Background
Few studies assessed myocardial inflammation using Cardiovascular Magnetic Resonance Imaging in Kawasaki disease (KD) patients.
Purpose
To quantify myocardial edema in KD patients using T2 ...mapping and explore the independent predictors of T2 values.
Study Type
Prospective.
Subjects
Ninety KD patients including 40 in acute phase (26 males, 65.0%) and 50 in chronic phase (34 males, 68.0%). Thirty‐one healthy volunteers (21 males, 70.0%).
Field Strength/Sequence
3.0 T T2‐weighted Turbo Spin Echo‐Short Time of Inversion Recovery sequence, True fast imaging with steady precession flash sequence and fast low‐angle shot 3D spoiled gradient echo sequence.
Assessment
T2 values were compared among KD groups and controls.
Statistical Test
Student's t test and Fisher's exact test; One‐way analysis of variance; Pearson correlation analysis; Receiver operating curve analysis; Multivariable linear regression.
Results
Global T2 value of KD patients in acute phase was the highest, followed by those of chronic‐phase patients and controls (38.83 ± 2.41 msec vs. 37.55 ± 2.28 msec vs. 36.05 ± 1.64 msec). Regional T2 values showed a same trend. There were no significant differences in global and regional T2 values between KD patients with and without coronary artery (CA) dilation, no matter in acute or chronic phase (all KD patients: P = 0.51, 0.51, 0.53, 0.72; acute KD: P = 0.61, 0.37, 0.33, 0.83; chronic KD: P = 0.65, 0.79, 0.62, 0.79). No significant difference was observed in global T2 values between KD patients with Z score > 5.0 and 2.0 < Z score ≤ 5.0 (P = 0.65). Multivariate analysis demonstrated that stage of disease (β = −0.123) and heart rate (β = 0.280) were independently associated with global T2 values.
Data Conclusion
The degree of myocardial edema was more severe in acute‐phase than in chronic‐phase KD patients. Myocardial edema persists in patients regardless of the existence or degree of CA dilation.
Evidence Level
2
Technical Efficacy
Stage 2
Background
Obesity is highly prevalent in patients with hypertrophic cardiomyopathy (HCM) and believed to influence its phenotype.
Purpose
To explore the effects of obesity on left ventricular (LV) ...remodeling and long‐term clinical course in Chinese patients with HCM.
Study Type
Longitudinal.
Population
A total of 247 patients with HCM classified according to body mass index (BMI) (normal weight: BMI = 18.0–22.9 kg/m2 N = 90; overweight: BMI = 23.0–24.9 kg/m2 N = 58; and obese: BMI ≥ 25 kg/m2 N = 99).
Field Strength/Sequence
3.0 T/Balanced steady‐state free precession sequence and phase‐sensitive inversion recovery late gadolinium enhancement (LGE) sequence.
Assessment
LV function and geometry were measured. LV peak strain analysis was performed. The presence and percentage of LGE in the LV were recorded. The endpoints including heart failure, sudden cardiac death, and overall composite outcome were assessed during a median follow‐up of 4.1 years (interquartile range, 3.0–6.2 years).
Statistical Tests
One‐way analysis of variance, Kruskal–Wallis test, or chi‐square test; Pearson correlation coefficient (r); multivariable linear regression analysis; Kaplan–Meier survival analysis; and Cox proportional hazards model analysis were conducted. A two‐tailed P‐value < 0.05 was considered statistically significant.
Results
Obese patients exhibited a significant progressive increase in LV mass compared with normal‐weight patients. The magnitude of all LV strain indices gradually and significantly decreased as BMI increased, whereas LV ejection fraction was not significantly different among BMI groups (P = 0.364). Multivariable linear regression analysis showed that obesity had a significant association with impaired strain indices as well as with indexed LV mass. Multivariable Cox model analysis retained obesity as an independent marker for future endpoints, and conveyed a > 3‐fold increase in risk compared with patients with normal weight (hazard ratio, 3.04; 95% confidence interval, 1.07–6.57).
Data Conclusion
Obesity is an important environmental modifier that is associated with adverse LV remodeling and is independently associated with future clinical outcomes in Chinese patients with HCM.
Level of Evidence
3
Technical Efficacy
Stage 2
Background
The majority of heart failure (HF) in hypertrophic cardiomyopathy (HCM) manifests as a phenotype with preserved left ventricular (LV) ejection fraction; however, the exact contribution of ...left atrial (LA) phasic function to HF with preserved ejection fraction (HFpEF) in HCM remains unresolved.
Purpose
To define the association between LA function and HFpEF in HCM patients using cardiac magnetic resonance imaging (MRI) feature tracking.
Study Type
Retrospective.
Population
One hundred and fifty‐four HCM patients (HFpEF vs. non‐HF: 55 34 females vs. 99 43 females).
Field Strength/Sequence
3.0 T/balanced steady‐state free precession.
Assessment
LA reservoir function (reservoir strain εs, total ejection fraction EF), conduit function (conduit strain εe, passive EF), booster‐pump function (booster strain εa and active EF), LA volume index, and LV global longitudinal strain (LV GLS) were evaluated in HCM patients.
Statistical Tests
Chi‐square test, Student's t‐test, Mann–Whitney U test, multivariate linear regression, logistic regression, and net reclassification analysis were used. Two‐sided P < 0.05 was considered statistically significant.
Results
No significant difference was found in LV GLS between the non‐HF and HFpEF group (−10.67 ± 3.14% vs. −10.14 ± 4.01%, P = 0.397), whereas the HFpEF group had more severely impaired LA phasic strain (εs: 27.40 22.60, 35.80 vs. 18.15 11.98, 25.90; εe: 13.80 9.20, 18.90 vs. 7.95 4.30, 14.35; εa: 13.50 9.90, 17.10 vs. 7.90 5.40, 14.15). LA total EF (37.91 29.54, 47.94 vs. 47.49 39.18, 55.01), passive EF (14.70 7.41, 21.49 vs. 18.07 9.32, 24.78), and active EF (27.19 17.79, 36.60 vs. 36.64 26.63, 42.71) were all significantly decreased in HFpEF patients compared with non‐HF patients. LA reservoir (β = 0.90 0.85, 0.96), conduit (β = 0.93 0.87, 0.99), and booster (β = 0.86 0.78, 0.95) strain were independently associated with HFpEF in HCM patients. The model including reservoir strain (Net Reclassification Index NRI: 0.260) or booster strain (NRI: 0.325) improved the reclassification of HFpEF based on LV GLS and minimum left atrial volume index (LAVImin).
Data Conclusion
LA phasic function was severely impaired in HCM patients with HFpEF, whereas LV function was not further impaired compared with non‐HF patients.
Level of Evidence
4
Technical Efficacy
Stage 3
Cardiac MRI feature-tracking (FT) with breath-holding (BH) cine balanced steady state free precession (bSSFP) imaging is well established. It is unclear whether FT-strain measurements can be reliably ...derived from free-breathing (FB) compressed sensing (CS) bSSFP imaging.
To compare left ventricular (LV) strain analysis and image quality of an FB CS bSSFP cine sequence with that of a conventional BH bSSFP sequence in children.
Prospective.
40 children able to perform BHs (cohort 1 12.1 ± 2.2 years) and 17 children unable to perform BHs (cohort 2 5.2 ± 1.8 years).
3T, bSSFP sequence with and without CS.
Acquisition times and image quality were assessed. LV myocardial deformation parameters were compared between BH cine and FB CS cine studies in cohort 1. Strain indices and image quality of FB CS cine studies were also assessed in cohort 2. Intraobserver and interobserver variability of strain parameters was determined.
Paired t-test, Wilcoxon signed-rank test, intraclass correlation coefficient (ICC), and Bland-Altman analysis. A P-value <0.05 was considered statistically significant.
In cohort 1, the mean acquisition time of the FB CS cine study was significantly lower than for conventional BH cine study (15.6 s vs. 209.4 s). No significant difference were found in global circumferential strain rate (P = 0.089), global longitudinal strain rate (P = 0.366) and EuroCMR image quality scores (P = 0.128) between BH and FB sequences in cohort 1. The overall image quality score of FB CS cine in cohort 2 was 3.5 ± 0.5 with acquisition time of 14.7 ± 2.1 s. Interobserver and intraobserver variabilities were good to excellent (ICC = 0.810 to 0.943).
FB CS cine imaging may be a promising alternative technique for strain assessment in pediatric patients with poor BH ability.
1 TECHNICAL EFFICACY: Stage 1.
Background
Understanding the impact of aortic regurgitation (AR) on hypertensive patients' hearts is important.
Purpose
To assess left ventricular (LV) strain and structure in hypertensive patients ...and investigate the relationship with AR severity.
Study Type
Retrospective.
Population
263 hypertensive patients (99 with AR) and 62 controls, with cardiac MRI data.
Field Strength/Sequence
Balanced steady‐state free precession (bSSFP) sequence at 3.0T.
Assessment
AR was classified as mild, moderate, or severe based on echocardiographic findings. LV geometry was classified as normal, concentric remodeling, eccentric hypertrophy, or concentric hypertrophy based on MRI assessment of LV mass/volume ratio and LV Mass index (LVMI). LV global radial peak strain (GRPS), global circumferential peak strain (GCPS), and global longitudinal peak strain (GLPS) were obtained by post‐processing bSSFP cine datasets using commercial software.
Statistical Tests
ANOVA, Kruskal–Wallis test, Spearman's correlation coefficients (r), chi‐square test, and multivariable linear regression analysis. A P value <0.05 was considered statistically significant.
Results
Hypertensive patients with AR had significantly lower LV myocardial strain and higher LVMI than the group without AR (GRPS 26.25 ± 12.23 vs. 34.53 ± 9.85, GCPS −17.4 ± 5.84 vs. −20.57 ± 3.57, GLPS −9.86 ± 4.08 vs. −12.95 ± 2.94, LVMI 90.56 ± 38.56 vs.58.84 ± 17.55). Of the 99 patients with AR, 56 had mild AR, 26 had moderate AR and 17 had severe AR. The degree of AR was significantly negatively correlated to the absolute values of LV GRPS, GCPS and GLPS (r = −0.284 – −0.416). LV eccentric hypertrophy increased significantly with AR severity (no AR 21.3%, mild AR 42.9%, moderate AR 73.1%, severe AR 82.4%). In multivariable analysis, the degree of AR was an independent factor affecting LV global strain and LVMI even after considering confounding factors (β values for global myocardial strain were −0.431 to −0.484, for LVMI was 0.646).
Data Conclusion
Increasing AR severity leads to decreased cardiac function and worse ventricular geometric phenotypes in hypertensive patients.
Level of Evidence
4
Technical Efficacy
Stage 3
Background
Mitral regurgitation (MR) is a comorbidity of myocardial infarction (MI), which may promote the incidence of adverse cardiovascular clinical events. However, it is not yet completely ...understood how MR in MI patients is associated with impaired myocardial deformation.
Purpose
To determine the damaging myocardium effects of MR in MI patients in terms of the global peak strain (PS) and left ventricular (LV) function, and evaluate the independent risk factors impacting LV deformation after MI.
Study type
Retrospective.
Population
One hundred eighty‐six MI patients (17.7% female) and 84 normal control subjects (27.4% female).
Field strength/sequence
3.0T; late gadolinium enhancement sequence, balanced steady‐state free precession.
Assessment
LV function and LV global PS (global radial peak strain GRPS; global circumferential peak strain GCPS; and global longitudinal peak strain GLPS) were compared among normal controls, MI without MR (MR−) and MI with MR (MR+, mild, moderate, severe) patients.
Statistical Tests
One‐way analysis of variance (ANOVA) test, Mann–Whitney U test, Kruskal–Wallis test, and multiple linear regressions were used. A P value <0.05 indicated statistically significant difference (two‐tailed).
Results
The MI (MR+) patients showed significantly lower LV global PS than both MI (MR−) and control groups in three directions (GRPS 16.66 ± 7.43%; GCPS −11.27 ± 4.27%; GLPS −7.75 ± 3.44%), and significantly higher LV end‐systolic (128.85 87.91, 188.01 mL) and end‐diastolic volumes (210.29 164.07, 264.00 mL) and significantly lower LV ejection fraction (38.23 ± 13.02%). Multiple regression analysis demonstrated that MR was independently associated with LV GCPS (β = −0.268) and GLPS (β = −0.320). LV infarct size was an independent indicator of LV GRPS (β = −0.215) and GCPS (β = −0.222). LV end‐diastolic volume was an independent indicator of LV GRPS (β = −0.518), GCPS (β = −0.503), and GLPS (β = −0.331).
Data Conclusion
MR may further exacerbate the reduction of LV global peak strains and function. The MR, infarct size, and LV end‐diastolic volume can be used as independent association indicators for LV global PS in MI (MR+) patients.
Level of Evidence: 4
Technical Efficacy Stage: 2
TOC Category: Chest.
Background
Type 2 diabetes mellitus (T2DM) and obesity often coexist and together contribute to left atrial (LA) functional abnormalities. However, little is known about the impact of body mass index ...(BMI) on LA strains measured using cardiac magnetic resonance feature tracking (MR‐FT).
Purpose
To investigate the additive effect of BMI on LA functional remodeling using MR‐FT as well as to explore abnormal atrioventricular interaction in T2DM patients.
Study Type
Retrospective.
Population
One hundred and fifty‐nine T2DM patients (53, 34, and 72 normal‐weight, overweight, and obese individuals) and 105 non‐diabetic controls (46, 32, and 27 normal‐weight, overweight, and obese individuals).
Field Strength/Sequence
3.0 T/balanced steady‐state free precession.
Assessment
LA reservoir strain (εs), conduit strain (εe), and active strain (εa) and their corresponding strain rates (SRs, SRe, SRa) were measured together with left ventricular (LV) radial, circumferential, and longitudinal peak strain, peak systolic strain rate, and peak diastolic strain rate.
Statistical Tests
Student's t‐test or Mann–Whitney U test, one‐way ANOVA, univariate and multivariate linear regression. A P value <0.05 was considered statistically significant.
Results
Compared to controls in the same BMI category, T2DM patients had significantly decreased reservoir and conduit function, while pump function was not significantly different (εa and SRa: P = 0.757 and 0.583 for normal‐weight, P = 0.171 and 0.426 for overweight, P = 0.067 and 0.330 for obese). LA strains were significantly correlated with BMI (r = −0.346 for εs, −0.345 for εe) in T2DM patients. Multivariable linear regression analysis indicated that BMI was independently associated with LA εs and εe, LV global longitudinal strain was independently associated with LA εs and εa, and LV circumferential peak diastolic strain rate was independently associated with LA εe.
Data Conclusion
These findings suggest that the coexistence of increased body weight and T2DM patients can exacerbate the impairment of LA strains and indicate abnormal atrioventricular interactions.
Level of Evidence
3
Technical Efficacy
Stage 3
Myocardial fibrosis is being increasingly recognised as a common final pathway of a wide range of diseases. Thus, the development of an accurate and convenient method to evaluate myocardial fibrosis ...is of major importance. Although T1 mapping is a potential alternative for myocardial biopsy, validation studies are limited to small numbers and vary regarding technical facets, and include only a restricted number of disease. A systematic review and meta-analysis was conducted to objectively and comprehensively evaluate the performance of T1 mapping on the quantification of myocardial fibrosis using cardiovascular magnetic resonance (CMR).
PubMed, EMBASE and the Cochrane Library databases were searched for studies applying T1 mapping to measure myocardial fibrosis and that validated the results via histological analysis. A pooled correlation coefficient between the CMR and histology measurements was used to evaluate the performance of the T1 mapping.
A total of 15 studies, including 308 patients who had CMR and myocardial biopsy were included and the pooled correlation coefficient between ECV measured by T1 mapping and biopsy for the selected studies was 0.884 (95% CI: 0.854, 0.914) and was not notably heterogeneous chi-squared = 7.44; P = 0.489 for the Q test and I^2 = 0.00%).
The quantitative measurement of myocardial fibrosis via T1 mapping is associated with a favourable overall correlation with the myocardial biopsy measurements. Further studies are required to determine the calibration of the T1 mapping results for the biopsy findings of different cardiomyopathies.
Malaria importation can be caused by cross-border movement either of both people and anopheline mosquitoes. However, there still lacks robust evidence of imported malaria caused by Plasmodium spp. ...infected anopheles along international border areas (border-spill malaria). The objectives of this study were to confirm whether an outbreak of Plasmodium vivax malaria is border-spill malaria and assess the effects of China's public health response along China-Myanmar border.
Epidemiological, parasitological and entomological investigations were conducted to investigate the outbreak of border-spill malaria. Meanwhile, comprehensive interventions were carried out to prevent further transmission and reintroduction of malaria.
Rapid diagnostic testing, microscopy and polymerase chain reaction were performed and the infections were confirmed as P. vivax. A total of 22 (9.21%) of 239 workers contracted P. vivax during the outbreak. Multivariate logistic regression analysis identified that the distance of worker shelters in China within 300 meters to the internally displaced person (IDP) camps in Myanmar was a risk factors associated with malaria infection (adjusted odds ratio 7.5920; 95% confidence interval, 2.6079-22.1013; P = 0.0002). After comprehensive interventions, malaria transmission was successfully interpreted and prevented at the project site till the completion of project on 14 January 2020, and recurrence of P. vivax malaria was not detected by the end of 2020.
This study provided robust evidence of border-spill malaria along China-Myanmar border. Malaria parasite reservoir and distance travelled by female anopheline mosquitoes are two determinants for border-spill malaria. The public health response to the outbreak indicates that the malaria surveillance and response system works well in preventing reintroduction of malaria. However, prevention of border-spill malaria is still a major challenge in the Yunnan border area, China.
Background
The pathophysiological changes in the remote myocardium after acute myocardial infarction (MI) remains less understood.
Purpose
To assess the inflammation in the remote myocardium post‐MI ...and its association with left ventricular (LV) remodeling using T2 mapping.
Study type
Prospective.
Animal Model and Subjects
Twelve pigs at 3‐day post‐MI, 6 pigs at 3‐month post‐MI, 6 healthy pigs; 54 patients at 3‐day and 3‐month post‐MI, 31 healthy volunteers;
Field Strength/Sequence
A 3 T MRI/ steady‐state free‐precession sequence for T2 mapping (animals: 0, 30, and 55 msec; human: 0, 25, and 55 msec), phase‐sensitive inversion recovery gradient echo for late gadolinium enhancement (LGE), balanced steady free‐precession sequence for cine.
Assessment
Infarcted myocardium was defined on LGE, remote T2 was measured on T2 maps. LV remodeling was evaluated as LV end‐diastolic volume change index between two scans using cine. CD68 staining was conducted to detect monocyte/macrophage.
Statistical Tests
Student‐t test and one‐way ANOVA were used to compare remote T2 with normal controls. The association of remote T2 with LV remodeling was assessed using linear regression. P values of <0.05 were used to denote statistical significance.
Results
Compared with healthy pigs, remote T2 significantly increased from 3 days to 3 months post‐MI (31.43 ± 0.67 vs. 33.53 ± 1.15 vs. 36.43 ± 1.07 msec). CD68 staining demonstrated the inflammation in remote myocardium post‐MI but not in healthy pigs. Significant remote myocardial alterations in T2 were also observed in human group (40.51 ± 1.79 vs. 41.94 ± 1.14 vs. 42.52 ± 1.71 msec). In patients, the 3‐month remote T2 (β = 0.432) and remote T2 variation between two scans (β = 0.554) were both independently associated with LV remodeling.
Conclusion
T2 mapping could characterize the abnormalities in the remote myocardium post‐MI, which was potentially caused by the inflammatory response. Moreover, variations in remote T2 were associated with LV remodeling.
Evidence Level
1
Technical Efficacy
Stage 3
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