Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. It has become an important public health issue causing increases in health care expenditures due to the growing elderly population. The prevalence of AF (2%) is now double that reported in the last decade.1 AF is present in 0.12% to 0.16% of those younger than 49 years, in 3.7% to 4.2% of those aged 60 to 70 years, and in 10% to 17% of those aged 80 years or older and is more common in males.1 Hypertension is the most frequently associated risk factor of AF followed by heart failure.2 Other associated cardiac diseases include coronary artery disease, valvular heart disease, and various cardiomyopathies. Noncardiac risk factors include diabetes mellitus, lipid disorders, chronic obstructive pulmonary disease, renal failure, and stroke.1
AF often begins in a paroxysmal fashion with acute symptoms of palpitations, lightheadedness, fatigue, and shortness of breath that result from increased ventricular rate, loss of atrial systole, and a reduction in left ventricular filling.2 It is important to note that as many as 33% of patients with AF may be asymptomatic.1 Paroxysmal periods of AF may last longer, and the clinical course progresses to persistent AF which can still be converted and then to permanent or chronic AF.2 The longer the patient remains in AF, the longer the atrial effective refractory period becomes, making conversion less likely.3 Thus, AF begets AF and pharmacological or electrical cardioversion is more likely when performed as soon as possible after AF develops.3 Permanent AF may result in 50% of patients who develop paroxysmal AF.2
Patients with AF have a 5-fold and 2-fold higher risk of stroke and death, respectively, as compared with the general population of the same age group. Stroke prevention is the mainstay of treatment of permanent AF, because embolic stroke is the primary driver of increased morbidity and mortality in all patients with chronic AF.1 Clot develops most frequently in the left atrial appendage but can develop even along the atrial wall due to the fibrillating, noncontracting atrium causing stasis of blood often called “smoke” on an echocardiogram. Undertreatment and noncompliance with anticoagulation are major challenges in the treatment of AF, especially in asymptomatic patients.4 Rate control versus rhythm control remains somewhat controversial, because a mortality benefit of a rhythm control strategy has not been demonstrated. However, restoration of sinus rhythm in patients with persistent AF improves symptoms and makes the likelihood of recurrence less.5 Pharmacological management of AF can be difficult at times with resultant side effects of antiarrhythmics. AF ablation solves many of the symptomatic problems with the arrhythmia and lessens the potential drug complications.6 Newly developed and approved left atrial occlusion devices are helpful in patients who cannot take or develop complications from anticoagulation therapy.7
Postoperative AF likely represents a mix of new-onset AF and exacerbation of AF in someone with a previous history of paroxysmal AF. Postoperative AF has additional etiological factors when applied to patients with associated risks to develop AF.8 Adrenergic stimulation from postoperative stress with high catecholamine levels from pain or inflammation result in tachycardia and hypertension which can precipitate AF.9 Intravascular volume overload can result in atrial stretch that results in AF.9 Mechanical irritation due to the location of surgery (intrathoracic) or the placement of chest tubes and intracardiac catheters are factors.8 Failure to continue preoperative β-blocker therapy or the requirement of inotropic drugs impact the incidence.9 Other clinical events that may increase the incidence of postoperative AF include mild hypothermia, hypercarbia and hypoxemia, hypokalemia and hypomagnesemia, endocrine disease, and neurological surgery.9,10 All of the above may increase atrial ectopy and the frequency of paroxysmal AF as well as alter atrial remodeling, increasing the likelihood of paroxysmal AF to persist.3,9 It is important to note that new-onset AF in the postoperative setting is not benign because it increases long-term mortality after coronary artery bypass grafting.11
In the current issue of Anesthesia & Analgesia, Alonso-Coello et al12 attempted to develop a clinical prediction model to assess prognosis in what they defined as “ new clinically important AF” in noncardiac surgery patients from the PeriOperative ISchemic Evaluation (POISE) I Trial.13 This trial, the largest randomized control trial in perioperative medicine ever undertaken, showed statistically and clinically significant cardiac protection but revealed an increase in all-cause mortality, strokes, bradycardia, and hypotension.14 The results of POISE I were criticized because of the potential for high doses of slow-release metoprolol to be administered, especially when patients were bradycardic.14 In POISE, they found that the overall incidence of AF was 2.5%, and patients randomly assigned to receive extended-release metoprolol had a reduced incidence. New AF was an independent risk factor for stroke at 30 days.
It is clear that prolonged arrhythmia monitoring will increase the diagnosis of AF, especially asymptomatic AF.15 Continuous monitoring demonstrates more AF than periodic examination or 12-lead electrocardiograms. In this study, electrocardiograms were obtained between 6 and 12 hours postoperatively and on postoperative day (POD) 1, POD2, and POD30. The authors rationalized that by using a definition of new AF defined as “clinically important” (associated with angina, acute heart failure, symptomatic hypotension, drug therapy, or cardioversion) that their retrospective analysis would reduce the likelihood of missing an AF event. Although, if asymptomatic AF occurred between POD2 and POD29, it could easily have been missed because the patients were not continuously monitored. However, the incidence of postoperative AF in noncardiac surgery peaks on POD1 to POD2 with most AF occurring by POD6.
The statistical analysis, which is an important component of this research, was clearly articulated, professionally conducted, and well reported. However, the model building efforts are somewhat limited by the nature of the available data that were not primarily collected for this purpose. For example, a reader might have reasons to suspect that this newly developed model is not as stable as it would need to be for clinical decision making. This is evidenced by the observation of dramatic changes of the risk estimates (ie, odds ratios) between the derivative cohort and the validation cohort in terms of age, intrathoracic surgery, and major vascular surgery (Table 2). Certainly, the consistency of the direction of the associations is comforting, but the ranking of the risks changes substantially between models. Additionally, the discrimination of the model actually increased in the validation cohort (C-statistic of 0.69 vs 0.72), and this is quite unusual. One possible explanation might be that the use of a hold-out sample is not as efficient as k-fold cross-validation as an internal validation method (transparent reporting of a multivariable prediction model for individual prognosis or diagnosis statement).16,17 This effort deserves further scrutiny before any clinical applications are applied, and like all efforts of this type, an external validation is needed before definitive use in clinical settings. Nevertheless, this model building effort is elegant, well articulated, and adds to the literature.
The independent risk factors in the derivation cohort were used to develop a point scoring system to identify high-risk patients who might develop AF. More points were given to factors with high odds ratios, and fewer points to those factors with lower but still significant odds ratios. Patients with a point total of 0 to 1 had a <1% chance of developing postoperative AF, and those with a point total of 5 to 6 had a >5% chance of developing postoperative AF. As expected, the patients who developed AF in this study had more cardiovascular complications, increased hospital length of stay, received more cardiac drugs, and had a higher all-cause mortality. Additionally, these patients received more antithrombotic medications; however, despite having a CHADS2 score of ≥4, only 33% of these patients received an oral anticoagulant drug at the time of discharge.
In summary, the independent predictors of age, intrathoracic surgery, major vascular surgery, and intraabdominal surgery in the derivation cohort have been well established previously.8 However, the assignment of points for each predictor to assess individual risk is novel. Although the overall number of patients that develop AF postoperatively in noncardiac surgery is high, its incidence as compared with cardiac surgery is small. Although 2 to 3 of 100 patients may develop postoperative AF after noncardiac surgery, 2 of 6 patients develop AF after cardiac surgery. Whether the aggressive preoperative identification and postoperative prophylaxis of AF will become a standard of care as in cardiac surgery remains to be seen and requires further study. This scoring system is a first attempt, and the authors should be applauded for their efforts. Meanwhile, clinicians should continue to treat risk factors of postoperative AF such as fluid overload, pain, electrolyte abnormalities, hyper- and hypotension, and other factors that can modulate the sympathetic nervous system and increase adrenergic stimulation. The failure to begin anticoagulants on discharge in AF patients is a particularly disturbing finding in this study. Physicians who manage patients perioperatively should be cognizant of this issue. Stroke is the primary driver of increased mortality in AF patients, and oral anticoagulation has been repeatedly shown to reduce mortality despite the challenges with compliance and increased bleeding risk.
Name: Roger L. Royster, MD.
Contribution: This author helped write the manuscript.
Name: Hao Deng, MBBS, MPH.
Contribution: This author helped write the manuscript.
Name: S. Patrick Whalen, MD, FHRS.
Contribution: This author helped write the manuscript.
This manuscript was handled by: Richard C. Prielipp, MD.
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