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JANAK MEHTA AWARD Table of Contents   
Year : 2010  |  Volume : 13  |  Issue : 2  |  Page : 130-137
Echocardiographic evaluation and comparison of the effects of isoflurane, sevoflurane and desflurane on left ventricular relaxation indices in patients with diastolic dysfunction


1 Consultant Cardiac Anesthesiologist, Woodlands Hospital & Medical Research Center Ltd, Kolkata, India
2 Consultant Cardiac Anesthesiologist Department of Anesthesiology & Intensive Care, Kolkata, India
3 Consultant Cardiac Anesthesiologist & Chief, Department of Anesthesiology & Intensive Care, Rabindranath Tagore International Institute of Cardiac Sciences, Kolkata, India

Click here for correspondence address and email

Date of Submission19-Oct-2009
Date of Acceptance31-Dec-2009
Date of Web Publication3-May-2010
 

   Abstract 

This prospective randomized study aims to evaluate and compare the effects of isoflurane, sevoflurane and desflurane (study drugs) on left ventricular (LV) diastolic function in patients with impaired LV relaxation due to ischemic heart disease using transesophageal Doppler echocardiography. After approval of the local ethics committee and informed consent, 45 patients scheduled for coronary artery bypass grafting surgery were enrolled in the study. Patients were selected by a preoperative Transthoracic Echocardiographic diagnosis of impaired relaxation or Grade 1 Diastolic Dysfunction. They randomly received fentanyl and midazolam anesthesia with 1 MAC of isoflurane (n=16), sevoflurane (n=14) or desflurane (n=15). Hemodynamic parameters and TEE derived ventricular diastolic relaxation indices before and after the study drug administration were compared. LV filling pressures were kept constant throughout the study period to exclude the effect of the loading conditions on diastolic function. Four patients in the sevoflurane group and three in the desflurane group were excluded from the study, after baseline TEE examination revealed normal diastolic filling pattern. All the three study drugs significantly reduced the systemic vascular resistance index with a significant increase in cardiac index. Mean arterial pressure was reduced by all the drugs, although the decrease was not statistically significant. Hemodynamic changes were comparable between all the three groups. In terms of LV relaxation indices, all three agents led to a significant improvement in diastolic function. Transmitral and Tissue Doppler E/A and Em/Am ratios improved significantly Transmitral and Tissue Doppler E/A and Em/Am ratios improved significantly accompanied by a significant decrease in deceleration time and isovolumetric relaxation time. The effect of all three agents on diastolic relaxation parameters was comparable. In conclusion , Isoflurane, sevoflurane and desflurane, do not appear to have a detrimental effect in patients with early diastolic dysfunction. On the contrary, these inhalational agents actually improve the LV relaxation. A significant reduction in afterload produced by these vapors can be a possible reason for these findings. The positive effect of these inhalational agents on LV relaxation can have a profound effect on the perioperative anesthetic management of patients with diastolic dysfunction.

Keywords: Desflurane, diastolic dysfunction, echocardiography, isoflurane, sevoflurane

How to cite this article:
Sarkar S, GuhaBiswas R, Rupert E. Echocardiographic evaluation and comparison of the effects of isoflurane, sevoflurane and desflurane on left ventricular relaxation indices in patients with diastolic dysfunction. Ann Card Anaesth 2010;13:130-7

How to cite this URL:
Sarkar S, GuhaBiswas R, Rupert E. Echocardiographic evaluation and comparison of the effects of isoflurane, sevoflurane and desflurane on left ventricular relaxation indices in patients with diastolic dysfunction. Ann Card Anaesth [serial online] 2010 [cited 2018 Sep 26];13:130-7. Available from: http://www.annals.in/text.asp?2010/13/2/130/62945



   Introduction Top


Abnormal ventricular diastolic function could cause clinical heart failure (HF) in 40 to 50% of patients despite their having normal systolic function. [1],[2] The situation is more alarming because the incidence of diastolic HF increases with age, approaching 50% in patients over 70 years of age. [3] Also, the condition is commonly associated with hypertension and diabetes mellitus, which are ever increasing among patients with ischemic heart disease. Diastolic HF may be associated with substantial morbidity and mortality; thus giving rise to enormous rise in health care budgets. Not surprisingly, the study of diastolic dysfunction has come to the forefront of clinical cardiovascular medicine research in recent times.

Clinically, diastolic dysfunction is measured both by transthoracic echocardiography and transesophageal echocardiography. Conventionally, transmitral pulsed wave Doppler and pulmonary venous Doppler were used to identify diastolic dysfunction. However, the major disadvantages of these techniques were their dependence on left ventricular loading conditions [4],[5] and a display of biphasic response to increasing disease severity. These limitations have led to the development of newer Doppler techniques of color M-mode Doppler and tissue Doppler which can assess diastolic dysfunction independent of preload conditions. [6]

Unrecognized diastolic dysfunction in the presence of near-normal systolic function can have adverse consequences like hemodynamic instability and acute pulmonary edema [7] in the perioperative period. Consequently, the modern day anesthesiologist must have an understanding of the effect of various anesthetic agents on ventricular diastolic function.

Interestingly, the effects of volatile agents, one of the commonest groups of anesthetic drugs in day to day clinical practice, on myocardial diastolic function are not yet well characterized. [8] In a study on chronically instrumented dogs with normal left ventricular (LV) function, Pagel et al. found 1 to 1.5 MAC of isoflurane and desflurane impaired LV relaxation by prolonging the time constant of isovolumetric relaxation. [9] Further, only a handful of studies have investigated the role of inhalational agents on ventricular diastolic function in a clinical context. In one of these studies, Houltz et al. conclude that isoflurane not only impaired early diastolic relaxation in coronary artery bypass graft (CABG) surgery patients, but also increased the LV end diastolic stiffness. [10] On the contrary, in a study on patients with normal heart, Oxorn et al. could not find any change in LV relaxation or stiffness with clinical doses of isoflurane. [11] To further complicate the matters, Neuhauser and coworkers. concluded that isoflurane does not exacerbate diastolic dysfunction, but, on the other hand, leads to normalization of impaired relaxation parameters. [12] These conflicting findings have led the leading cardiac anesthesiologists to conclude that "the effect of volatile agents on diastolic dysfunction ...await the application of bedside emerging technologies that have the sensitivity to quantitative indices of diastolic function". [8]

With this clinical background, this prospective, randomized study was carried out to evaluate the individual and comparative effects of isoflurane, sevoflurane and desflurane, on LV diastolic function in clinical setting, using the newer echocardiographic tissue Doppler techniques.


   Materials and Methods Top


After approval of the institutional ethics committee and written informed consent, 45 patients scheduled for CABG surgery were enrolled in the study. Patients were selected by a preoperative TTE diagnosis of grade 1 diastolic dysfunction. Patients with LV ejection fraction (EF) of less than 60%, regional wall motion abnormality (RWMA), previous myocardial infarction (MI), atrial fibrillation, valvular heart disease, hypertrophic obstructive cardiomyopathy (HOCM), pericardial disease and infiltrative myocardial disease,emergency CABG and patients on inotropes ,vasodilators and mechanical ventilation were excluded from the study

All preoperative medications, except ACE inhibitors, was continued until the morning of surgery. All the patients received tablet nitrazepam 10 mg the night before surgery and the morning of surgery. Upon arrival to the operation room, standard monitoring (5 lead ECG, SpO2 probe and noninvasive blood pressure) was attached. An 16G arterial cannula (Secalon; T, Becton Dickinson Critical Care Systems, Singapore) was inserted under local anesthesia in the femoral artery maintaining strict asepsis. After preoxygenation, intravenous induction of general anesthesia was performed using midazolam 0.05 mg/kg, fentanyl 5 - 10 ΅g/kg and titrated doses of propofol. Endotracheal intubation was performed using pancuronium bromide 0.1 mg/kg as neuromuscular blocking agent. Anesthesia was maintained in all the patients by 1 to 2 mg of midazolam and 100 to 200 ΅g of Fentanyl every 30 - 60 minutes till the start of study drugs. Supplemental doses of pancuronium bromide were administered as required. Ventilation was controlled to achieve arterial carbon dioxide tension (PaCO2) between 35 to 45 mm Hg and arterial oxygen tension (PaO2) >100 mm Hg. Positive end-expiratory pressure of 5 cm of H2O was applied in all patients. Inspired gas concentration of oxygen, carbon dioxide and inhalational agent was monitored for the study (Philips airway gas monitoring system Model M1026B, Philips Electronics N.V., Eindhoven, Netherlands).

After induction, an intermittent cardiac output measuring pulmonary artery catheter (Thermo dilution Venous Infusion Port/VIP Swan Ganz Catheter, Edwards Lifesciences, Irvine, CA) was placed via the right internal jugular vein into the pulmonary artery. For hemodynamic measurements, heart rate (HR), systolic, diastolic and mean arterial pressures (SBP, DBP and MAP) along with central venous pressures (CVP) and pulmonary artery pressures (PAP) were continuously recorded with a Philips monitoring system (Philips Intellivue MP60 Anesthesia Monitor, Philips Electronics N.V., Eindhoven, Netherlands). The pressure transducers were zeroed against atmospheric pressure and maintained at the midaxillary level throughout the operation all pressure recordings were carried out in the expiratory phase.

All measurements were performed after sternotomy during the preparation of the left internal mammary artery. At first, thermodilution cardiac output was measured in triplicate using a bolus of cold saline at each reading. The average of the three measurements was recorded. HR, MAP, CVP and pulmonary capillary wedge pressure (PCWP) were also recorded. Cardiac index (CI) and systemic vascular resistance index (SVRI) were calculated using standard formulae calculated by the hemodynamic monitor.

After recording of the hemodynamic parameters, a multiplane 7.0 MHz TEE probe with 64 transducers (Philips Model 21369A, Philips Medical Systems, Bothell, WA) was positioned carefully in the midesophagus of the patient. All patients then underwent a complete TEE evaluation with a commercially available ultrasound system (HP Sonos 4500, Andover, Massachusetts) according to the American Society of Echocardiography/Society of Cardiovascular Anesthesiologists (ASE/SCA) [13] guidelines. Only patients with an impaired ventricular relaxation pattern were included in the study. Impaired ventricular relaxation pattern is indicated by all of the following criteria: E/A ratio< 1; Deceleration Time>220 milliseconds; S/D ratio > 1 and Em/Am ratio < 1.

For the transmitral flow velocity recording, an optimal four-chamber mid-esophageal (ME) view of the heart was obtained and the Doppler sample volume placed at the level of the open leaflet tips in diastole. E, A and E/A ratio and the deceleration time of early diastolic filling were measured by pulsed wave (PW) Doppler [Figure 1].

For the pulmonary vein flow velocity recording, the transducer was positioned in the high mid-esophageal position and adjusted to obtain an optimal view of the left upper pulmonary vein. The sample volume was placed centrally in the vein approximately 0.5 - 1 cm distal from the orifice to the left atrium. Peak systolic velocity (S), peak diastolic velocity (D), peak reverse atrial velocity (A) and S/D ratio were recorded [Figure 2].

For tissue velocity recording, an optimal LV ME view was obtained and the Doppler sample volume was placed at the lateral mitral valve ring. Em, Am and Em/Am were recorded [Figure 3]. Isovolumetric relaxation time (IVRT) was calculated as described by Tekten et al. [Figure 4]. [16]

The images of three consecutive beats were recorded on a digital video disc (Pleomax DVD, Samsung Corporation, Korea). The images were further examined by an experienced TEE investigator who was blinded to the study drugs and the data collected was corroborated. The average of the measurements from three consecutive beats was taken for analysis.

After baseline measurements, patients were randomly assigned by a computer generated number to either receive 1 MAC of either sevoflurane or desflurane or isoflurane. The CVP and PCWP were kept constant by a titrated infusion of 6% Hydroxy Ethyl Starch (HES). After stabilization of end tidal study drug concentration (in a statistically comparable time period of one to two minutes for all patients) and filling pressures, the hemodynamic parameters and echocardiographic relaxation indices were measured again. After recording the repeat measurements, the study was terminated and the operation continued in the usual fashion.

Patient characteristics and comparison of medications received in the pre-operative and intraoperative periods were assessed with Kruskal-Wallis test (SPSS Version 10.0) and chi-square test. Hemodynamic and echocardiographic data within the group before and after the study drug intervention were compared with paired-sample t test. Changes in hemodynamic and echocardiographic parameters were compared between groups by using Kruskal-Wallis test. All data are presented as mean ± standard deviation. P values < 0.05 were considered significant.


   Results Top


After initial intraoperative echocardiographic assessment, seven patients (four in sevoflurane group and three in desflurane group) were diagnosed as having normal diastolic filling pattern and excluded from the study. Sixteen, 10 and 12 patients were treated with isoflurane, sevoflurane and Desflurane respectively. All the three groups were similar with respect to demographic data and pre-operative medications [Table 1]. Patients were also similar with respect to use of intraoperative anesthetic agents used during the study period excepting the study drugs [Table 2].

All the three groups were similar in terms of hemodynamic effects [Table 3]. All the three inhalational agents reduced MAP, although the decrease was not statistically significant. However, all of them decreased the SVRI significantly with statistically significant increases in CI [Table 4].

When the echocardiographic parameters were compared, it was evident that all the three inhalational agents had shifted the impaired LV relaxation to a more normal filling pattern. This was clearly seen from the improvement in E, E/A, Em and Em/Am ratio with statistically significant decrease in deceleration time and isovolumetric relaxation time [Table 5]. The S/D ratio remained above 1, post-study drug in all the three groups, thus ruling out these changes to be due to pseudo-normalization of LV filling. Also the maintenance of CVP and PCWP at baseline values excludes the possibility of pseudo-normalization. The consistent improvement in tissue Doppler parameters further rules out the effect of filling pressures, as these parameters are preload independent.

Also, all the three inhalational agents were similar with respect to Doppler echocardiographic parameters [Table 6]. However, there was a significant increase in Dvmax with Desflurane.


   Discussion Top


In summary, patients in all the three study groups were similar with respect to demographic characteristics and use of pre-operative and intraoperative medications excepting the study drugs. Hemodynamically, the study drugs decreased MAP and SVRI, with a statistically significant increase in CI. Comparing the echocardiographic parameters, the study drugs significantly improved impaired LV relaxation to a more normal filling pattern. However, in this regard, they were comparable between themselves.

The effects of volatile anesthetics on diastolic function in the normal and diseased heart have been incompletely understood.

Pagel et al. found clinical concentrations of isoflurane and desflurane impaired LV relaxation by prolonging IVRT was described by pagel and co workers. [9] On the contrary, Housmans et al. concluded that Isoflurane modestly enhanced isotonic relaxation of isolated ferret myocardium in vitro. [17] It was shown by Houltz et al. that isoflurane not only impaired early diastolic relaxation, but also increased the LV end diastolic stiffness, [10] Ihara et al. could not find any direct negative lusitropic effect for the inhalational agents. [18]

For accurate understanding of the effect of inhalational agents on diastolic function, the indices of diastolic relaxation have to be interpreted correctly. For example, a conclusion of diastolic dysfunction based on isovolumetric relaxation time (IVRT) must take into consideration the role of systemic vascular resistance (SVR).With a decreased SVR, the aortic pressure decreases and the aortic valve closes later leading to reduction in IVRT independent of relaxation. [19]

Similarly, ventricular diastolic function is extremely dependent on loading conditions. [4] An increase in preload will produce a pattern of transmitral filling similar to that seen in restrictive diastolic function without any contribution from the inhalational agents.

For these reasons, the present study was designed in such a way that the filling pressures (CVP and PCWP) were kept at baseline levels throughout data collection. Thus it can be safely concluded that the improvement in diastolic function with the three study drugs was actual and not due to a "pseudonormalization," which is associated with elevation in filling pressures. Further, in order to improve the accuracy of the data, tissue Doppler imaging was incorporated in the study. The main advantage of tissue Doppler over conventional PW Doppler is that it is less load dependent and does not display a biphasic response to increasing disease severity. [20]

Thus, the present study demonstrates that contrary to earlier published work, isoflurane, sevoflurane and desflurane in clinical concentrations actually lead to an improvement in impaired ventricular relaxation. The findings may have a direct relevance to the anesthetic management of patients with diastolic dysfunction. However, a number of studies have concluded that volatile agents do not directly alter the intrinsic viscoelastic properties of the myocardium. [21] The relative constancy of the diastolic pressure volume relation in humans after acute interventions including inhalational agents have led investigators to believe that LV compliance is rarely changed acutely. [22] In a frame by frame analysis of angiograms in 16 patients, Alderman et al. concluded that though acute hemodynamic interventions, produced changes in the diastolic pressure volume curve, they did not change the elasticity of the myocardium itself. [23]

In the possible absence of any effect of the study drugs on the intrinsic ventricular compliance, the investigators in these study believe that the improvement in ventricular relaxation by the inhalational agents is due to a concomitant and significant reduction in afterload produced by these agents. [24,25] [Table 4].

After load reduction may improve LV systolic performance by decreasing impedance to LV ejection and may also increase the rate of LV relaxation. The summated effect of these may contribute to improvement in LV diastolic filling and compliance [26]. Leite-Moreira et al. in a study on open chest rabbits concluded that afterload-induced changes in myocardial relaxation are a mechanism for diastolic dysfunction when afterload is elevated beyond certain limits and that load is an acute determinant of the end diastolic pressure-volume relationship. [27] the inhalational agents may improve diastolic performance [28] by improving ventricular efficiency.

The limitation of the study is the relatively small number of patients (n = 38) accepted for the investigation. In conclusion, isoflurane, sevoflurane and desflurane, do not appear to have a detrimental effect in patients with early diastolic dysfunction. Actually, these newer inhalational agents actually improve the LV relaxation. A significant reduction in afterload produced by these vapors can be a possible reason for these findings. Larger, prospective studies need to be conducted to extrapolate these findings in patients with more severe grades of diastolic dysfunction.

 
   References Top

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2.Groban L. Diastolic dysfunction in the elderly. J Cardiothorac Vasc Anesth 2005;19:228-36.  Back to cited text no. 2      
3.Zile MR, Brutsaert DL. New concepts in diastolic dysfunction and diastolic heart failure: Part I: diagnosis, prognosis and measurements of diastolic function. Circulation 2002;105:1387-93.  Back to cited text no. 3      
4.Nishimura RA, Abel MD, Hatle LK, Tajik AJ. Relation of pulmonary vein to mitral flow velocities by transesophageal Doppler echocardiography: Effect of different loading conditions. Circulation 1990;81:1488-97.  Back to cited text no. 4      
5.Berk MR, Xie GY, Kwan OL, Knapp C, Evans J, Kotchen T, et al. Reduction of left ventricular preload by lower body negative pressures alters Doppler transmitral filling patterns. J Am Coll Cardiol 1990;16:1387-92.   Back to cited text no. 5      
6.Garcia MJ, Thomas JD, Klein AL. New Doppler echocardiographic applications for the study of diastolic function. J Am Coll Cardiol 1998;32:865-75.  Back to cited text no. 6      
7.Gandhi SK, Powers JC, Nomeir AM, Fowle K, Kitzman DW, Rankin KM, et al. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med 2001;344:17-22.  Back to cited text no. 7      
8.Grogan K, Nyhan D, Berkowitz DE. Pharmacology of anesthetic drugs. In: Kaplan JA editor: Kaplan's Cardiac Anesthesia. Philadelphia: Saunders; 2006. p. 166.  Back to cited text no. 8      
9.Pagel PS, Kampine JP, Schmeling WT, Warltier DC. Alteration of the left ventricular diastolic function by desflurane, isoflurane and halothane in the chronically instrumented dog with autonomic nervous system blockade. Anesthesiology 1991;74:1103-14.  Back to cited text no. 9      
10.Houltz E, Caidahl K, Adin C, Gustavsson T, Ricksten SE. Effects of halothane and isoflurane on left ventricular diastolic function during surgical stress in patients with coronary artery disease. Acta Anaesthesiol Scand 1997;41:931-8.  Back to cited text no. 10      
11.Oxorn D, Edelist G, Harrington E, Tsang S. Echocardiographic assessment of the left ventricular filling during Isoflurane anesthesia. Can J Anaesth 1996;43:569-74.   Back to cited text no. 11      
12.Neuhδuser C, Mόller M, Welters I, Scholz S, Kwapisz MM. Effect of isoflurane on echocardiographic left ventricular relaxation indices in patients with diastolic dysfunction due to concentric hypertrophy and ischemic heart disease. J Cardiothorac Vasc Anesth 2006;20:509-14.   Back to cited text no. 12      
13.Shanewise JS, Cheung AT, Aronson S, Stewart WJ, Weiss RL, Mark JB, et al. ASE/SCA guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: Recommendations of the american society of echocardiography council for intraoperative echocardiography and the society for cardiovascular anesthesiologists task force for certification in perioperative transesophageal echocardiography. Anesth Analg 1999;89:870-84.   Back to cited text no. 13      
14.How to diagnose diastolic heart failure. European study group on Diastolic Heart Failure. Eur Heart J 1998;19:990-1003.   Back to cited text no. 14      
15.Benjamin EJ, Levy D, Anderson KM, Wolf PA, Plehn JF, Evans JC, et al. Determinants of Doppler indexes of left ventricular diastolic function in normal subjects (the Framingham Heart Study). Am J Cardiol 1992;70:508-15.  Back to cited text no. 15      
16.Tekten T, Onbasili AO, Ceyhan C, Unal S, Discigil B. Value of measuring myocardial performance index by tissue Doppler echocardiography in normal and diseased heart. Jpn Heart J 2003;44:403-16 .  Back to cited text no. 16      
17.Housmans PR, Murat I. Comparative effects of halothane, enflurane and isoflurane at equipotent anesthetic concentrations on isolated ventricular myocardium of the ferret. II. Relaxation. Anesthesiology 1988;69:464-71.   Back to cited text no. 17      
18.Ihara T, Shannon RP, Komamura K, Pasipoularides A, Patrick T, Shen YT, et al. Effects of anesthesia and recent surgery on diastolic function. Cardiovasc Res1994;28:325-36.   Back to cited text no. 18      
19.Zile MR, Nishimura RA, Gaasch WH. Hemodynamic loads and left ventricular diastolic function: Factors affecting the indices of isovolumetric and auxotonic relaxation. In: Gaasch WH, LeWinter MM editors. Left Ventricular Diastolic Dysfunction and Heart Failure: Philadelphia Lea and Febiger; 1993. p. 219.  Back to cited text no. 19      
20.Sohn DW, Chai IH, Lee DJ, Kim HC, Kim HS, Oh BH, et al. Assessment of mitral annulus velocity by Doppler tissue imaging in the evaluation of left ventricular diastolic function. J Am Coll Cardiol 1997;30:474-80.  Back to cited text no. 20      
21.Pagel PS, Warltier DC. Anesthetics and left ventricular function. In: Ventricular function. Warltier DC editor. Baltimore; Williams and Wilkins: 1995. p. 213-52.  Back to cited text no. 21      
22.Kass DA, Wolff MR, Ting CT. Diastolic compliance of hypertrophied ventricles is not acutely altered by pharmacologic agents influencing active processes. Am Intern Med 1993;119:166.   Back to cited text no. 22      
23.Alderman EL, Glantz SA. Acute hemodynamic interventions shift the diastolic pressure-volume curve in man. Circulation 1976;54:662-71.   Back to cited text no. 23      
24.Hettrick DA, Pagel PS, Warltier DC. Differential effects of isoflurane and halothane on aortic input impedance quantified using a three element Windkessel model. Anesthesiology 1995;83:361-3.   Back to cited text no. 24      
25.Lowe D, Hettrick DA, Pagel PS, Warltier DC. Influence of volatile anesthetics on left ventricular afterload in vivo: Differences between desflurane and sevoflurane. Anesthesiology 1996;85:112-20.   Back to cited text no. 25      
26.Little WC. Enhanced load dependence of relaxation in heart failure: Clinical implications. Circulation 1992;85:2326-8.   Back to cited text no. 26      
27.Leite-Moreira AF, Correia-Pinto J. Load as an acute determinant of end-diastolic pressure-volume relation . Am J Physiol Heart Circ Physiol 2001;280:H51-9.   Back to cited text no. 27      
28.Starling MR. Left ventricular-arterial coupling relations in the normal human heart. Am Heart J 1993;125:1659-66.  Back to cited text no. 28      

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Correspondence Address:
Emmanuel Rupert
Department of Cardiac Anesthesiology & Intensive Care, Rabindranath Tagore International Institute of Cardiac Science, #124, Mukundapur, off E M Bypass, Kolkata - 700 099
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.62945

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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]

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