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Eur J Cardiothorac Surg 1999;16:435-439
© 1999 Elsevier Science NL
Istituto Medico-Chirurgico di Cardiologia, Piazza, L. Miraglia, 80138 Napoli, Italy
Corresponding author. Present address: Corso Europa 72, 80127, Naples, Italy. Tel.: +39-081-643-055; fax: +39-081-714-5205
e-mail: adandrea{at}synapsis.it
| Abstract |
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Key Words: Atrial fibrillation Coronary artery bypass graft Postoperative arrhythmia
| 1. Introduction |
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Despite it is often regarded as a benign and self-limited condition, post-CABG AF may lead to severe complications, including systemic embolization and even significant haemodynamic instability [13].
The pathophysiological mechanisms responsible for the arrhythmia remain still unclear, although many studies have underlined the importance of different perioperative variables that appear independently related to its occurrence [116]. An increased age, preoperative beta-blockers withdrawal together with postoperative sympathetic activation and a history of preoperative paroxysmal supraventricular arrhythmias seem to play a major role, but many other factors appear to be involved somehow [416]. These apparently confounding results derive from the fact that only few studies comprised a satisfactory number of the different perioperative variables that might exert a possible influence on atrial arrhythmogenesis.
The aim of our paper was then to identify the clinical predictors of post-CABG AF, extending our analysis to all the preoperative, intraoperative and postoperative factors that might be potentially linked to its occurrence
| 2. Materials and methods |
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For each patient a complete preoperative echocardiographic evaluation had been performed using an Acuson XP10 ultrasound system (Mountain View, CA). Left atrial enlargement was defined as an anteroposterior M-mode diameter >41 mm measured in parasternal long-axis view.
Data collection was performed at the time of hospital discharge and consisted in filling a proper form containing all the preoperative, intraoperative and postoperative variables considered in all the patients (see Tables 13). In particular, preoperative episodes of paroxysmal AF were verified by accurate anamnesis.
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2.2. Postoperative protocols
Patients were weaned off of the ventilator as soon as they appeared haemodynamically stable, they presented no major bleeding, they were normothermic and conscious. Potassium and magnesium supplements were provided as necessary to maintain electrolytic balance within the normal range. For each patient heart rate, ECG lead II, arterial and central venous pressure were continuously monitored during their stay in the intensive care unit (ICU). Twelve-lead ECGs were routinely done until the day of discharge once a day or more, if necessary, to confirm any rhythm disturbance or ischemic incident. A postoperative echocardiogram was performed for those patients suspected of having a postoperative impairment of the systolic function of one or both the ventricles. An inotropic support with dobutamine was provided for a good deal of patients in order to achieve more rapidly a stable haemodynamic condition in the ICU. Further inotropic agents were then added only if ventricular contractility resulted frankly impaired and dobutamine alone did not prove to be sufficient in maintaining an adequate ejection fraction.
2.3. Statistics
The relation of all preoperative, intraoperative and postoperative factors with the occurrence of postoperative AF was performed using the chi-square and Student's t test. Differences were considered statistically significant when P<0.05. Univariate factors exhibiting a P-value of less than 0.05 were entered into multivariate logistic regression analysis in order to assess the independent correlates for AF. Again, statistical significance was obtained only for P-values less than 0.05.
| 3. Results |
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Multivariate logistic regression analysis identified left atrial enlargement, a history of prior episodes of paroxysmal AF and the severity of CAD to be independent correlates for AF. The OR and the P-value for each multivariate predictor are shown in Table 4.
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| 4. Discussion |
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Among the different factors possibly related to post-CABG AF occurrence, the patient's age, male sex and preoperative beta-blockers withdrawal turned out to be the most reliable predictors [79,11,12]. However, some authors underlined the importance of other variables, such as the type of cardioplegia approach and delivery [13,14], the existence of an obstructive disease of the seno-atrial and atrio-ventricular nodal arteries [15], the degree of right coronary artery stenosis [21], the development of postoperative fluid and electrolytes shifts and sympathetic activation [4,5]. Even an increased P wave duration might represent a risk factor [6,16], probably expressing an impaired intra-atrial and inter-atrial conduction.
Surprisingly, most of the major studies did not analyse the role exerted by left atrial enlargement and coronary artery disease severity on postoperative atrial arrhythmogenesis. These variables may alter atrial architecture and structure and were then included in our study in an attempt to test all the major factors that might be in some way related to post-CABG AF onset.
Our data suggest that the propensity to develop postoperative AF may be connected with the presence of advanced age, a greater body mass index, left atrial enlargement, a history of preoperative episodes of paroxysmal AF and finally a more severe coronary artery disease. Of these factors, only the last three seem to play an independent predictive role. A possible explanation might derive from the fact that AF needs a well-defined anatomical and electrical basis. In other words, greater left atrial dimensions, together with the structural changes that are likely to be associated with a more severe CAD and possibly also related to increased age and body mass index (i.e. atrial myocytes replacement with fibrous and/or adipose tissue) might constitute a fertile anatomical substrate for the development of post-CABG AF. This tendency could then be favoured by electrical triggering events. Prior episodes of paroxysmal AF, in fact, may predispose to further atrial tachyarrhythmias, acting through a complex electrophysiological remodeling of both the atria that finally leads to a progressive and spatially dyshomogeneous shortening of atrial relative and effective refractory periods [22]. On this basis, an ectopic impulse might encounter contiguous regions with different refractoriness and therefore propagate with different conduction velocities. As a result, if this phenomenon takes place at a microscopic level, it may generate multiple wavelets that could trigger and maintain the fibrillation process.
There are several final points raised by our study that need to be clarified. First, the relationship between the severity of CAD and postoperative occurrence of AF would apparently disagree with the lack of any predictive role played by the number of bypass grafts performed. A possible explanation might be inferred from the fact that the extension of CAD is not necessarily related to the number of vessels suitable for grafting. Furthermore, in accordance with previously reported studies [8,23], a depressed left ventricular function does not increase the risk of post-operative AF. Finally, additional valvular surgery does not seem to predispose to postoperative AF either. However, such a curious finding may be related to the small number of patients enrolled undergoing coronary surgery together with valve replacement.
| Footnotes |
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| References |
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