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Ann Thorac Surg 1996;61:1323-1327
© 1996 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery, New York Hospital-Cornell University Medical College, New York, and Department of Medicine, North Shore University Hospital, Manhasset, New York
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods.One hundred forty-two patients with depressed left ventricular function (ejection fraction < 0.40) undergoing coronary artery bypass grafting were randomized to either T3 or placebo treatment groups in a prospective, double-blind fashion. Triiodothyronine was administered as a 0.8 µg/kg intravenous bolus at the time of aortic cross-clamp removal followed by an infusion of 0.113 µg • kg-1 • h-1 for 6 hours. Patients were monitored for the development of arrhythmias during the first 5 postoperative days.
Results.The incidence of sinus tachycardia and ventricular arrhythmias were similar between groups. Triiodothyronine-treated patients had a lower incidence of atrial fibrillation (24% versus 46%; p = 0.009), and fewer required cardioversion (0 versus 6; p = 0.012) or anticoagulation (2 versus 10; p = 0.013) during hospitalization. Six patients in the T3 group versus 16 in the placebo group required antiarrhythmic therapy at discharge (p = 0.019).
Conclusions.Perioperative T3 administration decreased the incidence and need for treatment of postoperative atrial fibrillation.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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The development of atrial fibrillation is a common postoperative complication of cardiac operations. In patients undergoing coronary artery bypass grafting (CABG), an incidence ranging from 25% to 50% has been reported [1, 2]. Because sinus rhythm is usually restored, the problem was traditionally not considered to have a significant impact on outcome. However, hemodynamic instability due to the arrhythmia does occur, and large retrospective reviews support the conclusion that postoperative atrial fibrillation is associated with an increased incidence of stroke and malignant ventricular arrhythmias, as well as prolonged intensive care unit and hospital stays [3]. Therefore, cardiac surgeons are challenged to devise strategies to prevent its occurrence. Although a degree of success has been obtained with pharmacologic interventions [4–7], the effectiveness of these regimens is limited, particularly as the population of patients undergoing cardiac operations increases in age and severity of illness [8].
The relationship between chronic thyroid disease states and cardiac contractility is well established [9]. Various lines of evidence have documented that the biologically active thyroid hormone triiodothyronine (T3) can also act acutely to affect myocardial performance, as both an inotrope and a vasodilator [10, 11]. In light of these effects and with the observation that cardiopulmonary bypass results in a euthyroid sick or low T3 state, interest has focused on the potential benefits of perioperative T3 supplementation in patients undergoing cardiac operations.
The results from a randomized, double-blind, placebo-controlled, prospective clinical trial in which T3 was administered to high-risk patients undergoing CABG showed that perioperative T3 treatment resulted in increased cardiac output and lowered systemic vascular resistance compared with placebo-treated patients during the first 16 hours after operation [12]. Chronic hyperthyroidism, both overt and subclinical, increases the prevalence of atrial tachyarrhythmias [13]. Patients in this clinical trial were monitored for potential arrhythmogenesis. During the period of drug infusion, no differences in the incidence of atrial or ventricular tachyarrhythmias were detected [12]. In this report, we present evidence that perioperative T3 infusion was associated with a significant decrease in the development of atrial fibrillation observed after the first postoperative day.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Patients were randomly assigned to receive either triiodothyronine (Triostat; Smith Kline Beecham Pharmaceuticals) as a 0.8 µg/kg intravenous bolus at the time of aortic cross-clamp removal followed by an infusion of 0.113 µg • kg-1 • h-1 for 6 hours and a 3-hour taper halving the infusion to off or placebo treatment with 5% dextrose solution at the same infusion rates. Intraoperative and postoperative patient management did not differ between the two groups with the exception of study drug administration.
A standardized anesthesia and surgical protocol was applied in all cases. Cardiopulmonary bypass was performed using aortic and right atrial cannulation, an asanguineous prime solution, a membrane oxygenator, and nonpulsatile flow. Moderate hypothermia (bladder temperature, 30° to 32°C) was used routinely. Antegrade cardioplegic arrest was achieved with a cold blood high-potassium solution followed by additional doses administered antegrade and retrograde at 20-minute intervals. Cold (4°C) saline solution was applied topically to cool the myocardium. Standard surgical techniques were used to create the distal coronary anastomoses. Proximal vein graft anastomoses were performed with partial aortic occlusion during rewarming.
Patients were rewarmed to 36°C, and separation from cardiopulmonary bypass was accomplished by the gradual reduction of venous return to the bypass circuit. Inotropic support was initiated when needed during bypass separation to maintain cardiac contractility or if the cardiac index was less than 2.1 L • min-1 • m-2. Electrical pacing was instituted (atrial or atrioventricular) when needed to maintain a heart rate greater than 70 beats/min. Patients were continuously monitored in the cardiothoracic intensive care unit. Patients were weaned off mechanical ventilation based on hemodynamic stability, blood gas analysis, and level of alertness. Discharge from the cardiothoracic intensive care unit was generally accomplished after extubation and the discontinuation of all vasoactive infusions.
Cardiac rhythm was continuously monitored in the intensive care unit with bedside monitors and after intensive care unit discharge with telemetry. Twelve-lead electrocardiograms were obtained immediately postoperatively and on the first five mornings after the operation. Supraventricular and ventricular arrhythmias and respective treatment interventions were documented by the patient's nurse and supported by the inclusion of rhythm strips in the patient chart.
Sinus tachycardia was defined as sinus rates between 101 and 120 beats/min. Any narrow complex, regular tachycardia (with or without P waves) with a rate greater than 120 beats/min was defined as supraventricular tachycardia. Atrial fibrillation was documented when an irregularly irregular supraventricular rhythm was present in the absence of P waves. Episodes of atrial fibrillation that recurred or continued into the following 24-hour period were recorded as an additional episode. Ventricular tachycardia was defined as greater than three consecutive ventricular premature contractions at a rate greater than 100 beats/min. Arrhythmia data were collected and recorded for the first 5 postoperative days.
Supraventricular arrhythmia prophylaxis consisted of the routine administration of intravenous or oral digoxin, 0.25 mg per day, beginning on postoperative day 1. Administration of 25 mg of metoprolol by mouth or nasogastric tube two times a day was generally initiated on postoperative day 1 and continued throughout hospitalization except in patients with history of obstructive pulmonary disease or bradycardia, or with marked impairment of ventricular function.
Standardized protocols for the treatment of supraventricular and ventricular arrhythmias were adhered to during the course of the study. Blood gas abnormalities were corrected. Potassium, magnesium, and calcium were administered as needed to maintain serum concentrations greater than 4 mmol/L, 1.5 mEq/L, and 8.5 mg/dL, respectively. Sustained and nonsustained ventricular tachycardia and premature contractions that were more frequent than 6 per minute or multifocal were treated with lidocaine. Rapid heart rates (generally greater than 110 beats/min or associated with impaired hemodynamic performance) due to sinus or atrial or nodal tachycardia were controlled with intravenous ß-blocker (propranolol or metoprolol).
Rapid ventricular rates associated with atrial fibrillation were controlled with intravenous ß-blockers (propranolol or metoprolol) or calcium-channel blockers (verapamil or cardiazem). Patients were further treated with digitalis (1 g intravenously over 16 hours) and then maintained on daily digitalis therapy. Pharmacologic conversion to sinus rhythm with procainamide (intravenous infusion followed by oral dosing) was initiated when atrial fibrillation was persistent (>24 hours). Electrical cardioversion was attempted when atrial fibrillation resulted in hemodynamic instability or when clinically indicated in the setting of failure of pharmacologic conversion. Patients were routinely anticoagulated with heparin, warfarin, or both when atrial fibrillation persisted for longer than 36 hours.
Levels of T3 were measured preoperatively (baseline), 30 minutes after the start of cardiopulmonary bypass, and 30 minutes, 6 hours, and 24 hours after the initiation of the study drug infusion. Total serum thyroxine and thyrotropin levels were measured at the baseline time point. Hormone levels were determined by standard radioimmunoassay.
Of the 142 patients who were randomized, 6 patients in the placebo and 5 in the T3 groups, in whom atrial fibrillation was documented preoperatively, were excluded from analysis. For demographic, baseline, and one-time outcome variables, comparison of continuous variables across the two treatment groups was accomplished with a two-sample t test. Comparison of categoric variables across the groups was performed with the 
2 or Fisher's exact test (where applicable). For comparison of continuous outcome variables at multiple time points across treatment groups, repeated-measures analysis of variance was performed. Repeated-measures analysis of binary end-point data was used to compare binary outcomes across multiple time points and across treatment groups. All statistical tests were two-tailed. Statistical analysis was performed using SAS software (Cary, NC).
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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. The two groups did not differ with respect to any preoperative or intraoperative variables, including age, preoperative use of beta-adrenergic receptor blocking agents or digitalis, pulmonary disease, or ventricular function. Intraoperative variables are shown in Table 2. The two groups did not differ significantly with respect to perioperative mortality or dependence on postoperative ventilatory or inotropic support.
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In the first 24 hours after the operation, during the time period when serum T3 concentrations were elevated, there were no differences in the incidence of supraventricular or ventricular arrhythmias (Table 3). As shown in Table 4, there were no differences in the need for treatment of these arrhythmias during this same time period. Eighty percent of T3-treated and 79% of placebo-treated patients began prophylactic oral beta-blocker therapy within the first 2 days postoperatively. Prophylactic digitalis therapy was administered to 89% and 84% of T3- and placebo-treated patients, respectively.
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) (p < 0.01). As shown in Figure 1, most of these episodes (63% in each group) developed between postoperative days 2 and 4. Therapy for atrial fibrillation was initiated in the majority of patients in both groups. Correspondingly, a decrease in treatment interventions resulting from the presence of atrial fibrillation was observed in the T3 group (Table 6). Fewer patients in the T3-treated group required procainamide therapy at discharge or anticoagulation or cardioversion during hospitalization. By hospital discharge, nearly all patients had either spontaneously or pharmacologically converted to normal sinus rhythm.
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Certain patients are at increased risk of the development of atrial fibrillation. Age is the single most important variable [3, 17]. Chronic obstructive pulmonary disease and prior history of atrial arrhythmias are also significant risk factors in multivariate analysis [3]. In the present trial, patients were enrolled only in the presence of significant ventricular dysfunction with an ejection fraction of less than 0.40. The relatively older age and preponderance of comorbid factors are reflective of the nature of this cohort. Depressed ejection fraction, congestive failure, and ongoing ischemia are factors associated with an increased incidence of postoperative atrial fibrillation in univariate analysis [3] and were common in this group of patients. The 46% incidence of atrial fibrillation observed in our control group is greater than might be predicted considering that the majority of the study group received prophylactic ß-adrenergic receptor blockade. Although perioperative ß-blockade has been shown to decrease the incidence of postoperative atrial tachyarrhythmias [4–6], the degree of reported benefits have been variable [3, 4–6], and randomized, prospective studies have only been performed in younger, less critically ill patients [4–6, 18]. In a patient population such as ours, prophylactic ß-blockade would potentially be less effective.
At present, there is no reliable therapy available that is designed to reverse or prevent the surgical injury that causes postoperative atrial fibrillation. Augmented atrial hypothermia during cardioplegic arrest has been proposed, but experimental data and limited clinical experience have not been encouraging [14, 15]. Administration of diltiazem as a component of cardioplegia and as a 24-hour perioperative infusion was reported to decrease the incidence of atrial fibrillation in a small number of patients, presumably via prevention of calcium overload after reperfusion [15]. Although unexpected in light of the known association between chronic hyperthyroidism and atrial tachyarrhythmias, our findings suggest that acute thyroid hormone administration may represent a route through which the postischemic-reperfused atrium can be protected from developing an increased susceptibility to fibrillate. Although speculative, potential explanations include a T3-related attenuation of atrial ischemia-reperfusion injury, analogous to that which has been reported for the ventricle in numerous experimental studies [19–21]. The mechanism(s) through which T3 reduced ventricular stunning in these studies is not known. Various effects of T3 on high-energy phosphate metabolism [11] and membrane stability of intracellular organelles [22] have been suggested. The influence of vagal input on atrial activity is well established [23]. Perioperative vagal injury or inflammation is a potential source of postcardiotomy atrial dysrythmias [24]. The specific effects of T3 on vagal activity have not been studied, although data exist that suggest that thyroid hormone may have direct effects on neural tissue during development [25] and in the setting of cerebral ischemia [26]. Serum T3 concentrations were similar in the two study groups at 24 hours. Therefore, it seems unlikely that the decrease in prevalence in atrial fibrillation observed at 24 to 120 hours was a result of an acute or direct effect of T3 on the atrial myocyte at the time of onset of the arrhythmia. However, a latent effect on atrial myocyte ion flux [27] or adrenergic receptor expression [28] deserves further investigation. Alternatively, the ability of T3 to alter the gene expression of specific ion channels and plasma membrane enzymes, such as the plasma membrane sodium-potassium adenosine triphosphatase [9, 11], could potentially influence postoperative atrial activity.
Our current finding that T3 decreased the incidence of post-cardiopulmonary bypass atrial fibrillation requires confirmation in future clinical trials. Understanding these results requires a biological explanation for postoperative atrial fibrillation as well as for the potential sites at which T3 could modify its development. We have recently reported that although T3 treatment after CABG increased cardiac output and lowered systemic vascular resistance, it did not alter the routine management of perioperative hemodynamics and could not be recommended as a substitute for standard perioperative inotropic support therapy [12]. If indeed T3 administration alters the course of postoperative atrial arrhythmias, this would justify the reevaluation of routine T3 supplementation after CABG.
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Acknowledgments |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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We are indebted to the cardiothoracic surgeons of New York Hospital: Dr Nasser K. Altorki, Dr Jeffrey P. Gold, Dr Samuel Lang, and Dr Todd K. Rosengart, whose patients were enrolled in the study. We thank Dr Barbara Napolitano and Dr Martin Lesser for statistical consultation.
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Address reprint requests to Dr Klemperer, Department of Cardiothoracic Surgery, New York Hospital, 525 E 68th St, Rm A-827, New York, NY 10021.
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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