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Ann Thorac Surg 1997;63:1374-1381
© 1997 The Society of Thoracic Surgeons
Departments of Anesthesiology and Critical Care Medicine, Medicine, Surgery, and Biostatistics, Memorial Sloan-Kettering Cancer Center and Cornell University Medical College, New York, New York
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. Seventy consecutive patients without previous SVD were randomly allocated immediately after pneumonectomy or EPP to receive diltiazem (n = 35) or digoxin (n = 35). Diltiazem-treated patients received a slow intravenous loading dose of 20 mg, followed by 10 mg intravenously every 4 hours for 24 to 36 hours, then 180 to 240 mg orally daily for 1 month. Digoxin-treated patients received a 1-mg intravenous loading in the first 24 to 36 hours, then 0.125 to 0.25 mg orally daily for 1 month. A concurrent prospective cohort of 40 patients without previous SVD, who did not participate in the study and underwent pneumonectomy or EPP without prophylaxis, served as a comparison group for SVD occurrence. Serial Doppler echocardiograms were performed to assess cardiac function and all patients were continuously monitored with Holter recorders for 3 days. Data were analyzed by intent-to-treat.
Results. In patients undergoing standard or intrapericardial pneumonectomy, diltiazem prevented the overall incidence of postoperative SVD when compared with digoxin, 0 of 21 patients versus 8 of 25 patients, respectively, p < 0.005. When EPP patients were included in the analysis, diltiazem decreased the incidence of all SVD from 11 of 35 patients (31%) to 5 of 35 patients (14%) when compared with digoxin, p = 0.09. Digoxin-treated patients had a similar incidence of all SVD (31%) as concurrent controls (11 of 40 patients [28%]). The two treated groups did not differ in right or left atrial size, left ventricular ejection fraction, or right heart pressure. When all patients were combined, those in whom SVD developed were significantly older (65 ± 12 years versus 55 ± 11 years, p = 0.004) and had a longer median hospital stay (9 versus 6 days, p = 0.03), when compared with those in whom SVD did not develop, respectively. The subset of patients undergoing EPP had a greater incidence of atrial fibrillation and electrocardiographic changes suggestive of postoperative pericarditis than all other pneumonectomy patients.
Conclusions. Diltiazem was both safe and more effective than digoxin in reducing the overall incidence of SVD after standard or intrapericardial pneumonectomy. Digoxin therapy had no effect on the incidence of postoperative SVD and is not recommended for prophylaxis of SVD. Dysrhythmias after pneumonectomy or EPP occur in older patients and are associated with a greater length of hospital stay.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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After major pulmonary resection, supraventricular dysrhythmias (SVD) are most prevalent after pneumonectomy and are associated with increased postoperative morbidity and mortality [1–3]. For reasons that are unclear, we also noted that SVD occurring early after resection of non-small cell lung cancer is associated with decreased survival at 18 months [4]. Although digoxin has traditionally been used for the prophylaxis of SVD after pneumonectomy, its efficacy is unproven and it may be associated with untoward effects [5, 6]. The cause, optimum method of treatment, or potential benefit of prophylaxis of SVD remain unclear. We have shown increased right heart pressure, but not right atrial or ventricular size, to be associated with SVD after pulmonary resection [3]. It is not known whether SVD should be treated with drugs that attenuate the adrenergic response to operation (ie, ß blockers) or with those that may attenuate the pulmonary hypertensive response (ie, calcium channel blockers). However, ß blockers are frequently contraindicated in patients undergoing pulmonary resection because of associated bronchoreactive states.
Limited trials have examined the effects of verapamil as prophylaxis for SVD after pulmonary resection [7, 8]. This prospective study was designed to determine whether diltiazem, a calcium-channel blocker that may be more suitable due to fewer hemodynamic side effects than verapamil, is superior to digoxin in preventing SVD in patients undergoing pneumonectomy, a population known to be at highest risk for this complication. With the use of Doppler echocardiography, we sought to determine the influence of these drugs on perioperative cardiac function and right heart pressure.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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The 70 consecutive patients who underwent pneumonectomy (most commonly for lung cancer, n = 46) or EPP (most commonly for malignant mesothelioma, n = 24) were randomly allocated in the immediate postoperative period to a treatment group (see below). Preoperative evaluation consisted of routine blood tests, 12-lead ECG, and pulmonary function testing. A standard nomogram adjusting for sex, age, and height was used to calculate the percent of predicted values of the forced expired volume in 1 second and the percent of predicted values of the forced vital capacity in all patients [9].
Echocardiography
Preoperative awake supine transthoracic echocardiograms were performed before operation using a 2.5/2.0-MHz transducer for imaging and Doppler echocardiography (SONOS 1500; Hewlett Packard, Waltham, MA). Subsequent echocardiograms were performed on all patients on postoperative day 2 or 3 and once again on the first postoperative outpatient visit. All but two patients were in sinus rhythm at the time echocardiography was performed. Any evidence of pericardial disease or serial changes in ventricular size were recorded. Left ventricular ejection fraction was measured by established methods from M-mode parasternal views. Right and left atrial superior-to-inferior diameters were measured in the apical four-chamber view at end-systole from still frames. The apical four-chamber, parasternal, and the subxiphoid views were used to access the maximum tricuspid regurgitation jet (TRJ) Doppler velocity. The regurgitant jet was localized in the pulsed mode, then maximized and measured in the continuous wave mode at a sweep speed of 75 mm/s. The TRJ Doppler velocity was used to estimate right ventricular systolic pressure (RVSP) by a modification of the Bernoulli formula: RVSP = RAPe + (peak TRJ velocity)2 x 4. Right atrial pressure (RAPe) was estimated at rest in the supine position by assessing the response of the inferior vena cava to normal and deep inspiration in the subcostal view. A RAPe of 3 mm Hg was recorded when the inferior vena caval diameter was small (<15 mm) and collapsed during spontaneous respiration. A RAPe of 7 mm Hg was recorded when the inferior vena caval diameter was of normal size (<20 mm) and collapsed more than 50% only with deep inspiration. A RAPe of 17 mm Hg was recorded when the inferior vena caval diameter did not collapse more than 50% during deep inspiration [10]. All analyses were later made from videotape by one investigator (NR) blinded to treatment and patient end points.
Ambulatory Electrocardiography
Dual-lead ECG recordings (leads CM2 and CM1 or CM5) were made on Marquette 8500 Holter recorders. These recorders contain a digital clock to provide a time signal that is continuously recorded on the tape. The Holter tapes were digitized on a Marquette series 8000 scanner. The signal was sampled at 128 Hz. Sampling was triggered by the timing track on the tape to correct for flutter and wow of the recording or playback tape transport. QRS complex recognition and arrhythmia detection were done automatically by template matching. This system generates a beat by beat annotation of the ECG with a consistent and accurate time stamp for each QRS complex and classifies each complex as normal sinus, atrial or ventricular premature complex, or noise. The decisions made automatically by the computer were reviewed and corrected by an experienced technician and then by a cardiologist.
Anesthesia, Operation, and Perioperative Care
All patients were premedicated with midazolam and glycopyrrolate and received routine anesthetic management that consisted of isoflurane and nitrous oxide supplemented by intravenous fentanyl and morphine as needed. Pulmonary artery catheterization was not used routinely in this study. Intentional crystalloid restriction (<25 mL/kg) during operation was attempted in all patients. Operation was performed by experienced thoracic surgeons using standard thoracotomy approaches. Entry into the pericardial space or resection of pericardium were recorded. A pneumonectomy or EPP was carried out in a manner designed to completely resect all neoplastic disease. In 69 of 70 patients, mediastinal lymph node dissection was performed. Postoperative staging was done by histologic review of the resected specimen and all regional lymph nodes. Postoperative pain relief was provided to all patients by continuous administration of either epidural fentanyl administration (n = 34) or intravenous morphine patient-controlled analgesia (n = 36). Benzodiazepines were usually avoided. After an overnight stay in the postanesthesia care unit patients were transferred to the thoracic surgical floor on the first postoperative day. Intraoperative blood loss and fluid intake and output were recorded. Postoperative complications were recorded throughout the hospital stay and patients were monitored for complications as outpatients for 30 days.
Antiarrhythmic Prophylaxis
Upon arrival to the postanesthesia care unit patients were randomly assigned to one of two treatment groups. Group I patients (n = 35) received an intravenous loading dose of diltiazem 20 mg given over 30 minutes, followed by 10 mg intravenously every 4 hours for 24 to 36 hours. Diltiazem was temporarily discontinued for signs of systolic hypotension (<90 mm Hg) or bradycardia (heart rate, <50 beats/min). Beginning on the morning of postoperative day 2 patients received diltiazem 180 to 240 mg orally once daily for 30 days. Adjustments in the oral dose were made for patients weighing less than 50 kg, those who had a systolic blood pressure of less than 90 mm Hg, or those showing adverse effects to diltiazem. Venous blood was drawn to determine diltiazem level before the initiation of oral therapy in 19 of 35 randomly selected patients. Plasma diltiazem concentration was determined by high-performance liquid chromatography with ultraviolet detection by Hoechst Marion Roussel Laboratories (Kansas City, MO). Patients in group II (n = 35) received intravenous digoxin 0.5 mg loading, followed by two more doses of 0.25 mg intravenously 4 hours apart, for a total 1 mg of digoxin given over the first 24 to 36 hours, from admission to the postanesthesia care unit. Starting in the morning of postoperative day 2, patients received digoxin 0.125 to 0.25 mg orally once daily for 30 days. Adjustments in the digoxin dose were based on serum digoxin concentration, serum creatinine level, or onset of untoward effects. Venous blood was drawn to determine digoxin concentration before the initiation of oral therapy in all patients.
If an SVD developed while receiving diltiazem or digoxin, these patients were considered treatment failures. Once treatment failure occurred the primary physician was allowed either to maximize the assigned treatment drug or to crossover to the other study medication, as clinically indicated.
Measures of Clinical Outcome
The primary end point of supraventricular dysrhythmia was defined by a sustained cardiac rhythm other than sinus persisting for at least 15 minutes and documented on either ambulatory electrocardiography or 12-lead ECG. The association of hemodynamic compromise (systolic blood pressure <90 mm Hg or a 
20% decrease in systolic pressure) during SVD was recorded, as was evidence of myocardial ischemia. Other clinical end points recorded in the postoperative period were unexplained persistent sinus tachycardia (HR >140 beats/min, lasting 24 hours), myocardial infarction, respiratory failure, and death. The incidence of SVD was recorded during hospitalization and also noted if documented as outpatients within 30 days of operation. Need for intensive care admission (for any reason) and length of hospital stay were also recorded.
Statistical Analysis
The study was planned to include 70 patients on the basis of an expected incidence of SVD of 25% after pneumonectomy in untreated patients [1–3]. All analyses were performed on an intention-to-treat basis, and all p values are two-tailed. A p value less than 0.05 was considered significant. Statistical analysis was performed with software (SAS version 6.04). To determine the association of patient-, pulmonary function-, and echocardiography-specific factors with new-onset SVD, all variables were examined by univariate analysis (Student's t test or Fisher's exact test). A Wilcoxon rank sum test was used for estimated blood loss and fluid requirement. Length of hospital stay was analyzed by the Kaplan-Meier and log rank methods, with in-hospital deaths treated as censored observations. Data are presented as mean value ± standard deviation, unless otherwise indicated.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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. There was a statistically but not clinically important difference between the two treated groups in preoperative percent of predicted values of the forced expired volume in 1 second and arterial carbon dioxide tension (Table 1). For patients undergoing pneumonectomy for lung cancer the diltiazem group did not differ from the digoxin group with respect to the frequency of early stage (tumor stage I + II, 11 of 19 patients versus 7 of 19 patients), versus locally or advanced disease (tumor stage IIIA + IIIB + IV, 8 of 19 patients versus 12 of 19 patients), respectively, p = 0.33. Similarly, patients undergoing EPP did not differ in tumor stage between treatment groups, p = 0.39, or need for pericardial resection.
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When treated patients were combined, those in whom SVD developed were found to be older and had a significantly longer hospital stay (Table 2). However, right heart pressure, side of operation, and postoperative evidence of pericarditis by ECG did not differentiate patients in whom SVD did or did not develop (see Table 2). For patients undergoing pneumonectomy for lung cancer the SVD group did not differ from the non-SVD group with respect to the frequency of early tumor stage (5 of 7 patients versus 13 of 31 patients), versus locally advanced disease (2 of 7 patients versus 18 of 31 patients), respectively, p = 0.22.
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Primary End Points
The overall incidence of SVD and type of operation are shown in Table 3. Diltiazem-treated patients had a 14% incidence of SVD compared to 31% of those receiving digoxin, p = 0.09. The incidence of symptomatic SVD in the untreated cohort group of patients (11 of 40 patients; 28%) was similar to the incidence of SVD in digoxin-treated patients (31%). In 2 diltiazem-treated patients the drug was held for more than three half-lives (>12 hours) of the drug due to borderline systolic blood pressure (85 to 90 mm Hg) after EPP and more than 1 liter blood loss. Atrial fibrillation developed in these patients, which later responded to diltiazem therapy and converted to sinus rhythm. In another patient who received diltiazem, atrial fibrillation developed in conjunction with a persistent mediastinal shift to the right after a left EPP. The atrial fibrillation did not convert to sinus rhythm until 800 mL of air was aspirated from the left pleural cavity resulting in restoration of mediastinal contents to the midline. When the 2 patients who had an interruption of diltiazem therapy are omitted from the analysis, diltiazem was found to decrease the incidence of SVD significantly compared with digoxin (3 of 33 patients versus 11 of 35 patients, p = 0.035, Fisher's exact test). Diltiazem was highly effective in preventing all SVD in the subset of patients undergoing standard or intrapericardial pneumonectomy (p < 0.005; Table 3). In this subset, the difference in the proportion of patients who developed sustained atrial fibrillation while on diltiazem therapy (0 of 21) compared with those receiving digoxin (5 of 25) approached significance (p = 0.054).
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. Diltiazem-treated patients were continuously monitored for 64 ± 9 hours (range, 35 to 72 hours) and digoxin-treated patients for 67 ± 5 hours (range, 53 to 72 hours). Heart rate did not differ between treated groups at baseline before operation or at any other time point after operation. Similarly, the two groups did not differ in the severity of nonsustained ventricular or supraventricular ectopy (Table 4).
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). Right ventricular enlargement with preserved systolic function was seen in 3 patients, 1 of whom developed fatal acute respiratory distress syndrome. Median right atrial pressure estimation was 3 mm Hg throughout the study in both groups. The difference in RAPe values of 3, 7 or 17 mm Hg was not significant between the groups at all three study times.
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). The length of hospital stay did not differ between these two sets of patients. There was no difference in any parameter measured by Doppler echocardiography or ambulatory ECG between EPP or non-EPP patients.
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Side effects potentially related to diltiazem included dyspepsia (1 patient), peripheral edema (2), and rash (2 patients). Side effects potentially related to digoxin included nausea (2 patients) and symptomatic bradysrhythmia with Mobitz type-II second degree heart block despite a digoxin level of 0.8 to 1.2 ng/mL. These side effects occurred in some patients after discharge from the hospital and were self-limited, resolving in all patients after the assigned drug was discontinued.
Plasma digoxin concentrations (1.1 ± 0.5 ng/mL) were within our normal range (0.5 to 1.5 ng/mL) throughout the study. The mean plasma diltiazem level determined before the oral dose was 54 ± 66 ng/mL (range, 6 to 299 ng/mL; median, 32 ng/mL). In 16 of 19 patients (84%), the plasma diltiazem concentration was below the lower limit of the therapeutic range (79 to 294 ng/mL) [11]. Three of 5 patients in whom atrial fibrillation developed during diltiazem treatment had plasma diltiazem analysis with plasma concentrations of 17, 39, and 52 ng/mL, respectively.
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Digoxin has been used widely for the prophylaxis of SVD after thoracic operations without efficacy being proven in prospective trials and despite possible untoward effects [5, 6]. The predominant action of digoxin is on the atrioventricular node and is mediated by enhanced vagal tone. This may explain digoxin's lack of efficacy after thoracic operation, a period when vagal influences are withdrawn and adrenergic output is high [13, 14]. In our experience, patients who developed atrial fibrillation while receiving digoxin had ventricular response rates (120 to 180 beats/min) as rapid as untreated controls. Recently, the use of verapamil immediately after lobectomy or pneumonectomy was associated with a 50% reduction in overall atrial fibrillation after operation [8]. The high incidence of bradycardia (9%) and hypotension (14%) in this trial led to the early interruption of therapy in many patients. This high incidence of adverse cardiovascular effects may be explained by the relatively large dose of verapamil, a potent vasodilator with negative inotropic action, given as an initial bolus immediately after operation in patients who may be deliberately volume restricted. Comparative studies have generally shown diltiazem to exert less inhibition of vascular smooth muscle activity than nifedipine or verapamil in equimolar concentrations [15]. Because intravenous diltiazem has an efficacy similar to verapamil in treating acute supraventricular dysrhythmias with fewer adverse effects and requiring less hemodynamic monitoring, its introduction to clinical use has been met with enthusiasm [16–18].
Recently, prophylactic diltiazem was demonstrated to be effective in reducing the incidence of atrial fibrillation from 18% to 5% after coronary artery bypass grafting [19]. Other agents, such as flecainide or amiodarone, have been used to try to reduce the incidence of SVD after thoracic operations [20, 21]. Limitations of these studies are mostly related to the small sample size, patient selection, and dysrhythmia definition. In contrast to patients undergoing cardiac operation, use of ß blockers to prevent SVD after pulmonary operation has been avoided because of the potential of exacerbating postoperative bronchoconstriction.
The only consistent high risk predictor of SVD after thoracic operations has been older age [1, 3, 12, 22]. It is not surprising that advanced age is a strong predictor of postoperative SVD, because by 75 years of age only approximately 10% of normal sinus node pacemaker cells remain [23, 24]. We have previously found that increased right heart pressure but not fluid overload or right heart enlargement predisposes to clincially signficant SVD after major pulmonary resection [3]. In the current study, although digoxin-treated patients tended to have a higher right heart pressure, this was not significantly different from patients treated with diltiazem. Even when all patients were combined to determine the effect of right heart pressure on dysrhythmia occurrence there were no differences between the patients who did or did not develop SVD. To date, there is no evidence that preoperative pulmonary function impairment or postoperative hypoxia, hypercarbia, electrolyte imbalance (potassium or magnesium), or use of bronchodilators, are responsible for new onset SVD [2, 3, 12], although these have all been suggested as possible mechanisms.
Limitations of the Study
The rationale for not having a randomized control arm was twofold. First, because digoxin was used for prophylaxis as a routine by some of our surgeons, we considered for ethical reasons our digoxin group as standard therapy. Second, logistically the addition of a third arm to the study would have required doubling of the study sample size, and hence time, to address this important question. We acknowledge the use of "low-dose" intravenous diltiazem (10 mg intravenously every 4 hours) in the initial 24 to 36 hours of the study in comparison to the recommended therapeutic dose (approximately 5 to 15 mg/h in adults). The low dose of diltiazem was chosen due to the prophylactic nature of the study and lack of other reports on the safety of this drug after pneumonectomy. Because we have found diltiazem to be safe, it may be justified to determine the safety and efficacy of larger diltiazem doses in patients undergoing EPP.
In conclusion, our findings demonstrate that diltiazem is safe and effective in decreasing the overall incidence of SVD after pneumonectomy in comparison to digoxin. The routine use of digoxin for this purpose should be discouraged as it did not decrease the incidence of SVD below that of an untreated concurrent cohort or historic controls and its use may be associated with serious adverse effects. Dysrhythmias after pneumonectomy continue to be an important additional marker of poor cardiopulmonary reserve in older patients and are associated with a longer length of hospital stay. Larger trials are indicated to better define whether prevention of SVD improves outcome measures and decreases health care costs.
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Acknowledgments |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Address reprint requests to Dr Amar, Department of Anesthesiology and Critical Care Medicine, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, New York, NY 10021.
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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