced coronary circulation. We therefore can only speculate that occlusion of the venous graft may have resulted in undetected myocardial infarction leading to lethal arrhythmias. If a myocardial infarction occurs late after LVAR, even previous arrhythmia ablation procedures may not be able to prevent this kind of new lethal arrhythmia, and, overall, placement of an ICD may be the most efficacious approach.
4.1. Limitations of the study
Ideally, a prospective, randomized multicenter trial would be desirable to clarify the best treatment with regard to anti-arrhythmic treatment for patients with LV-aneurysms. However, there are shortcomings regarding the generalizibility and practical difficulties in performing such a randomized trial. Carefully conducted observational studies are also of significant value [25], and studies as ours may help to increase knowledge in as much as all our LVAR-patients were treated without concomitant anti-arrhythmic surgery compromising a comparably large, uniform patient cohort.
This retrospective study lacks objective data on arrhythmias. However, sudden death is usually arrhythmogenic in nature [5,6], and we observed a significant association between late sudden death and ventricular tachyarrhythmias necessitating treatment in the first postoperative days. This finding provides some reassurance that the observed sudden deaths were likely caused by arrhythmias. Our study also lacks data on postoperative ventricular dimensions. We therefore cannot exclude that residual ventricular dilatation may have contributed to the supposed arrhythmogenic deaths.
| 5. Conclusion |
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| Acknowledgments |
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| References |
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