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(Circulation. 2005;112:3247-3255.)
© 2005 American Heart Association, Inc.
Cardiovascular Surgery |
From the Division of Cardiovascular Surgery, St. Vincent Mercy Medical Center (A.Z., T.A.S., C.J.R., S.J.D., A.S.S., R.H.H.), Toledo, Ohio; Division of Cardiovascular Surgery, St. Lukes Hospital (A.Z., T.A.S., C.J.R., S.J.D., A.S.S., R.H.H.), Maumee, Ohio; and Departments of Surgery (A.Z., T.A.S., C.J.R., S.J.D., A.S.S.) and Medicine (R.H.H.), Medical University of Ohio, Toledo, Ohio.
Correspondence to Robert H. Habib, PhD, Director, Cardiopulmonary Research, St. Vincent Mercy Medical Center, 2213 Cherry St, ACC Bldg, Suite 309, Toledo, OH 43608. E-mail Robert_Habib{at}mhsnr.org
Received April 4, 2005; revision received August 30, 2005; accepted September 1, 2005.
| Abstract |
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Methods and Results This was a retrospective analysis of the incidence of AF in terms of body mass index (BMI). A total of 8051 consecutive cardiac surgery patients (1994 to 2004; mean age 64 [SD 11] years; 5372 men [67%]) who were free of any history of preoperative AF or flutter were included in the analysis. This series included 3164 obese patients (39%; median age 62 years) and 4887 nonobese patients (61%; median age 66 years), who were further divided on the basis of BMI (kg/m2) into 6 groups: BMI <22 kg/m2, 22
BMI
25 kg/m2 (normal), 25<BMI
30 kg/m2 (overweight), 30<BMI
35 kg/m2 (obese I), 35<BMI
40 kg/m2 (obese II), and BMI >40 kg/m2 (obese III). Unadjusted AF incidence was similar in obese and nonobese patients (n=742 [23.5%] versus n=1068 [21.9%], respectively; P=0.099). Covariate-adjusted ORs for AF were systematically greater for larger patients than for patients in the normal group (adjusted OR [95% CI]=1.18 [1.00 to 1.40], 1.36 [1.14 to 1.63], 1.69 [1.35 to 2.11], and 2.39 [1.81 to 3.17] for overweight, obese I, obese II, and obese III, respectively). Other AF predictors included age (adjusted OR=1.52 [95% CI 1.46 to 1.58] per 10 years), mitral valve surgery (adjusted OR=2.42 [95% CI 1.92 to 3.06]), aortic valve surgery (adjusted OR=1.79 [95% CI 1.45 to 2.22]), chronic obstructive pulmonary disease (adjusted OR=1.28 [95% CI 1.12 to 1.46]), male gender (adjusted OR=1.24 [95% CI 1.10 to 1.40]), preoperative ß-blocker use (adjusted OR=1.17 [95% CI 1.05 to 1.32]), vascular disease (adjusted OR=1.18 [95% CI 1.05 to 1.32]), white race (adjusted OR=1.33 [95% CI 1.07 to 1.66]), history of arrhythmia other than AF/flutter (adjusted OR=0.80 [95% CI 0.68 to 0.96]), ejection fraction <40% (adjusted OR=1.16 [95% CI 1.03 to 1.31]), left main disease (adjusted OR=1.15 [95% CI 1.00 to 1.32]), and off-pump surgery (adjusted OR=0.61 [95% CI 0.44 to 0.83]). The obesity-AF association was confirmed in 4 1-to-1 propensity-matched obese versus nonobese comparisons and in 2 separate derivation/validation subcohort analyses.
Conclusions Obesity is an important determinant of new-onset AF after cardiac surgery. Future postoperative AF risk models should incorporate BMI or obesity levels. Studies examining the efficacy of AF-minimizing prophylactic interventions in high-BMI patients, particularly in the elderly, may be warranted.
Key Words: arrhythmia cardiopulmonary bypass complications multivariate analysis propensity matching
| Introduction |
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New-onset AF is the most common complication after cardiac surgery (20% to 40%) and is linked to other serious perioperative complications (eg, stroke), prolonged hospital stays, increased frequency of readmissions, and greater operative mortality.613 Moreover, 1 group has demonstrated a significantly worse 0- to 4-year survival in CABG patients who develop postoperative AF.14 Obesity is increasingly more prevalent among cardiac surgery patients, with
40% of CABG patients having a body mass index (BMI) >30 kg/m2.15 Whether and to what extent this prevalence of obesity explains new-onset AF in this surgical population is not fully known. To date, no studies exploring predictors of AF after cardiac surgery have linked increased body size or obesity to this complication.613
We reasoned that the association of left atrial enlargement with increasing adiposity in adult cardiac surgery patients is most likely similar to that in the general adult population.4,16 In fact, the increased potential of other cardiovascular risk factors (eg, hypertension and left ventricular dysfunction) in this surgical cohort are likely to exacerbate this effect. The primary objective of the present study was to elucidate the role of body size (with primary emphasis on BMI) in the development of postoperative AF after cardiac surgery.
| Methods |
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98% of on-pump patients. This investigation was approved by the institutional review boards at both hospitals. Because of the retrospective nature of the study, requirement for informed consent was waived. Clinical data for all patients were collected prospectively and entered into identical cardiac surgery databases at both institutions as described previously.15 Collected variables included demographics, risk factors and comorbidities, preoperative medications, operative data, and postoperative complications and outcomes. All entries were based on definitions of the Society of Thoracic Surgeons and were regularly reported to the national cardiac surgery database. The single end point in this investigation was new-onset AF (occurring anytime perioperatively through hospital discharge), which was collected as a postoperative complication. AF was diagnosed on the basis of an ECG, telemetry (100% of patients), or physician findings and was confirmed from hospital or physician chart notes and discharge summaries. Database quality checks for missing values and incorrect entries were performed routinely. Additionally, complication rates and resource utilization (transfusion, cardiovascular intensive care unit [CVICU]/hospital stays) were always cross-checked for the separate CVICU and cardiac surgery databases, as well as against patients discharge summaries and hospital medical chart attestation (or coding summary).
Postoperative Medications
Aspirin and ß-blockers use was consistent throughout this 1994 to 2004 series. Aspirin (325 mg via nasogastric tube) was always given to patients on arrival at the CVICU and was decreased to 162 mg PO daily on postoperative day 1. In all patients, ß-blockers were routinely given by mouth until the morning of surgery and reinstituted soon after surgery, being given intravenously in the CVICU if the patient was unable to swallow pills. Accordingly, time of ß-blocker withdrawal (if any) was minimized in the present series of patients. Amiodarone (intravenous or by mouth) was always used after onset of AF, including intraoperatively. Since July 1999, postoperative prophylactic amiodarone (daily 200 mg PO started on postoperative day 1) has been used routinely in all patients. An ACE inhibitor was used routinely in patients, including those who were taking one preoperatively, who were in congestive heart failure or who had low ejection fraction (<35%), if hemodynamically tolerated (systolic blood pressure >100 mm Hg).
Data Analysis and Statistical Methods
Patients were divided into those who developed the complication (AF) versus those who did not (No-AF). BMI (in kg/m2) and body surface area (BSA; in m2) were used to characterize the role of patient size and adiposity and were considered both as continuous and categorical variables (6 categories each). BMI was derived as the weight (in kilograms) divided by the square of height (in meters). BMI categories were largely based on the World Health Organization/National Institutes of Health classification scheme17 as follows: BMI <22 kg/m2 (underweight), 22
BMI
25 kg/m2 (normal), 25<BMI
30 kg/m2 (overweight), 30<BMI
35 kg/m2 (obese I), 35<BMI
40 kg/m2 (obese II), and BMI >40 kg/m2 (obese III). BSA was calculated with the Mosteller formula as BSA (m2)=[(height (cm)xweight (kg)]/3600)1/2 and categorized as follows: BSA <1.5 m2 (very small), 1.5
BSA
1.75 m2 (small), 1.75<BSA
2.0 m2 (intermediate), 2.0<BSA
2.25 m2 (large I), 2.25<BSA
2.5 m2 (large II), and BSA >2.5 m2 (large III).
Continuous data were expressed as mean (SD). Baseline variables for AF versus No-AF groups were compared by use of the Wilcoxon rank sum test, t test, or the
2 test as appropriate. A 2-sided P<0.05 was considered statistically significant. Body sizeAF relations were derived with and without adjustment for clinical and operative confounders via multivariable logistic regression techniques for (1) all cardiac surgery and (2) isolated CABG patients. Separate multivariable model analyses were performed with either BMI and BSA to define body size. Here, "normal" BMI and "intermediate" BSA were used as reference categories, respectively, when size was described as a categorical variable. For CPB, short-duration CPB (
60 minutes) was used as the reference category, with "off-pump" included as a subgroup. Covariates selected for adjustment were based on prior reports613 and included all the variables listed in Table 1 in addition to a month-of-surgery variable, which varied between 1 (January 1994) and 132 (December 2004). Regression model selection was done with backward elimination (Wald statistic, confirmed by forward and stepwise selection). A P<0.05 significance level was used for model inclusion and P>0.1 for exclusion (SPSS version 10.0, SPSS Inc).
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The obesity-AF association derived in the primary multivariable analysis was further confirmed via additional complementary analyses. First, we compared AF incidence in 1-to-1 or greedy (ie, no shared or repeated matches) propensity-matched obese (BMI >30 kg/m2) versus nonobese (BMI
30 kg/m2) isolated CABG patient groups. Here, a total of 4 matched patient group pairs were obtained via a nonparsimonious obese model18,19 that incorporated all variables in Table 1 except for body size. These were as follows: obese (all) versus nonobese, obese I versus nonobese, obese II versus nonobese, and obese III versus nonobese. Propensity score matching was strict, with a maximum of ±1% score difference to ensure that all covariates (demographics, risk factors, and operative data) for the obese versus nonobese comparisons groups, other than size, were statistically similar. Here, a significantly greater difference in AF incidence after matching would indicate a link between obesity (or size) and AF while controlling for confounders. Second, we used 2 additional analyses in which the 8051 patients were divided into derivation (n=4026) and validation (n=4025) subcohorts of equal size (1) via random selection without replacement of the derivation group and (2) based on time of surgery, with recent patients (September 1999 to December 2004) used as the derivation group and remote patients used as the validation cohort (January 1994 to September 1999).
| Results |
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AF patients were characterized by a higher incidence of hypertension, chronic obstructive pulmonary disease, peripheral and/or cerebrovascular disease (vascular disease), congestive heart failure, triple-vessel disease, and left main disease; lower ejection fractions; less preoperative use of digitalis, diuretics, or steroids; and low cardiac output (use of intra-aortic balloon pump). Current smokers, patients with angina (any kind), and preoperative ß-blocker use were less frequent among AF patients. Operatively, valve surgery and increasing time on CPB (Figure 1, bottom; P<0.001) were associated with increased frequency of AF, whereas off-pump (CPB=0) surgery was associated with less AF both before and after age adjustment.
Role of Body Size in New-Onset AF
Of 8051 overall study patients, 3164 were obese (39.3%; median age 62 years; BMI >30 kg/m2) and 4887 were nonobese (61%; median age 66 years). The overall unadjusted AF rates in obese (742 of 3164; 23.5%) versus nonobese (1068 of 4887; 21.9%) patients were similar (P=0.099); however, the mean age of cardiac surgery patients decreased systematically for increasing BMI categories (both P<0.001; Figure 2). When BMI was considered as a continuous variable (Table 2), unadjusted BMI was significantly associated with AF (OR 1.01, 95% CI 1.00 to 1.02; P=0.046), equivalent to a 1% increase in AF incidence per 1-kg/m2 increase in BMI. This effect was increased after adjustment for age (OR=1.03; P<0.001) and other covariates (OR=1.04; P<0.001). These findings were largely mirrored when BMI was included as a categorical variable (Table 2; Figure 2). Age-adjusted AF rates were increased from lowest to highest BMI groups (P<0.001): 20.0%, 19.8%, 21.8%, 23.3%, 26.59%, and 33.2%, respectively. The corresponding analyses when BSA was used for body size instead of BMI are provided in the online-only Data Supplement (Table I, Figure I).
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Multivariable Analyses
With adjustment for covariates, underweight (OR 0.97, 95% CI 0.73 to 1.27) and normal (OR 1.0 [reference]) BMI groups were equally likely to develop AF. The adjusted ORs for developing AF were systematically greater for the larger patients (1.18 [95% CI 1.00 to 1.40], 1.36 [95% CI 1.14 to 1.63], 1.69 [95% CI 1.35 to 2.11], and 2.39 [95% CI 1.81 to 3.17] for overweight, obese I, obese II, and obese III, respectively). In case of BSA (Table I in the Data Supplement), the risk-adjusted OR for AF was increased systematically from smallest (OR [very small]=0.67 [95% CI 0.43 to 1.06]) to largest (OR [large III]=2.60 [95% CI 1.87 to 3.63]).
Results of the multivariable logistic regression models for AF, with patient size represented by 6 BMI categories, for all cardiac surgery and isolated CABG are shown in Table 3. The model discriminated between AF and No-AF fairly well (area under the receiver operator characteristic curve 0.68 and 0.67 [isolated CABG]), and the model calibration was good (Hosmer-Lemeshow [goodness-of-fit test]: P=0.36 and 0.58 [isolated CABG]). Other than BMI category, predictors of AF included age (adjusted OR 1.52 [95% CI 1.46 to 1.58] per 10 years), mitral valve surgery (adjusted OR 2.42 [95% CI 1.92 to 3.06]) and aortic valve surgery (adjusted OR 1.79 [95% CI 1.45 to 2.22]), chronic obstructive pulmonary disease (adjusted OR 1.28 [95% CI 1.12 to 1.46]), male gender (adjusted OR 1.24 [95% CI 1.10 to 1.40]), preoperative ß-blockers (adjusted OR 1.17 [95% CI 1.05 to 1.32]), vascular disease (adjusted OR 1.18 [95% CI 1.05 to 1.32]), white race (adjusted OR 1.33 [95% CI 1.07 to 1.66]), history of arrhythmia other than AF/flutter (adjusted OR 0.80 [95% CI 0.68 to 0.96]), ejection fraction <40% (adjusted OR 1.16 [95% CI 1.03 to 1.31]), left main disease (adjusted OR 1.15 [95% CI 1.00 to 1.32]), and off-pump surgery (adjusted OR 0.61 [95% CI 0.44 to 0.83]). Obviously, for isolated CABG patients only, the model did not include mitral and aortic valve surgery as predictor variables. Also, left main disease, triple-vessel disease, and vascular disease were no longer significant predictors. Preoperative congestive heart failure was a predictor of AF in the CABG-only subpopulation.
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Validation of Findings
Propensity-Matched Comparisons
Of the 6749 isolated CABG patients, 2712 (40.2%) were obese (BMI >30 kg/m2). The derived propensity score model for obese versus nonobese patients was of good calibration (Hosmer-Lemeshow P=0.59) and good discrimination (area under the receiver operator characteristic curve 0.74). Obese versus nonobese propensity scores were substantially different (0.457±0.149 versus 0.358±0.134; P<0.001) and increased systematically and significantly with increasing BMI category (online Data Supplement; Figure II, top; P<0.001, all pairwise and overall [trend]). Greedy 1-to-1 matchings were obtained for 2360 (87%) of 2712 when all obese patients were matched as 1 group. Nearly all patients were matched when obese subgroups were matched separately: 1730 obese III (99.5%), 659 obese II (100%), and 314 obese I (100%). In all cases, with the exception of size variables, all demographics, risk factors, preoperative medications, and operative variables (grafting and CPB) were similar for the matched comparison groups (see Table 1 for list). Overall, the incidence of new-onset AF was significantly greater in obese than in nonobese patients (P<0.001), mostly owing to the increased rate of AF in moderately and severely obese patients (obese II and III; Data Supplement Figure II, bottom).
Derivation Versus Validation Subcohort Analyses
Figure 3 shows the derived adjusted OR for developing new-onset AF for each of the BMI categories (normal=reference category) compared with those derived in the overall population using independent derivation and validation subpopulations of equal size. The derived BMI-AF associations were similar for the 2 subcohorts and were within the confidence bounds derived from the overall cardiac surgery series. This finding was true when the patient subgroups were based on random selection (Figure 3, top) or based on date of surgery (Figure 3, bottom). Importantly, in the latter case, the derivation (recent) group included patients for whom postoperative amiodarone prophylaxis began on postoperative day 1, whereas this was not true for the overwhelming majority (3861 [96%] of 4025) of the validation (remote) cohort.
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| Discussion |
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Prior studies have demonstrated that advanced age, history of AF, male gender, digoxin use, hypertension, longer CPB cross-clamp time, chronic obstructive pulmonary disease, valve surgery, postoperative withdrawal of ß-blockers, and postoperative low cardiac output increase the risk of developing new-onset AF after cardiac surgery.613 Many of these factors were confirmed in our present analysis of a large cardiac surgery population (Table 3). Others have also investigated the possible role of ECG characteristics, and they have linked prolonged P-wave duration (indicative of intra-atrial conduction delay) and increased PR interval to postoperative AF.13 No previous studies have previously associated obesity or large body habitus with increased AF after cardiac surgery.
The primary finding in the present study is that we demonstrated, for the first time, the existence of a strong independent association between increasing body size (especially obesity) and new-onset postoperative AF in cardiac surgery patients. These results were confirmed via multiple complementary analyses, which included (1) comparisons of AF rates in obese versus nonobese groups (and subgroups) that were closely matched for all other covariates and AF predictors via propensity modeling techniques and (2) 2 comparisons of covariate-adjusted AF-BMI category relations (Figure 3) in equally sized independent derivation/validation cohorts based on random selection and chronological order (time of surgery).
This multivariable modeling also showed, that after risk adjustment, off-pump CABG surgery was associated with a significantly lower incidence of new-onset postoperative AF (Table 3). The following CPB-related mechanisms may have contributed to these findings: (1) Myocardial ischemia during CPB is global compared with localized or regional ischemia during off-pump surgery; (2) myocardial injury (elevated creatine kinase-MB) is more common in CPB versus off-pump patients; and (3) increased inflammatory injury to all organs with CPB is mediated by complement activation, cytokine release, endothelial activation, and neutrophil induction and adhesion. The latter can lead to abnormal gas exchange and electrolyte imbalance, both of which can contribute to atrial irritability.
Potential Mechanisms of the AF-Obesity Association
Left atrial enlargement, a recognized precursor of AF, is strongly correlated with increasing BMI or adiposity.16,20,21 Other factors characterizing obesity are ventricular remodeling,22 elevated plasma volume,23 autonomic tone,24 ventricular diastolic dysfunction,25 and enhanced neurohormonal activation.26 These too can contribute to left atrial dilatation and its electrical dysfunction. Also, increased oxidative stress27 and/or lipoapoptosis,28 which are seen with increasing adiposity, may lead to myocardial structural changes (including atrial changes) such that the likelihood of AF is increased.
Our finding of an association between increasing body size and new-onset AF after cardiac surgery is in concert with the recent study by Wang and colleagues4 in the general adult population (Framingham Heart Study). There, they described an association between greater incidence of newly diagnosed AF over time with increasing body size. Importantly, they showed via echocardiography data that left atrial dilatation is a critical intermediate phenotype and a physiologically plausible and mechanistic explanation for the obesity-AF association. This is further supported by another population-based study by Pritchett et al,16 who found a similar association between large atrial size and greater AF/flutter incidence. There, they found a 13.6% AF/flutter rate in the upper quartile of left atrial size (quartile IV) compared with lower rates in quartiles I, II, and III (1.1%, 1.7%, and 2.3%, respectively). We do not routinely collect data on left atrial size in cardiac surgery patients and are unable to provide the corresponding data in this retrospective surgical population. However, we suggest that the distribution of left atrial size as a function of BMI is likely similar to that of the general adult population.4,16
Diabetes mellitus has been associated with increased AF in the general adult population, most notably by Kannel and colleagues29 from the Framingham Heart Study. Incidence of diabetes is also systematically greater with increasing obesity.30 Yet, the present data, similar to what has been reported in several recent large analyses,713 did not indicate the presence of an independent association between new-onset postoperative AF and diabetes. Although a diabetes effect in this form of AF may be implicit in the AF-obesity association, this possibility is downplayed by the fact that as in most of the other cardiac surgery series,713 the incidence of diabetes in the AF versus No-AF cohorts was essentially identical (Table 1). This may indicate a distinctly different role for diabetes in the development of new-onset postoperative AF versus AF in the general adult population. Elucidation of this role is outside the scope of our present report.
Study Limitations
This study is characterized by several important strengths that support the primary finding of increasing new-onset AF with increasing patient adiposity after cardiac surgery. These included the large study population (n=8051), the number of AF cases analyzed (n=1810), the multiple converging complementary statistical analyses, and finally, supporting data from the nonsurgical general population by other authors.4,16 Yet, several study limitations are worth noting. Most obvious is the aforementioned lack of direct left atrial data to support the left atrial dilatation mechanistic explanation that we propose. Although likely true, a BMIleft atrial size relation in cardiac surgery patients specifically is more relevant. Second, we cannot exclude the possibility that episodes of AF were missed in some patients because of their minimal and or short-lived nature and that these patients were grouped as No-AF. The prevalence of AF we report in the present series of patients lies within the range of the national data reported by the Society of Thoracic Surgeons. However, it appears unlikely that such misclassifications would occur disproportionately among the different size groups, and therefore, they should have minimal effects on the results reported here. In addition, such random misclassification might have led to a conservative bias. Third, the present study is a retrospective, nonrandomized analysis from 1 surgical team serving 2 hospitals; however, all postoperative complications were prospectively and rigorously tracked and reported to the Society of Thoracic Surgeons national cardiac surgery database. Large observational studies have been shown to closely predict the results of corresponding randomized trials.31,32 To minimize the potential inaccuracies of nonrandomized retrospective data, we implemented several analytical methods, including propensity modeling and matching,18,19 in addition to 2 separate derivation and validation cohort analysis comparisons. We contend that the fact that all the methods we used converged to produce the same result significantly advances our primary findings.
| Conclusions |
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| Acknowledgments |
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| Footnotes |
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N. Echahidi, P. Pibarot, G. O'Hara, and P. Mathieu Mechanisms, Prevention, and Treatment of Atrial Fibrillation After Cardiac Surgery J. Am. Coll. Cardiol., February 26, 2008; 51(8): 793 - 801. [Abstract] [Full Text] [PDF] |
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M. A. Albert, N. Halevy, and E. M. Antman Preoperative Evaluation for Cardiac Surgery Card. Surg. Adult, January 1, 2008; 3(2008): 261 - 280. [Full Text] |
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D. P. Mason, D. H. Marsh, J. M. Alster, S. C. Murthy, A. M. McNeill, M. M. Budev, A. C. Mehta, G. B. Pettersson, and E. H. Blackstone Atrial Fibrillation After Lung Transplantation: Timing, Risk Factors, and Treatment Ann. Thorac. Surg., December 1, 2007; 84(6): 1878 - 1884. [Abstract] [Full Text] [PDF] |
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N. Echahidi, D. Mohty, P. Pibarot, J.-P. Despres, G. O'Hara, J. Champagne, F. Philippon, P. Daleau, P. Voisine, and P. Mathieu Obesity and Metabolic Syndrome Are Independent Risk Factors for Atrial Fibrillation After Coronary Artery Bypass Graft Surgery Circulation, September 11, 2007; 116(11_suppl): I-213 - I-219. [Abstract] [Full Text] [PDF] |
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N. Echahidi, P. Pibarot, J.-P. Despres, J.-M. Daigle, D. Mohty, P. Voisine, R. Baillot, and P. Mathieu Metabolic Syndrome Increases Operative Mortality in Patients Undergoing Coronary Artery Bypass Grafting Surgery J. Am. Coll. Cardiol., August 28, 2007; 50(9): 843 - 851. [Abstract] [Full Text] [PDF] |
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Writing Committee Members, V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: full text: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Europace, September 1, 2006; 8(9): 651 - 745. [Full Text] [PDF] |
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V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society J. Am. Coll. Cardiol., August 15, 2006; 48(4): e149 - e246. [Full Text] [PDF] |
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W. J. Manning and E. V. Gelfand Left Atrial Size and Postoperative Atrial Fibrillation: The Volume of Evidence Suggests it Is Time to Break an Old Habit J. Am. Coll. Cardiol., August 15, 2006; 48(4): 787 - 789. [Full Text] [PDF] |
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V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society Circulation, August 15, 2006; 114(7): e257 - e354. [Full Text] [PDF] |
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M. A. Arias Prevention of atrial fibrillation following cardiac surgery. JAMA, May 17, 2006; 295(19): 2247 - 2247. [Full Text] [PDF] |
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M. A. Arias, J. Sanchez-Gila, and D. Amar Obesity As a Risk Factor for Developing Postoperative Atrial Fibrillation Chest, March 1, 2006; 129(3): 828 - 829. [Full Text] [PDF] |
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