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 Table of Contents  
ORIGINAL ARTICLE
Year : 2021  |  Volume : 9  |  Issue : 1  |  Page : 46-53

Evaluation of idiopathic dilated cardiomyopathy with cardiac magnetic resonance imaging


1 Department of Radiodiagnosis, Sher-i-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India
2 Department of Cardiology, Sher-i-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India

Date of Submission21-Nov-2020
Date of Acceptance25-Feb-2021
Date of Web Publication30-Mar-2021

Correspondence Address:
Dr. Arshed Hussain Parry
Department of Radiodiagnosis, Sher-i-Kashmir Institute of Medical Sciences, Srinagar - 190 011, Jammu and Kashmir
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/heartindia.heartindia_52_20

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  Abstract 


Purpose: The present study was aimed to assess the prevalence, location, and patterns of late gadolinium enhancement (LGE) in idiopathic dilated cardiomyopathy (DCM) on cardiac magnetic resonance (CMR) imaging and to correlate the left ventricular (LV) functions obtained by cine CMR with the values obtained by echocardiography.
Methods: This was a prospective single-center study covering a 2-year study period. The authors studied the prevalence, location, and patterns of LGE in idiopathic DCM on CMR and correlated the ventricular functions obtained by CMR with those obtained by echocardiography.
Results: LGE was seen in 18/40 (45%) and was absent in 22/40 (55%) of patients. With regard to location, septal enhancement was the most common, seen in 8 (20%) followed by free-wall enhancement in 4 (10%) and a concomitant septal and free-wall enhancement in 6 (15%). In terms of pattern, midwall enhancement was observed in 10 (25%), subepicardial in 2 (5%), subendocardial in 4 (10%), and focal and transmural enhancement in 1 each. The maximum correlation for calculation of LV ejection fraction (EF) was obtained between CMR and two-dimensional echocardiography (P = 0.442).
Conclusion: CMR is an accurate tool to determine the phenotype of DCM by identifying the presence, location, and pattern of LGE which has a prognostic value and is used to guide management. CMR is the most accurate assessment tool for the calculation of EF and other volumetric variables in DCM.

Keywords: Cardiac magnetic resonance imaging, dilated cardiomyopathy, echocardiography, late gadolinium enhancement, ventricular functions


How to cite this article:
Khan IA, Parry AH, Paul I, Choh NA, Shaheen FA, Singh M, Khan KA. Evaluation of idiopathic dilated cardiomyopathy with cardiac magnetic resonance imaging. Heart India 2021;9:46-53

How to cite this URL:
Khan IA, Parry AH, Paul I, Choh NA, Shaheen FA, Singh M, Khan KA. Evaluation of idiopathic dilated cardiomyopathy with cardiac magnetic resonance imaging. Heart India [serial online] 2021 [cited 2021 Apr 17];9:46-53. Available from: https://www.heartindia.net/text.asp?2021/9/1/46/312492




  Introduction Top


Dilated cardiomyopathy (DCM) represents alteration in ventricular morphology and function secondary to various pathological conditions of cardiac muscle.[1] DCM is characterized by an increase in diameter and volume of the left or both ventricles (left ventricular internal diastolic diameter >56 mm) and leading to an impaired ventricular systolic function (ejection fraction [EF] <40%) that is not secondary to or cannot be exclusively justified by abnormal loading conditions (e.g., valve disease and hypertension) or by the concomitant coronary artery disease (CAD).[2],[3],[4],[5],[6] The wide gamut of phenotypic expressions of DCM has recently led to the inclusion of a new category of patients under the umbrella of DCM. These include patients who demonstrate isolated left ventricular (LV) dilatation in the absence of impaired systolic function and hypokinetic but nondilated LV (hypokinetic non-DCM).[7]

DCM is the most common cardiomyopathy worldwide with an estimated prevalence of 40–50 cases per 100,000 adult population.[8],[9] Clinical manifestations of DCM vary widely from asymptomatic to mild systolic dysfunction characterized by effort fatigability to gross LV dysfunction characterized by heart failure. LV dysfunction determines the severity of clinical symptoms. DCM can also manifest as supraventricular or ventricular arrhythmias and sudden cardiac death.[10] Most common cause of DCM is idiopathic (50%) followed by familial (20%–35%), drugs, alcohol, peripartum, and postviral.[11] Idiopathic DCM has a multifactorial etiology consisting of genetic mutations and exposure to various environmental insults causing myocardial damage and leading to ventricular dysfunction.[11]

Transthoracic echocardiography is currently the principal imaging tool for the diagnostic evaluation of cardiomyopathy.[12] Two methods are used in echocardiography which are M-mode and two-dimensional echocardiography (2D-echo). M-mode echocardiography uses leading-edge to leading-edge principle as recommended by the American Society of Echocardiography.[13] 2D-echo uses method of discs with manual planimetry of the endocardial border in end-diastolic (largest frame) and end-systolic (smallest frame) frames.[14],[15]

2D-echo findings in DCM include LV dilatation (with or without right ventricular dilatation), myocardial thinning, and decreased systolic function in the form of reduced (LVEF <40%). Associated findings may include mitral or aortic regurgitation due to the change in the dimensions of valve annulus with resultant poor coaptation of the valve leaflets.[16],[17]

Various international cardiac associations have advocated the use of cardiac magnetic resonance (CMR) imaging as a gold-standard technique in the evaluation of cardiomyopathies.[18] Recent technical advances in magnetic resonance imaging (MRI) technology such as the development of high magnetic field strengths, surface coil channels, and improved post-processing techniques have catapulted CMR into the category of chief imaging tools for the assessment of cardiomyopathies.[19] Cine MRI helps in accurate measurement of cardiac chamber size, ventricular function, and regional wall motion abnormalities such as hypokinesia or dyskinesia and myocardial mass.[20] Contrast-enhanced imaging using fast gradient-echo sequences with a preparatory inversion pulse called as late gadolinium enhancement (LGE) technique are of immense value for the characterization of myocardial tissue including detection of focal myocardial disease (necrosis/fibrosis). The presence, location, and patterns of myocardial LGE provide crucial information regarding the characterization of DCM as some locations and patterns of LGE carry a poorer prognosis compared to others and warrant action.[21] LGE helps in deciding which patients can potentially benefit from prophylactic implantable cardioverter-defibrillator (ICD) placement to circumvent sudden cardiac death.[22]

The present study was aimed to evaluate idiopathic DCM patients using CMR, to assess the prevalence, locations, and various patterns of LGE in idiopathic DCM on CMR and comparatively assess echocardiography and CMR in the calculation of various LV volumetric variables.


  Methods Top


Study design and patient cohort

This was a prospective single-center study covering a 2-year study period. The study was approved by the Institutional Ethical Committee of our institution, and informed consent was obtained from all patients.

Patients suspected of having DCM on clinical evaluation and subsequently confirmed by the World Health Organization/International Society and Federation of Cardiology definition, based on reduced LVEF and elevated LV end-diastolic volume indexed to body surface area, compared to age- and sex-specific reference values were recruited in this study.[23] Among all potentially eligible patients (n = 161), patients with ischemic heart disease (defined as ≥50% luminal stenosis on invasive coronary angiography or noninvasive testing such as coronary computed tomography angiography), cardiomyopathy due to endocrinopathies, HIV-induced cardiomyopathy, stress-induced cardiomyopathy, infiltrative cardiomyopathy, hypertrophic cardiomyopathy, valvular disease, hypertensive heart disease, cardiomyopathy due to autoimmune diseases, alcohol- and drug-induced cardiomyopathy, and restrictive cardiomyopathy patients were excluded from the study.

Only 40 patients finally received a diagnosis of idiopathic DCM and were evaluated with contrast-enhanced CMR after preliminary echocardiography. CMR was performed within 2 weeks of preliminary echocardiographic study. Based on the results of CMR, five patients (with subendocardial or transmural pattern of enhancement or significant wall motion abnormalities) were subjected to conventional three vessel coronary angiography.

Examination techniques and imaging protocols

Echocardiography

All echocardiographic studies were performed on the Aloka ultrasonography system (Hitachi, Japan). M-mode and 2D echocardiography were performed by two experienced cardiologists.

M-mode echo, using leading-edge to leading-edge principle, calculated EF by cube method (end-diastolic volume [EDV] – end-systolic volume [ESV]/ESV where EDV (EDV = EDD3) and ESV (ESV = ESD3).[22]

2D-echo was performed by Simpson's biplane method of discs with manual planimetry of LV endocardial border in end-diastolic (largest) and end-systolic (smallest) frames.

A standardized protocol was performed with cross-sectional imaging of left ventricle immediately distal to mitral valve tips and apical two-dimensional imaging based on orthogonal 2- and 4-chamber views, and area tracings of the LV endocardial border in the apical 2- and 4-chamber views in both end-diastolic and end-systolic were used to calculate LVEF.[22],[23],[24]

Cardiac magnetic resonance imaging

All CMR studies were performed on 1.5 Tesla MR system (MAGNETOM Avanto, Siemens Medical System, Erlangen, Germany). After the preliminary localizing sequence, the imaging protocol included as follows:

  1. Turbo spin-echo (TSE) sequences for morphology
  2. Cine steady-state free precession (SSFP) sequences in 4-chamber long-axis and 2-chamber vertical long-axis and short-axis views for the estimation of ventricular volumes, function, and myocardial thickness. Breath-hold cine MR images were obtained using TR of 47.1 ms, TE of 1.57 ms, 256 × 176 matrix, and 240 mm × 340 mm field of view with slice thickness of 6 mm and an interslice gap of 20%
  3. Postcontrast dynamic perfusion imaging using balanced cine SSFP performed for the first-pass imaging of myocardium immediately after injection of contrast (gadolinium diamide-Omniscan, GE Healthcare) at doses of 0.1 mmol/kg using a power injector followed by 20 ml saline flush
  4. LGE imaging with T1-weighted inversion recovery TSE imaging was performed at 10–15 min following injection of 0.1 mmol/kg of contrast. The imaging parameters used were TR of 445 ms, TE of 1.22 ms, flip angle of 50°, 256 × 176 matrix, and a slice thickness of 8 mm with no interslice gap. An appropriate inversion time (TI) was chosen for each measurement to null the signal intensity of normal myocardium (250–360 ms) to clearly depict any abnormal delayed enhancement of myocardium.


The sequences were taken in short-axis, 2-chamber, and 4-chamber planes.

The basal short-axis view was taken just ahead of atrioventricular ring, and subsequent cines were taken in 1 cm steps toward LV apex. An average of 10 short-axis segments were taken to encompass the entire LV. Obtained data were then analyzed on a Siemens MR workstation. End-diastolic and end-systolic images were chosen as images having maximum and minimum LV diameters. Short-axis end-diastolic and end-systolic endocardial borders were traced manually for each slice, then multiplied by slice thickness, and finally added up to obtain EDV and ESV. EF was then calculated as EDV-ESV/EDV. Papillary muscles were excluded from the measurement, and care was taken not to include the left atrium in volumetry in end-systolic phase.

Coronary angiography

Conventional three-vessel coronary angiography was performed in selected patients (those with the ischemic pattern of enhancement and significant wall motion abnormalities on CMR) after taking proper consent for the invasive procedure.

Statistical analysis

Statistical analysis was performed using the Statistical Package for the Social Sciences (SPSS Inc., Chicago, IL, USA, version 21.0). Continuous variables were expressed as mean, ranges, and standard deviation, whereas categorical variables were expressed as counts and percentages. Two sample Student's t-test was used for comparison of continuous variables. P < 0.05 was considered statistically significant. Bland–Altman plot analysis was used to assess the agreement between different quantitative measurements.[25]


  Results Top


The study cohort included 27 (67.5%) males and 13 (32.5%) females. The mean age of the patients was 52.78 years with a range of 20–75 years.

Electrocardiogram findings

The most common electrocardiogram (ECG) finding was poor R-wave progression (15; 37.5%) followed by left bundle branch block (13; 32.5%) of patients. The ECG changes are summarized in [Table 1].
Table 1: Pattern of electrocardiogram findings in idiopathic DCM patients

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Contrast-enhanced CMR findings

  1. Prevalence of LGE: Absence of LGE was seen in 55% (22/40) of patients whereas 18/40 (45%) showed LGE [Figure 1]
  2. Location of LGE: Interventricular septal LGE was seen in 8 (20%) [Figure 2], free-wall LGE was seen in 4 (10%), and a concomitant septal and free-wall LGE was observed in 6 (15%)
  3. Patterns of LGE: Midwall enhancement was observed in 10 (25%) [Figure 2], subepicardial in 2 (5%), subendocardial in 4 (10%) [Figure 3], focal in 1 (2.5%), and 1 patient showed transmural enhancement. The ischemic pattern of enhancement including subendocardial and transmural enhancement did not correspond to any vascular territory, had no significant history or ECG feature consistent with myocardial infarction, and their coronary angiographic examination was normal.
Figure 1: Steady-state free precession cine images in 4-chamber (a), 2-chamber (b), and short-axis (c) views in a 52-year-old man with idiopathic DCM reveal dilated left ventricle which was hypokinetic. Corresponding LGE inversion recovery image in short axis (d) does not reveal any myocardial enhancement

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Figure 2: (a and b) Inversion recovery-prepared fast low-angle shot images in short-axis view in two different patients of idiopathic DCMshowing linear midwall myocardial enhancement (red arrows) in interventricular septum

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Figure 3: LGE inversion recovery-prepared fast low-angle shot images in 2-chamber (a) and short-axis (b) planes in a 48-year-old patient of idiopathic DCM showing subendocardial enhancement in posterior interventricular wall (red arrows). The patient was subjected to conventional angiography which was normal. LGE images in another patient of idiopathic DCM in short-axis (c) and 4-chamber (d) views revealing subendocardial enhancement in midinterventricular septum (red arrows) with normal subsequent coronary angiography

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Echocardiography and CMR volumetric findings

Mean LVEF calculated was 46.03% by M-mode echo, 38.92% by 2D-echo, and 37.58% by CMR. Values of EF obtained by M-mode echo were higher compared to 2D-echo and CMR in decreasing order of magnitude. The mean LVEF, LV-EDV, and LV-ESV from all the techniques are shown in [Table 2]. The maximum correlation in the measurement of LVEF was noted between CMR and 2D-echo values (P = 0.442) whereas mean LVEF values calculated by the M-mode echo and CMR were significantly different from each other (P < 0.05), demonstrated in Bland–Altman graphs in [Figure 4], [Figure 5], [Figure 6] and [Table 3].
Figure 4: Bland–Altman graph between two-dimensional echocardiography and M-mode echo for ejection fraction

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Figure 5: Bland–Altman graph between two-dimensional echocardiography and CMR for ejection fraction

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Figure 6: Bland–Altman graph between M-mode echo and CMR for ejection fraction

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Table 2: Comparison of volumetric measurements between M-mode echocardiography, 2D echocardiography, and CMR imaging

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Table 3: Mean difference, correlation coefficient, t-test, Bland-Altman limits, and total range of agreement (±1.96 standard deviation) for the comparison of ejection fraction between echo (M-mode and 2D) and CMR

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Mean EDV/ESV values were 185.5/132.3 ml by 2D-echo and 192.7/141.6 ml by CMR. Both EDV and ESV were underestimated by 2D-echo as compared to CMR. The EDV and ESV by 2D-echo and CMR revealed wide limits of agreement despite very good correlation (0.57 for EDV and 0.75 for ESV) as shown in [Table 4] and demonstrated in [Figure 7] and [Figure 8].
Figure 7: Bland–Altman graph between two-dimensional echocardiography and CMR for end diastolic volume

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Figure 8: Bland–Altman graph between two-dimensional echocardiography and CMR for end systolic volume

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Table 4: Mean difference, correlation coefficient, t-test, Bland-Altman limits, and range of agreement (±1.96 standard deviation) for the comparison between end-diastolic volume and end-systolic volume by echocardiography (two-dimensional) and CMR imaging

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  Discussion Top


CMR is the gold-standard investigation for the evaluation of ventricular morphology, chamber volumes, EF, and ventricular muscle thickness and muscle mass. CMR is not hampered by the poor acoustic windows, unlike echocardiography. In addition, CMR helps in the characterization of myocardial muscle which aids in the etiological diagnosis of cardiomyopathies.[10] Contrast-enhanced CMR referred to as LGE is the most valuable parameter to establish a proper diagnosis of cardiomyopathy.

Gadolinium-based contrast agents are extracellular contrast agents that do not permeate across an intact myocyte cell membrane.[26] The normal myocardium is composed of densely packed viable cells that do not allow entry of gadolinium chelates into the myocardial muscle. Thus, there is no appreciable enhancement of normal myocardium. However, in the setting of myocyte injury, there is disruption of cell membrane with consequent free entry of gadolinium chelates into the cells with resultant contrast enhancement. In chronic myocardial injury, there is replacement of myocytes with collagenous tissue leading to increased gadolinium uptake and hyperenhancement.[26] Ischemic cardiomyopathy is characterized by LGE in the subendocardial or transmural myocardium in a particular vascular territory. In contradiction, nonischemic cardiomyopathy is associated with midmyocardial or epicardial or subendocardial enhancement not following any vascular territory.[27] Therefore, the pattern of LGE furnishes important clues to the etiological diagnosis of cardiomyopathy. It has been reported that midwall myocardial fibrosis in DCM patients is a predictor of ventricular arrhythmias and sudden cardiac death.[27]

In the largest study of 874 idiopathic DCM patients till date, it was found that the presence of LGE is a major risk factor for adverse outcomes and the amount or extent of LGE does not determine the outcome as even a small amount of LGE predicted a substantial increase in risk. It was also found that location and pattern of LGE are equally important in determining the risk of sudden cardiac death as combined septal and free-wall enhancement is associated with the highest risk followed by septal enhancement and free wall has the least risk. Similarly, subepicardial and multiple patterns of LGE were more risky compared to midwall and focal patterns of LGE.[21]

In the current study, 40 patients of DCM were evaluated with echocardiography and contrast-enhanced CMRI.[28]

The patterns of LGE observed in the current study are in concordance with a study conducted by McCrohon et al. to differentiate heart failure related to CAD and DCM who found that of the DCM population, 59% had no enhancement thus helping differentiate DCM from CAD, whereas in 13% of patients, ischemic pattern of enhancement was seen who had normal coronary angiography.[28]

Wu et al. in a study to visualize the presence, location, and transmural extent of healed Q-wave and non-Q-wave infarcts performed 82 MRI examinations in three subgroups of patients consisting of patients with healed myocardial infarction, patients with nonischemic cardiomyopathy, and healthy volunteers and found that 91% of patients with infarcts imaged at 3 months and all of 19 patients imaged at 14 months showed myocardial hyperenhancement whereas none of the 20 patients with nonischemic cardiomyopathy or the 11 healthy volunteers showed hyperenhancement.[29]

Bello et al. in a gadolinium-enhanced cardiac MRI study of 45 patients with chronic stable heart failure found that 100% of patients with ischemic cardiomyopathy (n = 28) showed hyperenhancement whereas hyperenhancement was found in only 12% of patients with nonischemic cardiomyopathy and 88% of nonischemic patients did not show any enhancement.[30]

Taking coronary angiography as arbitrator, and considering the enhancement pattern, the clinical diagnosis in 12.5% of our DCM population – patients with ischemic pattern of enhancement was either partly or wholly incorrect, which has important therapeutic implications. These findings of the ischemic pattern of myocardial enhancement may be explained by the occurrence of recanalization of coronary arteries after an occlusive coronary event or embolization from an unstable but minimally stenotic atherosclerotic plaque which has been reported earlier.[31],[32] Thus, it may be possible that these patients are wrongly labeled as idiopathic DCM as they have a normal coronary angiography, but actually, the underlying cause of DCM lies in the unobstructed coronaries. This finding is also supported by autopsy studies in DCM, as demonstrated by Roberts et al. that visible scars were found in only 14% of patients with idiopathic DCM at necropsy.[33] However, virtually all patients with congestive heart failure and significant CAD demonstrate gross myocardial scarring at autopsy, even in those without clinical history of myocardial infarction, angina, or Q-waves.[34] The midwall enhancement seen in DCM probably reflects the focal segmental fibrosis at autopsy.[35],[36]

Mean LVEF calculated was 46.03% by M-mode echo, 38.92% by 2D-echo, and 37.58% by CMR. M-mode echo showed comparatively higher values of EF followed by 2D-echo and MRI. The maximum correlation in the measurement of LVEF was noted between CMR and 2D-echo values (P = 0.442) whereas M-mode echo and CMR-EF values were significantly different from each other (P < 0.05). The EDV and ESV calculated by 2D-echo and CMR revealed wide limits of agreement despite very good correlation (0.57 for EDV and 0.75 for ESV). Thus, the maximum agreement between various volumetric measurements was observed between 2D-echo and CMR.

Bellenger et al. in a study to compare LVEF and ventricular volumes in patients with chronic stable heart failure by M-mode echo, 2D-echo, radionuclide ventriculography, and CMR performed within 4 weeks of each other found that EF calculated by each technique was significantly different from all other techniques (P < 0.0001) except CMR and 2D-echo EF which were not significantly different. EF was overestimated by M-mode as compared to 2D-echo which in turn overestimated as compared to CMR.[37]

Gruszczyńska et al. found moderate-to-strong correlation between CMR and 2D-echo in the assessment of LV functions and mass in patients with heart failure.[38]

These results suggest that for the estimation of ventricular functions, no single method of assessment can be assumed to be universal. Echocardiography owing to its widespread availability is the most common used modality. However, it is dependent on certain geometric assumptions for the estimation of ventricular functions which do not hold valid in dilated hearts as they assume spherical shape with alteration of length and diameter of ventricle.[39] 2D-echo although less frequently used as compared to M-mode echo is comparatively more accurate method of assessment.[40] CMR by virtue of its unique ability to acquire high-resolution multiplanar images is not dependent on geometric assumptions for the calculation of ventricular functions. This has been further improved by the availability of sophisticated postprocessing software to calculate ventricular functions. Thus, a high accuracy and lack of any ionizing radiation make CMR the method of choice to calculate ventricular functions in DCM.


  Conclusion Top


CMR is an effective tool to study the phenotype of DCM and identify the presence, location, and patterns of enhancement which is prognostically important. LGE, an imaging surrogate of myocardial fibrosis, predisposes to conduction abnormalities, ventricular arrhythmias, and ventricular dysfunction. Identification of such patients and timely placement of a pacemaker or an ICD can prevent sudden cardiac death in these patients. In addition, CMR is the preferred technique in assessing the EF and volumetry in DCM patients because of its three-dimensional approach and lack of any geometric assumptions and least interobserver variation.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Ethical approval

The study was approved by the Institutional Ethical committee of Sher-i-Kashmir Institute of Medical Sciences, Srinagar under number SIMS-1-31/IEC-SKIMS/2014-67.

Authors' contributions

K.I, P.A, C.N, S.F and S.M conceptualized the study and collected and analyzed the data. P.A and K.I wrote the manuscript which was assisted by P.I. K.I, P.A and P.I performed statistical analysis. K.K performed the echocardiography and provided the clinical data.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
 
 
    Tables

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



 

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