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Cardiac Imaging |
1 From the Departments of Cardiology (Y.K., H.M., H.K., J.A., T.I.) and Radiology (H.H.), Ehime Prefectural Imabari Hospital, 4–5-5 Ishii-chou, Imabari, 794-0006, Ehime, Japan; Department of Radiology (T.M., S.N.) and Second Department of Internal Medicine (J.H.), Ehime University School of Medicine, Ehime, Japan; and Department of Biostatistics/Epidemiology and Preventive Health Sciences, School of Health Sciences and Nursing, University of Tokyo, Tokyo, Japan (M.N., Y.O.). From the 2002 RSNA Annual Meeting. Received March 22, 2003; revision requested June 13; final revision received July 27, 2004; accepted August 16. Address correspondence to Y.K. (e-mail: yasushi@koyamasan.com).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Ethics committee approval and informed consent were obtained. In 58 patients (51 men and seven women; mean age, 62 years ± 12 [standard deviation]) who had experienced an acute MI and undergone successful angioplasty, two-phase (acquisitions at 45 seconds and 7 minutes) contrast-enhanced CT was performed in the acute (mean interval between treatment and CT, 37 hours ± 4) and intermediate (mean interval, 28 days ± 4) periods and for long-term (mean interval, 12 months ± 4) follow-up. CT images were reviewed for an early perfusion defect (ED) at 45 seconds and for late enhancement (LE) and a residual perfusion defect (RD) at 7 minutes. Myocardial enhancement patterns and WT were assessed, and LV ejection fraction (LVEF) and percentage decrease in WT were calculated. The patient group was subdivided into three groups according to enhancement pattern: Group 1 included patients with LE but no ED or RD; group 2, patients with ED and LE but no RD; and group 3, patients with ED, LE, and RD. Fisher exact testing was used to measure categorical response. Paired and unpaired t tests were used for comparison between two groups (points); Tukey-Kramer multiple comparison and repeated-measures analysis of variance were used for comparisons between the three groups. P < .05 was considered to indicate a significant difference.
RESULTS: In group 3 (n = 36), WT in infarcted area was significantly reduced at the intermediate and long-term CT examinations (P < .001). At the intermediate and long-term examinations, percentage decrease in WT was greater in group 2 (n = 10) than in group 1 (n = 12) (P < .05 for intermediate and P < .001 for long-term examination) and was greatest in group 3 (P < .001 for both examinations). LVEF was poorest in group 3 and best in group 1.
CONCLUSION: Two-phase contrast-enhanced CT proved useful in predicting LV functional recovery and WT in patients who had experienced acute MI and undergone successful angioplasty.
© RSNA, 2005
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Because the prognosis of patients who have experienced an acute myocardial infarction (MI) depends on their myocardial reperfusion status, the assessment of microvascular flow after reperfusion therapy is of great importance.
Conventionally, myocardial perfusion is evaluated mainly by using nuclear imaging techniques (7,8). Contrast material–enhanced magnetic resonance (MR) imaging (9–12) and myocardial contrast echocardiography (13–15) are also common procedures that can be employed to assess myocardial perfusion. Electron-beam CT also provides reliable information on myocardial perfusion (16). In a case report, contrast-enhanced helical CT revealed an early myocardial perfusion defect and late enhancement in acute MI, and these findings agree with those observed at nuclear imaging and contrast-enhanced MR imaging (17), suggesting a possible use for contrast-enhanced helical CT in myocardial perfusion assessment.
The goal of this study was to investigate whether two-phase contrast-enhanced CT findings serve as predictors of changes in left ventricular function and wall thickness in patients who have experienced acute MI and have undergone successful reperfusion therapy.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Inclusion Criteria
Inclusion criteria consisted of the following:
1. The presence of typical symptoms of acute MI associated with ECG changes and a serum concentration of creatine kinase (CK) of more than twice the upper limit of normal with more than 5% of the isoenzyme CK-MB in the serum.
2. A first acute MI that was related to a single coronary artery.
3. Successful coronary angioplasty of the totally or subtotally occluded infarct-related artery (Thrombolysis in Myocardial Infarction [TIMI] grade 0 or 1) within 12 hours after the onset of chest pain. In brief, TIMI grade 0 perfusion indicates that there is no antegrade flow beyond the point of occlusion, grade 1 indicates minimal incomplete perfusion of a contrast medium around the clot, grade 2 (partial perfusion) indicates complete but delayed perfusion of the distal coronary bed with a contrast medium, and grade 3 (complete perfusion) indicates antegrade flow to the entire distal coronary bed at a normal rate.
4. Residual stenosis of less than 50% after angioplasty.
Exclusion Criteria
Exclusion criteria consisted of the following:
1. Renal failure (serum creatinine level > 1.5 mg/dL [132.6 µmol/L] and/or blood urea nitrogen level > 21 mg/dL [7.5 µmol/L]).
2. Restenosis of 50% or greater at coronary angiography during follow-up.
3. Inadequate CT imaging and/or cine angiographic results.
4. Lipid degeneration or calcification in the myocardium on non–ECG-gated 10-mm-thick plane scans obtained before the contrast-enhanced CT examination was performed.
Seven patients were excluded from the analysis because of the following reasons: Their cineangiograms were inadequate for evaluation of TIMI flow grade (n = 2), they had incomplete coronary recanalization (residual stenosis 
50% owing to distal embolization) (n = 1), restenosis was detected at coronary angiography during follow-up (n = 2), or their CT images were inadequate because of atrial fibrillation (n = 1) or body movement (n = 1).
Final Study Population
Therefore, this study is based on data from 58 evaluable patients (mean age, 62 years ± 12 [standard deviation]; age range, 39–84 years): 51 men (mean age, 62 years ± 11; age range, 39–83 years) and seven women (mean age, 66 years ± 14; age range, 46–84 years). According to results of unpaired t testing, there were no significant differences between the male and the female patients in terms of age. The left anterior descending artery was involved in 31 patients, the right coronary artery was involved in 23 patients, and the circumflex artery was involved in four patients. Fifty-seven patients (98%) underwent stent placement, and one patient (2%) underwent balloon angioplasty. Regarding the final TIMI grade, 56 patients (97%) had TIMI grade 3 reflow, and two patients (3%) had TIMI grade 2 reflow.
Study Protocol
Coronary angiography was performed in all 58 patients who underwent angioplasty. In the acute phase study, conventional left ventriculography was performed immediately after coronary angioplasty, which was performed by one of three cardiologists (T.I., H.M., and J.H., with 25, 23, and 30 years of clinical practice, respectively), to assess end-diastolic volume (EDV), end-systolic volume (ESV), and ejection fraction (EF). Two-phase contrast-enhanced CT was performed within 48 hours (mean interval, 37 hours ± 4) after direct angioplasty. In the intermediate phase study, both coronary angiography and left ventriculography were performed a mean of 27 days ± 3 after direct angioplasty, and two-phase contrast-enhanced CT was performed a mean of 28 days ± 4 after direct angioplasty. In the long-term study, two-phase contrast-enhanced CT was performed 12 months ± 4 after direct angioplasty. The biplanar angiographic system used for coronary angiography and conventional left ventriculography was an Integris V3000 (Philips Medical Systems, Best, the Netherlands). A Cardio 500 analysis system (Kontron Electronik, Munich, Germany) was used for performing quantitative coronary angiography and assessing cardiac function. During the infusion of the contrast medium (Optiray [320 milligrams of iodine per milliliter]; Yamanouchi, Tokyo, Japan) at a rate of 8 mL/sec to a total of 35 mL, biplanar images were obtained at a filming rate of 30 images per second.
Two-Phase Contrast-enhanced CT
The helical CT scanner used was a single–detector row Proceed SA (GE-Yokogawa Medical Systems, Tokyo, Japan) with a gantry rotation speed of 0.8 second. Patients were asked to lie supine on the CT table and inhale oxygen at a rate of 3 L/min while the scanning parameters were prepared.
The scanning protocol was based on that used in a previous study involving electron-beam CT (16) and was as follows: Nonionic iodinated contrast medium (iopamidol, Iopamiron [300 milligrams of iodine per milliliter]; Nihon Schering, Osaka, Japan) was intravenously administered at a rate of 1.5 mL/sec for the first acquisition for the early image. The early image was obtained 45 seconds after the start of contrast medium administration; the same contrast medium was then infused at a rate of 0.1 mL/sec for the second acquisition for the late image. The late image was obtained 7 minutes after the start of contrast medium administration; a total of 150 mL of the contrast medium was used (Fig 1). The ECG trace was recorded during scanning so that we could determine triggers and identify the diastolic image data set. Patients were asked to hold their breath during whole-heart scanning. Scanning parameters were as follows: collimation, 3 mm; table feed, 3 mm per rotation; and number of rotations, 40 (at a rate of 12 cm every 32 seconds). The tube current and voltage were 200 mA and 140 kV, respectively.
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The diastolic image data set, which was extracted with reference to the R wave of the recorded ECG trace, was used to assess myocardial enhancement pattern and wall thickness. The 3-mm-thick cardiac short-axis images were reconstructed by using the double-oblique method (Fig 2). All measurements were performed by using a ZIO-M900 workstation (ZIO Software, Tokyo, Japan).
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We defined a myocardial perfusion defect (a dark zone) on the early-phase images (those obtained 45 seconds after contrast material administration) as an early perfusion defect, the presence of smaller dark regions in the subendocardium surrounded by partially enhanced myocardium on the late-phase images (those obtained 7 minutes after contrast material administration) as a residual perfusion defect, and the presence of an enhanced zone on the late-phase images as late enhancement.
Regions of interest were created for one-third of the area of each finding (early perfusion defect, residual defect, and late enhancement) and were placed over the center of each area. A region of interest of the same size, which was at least greater than 50 mm2, was also placed over a remote noninfarcted area on the opposite side of the infarct-related area so that we could measure the mean attenuation. This was performed by the same four investigators (T.I., Y.K., H.H., and T.M.) working in consensus.
Enhancement Patterns
Several enhancement patterns theoretically exist; however, all enhancement could actually be classified into one of the following three patterns: group 1, in which there is an absence of early perfusion defect in the early phase and a presence of late enhancement without residual perfusion defect in the late phase; group 2, in which there is a presence of early perfusion defect in the early phase and a presence of late enhancement without residual perfusion defect in the late phase; and group 3, in which there is a presence of early perfusion defect in the early phase and a presence of both late enhancement and residual perfusion defect in the late phase (Fig 3).
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In the long-term study, a scar was defined according to published criteria based on autopsy data (19). If the myocardial segment was thin on the early-phase images (wall thickness, <6 mm), the patient was given a diagnosis of transmural scar formation.
Analysis of Conventional Coronary Angiographic and Left Ventriculographic Results
All patient-identifying information on the coronary angiograms was obscured; the angiograms were then randomized. Two cardiologists (H.M. and H.K., with 23 and 14 years of clinical practice, respectively), who were blinded to patient clinical outcome, classified in simultaneous consensus the antegrade contrast material flow in the infarct-related artery on the final coronary angiograms according to the criteria established by the TIMI study group. All patient-identifying information on the conventional left ventriculograms was obscured; the ventriculograms were then randomized. Two observers (J.H. and J.A., with 30 and 14 years of clinical practice, respectively) measured EDV and ESV and calculated the left ventricular EF by using the area-length method (20) and working in consensus.
Determination of Peak CK Level and CK-MB Fraction
Immediately after reperfusion therapy, blood was collected every 4 hours, and J.A. determined the maximum values of serum CK and the isoenzyme CK-MB.
Determination of Ischemic Time
Ischemic time was measured by J.A. and was defined as the interval from the onset of the symptoms to the time at which the first balloon inflation was performed.
Statistical Analysis
All data are expressed as means ± standard deviations. The Fisher exact test was used for comparing the frequencies of sex and culprit artery among the groups (group 1, group 2, and group 3). The Tukey-Kramer multiple comparison test was used for comparing age among the groups. An unpaired t test was used for comparing mean CT values in regions of interest of noninfarcted area, and the Tukey-Kramer multiple comparison test was used for comparing CT values between three areas (the region of interest of the noninfarcted area, the region of interest of the late enhancement area, and the region of interest of the residual perfusion defect area). The Tukey-Kramer multiple comparison test was also used for comparing ages, CK levels, CK-MB fractions, and ischemic time between the groups.
A paired t test was used for two-point comparisons (between the acute and the intermediate phase study) of EDV, ESV, and EF in each group. The Tukey-Kramer multiple comparison test was also used for group comparisons of EDV, ESV, and EF at two points (the acute and intermediate phase studies).
Regarding the wall thickness of the noninfarcted area, repeated analysis of variance measurement of groups, time points (the acute phase, intermediate phase, and long-term studies), and their interaction terms was performed. As a covariance structure among the time points, compound symmetry was assumed and robust variance was used.
Regarding the wall thickness of the infarcted area, heterogeneity among individuals in the degree of damage due to infarction was expected, so we used the wall thickness at the acute phase study as an adjusting factor; repeated-measures analysis of variance with groups, time points (the intermediate phase and long-term studies), and their interaction terms was then performed. As a covariance structure among the time points, compound symmetry was assumed and robust variance was used.
The Tukey-Kramer multiple comparison test was used for group comparisons of percentage decrease in wall thickness at two points (the intermediate phase and long-term studies). A paired t test was used for two-point comparisons (between the intermediate phase and the long-term study) of percentage decrease in wall thickness in each group. P < .05 was considered to indicate a statistically significant difference. The statistical analyses were performed by using SAS version 8.2 (SAS Institute, Cary, NC).
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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EDV, ESV, and EF in Acute and Intermediate Phase Studies: Intra- and Intergroup Comparisons
In group 1, between the time of the acute phase and the time of the intermediate phase study, the EDV did not change significantly (value at acute phase study, 129 mL ± 24; value at intermediate phase study, 121 mL ± 29 [P = .069]), the ESV decreased (value at acute phase study, 51 mL ± 11; value at intermediate phase study, 28 mL ± 8 [P < .001]), and the EF improved (value at acute phase study, 60% ± 11; value at intermediate phase study, 76% ± 8 [P < .001]). In group 2, EDV, ESV, and EF did not change significantly: EDV decreased from 122 mL ± 24 to 115 mL ± 26, ESV decreased from 46 mL ± 12 to 43 mL ± 14, and EF increased from 62% ± 7 to 63% ± 8. In group 3, EDV increased from 121 mL ± 35 to 148 mL ± 37 (P < .001), ESV increased from 44 mL ± 21 to 72 mL ± 30 (P < .001), and EF decreased from 64% ± 11 to 52% ± 13 (P < .001). In the acute phase study, no significant differences were noted in EDV, ESV, or EF among the three groups.
In the intermediate phase study, the EDV in group 3 was the largest among the three groups (P < .05), the ESVs in groups 1 and 2 were smaller than the ESV in group 3 (P < .001 and P < .01, respectively), and the EF in group 1 was higher than that in group 3 (P < .001) and group 2 (P < .05). The EF in group 2 was higher than that in group 3 (P < .05).
Wall Thickness and Percentage Decrease in Wall Thickness
The wall thickness values in the noninfarcted area at three time points—the acute phase, intermediate phase, and long-term studies, respectively—were 12.0 mm ± 1.7, 12.2 mm ± 1.7, and 11.8 mm ± 1.7 in group 1; 11.0 mm ± 1.7, 11.1 mm ± 1.6, and 11.0 mm ± 1.7 in group 2; and 11.5 mm ± 2.1, 11.5 mm ± 2.0, and 11.2 mm ± 1.8 in group 3. There were no significant differences between the time points (P = .058), the groups (P = .330), or their interactions (P = .181) according to results of repeated-measures analysis of variance.
The wall thickness values in the infarcted area at three time points—the acute phase, intermediate phase, and long-term studies, respectively—were 11.7 mm ± 1.3, 11.6 mm ± 1.3, and 11.6 mm ± 1.5 in group 1; 11.1 mm ± 2.1, 9.1 mm ± 1.7, and 8.1 mm ± 1.7 in group 2; and 11.1 mm ± 1.9, 6.1 mm ± 1.7, and 4.8 mm ± 1.5 in group 3. There were no significant differences (P = .657) in wall thickness at the acute phase study among the groups. However, according to results of repeated-measures analysis of variance, there were significant differences within each group (P < .001) and among time points (P = .001), their interactions (P < .001), and adjusting factors (P = .001).
In group 3, 21 patients (58%) with transmural early perfusion defect were found to have scar formation. Figure 5 shows typical images obtained at the long-term study (in the same patients as in Fig 4) in these three groups.
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In terms of percentage decrease in wall thickness of the infarcted areas, there were no significant differences between group 1 and group 2 at the intermediate phase and long-term studies. The percentage decrease in wall thickness in group 3 at the long-term study was greater than that at the intermediate phase study (P < .001).
At the intermediate phase study, the percentage decrease in wall thickness of the infarcted areas in group 1 (0.4% ± 1.7) was the lowest among the three groups (group 2: 17.6% ± 9.8, P < .05; group 3: 44.4% ± 15.9, P < .001). The percentage decrease in wall thickness in group 3 was greater than that in group 2 (P < .001).
At the long-term study, the percentage decrease in wall thickness in group 3 (56.1% ± 4.2) was the highest among the three groups (group 1: 0.9% ± 3.6, P < .001; group 2: 26.5% ± 10.7, P < .001). The percentage decrease in wall thickness in group 2 was greater than that in group 1 (P < .001).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Although revascularization of the epicardial coronary arteries (improvement of TIMI grade flow) is necessary for the myocardium to be salvaged, this is not enough to ensure myocardial recovery. That is, successful revascularization of epicardial coronary arteries is not equal to successful reperfusion at the microvascular level. In this study, we detected three enhancement patterns among the 56 patients with TIMI grade 3 flow; the variability in enhancement pattern indicates that there is variability in the extent of microvascular damage. The least extensive recovery of left ventricular function was observed in patients who had both an early and a residual perfusion defect, namely, those in group 3. That is, they might not have complete reperfusion at the microvascular level, while those patients who did not have an early or a residual perfusion defect (group 1) might experience a complete recovery of left ventricular function, which might be indicative of successful reperfusion at both the epicardial and the microvascular level.
Importance of an Early Defect
Contrast medium is thought to reach the microvascular bed in the early phase after intravenous administration. A study involving electron-beam CT (16) revealed that myocardial enhancement in the early phase reflected the volume of the vascular bed.
Reduced signal intensity on first-pass contrast-enhanced MR images has been shown to indicate reduced blood flow (28). Therefore, an early perfusion defect observed by using CT would also reflect a decrease in the volume of the vascular bed—that is, a decrease in the myocardial blood flow.
Using an experimental infarct-reperfusion model in dogs, Braunwald and Kloner (29) classified the condition of myocardial tissue into four layers beginning from the endocardial side. The first layer corresponded to a viable and very thin myocardium that received oxygen directly from the left ventricle; the second layer, to myocardial necrosis with extensive capillary (microcirculation) disorder; the third layer, to myocardial necrosis in which blood supply was preserved to some extent; and the fourth layer, to stunned myocardium that had escaped necrosis. The early perfusion defect in our study may correspond to the second and third layers—that is, to tissue with moderate to severe microvascular damage and myocardial necrosis—because the wall thickness in groups 2 and 3 had significantly decreased. In particular, 21 (58%) patients with a transmural early perfusion defect in group 3 developed myocardial scar formation about 12 months after reperfusion therapy. Our findings are supported by the results of an MR imaging–based study, which showed that 68% of patients with microvascular obstruction in the postinfarction period had a thinning of the ventricular wall consistent with scar formation at 6 months (30).
Importance of Residual Defect and Late Enhancement
After the contrast medium reaches the microvascular bed, it gradually flows into the interstitium (extracellular space), stays there, and is then washed out slowly. Therefore, myocardial enhancement in the late phase mainly reflects the characteristics of the interstitium—that is, the volume of the interstitial space (16). When myocardial cells are damaged and the cell number decreases after an acute MI, the volume of the interstitial space increases.
In the present study, when a residual perfusion defect was detected, as it was in group 3, functional recovery was not observed. However, when an early perfusion defect turned into late enhancement, as happened in group 2, deterioration of left ventricular function was minimal or less than that observed in group 3. We speculate that the area of residual perfusion defect might correspond to the second layer (myocardial necrosis with extensive capillary disorder) of the Braunwald classification and that late enhancement might correspond to the third layer, where blood supply is preserved to some degree, indicating possible residual myocardial viability.
In this study, the percentage decrease in wall thickness in group 3 was significantly greater than that in group 2—that is, the residual perfusion defect in group 3 indicated that there was less antegrade microvascular flow beyond the point of microvascular obstruction in group 3 than in group 2. As a result of incomplete perfusion at the microvascular level, the percentage decrease in wall thickness in group 3 was greater than that in group 2 in the intermediate phase and long-term studies.
Given our results, we may conclude that a residual perfusion defect indicated a necrotic area caused by severe microvascular obstruction—the so-called no-reflow phenomenon (31) that is caused by the presence of red blood cells and necrotic debris (32) in the "wavefront" of ischemic necrosis (33,34).
In general, there is a consensus that delayed hyperenhancement at MR imaging reflects nonviable myocardium (30). However, other studies involving humans revealed that 3–5 days after a reperfused MI, some regions of enhancement recovered function 3 months later (10,35). In our study, late enhancement was also observed in both group 1 and group 2, indicating that the area of late enhancement includes viable myocardium, at least in part, at examinations performed within 48 hours of reperfusion therapy. An MR imaging–based study in rats that involved occluding the coronary artery for 30 minutes and for 2 hours revealed that the enhanced zone was time dependent (ie, it decreased in size over time), and the true infarct size corresponded to the enhancement size at 21 minutes ± 4 (36). On late images, which were acquired 7 minutes after the start of the administration of the contrast medium in that study, the true infarct size might have be overestimated; however, the contrast medium had been slowly injected at 0.1 mL/sec (to a total of 37.5 mL) after the bolus injection at 1.5 mL/sec (to a total of 112.5 mL). The total dose and injection rate of the bolus and/or the continuous injection of the contrast medium might have had an effect on the size of the enhancing lesion, although these factors were not investigated in that study.
After successful reperfusion therapy, both the wall thickness and the microvasculature change dynamically during the acute healing stage. Therefore, in the clinical setting, we assume that the timing of the CT examination after reperfusion therapy is important in assessing late enhancement with contrast-enhanced CT.
However, this concept of these enhancement patterns and their combinations at CT has not attained wide acceptance, and because CT can also help define the depth and extent of early and residual perfusion defects and late enhancement, the sizes of these parameters in comparison with the infarct size should be investigated in future studies.
Study Limitations
In this study, because the images were read concurrently by four observers and we could not compare interobserver and intraobserver agreement, interobserver and intraobserver reliabilities were not confirmed.
Regarding the x-ray exposures during two-phase contrast-enhanced CT, the radiation dose for one acquisition was 9.4 mGy. In our protocol, we performed three two-phase contrast CT studies, for a radiation dose of 18.8 mGy for each study and a total of 56.4 mGy, which does not include the fluoroscopy dose at angioplasty and angiography. Although x-ray exposure dose was high in this study, our results suggest that if two-phase contrast-enhanced helical CT was performed once within 48 hours after reperfusion therapy, the enhancement patterns could be evaluated and these enhancement patterns would serve to predict left ventricular function and wall thickness, while the x-ray exposure at this examination would be 18.8 mGy—exactly the same exposure incurred when nonoverlapping reconstructions are used. Additionally, the exposed range (12 cm) for a two-phase cardiac CT examination is smaller than that for a three-phase abdominal CT examination. Therefore, when one considers the useful information obtained from the myocardial studies, the radiation dose seems to be acceptable for patients with heart disease that may threaten their lives.
In conclusion, in patients with acute MI, the myocardial enhancement pattern at two-phase contrast-enhanced CT performed after reperfusion therapy can serve as a predictor of left ventricular functional recovery and wall thickness.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Authors stated no financial relationship to disclose.
Author contributions: Guarantors of integrity of entire study, Y.K., T.M., T.I., J.H.; study concepts and design, Y.K., T.M., T.I., J.H.; literature research, Y.K., H.M., T.M., H.H., H.K., T.I., J.H.; clinical studies, Y.K., H.M., T.M., H.H., H.K., S.N., J.A., T.I., J.H.; experimental studies, Y.K., T.M., S.N., J.A., T.I., J.H.; data acquisition, Y.K., H.M., T.M., H.H., H.K., J.A.; data analysis/interpretation, Y.K., T.M., H.H., H.K., T.I., J.H.; statistical analysis, Y.O., M.N., Y.K.; manuscript preparation, Y.K.; manuscript definition of intellectual content, Y.K., T.M.; manuscript editing and final version approval, all authors; manuscript revision/review, Y.K., T.M., T.I., M.N., Y.O., J.H.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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