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    Abstract
    Introduction
    Materials and Me...
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    Results
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ORIGINAL ARTICLE Table of Contents   
Year : 2009  |  Volume : 12  |  Issue : 1  |  Page : 10-16
Effect of single intraoperative dose of amiodarone in patients with rheumatic valvular heart disease and atrial fibrillation undergoing valve replacement surgery


Department of Cardiac Anaesthesia, Cardio Thoracic Sciences Centre, All India Institute of Medical Sciences, New Delhi - 110 029, India

Click here for correspondence address and email

Date of Submission10-Mar-2008
Date of Acceptance31-Jul-2008
 

   Abstract 

Maintenance of sinus rhythm (SR) is superior to rate control in atrial fibrillation (AF). In order to achieve SR, we administered single-dose intravenous amiodarone intraoperatively and evaluated its effect on conversion of rheumatic AF to SR in patients undergoing valvular heart surgery. Patients were randomly assigned to amiodarone ( n = 42) or control ( n = 40) group in a double blind manner. The amiodarone group received amiodarone (3 mg/kg) intravenously prior to the institution of cardiopulmonary bypass and the control group received the same volume of normal saline. In the amiodarone group, the initial rhythm after the release of aortic cross clamp was noted to be AF in 14.3% ( n = 6) and remained so in 9.5% ( n = 4) of patients till the end of surgery. In the control group, the rhythm soon after the release of aortic cross clamp was AF in 37.5% ( n = 15) ( p = 0.035) and remained so in 32.5% ( n = 13) of patients till the end of surgery ( p = 0.01). At the end of first post-operative day 21.4% ( n = 9) of patients in amiodarone group and 55% ( n = 22) of patients in control group were in AF ( p = 0.002). The requirement of cardioversion/defibrillation was 1.5 (±0.54) in amiodarone group and 2.26 (±0.73) in the control group ( p = 0.014), and the energy needed was 22.5 (±8.86) joules in the amiodarone group and 40.53 (±16.5) in the control group ( p = 0.008). A single intraoperative dose of intravenous amiodarone increased the conversion rate of AF to normal sinus rhythm, reduced the need and energy required for cardioversion/defibrillation and reduced the recurrence of AF within one day.

Keywords: Amiodarone, atrial fibrillation, rheumatic heart disease, valvular heart disease

How to cite this article:
Selvaraj T, Kiran U, Das S, Chauhan S, Sahu B, Gharde P. Effect of single intraoperative dose of amiodarone in patients with rheumatic valvular heart disease and atrial fibrillation undergoing valve replacement surgery. Ann Card Anaesth 2009;12:10-6

How to cite this URL:
Selvaraj T, Kiran U, Das S, Chauhan S, Sahu B, Gharde P. Effect of single intraoperative dose of amiodarone in patients with rheumatic valvular heart disease and atrial fibrillation undergoing valve replacement surgery. Ann Card Anaesth [serial online] 2009 [cited 2019 Jul 20];12:10-6. Available from: http://www.annals.in/text.asp?2009/12/1/10/42881



   Introduction Top


Atrial fibrillation (AF) is one of the most commonly encountered and sustained cardiac arrhythmia in clinical practice. [1] In developing countries, rheumatic mitral stenosis (MS) is the most frequent underlying condition in patients with AF. AF is associated with the risk of thromboembolic complications in 17%-18% of patients. [2],[3]

The Pharmacological Intervention in Atrial Fibrillation (PIAF) trial suggested that the maintenance of normal sinus rhythm (NSR) in patients with AF leads to symptomatic improvement. [4] However, the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study did not show any mortality benefit by the maintenance of sinus rhythm. [1] These two studies were, however, conducted in patients with AF of non-rheumatic aetiology. Furthermore, the issue of rate control versus rhythm control has not been critically evaluated in patients with rheumatic heart disease (RHD).

The presence of AF after mitral valve replacement (MVR) is associated with a worse New York Heart Association (NYHA) functional class, increased transmitral gradients, and larger areas of both atria. [5] Maintenance of NSR is superior to ventricular rate control in patients with rheumatic AF with respect to effects on exercise capacity, quality of life, morbidity, and possibly mortality. [6] Hence, special efforts should be made to correct AF during surgery. [6] NSR is difficult to achieve and maintain in patients with RHD. According to one of the reports, mitral valve surgery restored NSR in only 8.5% of patients with chronic AF. [7]

Among all the anti-arrhythmic drugs evaluated for AF, amiodarone has shown the most promising results with successful conversion and maintenance of NSR achieved in 50%-70% of patients. [8],[9],[10] Oral amiodarone therapy needs frequent visits to the hospital and intense monitoring for side effects. However, the onset of the anti-arrhythmic effect of intravenous amiodarone is rapid. [11],[12]

Reports regarding the use of intraoperative intravenous amiodarone in patients with AF of rheumatic origin, undergoing valvular heart surgery seem to be scarce. We evaluated the effect of intraoperative single-dose intravenous amiodarone to convert AF into NSR in patients undergoing valvular heart surgery.


   Materials and Methods Top


The study protocol was approved by the institutional ethics committee. The study was performed in a prospective randomized case control manner. Three hundred consecutive patients with rheumatic valvular heart disease and undergoing elective valve replacement surgery under cardiopulmonary bypass (CPB) were screened for participating in this study. The patients who were in NYHA class II or III and having persistent chronic AF (more than one year) were included in this study.

Pregnancy, resting heart rate of < 50/min, uncontrolled heart failure, sick sinus rhythm, atrioventricular block and serum creatinine > 2 mg/dl were considered criteria for exclusion from the study. Patients receiving cimetidine, phenytoin, cholestyramine, and cyclosporine for therapeutic reasons and those who were either allergic to amiodarone or had received amiodarone therapy in the past four months were also excluded from the study. Patients with thyroid disease, and high value of serum aspartate and alanine amino transferase (concentrations more than four times the upper limit of normal) were excluded from the study.

Out of the total eligible 130 patients, 82 consented to be included in the study. These patients were randomly assigned in a double blind fashion to either amiodarone group (42 patients) or control group (40 patients).

The preoperative left atrial size was measured using M-mode transthoracic echocardiography in parasternal long axis view. All the patients received the morning dose of beta blockers and calcium channel blockers, and digoxin was omitted on the day of surgery. All the patients were premedicated with intramuscular injection of morphine 0.1 mg/kg and promethazine 0.5 mg/kg, 45 min prior to induction.

In the operation theatre, electrocardiogram (ECG), pulse oximetry (SpO 2 ) and non-invasive blood pressure monitoring were commenced. After establishing intravenous cannula and arterial line, general anaesthesia was induced by administering the following drugs intravenously: 2 µg/kg of fentanyl, 0.02 mg/kg of midazolam, 5 mg/kg of thiopentone and 0.9 mg/kg of rocuronium. Trachea was intubated with an endotracheal tube of appropriate size. Anaesthesia was maintained with incremental doses of fentanyl, midazolam, isoflurane and pancuronium. The right internal jugular vein was cannulated with triple lumen central venous catheter. Injection ceftazidine 25 mg/kg, methyl prednisolone 30 mg/kg and epsilon aminocaproic acid (EACA) 100 mg/kg were administered intravenously to all the patients as a part of the institutional protocol. Injection EACA 100 mg/kg was repeated during and following CPB.

In the amiodarone group, amiodarone 3 mg/kg (total dose diluted in 100 ml of normal saline) was started prior to skin incision and administered through the central venous route over a period of 30 min. In the control group, the same volume of normal saline was infused in a similar fashion. The drug or saline was prepared and administered in a random (sealed envelope technique) manner by a resident doctor who was not involved in patient care. The anaesthesiologist involved in patient care in operating room or ICU was blinded to the patient group. The frequency of occurrence of bradycardia (defined as less than 60 HR (heart rate)/min) and hypotension (defined as systolic blood pressure (BP) < 90 mmHg) was noted. If either of the two occurred, amiodarone infusion was temporarily discontinued. Preload was optimized to achieve CVP of 10 mmHg as a measure to treat hypotension during the infusion of amiodarone. Inotrope infusion was initiated to treat persistent hypotension despite preload optimisation. Amiodarone infusion was restarted after achieving haemodynamic stability. As per the institutional protocol, bradycardia was treated with epicardial pacing. Pre-CPB conversion of AF to NSR, if any, was observed.

Heparin 4 mg/kg was administered intravenously to achieve adequate anticoagulation-activated clotting time of 480 s. The valve replacement surgery was performed under CPB with mild hypothermia using standard extracorporeal techniques. CPB circuit was primed with lactated Ringer's solution and/or packed red blood cells to achieve haematocrit of more than 24% on CPB. Myocardial protection was achieved by infusing cold (4°C) St. Thomas' solution-based crystalloid-blood (1:4) cardioplegic solution into the root of the aorta after aortic cross clamping (ACC). As per the institutional protocol, nitroglycerine infusion 0.5 µg/kg/min was started at the onset of CPB to achieve adequate rewarming. All the patients were rewarmed to 36°C. Serum potassium levels were optimised to 4-4.5 mEq/l by adding incremental doses (5 mEq) of potassium chloride to the venous reservoir in the extracorporeal circuit. An incremental dose of magnesium sulphate starting from 10 mg/kg was added to the CPB circuit if hypomagnesaemia was detected.

Initial rhythm after the release of ACC was noted. If it was AF, cardioversion was attempted with internal paddles with stepwise increasing energy (10 J, 20 J, 30 J monophasic). If HR was less than 60/min, atrial pacing (epicardial) was initiated. If the patient had ventricular fibrillation (VF) or ventricular tachycardia (VT), this was also treated with internal defibrillation with stepwise increasing energy. If the patient had atrioventricular block A-V sequential pacing (epicardial) was initiated.

Dopamine was started for inotropic support if hypotension was encountered. Adrenaline was added as a second inotropic agent to treat persistent hypotension despite 10 µg/kg/min of dopamine infusion. Aorta was decannulated after reversal of residual action of heparin by administration of protamine sulphate (6 mg/kg) intravenously. After surgical closure, the patient was transferred to the post-operative ICU. A 5-lead ECG was continuously monitored.

The following were primary outcome parameters: AF at release of ACC, number of shocks and response to cardioversion/defibrillation, amount of energy needed for cardioversion/defibrillation, the recurrence of AF at the end of surgical procedure, in the first 24 hours of post-operative period and at the time of discharge, need for temporary pacemaker and ventricular rate in patients with AF at first post-operative day.


   Statistics Top


Continuous variables in the two groups were compared by student's t test. Categorical variables were compared by the chi-square test. A p value < 0.05 was considered to be statistically significant. Statistical analysis was performed using the SPSS 11.5 software (SPSS Inc, 233, South Wacker Drive, 11th floor, Chicago, IL, USA).


   Results Top


There were no significant differences in the patient characteristics and demographic data between the two groups [Table 1].

The intraoperative data of both the groups is summarised in [Table 2]. There was no significant difference in the mean basal heart rate. The difference in the HR before and 5 min after drug infusion in the amiodarone group was +9.55 (±13.59)/min, significantly ( p < 0.001) more than the difference in the HR before and five minutes after drug infusion in the control group -1.3 (±6.3)/min. Two patients had bradycardia during the infusion of amiodarone; however, this was statistically not significant ( p = 0.162). There was no hypotension in any of the patients of both the groups during the infusion of the study drug or the placebo.

On release of ACC, NSR was observed in 31 patients (73.8%) in the amiodarone group and 17 patients (58.5%) in the control group. AF was observed in 6 patients (14.3%) in the amiodarone group and 15 patients (37.5%) in the control group ( p = 0.035). [Table 3] These differences in between the two groups are statistically significant ( p = 0.035) in respect to AF at ACC release.

Seventy-five percent ( n = 6 out of 8) of the patients in the amiodarone group, and 47.4% ( n = 9 out of 19) in the control group reverted to NSR after cardioversion ( p = 0.187). The need of number of cardioversion/defibrillation and the amount of energy needed for cardioversion/defibrillation needed was less in the amiodarone group [Table 3]. The recurrence of AF at the end of surgery, in the post-operative ICU, at the end of first post-operative day and before discharge was significantly higher in the control group as compared with the amiodarone group [Table 3]. In the amiodarone group, 14.3% ( n = 2 out of 14) of the patients taking b blockers developed AF as compared to 25% ( n = 7 out of 28) of patients not taking it ( P = 0.425). In the control group, 46.7% ( n = 7 out of 15) of patients taking b blocker developed AF as compared with, 60% ( n = 15 out of 25) not taking it ( P = 0.412). The mean ventricular rate in patients with AF was significantly different between the two groups: 72.9 ± 11.27/min in the amiodarone group and 92 ± 15.3/min in the control group ( P = 0.002).

Significantly higher number of patients in the amiodarone group, i.e. 40.5% ( n = 17) required temporary pacemaker in comparison to 20% ( n = 8) in control group ( P = 0.04) [Table 3]. There was no significant difference in the duration of pacing between the two groups (10.41 ± 5.66 h in the amiodarone group as compared to 10.38 ± 4.95 h in the control group, p = 0.988). Twenty-four hours after the surgery, no patients in either group required a pacemaker.

There was no significant difference in the need for inotropes in the operation theatre ( P = 0.442) or in the post-operative care unit ( p = 0.836) between the two groups and extubation time. The ICU stay was significantly prolonged in the control group (47.33 ± 7.09 h) as compared with the amiodarone group (41.67 ± 4.97 h, ( p < 0.001)). However, we did not randomise all the factors affecting the ICU stay; therefore, we are considering it is an incidental finding in our study.

Five patients in the amiodarone group and nine in the control group had hypotension ( p = 0.202) after surgery. Post-operative bradycardia was observed in sixteen patients in the amiodarone group and six in the control group (P=0.018).

In the amiodarone group, 7 out of the 9 patients who developed AF at first post-operative day had LA size ≥ 60 mm.


   Discussion Top


AF is one of the most common, sustained cardiac arrhythmia encountered in clinical practice. [1] The loss of atrial systole and rapid ventricular rate may cause haemodynamic deterioration in patients with RHD.

Benefits of restoring NSR in patients with rheumatic AF are relief of symptoms, prevention of fast ventricular rate induced dysfunction, improved exercise capacity, improved quality of life, possible reduction in embolic strokes and improved survival. [6] Newer anti-arrhythmics such as flecainide, propafenone and cibenzoline are less useful in established AF. [13]

The AFFIRM study and PIAF trail concluded that the rhythm control strategy offered no survival advantage over the rate control strategy. [1],[4] In AFFIRM study, the mean age was 69.7 ± 9 years, 70.8% had history of hypertension, 38.2% had history of coronary artery disease, only 4.9% of total patients had valvular heart disease and the incidence of rheumatic valvular heart disease is not reported. The study was performed in non-rheumatic AF and in non-surgical patients. Hence, it is difficult to apply the results of this study in patients with RHD undergoing valve replacement surgery. In contrast to the AFFIRM study, the author's subjects had valvular heart disease secondary to RHD; therefore, it may not be prudent to compare the two studies on par.

In a study, NSR was re-established only in 8.5% of patients with AF who underwent mitral valve surgery, which included valve repair and replacement. [7] The potential complications of AF include haemodynamic compromise during the immediate post-operative period. Hence, it is recommended to use concomitant anti-arrhythmic procedures or medication for all patients with AF who undergo mitral valve surgery. [7]

In the Stroke Prevention in Atrial Fibrillation Trial, intolerance to warfarin therapy leads to withdrawal in up to 38%. [14],[15],[16] In contrast, contraindications to amiodarone, including active hepatitis and hyperthyroidism occur less frequently than those for warfarin. [17] The incidence of drug withdrawal due to intolerable side effects is less for amiodarone than (less than 12% per year) warfarin. [18],[19],[20] Therefore, conversion to NSR is the only best option available to patients who have clinical conditions contraindicating the use of warfarin or those intolerant to it.

Pre-treatment with oral amiodarone and direct current cardioversion resulted in NSR restoration in approximately 80.6% of non-surgical patients with persistent AF after an initial unsuccessful attempt in a study performed by Kosior et al . [21] However, the onset of anti arrhythmic effect of oral amiodarone takes 7-10 days; complete anti-arrythmic effects may not be noticed for up to 10 weeks. However, the onset of the anti-arrhythmic effect of intravenous amiodarone is rapid. [11],[12]

Low-dose oral amiodarone was found to be safe and effective in restoring and maintaining NSR after balloon mitral valvotomy in patients with AF and RHD. [22] Short-term amiodarone (high oral dose) with or without electrical cardioversion was effective and safe in the treatment of chronic rheumatic AF after mitral valve surgery. [23] Prophylactic oral amiodarone was shown to reduce the incidence of new onset AF in patients undergoing open heart surgery. [24],[25] However, literature is scarce on the therapeutic role of intravenous amiodarone in the treatment of chronic rheumatic AF in patients undergoing for mitral valve surgery.

The authors of this study observed a significant reduction in the incidence of AF in the amiodarone group. The need of cardioversion/defibrillation and the energy needed was less in the amiodarone group; similar observations were made by other authors as well. [26] Even in patients whose rhythm was not converted to NSR, amiodarone decreased the ventricular rate significantly. [27] Therefore, amiodarone may be effective to either convert the rhythm to NSR or controlling the fast ventricular rate.

Patients with LA dimensions between 46 mm and 60 mm who are significantly compromised by AF can often be maintained in NSR with amiodarone therapy. [18] In the amiodarone group, 7 out of 9 patients who developed AF (at the first post-operative day) had LA size ≥ 60 mm. Hence, the recurrence of AF is common in patients with larger LA size.

The low arrhythmogenicity and negligible negative inotropic effect of amiodarone makes it particularly useful in treating high-risk patients prone to sudden cardiac death. [28] The authors in this study did not observe significant incidence of hypotension in the amiodarone group. There was significant increase in the incidence of bradycardia in the amiodarone group (38%) as compared with 15% in the control group. The need of temporary epicardial pacing was significantly high in the amiodarone group (40.5%) as compared with the control group (20%). However, there was no significant increase in the duration of pacing in the amiodarone group. However, in the amiodarone group, out of 16 patients who developed bradycardia, 13 were also on b blocker (p ≤ 0.001). This may explain the high incidence of bradycardia in the amiodarone group because of the additive effect of the two drugs on the conduction system.

In a report, intravenous amiodarone was found to be well tolerated and did not increase the risk of post-operative complications. [24] This finding was confirmed by the authors of this study as well.

One of the limitations of this study was that the authors did not continue the amiodarone therapy in the post-operative period. Since amiodarone has shown to decrease the recurrence of AF, the higher incidence of AF in this study might be due to the non-continuance of amiodarone in the post-operative period. The small size of study population is another limitation of our study. Future trials with more subjects participating in the study and long-term follow-up may aid in identifying the role of amiodarone in patients with rheumatic AF undergoing valvular heart surgery.


   Conclusion Top


A single intra operative dose of intravenous amiodarone increases the incidence of conversion of AF to NSR. When AF persisted, use of amiodarone reduces the frequency of need for cardioversion and the energy required for it. Recurrence of AF until hospital discharge and occurrence of fast ventricular rate is also reduced.


   Acknowledgement Top


We acknowledge the assistance of Mr. Ashish Datt Upadhayay for statistical analysis. This original article was presented in the 11 th annual conference of Indian association of cardiovascular and thoracic anaesthesiologists, Gandhinagar, Gujarat, India, on 23 February 2008.



 
   References Top

1.Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, et al . Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators: A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002;347:1825-33.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Kannel WB, Abbott RD, Savage DD, McNamara PM. Epidemiologic features of chronic atrial fibrillation: the Framingham Study. N Engl J Med 1982;306:1018-22.  Back to cited text no. 2  [PUBMED]  
3.Alpert JS, Petersen P, Godtfredsen J. Atrial fibrillation: Natural history, complications, and management. Annu Rev Med 1988;39:41-52.   Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Hohnloser SH, Kuck KH, Lilienthal J. Rhythm or rate control in atrial fibrillation-Pharmacological Intervention in Atrial Fibrillation (PIAF): A randomized trial. Lancet 2000;356:1789-94.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Vaturi M, Sagie A, Shapira Y, Feldman A, Fink N, Strasberg B, et al . Impact of atrial fibrillation on clinical status, atrial size and hemodynamics in patients after mitral valve replacement. J Heart Valve Dis 2001;10:763-6.   Back to cited text no. 5  [PUBMED]  
6.Vora A, Karnad D, Goyal V, Naik A, Gupta A, Lokhandwala Y, et al . Control of rate versus rhythm in rheumatic atrial fibrillation: A randomized study. Indian Heart J 2004;56:110-67.   Back to cited text no. 6  [PUBMED]  
7.Raine D, Dark J, Bourke JP. Effect of mitral valve repair/replacement surgery on atrial arrhythmia behavior. J Heart Valve Dis 2004;13:615-21.   Back to cited text no. 7  [PUBMED]  
8.Roy D, Talajic M, Dorian P, Connolly S, Eisenberg MJ, Green M, et al Amiodarone to prevent recurrence of atrial fibrillation: Canadian Trial of Atrial Fibrillation Investigators. N Engl J Med 2000;342:913-20.  Back to cited text no. 8    
9.Chun SH, Sager PT, Stevenson WG, Nademanee K, Middlekauff HR, Singh BN. Long-term efficacy of amiodarone for the maintenance of normal sinus rhythm in patients with refractory atrial fibrillation or flutter. Am J Cardiol 1995;76:47-50.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Kochiadakis GE, Igoumenidis NE, Marketou ME, Solomou MC, Kanoupakis EM, Vardas PE. Low-dose amiodarone versus sotalol for suppression of recurrent symptomatic atrial fibrillation. Am J Cardiol 1998;81:995-8.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Installe E, Schoevaerdts JC, Gadisseux P, Charles S, Tremouroux J.none Intravenous amiodarone in the treatment of various arrhythmias following cardiac operations. J Thorac Cardiovasc Surg 1981;81:302-8.   Back to cited text no. 11  [PUBMED]  
12.Singh BN, Vaughan Williams EM.none The effect of amiodarone: A new anti-anginal drug, on cardiac muscle. Br J Pharmacol 1970;39:657-67.   Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Levy S. Pharmacologic management of atrial fibrillation: Current therapeutic strategies, Am heart J 2001;141;S15-21.  Back to cited text no. 13    
14.Preliminary report of the stroke prevention in atrial fibrillation study. N Engl J Med 1990;322:863-8.   Back to cited text no. 14    
15.Petersen P, Boysen G, Godtfredsen J, Andersen ED, Andersen B. Placebo-controlled, randomised trial of warfarin and aspirin for prevention of thromboembolic complications in chronic atrial fibrillation: The Copenhagen AFASAK study. Lancet 1989;1:175-9.   Back to cited text no. 15  [PUBMED]  
16.Connolly SJ, Laupacis A, Gent M, Roberts RS, Cairns JA, Joyner C.none Canadian Atrial Fibrillation Anticoagulation (CAFA) Study. J Am Coll Cardiol 1991;18:349-55.   Back to cited text no. 16  [PUBMED]  
17.Mason JW.none Amiodarone. N Engl J Med 1987;316:455-66.  Back to cited text no. 17  [PUBMED]  
18.Brodsky MA, Allen BJ, Walker CJ 3rd, Casey TP, Luckett CR, Henry WLnone . Amiodarone for maintenance of sinus rhythm after conversion of atrial fibrillation in the setting of a dilated left atrium. Am J Cardiolnone 1987;60:572-5.   Back to cited text no. 18    
19.Gold RL, Haffajee CI, Charos G, Sloan K, Baker S, Alpert JS.none Amiodarone for refractory atrial fibrillation. Am J Cardiol 1986;57:124-7.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]
20.Blevins RD, Kerin NZ, Benaderet Dnone , Frumin H, Faitel K, Jarandilla R, et al . Amiodarone in the management of refractory atrial fibrillation. Arch Intern Mednone 1987;147:1401-4.  Back to cited text no. 20    
21.Kosior DA, Wozakowska-Kap?on B, Jasik M, Kiliszek M, Rabczenko D, Opolski G. Amiodarone after unsuccessful direct-current cardioversion of persistent atrial fibrillation. Kardiol Pol 2005;63:585-92.  Back to cited text no. 21    
22.Kapoor A, Kumar S, Singh RK, Pandey CM, Sinha N. Management of persistent atrial fibrillation following balloon mitral valvotomy: Safety and efficacy of low-dose amiodarone. J Heart Valve Disnone 2002;11:802-9.  Back to cited text no. 22    
23.Skoularigis J, Rφthlisberger C, Skudicky D, Essop MR, Wisenbaugh T, Sareli P. Effectiveness of amiodarone and electrical cardioversion for chronic rheumatic atrial fibrillation after mitral valve surgery. Am J Cardiol 1993;72:423-7.  Back to cited text no. 23    
24.Guarnieri T, Nolan S, Gottlieb SO, Dudek A, Lowry DR. Intravenous amiodarone for the prevention of atrial fibrillation after open heart surgery: the amiodarone reduction in coronary heart (ARCH) trial. J Am Coll Cardiol 1999;34:343-7.  Back to cited text no. 24  [PUBMED]  [FULLTEXT]
25.White CM, Giri S, Tsikouris JP, Dunn A, Felton K, Reddy P, et al . A comparison of two individual amiodarone regimens to placebo in open heart surgery patients. Ann Thorac Surg 2002;74:69-74.  Back to cited text no. 25  [PUBMED]  
26.Sagristą-Sauleda J, Permanyer-Miralda G, Soler-Soler Jnone . Electrical cardioversion after amiodarone administration. Am Heart J none 1992;123:1536-42.  Back to cited text no. 26    
27.Hohnloser SH, Meinertz T, Dammbacher T, Steiert K, Jδhnchen E, Zehender M, et al .none Electrocardiographic and antiarrhythmic effects of intravenous amiodarone: Results of a prospective, placebo-controlled study. Am Heart J 1991;121:89-95.   Back to cited text no. 27    
28.Hohnloser SH, Klingenheben T, Singh BN. Amiodarone-associated proarrhythmic effects: A review with special reference to torsade de pointes tachycardia. Ann Intern Med 1994;121 :529-35 .  Back to cited text no. 28  [PUBMED]  [FULLTEXT]

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Correspondence Address:
Usha Kiran
Department of Cardiac Anaesthesia, 7th floor, Cardiothoracic Sciences centre, All India Institute of Medical Sciences, New Delhi - 110 029
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.42881

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    Tables

  [Table 1], [Table 2], [Table 3]

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