Cardiac Magnetic Resonance T1 Mapping Research Articles

Myocardial extracellular volume derived from contrast-enhanced chest computed tomography in longitudinal evaluation of cardiac toxicity in patients treated with immune checkpoint inhibitors.

The immune-related adverse effects after immune checkpoint inhibitors (ICIs) treatment have always been a hot topic. Although the incidence of myocarditis is not high among the related adverse effects, the mortality rate is extremely high once it occurs. In the past, the risk of cancer therapy-related cardiac dysfunction (CTRCD) after drug treatment was evaluated based on imaging examinations, but this evaluation still had certain limitations. Currently, the extracellular volume (ECV) score measurement calculated using cardiac magnetic resonance T1 mapping has become a reliable method for evaluating myocardial toxicity and computed tomography (CT) examination may become an alternative. This study aimed to longitudinally evaluate the cardiac toxicity of patients treated with ICIs using myocardial ECV derived from contrast-enhanced chest CT. A total of 500 patients with III-IV lung cancer and esophageal cancer treated with ICIs were evaluated. Participants underwent baseline examination and at least 1 follow-up examination after treatment. Contrast-enhanced chest CT-ECV, left ventricular ejection fraction (LVEF), and measurement of cardiac troponin T (cTnT) were conducted before the first treatment, 3-6 months after the first treatment, and about 12 months after the first treatment, respectively. The ECV value of the middle part of the left ventricular septum was evaluated on CT venography and plain scan, the LVEF value was evaluated by color Doppler ultrasound, and the quantity of cTnT was detected by chemiluminescence. Cancer therapy-related cardiac dysfunction was recorded. The mean baseline LVEF value was 68.51%±4.81% (N0=500), and those of LVEF1, LVEF2, and LVEF3 were 68.77%±4.30%, 68.16%±3.59%, and 66.23%±4.20%, respectively (N1=500, N2=467, and N3=361, respectively). There was no significant difference between LVEF1, LVEF2, and LVEF0 (P1=0.095, P2=0.062), whereas LVEF3 was significantly lower than LVEF0 (P<0.001). The average baseline cTnT0 value was 7.42±3.95 (N0=500). The values of cTnT1, cTnT2, and cTnT3 were 10.05±11.40, 12.24±13.59, and 14.54±14.49, respectively (N1=500, N2=467, N3=361). The values of cTnT1, cTnT2, and cTnT3 were significantly higher than cTnT0 (P1<0.001, P2<0.001, P3<0.001). The average ECV0 was 47.14%±7.48% (N0=500). ECV1, ECV2, and ECV3 were 50.85%±6.79%, 53.44%±6.96% and 52.64%±7.58% respectively (N1=500, N2=467 and N3=361). ECV1, ECV2, and ECV3 were significantly higher than ECV0 (P1<0.001, P2<0.001, P3<0.001). CTRCD occurred in 49 patients. There were significant differences between the CTRCD (+) group and the CTRCD (-) group in cTnT1, cTnT2, and cTnT3 (P1<0.001, P2<0.001, and P3<0.001, respectively) and in ECV1, ECV2, and ECV3 (P1=0.039, P2=0.041, and P3=0.013, respectively). CT-ECV began to increase at the early stage after the treatment of ICIs. CT-ECV is a potential biomarker for dynamically monitoring the cardiac toxicity of tumor patients after receiving ICIs. ECV may be used to speculate the CTRCD caused by the treatment of ICIs.

Kiosk 8R-TB-04 - Cardiac Magnetic Resonance T1 Mapping and Strain in Patients with Crohn’s Disease and Endoscopic Assessment of Inflammation

Kiosk 8R-TB-04 - Cardiac Magnetic Resonance T1 Mapping and Strain in Patients with Crohn’s Disease and Endoscopic Assessment of Inflammation

Potential for intramyocardial fibrosis detection based on estimation of extracellular volume using dual-energy computed tomography

An increase in left ventricular (LV) extracellular volume (ECV) is an important parameter of LV morphology and is considered synonymous with myocardial fibrosis, as well as a reliable marker of myocardial injury and impaired cardiac function. Accurate methods for detecting and assessing myocardial fibrosis are very important for clinical practice. The current standard for myocardial fibrosis imaging is delayed gadolinium enhanced cardiac magnetic resonance imaging (MRI) or T1 mapping, but these techniques have limitations. They can be avoided by using dual-energy computed tomography (DECT), which makes it possible to identify myocardial fibrosis, including small-focal fibrosis, in two different ways (subtraction technique and iodine density measurement technique). The literature analysis carried out by the authors showed good comparability of MRI and DECT results in determining ECV in patients with various heart diseases of both ischemic and non-ischemic nature, including cardiomyopathies, aortic stenosis, pulmonary hypertension, sarcoidosis, and amyloidosis. In addition, the use of DECT to identify myocardial fibrosis is also possible if cardiac inflammation is suspected. In addition to evaluating the effectiveness of DECT compared with MRI, different scanning protocols were analyzed, since there is currently no consensus on the optimal contrast administration regimen. The issue of radiation exposure in modern DECT scanners is also separately considered. The authors showed that DECT is an important tool for determining ECV, which is of interest for clinical practice.

Association of Lipoprotein(a) Levels With Myocardial Fibrosis in the Multi-Ethnic Study of Atherosclerosis.

Lipoprotein(a) (Lp[a]) has been identified as an emerging risk factor for adverse cardiovascular (CV) outcomes, including heart failure. However, the connections among Lp(a), myocardial fibrosis (interstitial and replacement), and cardiac remodeling as pathways to CV diseases remains unclear. This study investigated the relationship between Lp(a) levels and myocardial fibrosis by cardiac magnetic resonance (CMR) T1 mapping and late gadolinium enhancement, as well as cardiac remodeling by cine CMR, in the MESA (Multi-Ethnic Study of Atherosclerosis) cohort. The study included 2,040 participants with baseline Lp(a) measurements and T1 mapping for interstitial myocardial fibrosis (IMF) evaluation in 2010. Lp(a) was analyzed as a continuous variable (per log unit) and using clinical cutoff values of 30 and 50mg/dL. Multivariate linear and logistic regression were used to assess the associations of Lp(a) with CMR measures of extracellular volume (ECV fraction [ECV%]), native T1 time, and myocardial scar, as well as parameters of cardiac remodeling, in 2,826 participants. Higher Lp(a) levels were associated with increased ECV% (per log-unit Lp[a]; β=0.2%; P=0.007) and native T1 time (per log-unit Lp[a]; β=4%; P< 0.001). Similar relationships were observed between elevated Lp(a) levels and a higher risk of clinically significant IMF defined by prognostic thresholds per log-unit Lp(a) of ECV% (OR: 1.20; 95%CI: 1.04-1.43) and native T1 (OR: 1.2; 95%CI: 1.1-1.4) equal to 30% and 955ms, respectively. Clinically used Lp(a) cutoffs (30 and 50mg/dL) were associated with greater prevalence of myocardial scar (OR: 1.85; 95%CI: 1.1-3.2 and OR: 1.9; 95%CI: 1.1-3.4, respectively). Finally, higher Lp(a) levels were associated with left atrial enlargement and dysfunction. Elevated Lp(a) levels are linked to greater subclinical IMF, increased myocardial scar prevalence, and left atrial remodeling.

Role of cardiac magnetic resonance T1 mapping in comparison to T2* for cardiac iron overload assessment in transfusion-dependent thalassemia major patients

BackgroundCardiac complications are the leading cause of death in transfusion-dependent thalassemia major (TDT) patients due to increased cardiac iron overload (CIO), so this study’s purpose is to assess the diagnostic utility of cardiac magnetic resonance T1 mapping in correlation to T2* for the assessment of CIO in TDT patients. This prospective case–control study involved 55 TDT patients and 30 age- and gender-matched healthy controls. All the patients underwent assessment of myocardial T2*, and native T1 values by conventional cardiac magnetic resonance imaging, and native T1 mapping technique to assess the CIO. Comparison and association between T2*, and native T1 values among TDT patients were studied.ResultsA statistically significant difference is noted between control and patient groups in regard to mean T2* and native T1 values (P = 0.03 and 0.01, respectively). The mean native T1 value in TDT patients was lower than in the control group (992 ± 54 vs. 1234 ± 42), respectively, with a statistically significant P value of 0.04. The study evoked a statistically significant strong positive association, and correlation was noted between measured T2* and native T1 values (r = 0.84, P value = 0.001), while a moderate negative association was observed between native T1 values and S. ferritin levels (r = − 0.53, P value = 0.02).ConclusionsNative T1 mapping is a non-invasive promising complementary technique to T2* that helps to detect cardiac iron overload in TDT patients, as it is strongly associated with T2*. Also, native T1 value can differentiate mild, moderate, severe, and no cardiac iron overload.

Association of epicardial adipose tissue on magnetic resonance imaging with cardiovascular outcomes: Quality over quantity?

Abstract Background Quantity of epicardial adipose tissue (EAT) has been associated with poor cardiovascular outcomes. As suggested by computed tomography (CT) studies the quality of EAT may be of incremental prognostic value. Cardiac magnetic resonance (CMR) is the gold-standard for tissue characterization, however, has never been applied for EAT quality assessment. Objectives To investigate EAT quality measured on CMR T1 mapping as predictor of outcome in an all-comer cohort. Methods We measured EAT area (EATA) and T1 time (EAT-T1) in a four-chamber views (Figure 1) and tested for association with clinical, demographic, and laboratory parameters using linear regression models. We used Cox-regression analyses to test the association between EATA and EAT-T1 with a composite endpoint of non-fatal myocardial infarction, heart failure hospitalization, and all-cause death. Results A total of 966 participants were included (47.2% female, mean age: 58.4years). Mean EATA was 7.3cm2 and mean EAT-T1 was 268ms. On linear regression EAT-T1 was not associated with markers obesity, dyslipidemia or co-morbidities such as diabetes (p&amp;gt;0.05 for all). During a follow-up of 57.7 months, a total of 280 (29.0%) events occurred. EAT-T1 was independently associated (adj. HR: 1.003, 95%-CI: 1.000 – 1.005, p=0.029, Figure 2) with the composite endpoint when adjusted for established clinical risk factors including age, sex, natriuretic peptide levels, left and right ventricular function, arterial hypertension, body mass index, and coronary artery disease. Conclusion In an all-comer CMR cohort, EAT quality, as measured on CMR T1-times, but not EAT quantity is independently associated with a composite endpoint of non-fatal myocardial infarction, heart failure hospitalization, and all-cause death.Figure 1.Regions of interestFigure 2.Kaplan Meier Curves

Myocardial structural and functional changes in cardiac amyloidosis - insights from a prospective observational patient registry

Abstract Background Within the last decade, cardiac amyloidosis (CA) has been acknowledged as a significant cause of heart failure and patients who are affected face a dismal prognosis, especially in later stages of the disease. The pathophysiological hallmark of cardiac amyloidosis (CA) is the deposition of amyloid within the myocardium. Consequently, extracellular volume (ECV) of affected patients increases. However, studies on ECV progression over time and its' impact on prognosis are lacking. Objectives We aimed to investigate the progression of ECV and its prognostic impact in CA patients. Methods Serial cardiac magnetic resonance (CMR) examinations, including ECV quantification were performed in consecutive CA patients. Results Between 2012 and 2021, 103 CA patients underwent baseline and follow-up CMR, including ECV quantification. Median ECVs at baseline of the total (n = 103), transthyretin [(ATTR) n = 80], and [light chain (AL) n = 23] CA cohorts were 48.0%, 49.0%, and 42.6%. During a median follow-up period of 12 months, ECV increased significantly in all cohorts (48.0% to 50.5%, p&amp;lt;0.001; 49.0% to 50.5%, p&amp;lt;0.001; 42.6% to 50.6%, p = 0.026). Separate analyses for treatment-naïve (n = 14) and treated (n = 66) ATTR patients revealed that the median change of ECV from baseline to follow-up was significantly higher among untreated patients (5.5% versus 2.7%, p = 0.035). Survival analyses demonstrated that median change of ECV was an independent (adjusted for troponin t and NT-proBNP) predictor of outcome in all CA cohorts [total: hazard ratio (HR): 1.114, 95% confidence-interval (CI): 1.045 – 1.189, p&amp;lt;0.001; ATTR: HR: 1.099, 95% CI: 1.014 – 1.192, p = 0.022; AL: HR: 1.142, 95% CI: 1.006 – 1.297, p = 0.040]. Conclusions The present study demonstrates that ECV, quantified by CMR T1 mapping, increases significantly in CA patients over the course of 12 months. While ECV increased, irrespective of amyloid type our analyses showed the highest increase among untreated ATTR patients. Moreover, the change of ECV was an independent predictor of adverse outcomes in AL, as well as ATTR patients emphasizing the usefulness of CMR T1 mapping in the management of CA patients.Figure 1.Dot PlotsFigure 2.Kaplan Meier Curves

Arrhythmic form of mitral valve prolapse: presentation, risk stratification and management

Abstract Background Mitral valve prolapse (MVP) is a common finding that has been considered as benign condition for a long time. However, some anatomic forms have been recently recognized to be associated with life-threatening ventricular arrhythmia and sudden cardiac death (SCD), recently known as arrhythmic MVP (AMVP). Objectives This study is aiming to clinically characterize and risk stratify patients with malignant phenotype of MVP of high risk for ventricular arrhythmia which may lead to SCD. We aim to explore characteristics and assess potential markers for MVP induced ventricular arrhythmia that might need monitoring and follow up with medical or invasive treatment as implantable cardioverter-defibrillator, catheter ablation or even surgical repair. Methods A prospective cohort study of 45 (age 35±8, 29 females), consecutive patients with MVP and/or mitral annular disjunction (MAD) and comprehensive clinical arrhythmia on resting electrocardiography (ECG) or 48-hours Holter monitoring , Doppler echocardiography and contrast based cardiac magnetic resonance (CMR) characterization were identified. Patients were followed-up for a period of maximum one year to identify any further management needed. Results Frequent ventricular arrhythmia was evidently seen associated to MVP (69% with at least ventricular ectopy ≥5%), as well as complex ventricular arrhythmia (31% with sustained or non-sustained ventricular tachycardia ) P&amp;lt;0.001. AMVP was strongly associated with premature ventricular contractions (PVCs) having Right bundle branch block (RBBB) morphology on ECG and late gadolinium enhancement (LGE) on CMR (all p&amp;lt;0.05). Furthermore, it was shown to be associated with bileaflet prolapse and higher left ventricular volumes, however not statistically significant. On Follow-up, Out of 36 patients with ventricular arrhythmia, 64% were controlled on medical anti-arrhythmic and some others were referred either for ablation after worsening of symptoms despite of medical treatment (27.8%), implantable cardioverter-defibrillator device for secondary VT prophylaxes (5.6%) or surgery (2.8%) due to progression in mitral regurgitation severity and deterioration of symptoms. Conclusion In this small cohort study, characteristic form of MVP was found to be associated with ventricular arrhythmia more common in the form of frequent PVCs and less common in the complex form. Although majority of patients were controlled on medical treatment, few patients required further invasive management despite of medical treatment . Thus, arrhythmia associated with a special form of MVP could be life threatening and needs close monitoring, long follow-up and proper management approach to prevent SCD. Large prospective studies with comprehensive approach and long term follow up is pivotal. CMR T1 mapping and electro anatomical CARTO mapping could help in better detection and proper defining of arrhythmia substrate in future studies.AMVP illustration

Chemotherapy effect on myocardial fibrosis markers in patients with gynecologic cancer and low cardiovascular risk.

Patients with gynecologic cancers experience side effects of chemotherapy cardiotoxicity. We aimed to quantify cardiac magnetic resonance (CMR) markers of myocardial fibrosis in patients with gynecologic cancer and low cardiovascular risk who undergo chemotherapy. This study is part of a registered clinical research. CMR T1 mapping was performed in patients with gynecologic cancer and low cardiovascular risk undergoing chemotherapy. The results were compared with those of age-matched healthy control subjects. 68 patients (median age = 50 years) and 30 control subjects were included. The median number of chemotherapy cycles of patients was 9.0 (interquartile range [IQR] 3.3-17.0). Extracellular volume fraction (ECV) (27.2% ± 2.7% vs. 24.5% ± 1.7%, P < 0.001) and global longitudinal strain (-16.2% ± 2.8% vs. -17.4% ± 2.0%, P = 0.040) were higher in patients compared with controls. Patients with higher chemotherapy cycles (>6 cycles) (n=41) had significantly lower intracellular mass indexed (ICMi) compared with both patients with lower chemotherapy cycles (≤6 cycles) (n=27) (median 27.44 g/m2 [IQR 24.03-31.15 g/m2] vs. median 34.30 g/m2 [IQR 29.93-39.79 g/m2]; P = 0.002) and the control group (median 27.44 g/m2 [IQR 24.03-31.15 g/m2] vs. median 32.79 g/m2 [IQR 27.74-35.76 g/m2]; P = 0.002). Patients with two or more chemotherapy regimens had significantly lower ICMi compared with both patients with one chemotherapy regimen (27.45 ± 5.16 g/m2 vs. 33.32 ± 6.42 g/m2; P< 0.001) and the control group (27.45 ± 5.16 g/m2 vs. 33.02 ± 5.52 g/m2; P < 0.001). The number of chemotherapy cycles was associated with an increase in the ECV (Standard regression coefficient [β] = 0.383, P = 0.014) and a decrease in the ICMi (β = -0.349, P = 0.009). Patients with gynecologic cancer and low cardiovascular risk who undergo chemotherapy have diffuse extracellular volume expansion, which is obvious with the increase of chemotherapy cycles. Myocyte loss may be part of the mechanism in patients with a higher chemotherapy load. http://www.chictr.org.cn, identifier ChiCTR-DDD-17013450.

Myocardial Fibrosis and Cardiomyopathy Risk: A Genetic Link in the MESA.

Common genetic variants are associated with risk for hypertrophic cardiomyopathy and dilated cardiomyopathy and with left ventricular (LV) traits. Whether these variants are associated with myocardial fibrosis, an important pathophysiological mediator of cardiomyopathy, is unknown. Multi-Ethnic Study of Atherosclerosis participants with T1-mapping cardiac magnetic resonance imaging in-whom extracellular volume was assessed, and genotyping information was available were included (N=1255). Log extracellular volume (%) was regressed on 50 candidate single nucleotide polymorphisms (previously identified to be associated with hypertrophic cardiomyopathy, dilated cardiomyopathy, and LV traits) adjusting for age, sex, diabetes, blood pressure, and principal components of ancestry. Ancestry-specific results were pooled by fixed-effect meta-analyses. Gene knockdown experiments were performed in human cardiac fibroblasts. The SMARCB1 rs2186370 intronic variant (minor allele frequency: 0.18 in White and 0.50 in Black participants), previously identified as a risk variant for dilated cardiomyopathy and hypertrophic cardiomyopathy, was significantly associated with increased extracellular volume (P=0.0002) after adjusting for confounding clinical variables. The SMARCB1 rs2070458 locus previously associated with increased LV wall thickness and mass was similarly significantly associated with increased extracellular volume (P=0.0002). The direction of effect was similar in all 4 ancestry groups, but the effect was strongest in Black participants. The variants are strong expression quantitative loci in human LV tissue and associated with genotype-dependent decreased expression of SMARCB1 (P=7.3×10-22). SMARCB1 knockdown in human cardiac fibroblasts resulted in increased TGF (transforming growth factor)-β1-mediated α-smooth muscle actin and collagen expression. Common genetic variation in SMARCB1 previously associated with risk for cardiomyopathies and increased LV wall thickness is associated with increased cardiac magnetic resonance imaging-based myocardial fibrosis and increased TGF-β1 mediated myocardial fibrosis in vitro. Whether these findings suggest a pathophysiologic link between myocardial fibrosis and cardiomyopathy risk remains to be proven.

Risk prediction in patients with classical low-flow, low-gradient aortic stenosis undergoing surgical intervention.

Classical low-flow, low-gradient aortic stenosis (LFLG-AS) is an advanced stage of aortic stenosis, which has a poor prognosis with medical treatment and a high operative mortality after surgical aortic valve replacement (SAVR). There is currently a paucity of information regarding the current prognosis of classical LFLG-AS patients undergoing SAVR and the lack of a reliable risk assessment tool for this particular subset of AS patients. The present study aims to assess mortality predictors in a population of classical LFLG-AS patients undergoing SAVR. This is a prospective study including 41 consecutive classical LFLG-AS patients (aortic valve area ≤1.0 cm2, mean transaortic gradient <40 mmHg, left ventricular ejection fraction <50%). All patients underwent dobutamine stress echocardiography (DSE), 3D echocardiography, and T1 mapping cardiac magnetic resonance (CMR). Patients with pseudo-severe aortic stenosis were excluded. Patients were divided into groups according to the median value of the mean transaortic gradient (≤25 and >25 mmHg). All-cause, intraprocedural, 30-day, and 1-year mortality rates were evaluated. All of the patients had degenerative aortic stenosis, with a median age of 66 (60-73) years; most of the patients were men (83%). The median EuroSCORE II was 2.19% (1.5%-4.78%), and the median STS was 2.19% (1.6%-3.99%). On DSE, 73.2% had flow reserve (FR), i.e., an increase in stroke volume ≥20% during DSE, with no significant differences between groups. On CMR, late gadolinium enhancement mass was lower in the group with mean transaortic gradient >25 mmHg [2.0 (0.0-8.9) g vs. 8.5 (2.3-15.0) g; p = 0.034), and myocardium extracellular volume (ECV) and indexed ECV were similar between groups. The 30-day and 1-year mortality rates were 14.6% and 43.8%, respectively. The median follow-up was 4.1 (0.3-5.1) years. By multivariate analysis adjusted for FR, only the mean transaortic gradient was an independent predictor of mortality (hazard ratio: 0.923, 95% confidence interval: 0.864-0.986, p = 0.019). A mean transaortic gradient ≤25 mmHg was associated with higher all-cause mortality rates (log-rank p = 0.038), while there was no difference in mortality regarding FR status (log-rank p = 0.114). In patients with classical LFLG-AS undergoing SAVR, the mean transaortic gradient was the only independent mortality predictor in patients with LFLG-AS, especially if ≤25 mmHg. The absence of left ventricular FR had no prognostic impact on long-term outcomes.

Anderson-Fabry disease cardiomyopathy: an update on epidemiology, diagnostic approach, management and monitoring strategies.

Anderson-Fabry disease (AFD) is an X-linked lysosomal storage disorder caused by deficient activity of the enzyme alpha-galactosidase. While AFD is recognized as a progressive multi-system disorder, infiltrative cardiomyopathy causing a number of cardiovascular manifestations is recognized as an important complication of this disease. AFD affects both men and women, although the clinical presentation typically varies by sex, with men presenting at a younger age with more neurologic and renal phenotype and women developing a later onset variant with more cardiovascular manifestations. AFD is an important cause of increased myocardial wall thickness, and advances in imaging, in particular cardiac magnetic resonance imaging and T1 mapping techniques, have improved the ability to identify this disease non-invasively. Diagnosis is confirmed by the presence of low alpha-galactosidase activity and identification of a mutation in the GLA gene. Enzyme replacement therapy remains the mainstay of disease modifying therapy, with two formulations currently approved. In addition, newer treatments such as oral chaperone therapy are now available for select patients, with a number of other investigational therapies in development. The availability of these therapies has significantly improved outcomes for AFD patients. Improved survival and the availability of multiple agents has presented new clinical dilemmas regarding disease monitoring and surveillance using clinical, imaging and laboratory biomarkers, in addition to improved approaches to managing cardiovascular risk factors and AFD complications. This review will provide an update on clinical recognition and diagnostic approaches including differentiation from other causes of increased ventricular wall thickness, in addition to modern strategies for management and follow-up.

Endogenous Sex Hormone Levels and Myocardial Fibrosis in Men and Postmenopausal Women

BackgroundSex hormone (SH) imbalances have been linked to a higher risk of heart failure in both sexes. However, mechanisms that underlie this relationship remain unclear. We examined the association of baseline SH with interstitial and replacement myocardial fibrosis in the MESA (Multi-Ethnic Study of Atherosclerosis) using cardiac magnetic resonance (CMR) T1 mapping and late gadolinium enhancement (LGE). ObjectivesThe purpose of this study was to assess the link between baseline sex hormone levels and myocardial fibrosis in the MESA cohort using CMR. MethodsA total of 2,324 participants (men and postmenopausal women [PMW]) were included in the MESA with SH measured at baseline and had underwent CMR 10 years later. All analyses were stratified by sex and age. Regression models were constructed to assess the associations of baseline SH with extracellular volume (ECV)% and native T1 time and with LGE. Higher native T1 time and ECV% are interpreted as evidence of increasing interstitial myocardial fibrosis (IMF). Given the limited number of myocardial scars present in PMW, analysis of LGE was limited to men. ResultsAmong older men (age ≥65 years), a 1-SD increment higher free testosterone was significantly associated with 2.45% lower ECV% and 21.5% lower native T1 time, while a 1-SD increment higher bioavailable testosterone was associated with 12.5% lower native T1 time. A 1-SD increment greater sex hormone-binding globulin level was associated with 1% higher ECV%. Among PMW of 55 to 64 years, a 1-SD increment higher total testosterone was associated with 9.5% lower native T1 time. Higher levels of estradiol in older men were independently associated with higher odds of having a myocardial scar (OR: 4.10; 95% CI: 1.35-12.40; P = 0.01). ConclusionsAmong older men, SH imbalances at initial evaluation were independently associated with CMR defined IMF and replacement fibrosis, respectively; while increasing total testosterone in middle-aged PMW was associated with lesser marker of IMF.

Early detection and serial monitoring during chemotherapy-radiation therapy: Using T1 and T2 mapping cardiac magnetic resonance imaging.

To confirm the ability of native T1 and T2 values in detecting and monitoring early myocardial injuries of chest radiotherapy in neoplasm patients. Fifteen participants received non-anthracycline chemotherapy and chest radiotherapy, and 30 age/gender-matched controls were enrolled in this prospective study. Cardiac magnetic resonance scans were performed within 2 days, 3 months, and 6 months after chest radiotherapy. Myocardial native T1 and T2 values were measured in irradiated and nonirradiated areas. Meanwhile, the parameters of left ventricular function and left ventricular myocardial strain were obtained. There were no significant differences in left ventricular function, native T1, T2, and strain between patients and controls before chest radiotherapy. In 15 participants who were followed up for 6 months, there was a significant change only in left ventricular ejection fraction (LVEF) among baseline and the first follow-up (P = 0.021), while the adjusted P-value was higher than 0.05 after Bonferroni correction, as well as other parameters. Native T1 values were elevated at 3 and 6 months in irradiated areas compared with baseline (1,288.72 ± 66.59 ms vs. 1,212.51 ± 45.41 ms; 1,348.01 ± 54.16 ms vs. 1,212.51 ± 45.41 ms; P < 0.001 for both). However, T2 values only changed at 3 months in irradiated areas compared with baseline (44.21 ± 3.35 ms vs. 39.14 ± 1.44 ms; P = 0.006). Neither the native T1 nor T2 values changed in nonirradiated areas during the follow-up period (all P > 0.05). There were no significant differences in strain changes during the follow-up period (all P > 0.05). Native T1 and T2 values elevated at 3 months after chest radiotherapy, whereas LVEF showed no significant change during the 6-month follow-up.

Myocardial oedema contributes to interstitial expansion and associates with mechanical and electrocardiographic changes in takotsubo syndrome: a CMR T1 and T2 mapping study.

myocardial oedema is largely represented in takotsubo syndrome (TTS) and may contribute to alter the myocardium morphology and function. The aim of the study is to describe relationships between oedema, mechanical, and electrical abnormalities in TTS. the study included n = 32 hospitalized TTS patients and n = 23 controls. Cardiac magnetic resonance (CMR) with tissue mapping and feature tracking was performed with concomitant 12-lead electrocardiogram (ECG) recording. Mean age of TTS was 72 ± 12 years old, 94% women. Compared with controls, patients had higher left ventricular (LV) mass, worse systolic function, higher septal native T1 (1116 ± 73 msec vs. 970 ± 23 msec, P < 0.001), T2 (56 ± 5 msec vs. 46 ± 2 msec, P < 0.001), and extracellular volume (ECV) fraction (32 ± 5% vs. 24 ± 1%, P < 0.001). TTS patients had higher apicobasal gradient of T2 values (12 ± 6 msec vs. 2 ± 6 msec, P < 0.001); basal LV wall displayed higher native T1, T2, and ECV (all P < 0.002) but similar circumferential strain against controls (-23 ± 3% vs. -24 ± 4%, P = 0.351). In the TTS cohort, septal T2 values showed significant correlations with native T1 (r = 0.609, P < 0.001), ECV (r = 0.689, P < 0.001), left ventricular ejection fraction (r = -0.459, P = 0.008) and aVR voltage (r = -0.478, P = 0.009). Negative T-wave voltage and QTc length correlated with apicobasal T2 mapping gradient (r = 0.499, P = 0.007 and r = 0.372, P = 0.047, respectively) but not with other tissue mapping measurements. CMR T1 and T2 mapping demonstrated increased myocardial water content conditioning interstitial expansion in acute TTS, detected even outside areas of abnormal wall motion. Oedema burden and distribution associated with mechanical and electrocardiographic changes, making it a potential prognostic marker and therapeutic target in TTS.

Comprehensive cardiac magnetic resonance T1, T2, and extracellular volume mapping to define Duchenne cardiomyopathy

BackgroundCardiomyopathy is the leading cause of death in Duchenne muscular dystrophy (DMD). Cardiac magnetic resonance (CMR) parametric mapping sequences offer insights into disease pathophysiology. We propose a novel approach by leveraging T2 mapping in conjunction with T1 and extracellular volume (ECV) mapping to perform a virtual myocardial biopsy. While previous work has attempted to describe myocardial changes in DMD, our inclusion of T2 mapping enables comprehensive categorization of myocardial tissue characteristics of fibrosis, edema, and fat to better understand the pathological composition of the myocardium with disease progression. MethodsDMD patients (n = 49; median: 12 years-old) underwent CMR, including T1, T2, and ECV. Categories were defined as normal, isolated high T1 (normal ECV, high T1, normal T2), fibrosis (high ECV, normal or high T1, normal T2), edema (normal or high ECV, normal or high T1, high T2), fat (normal ECV, low T1, high T2) or fibrofatty (high ECV, low T1, high T2). ResultsMedian left ventricular ejection fraction (LVEF) was 59% with 27% having LVEF < 55%. Those with normal LVEF and no late gadolinium enhancement (37%) were younger in age (10.5 ± 2.6 vs. 15.0 ± 4.3 years-old, p < 0.001). Native T1 was elevated in at least one slice in 82% of patients. Those with high T2 at any slice (27%) were older (p = 0.005) and had lower LVEF (p = 0.005) compared with subjects with normal T2 (73%). The most common myocardial characterization was fibrosis (43%) followed by isolated high T1 (24%). Of the 13 with high T2, ten were categorized as edema, two as fibrofatty, and one as fat. ConclusionCMR parametric mapping sequences offer insights into Duchenne cardiomyopathy pathophysiology, which should drive development of therapeutic interventions aimed at these targets. Myocardial fibrosis is common in DMD. Patients with elevated T2 were older and had lower LVEF. Though fat infiltration was present, the majority of subjects with elevated T2 met criteria for myocardial edema.

Left Ventricular Adverse Remodeling in Ischemic Heart Disease: Emerging Cardiac Magnetic Resonance Imaging Biomarkers

Post-ischemic left ventricular (LV) remodeling is a biologically complex process involving myocardial structure, LV shape, and function, beginning early after myocardial infarction (MI) and lasting until 1 year. Adverse remodeling is a post-MI maladaptive process that has been associated with long-term poor clinical outcomes. Cardiac Magnetic Resonance (CMR) is the best tool to define adverse remodeling because of its ability to accurately measure LV end-diastolic and end-systolic volumes and their variation over time and to characterize the underlying myocardial changes. Therefore, CMR is the gold standard method to assess in vivo myocardial infarction extension and to detect the presence of microvascular obstruction and intramyocardial hemorrhage, both associated with adverse remodeling. In recent times, new CMR quantitative biomarkers emerged as predictive of post-ischemic adverse remodeling, such as T1 mapping, myocardial strain, and 4D flow. Additionally, CMR T1 mapping imaging may depict infarcted tissue and assess diffuse myocardial fibrosis by using surrogate markers such as extracellular volume fraction, which may predict functional recovery or risk stratification of remodeling. Finally, there is emerging evidence supporting the utility of intracavitary blood flow kinetic energy and hemodynamic features assessed by the 4D flow CMR technique as early predictors of remodeling.

Effect of ticagrelor and prasugrel on remote myocardial inflammation in patients with acute myocardial infarction with ST-elevation: a CMR T1 and T2 mapping study.

Acute myocardial ischaemia triggers a non-specific inflammatory response of remote myocardium through the increase of plasma concentrations of acute-phase proteins, which causes myocardial oedema. As ticagrelor has been shown to significantly decrease circulating levels of several pro-inflammatory cytokines in patients after acute myocardial infarction with ST-elevation (STEMI), we sought to investigate a potential suppressive effect of ticagrelor over prasugrel on cardiac magnetic resonance (CMR) T1 and T2 values in remote myocardium. Ninety STEMI patients were prospectively included and randomised to receive either ticagrelor or prasugrel maintenance treatment after successful primary percutaneous coronary intervention. Patients underwent CMR after 2-7 days. The protocol included long and short axis cine imaging, T1 mapping, T2 mapping and late gadolinium enhancement imaging. After excluding 30 patients due to either missing images or insufficient quality of the T1 or T2 maps, 60 patients were included in our analysis. Of those, 29 patients were randomised to the ticagrelor group and 31 patients to the prasugrel group. In the remote myocardium, T1 values did not differ between groups (931.3 [919.4-950.4] ms for ticagrelor vs. 932.6 [915.5-949.2] ms for prasugrel (p = 0.94)), nor did the T2 values (53.8 ± 4.6 ms for ticagrelor vs. 53.7 ± 4.7 ms for prasugrel (p = 0.86)). Also, in the infarcted myocardium, T1 and T2 values did not differ between groups. In revascularised STEMI patients, ticagrelor maintenance therapy did not show superiority over prasugrel in preventing early remote myocardial inflammation as assessed by CMR T1 and T2 mapping.

Abstract 9934: Albuminuria Entails Myocardial Fibrosis at the Population Level: The MESA STUDY

Introduction: Microalbuminuria(MA) is an established predictor of CVD. Experimental and small observational studies have shown an association between MA and myocardial fibrosis(MF) among patients with type two diabetes mellitus (DM). However, the relationship to MF in a community-based population is unknown. Hypothesis: We hypothesize that participants with MA will have higher rates of MF measured by cardiac magnetic resonance T1(CMR-T1) mapping. Methods: A total of 1,010 men (mean age:68±9) and 1,003 women (mean age: 70 ± 9) who had both urine albumin and creatinine measurements and CMR-T1 for evaluation of MF were included in MESA visit 5. To study the association of MA among various populations, analyses were then stratified by diabetes stage and by sex. Multivariable linear regression models were constructed to assess the associations of MA with ECV and native T1 time. Results: Higher levels of MA were independently associated with greater evidence of MF (Fig.A). Participants with worse severity of MF (defined as ECV &gt;30%), that were men, or had either history of pre-DM or DM had significantly higher levels of MA, whereas no difference in MA levels were found in women (Fig.B). Among men only, each 1-SD increment greater MA levels was significantly associated with 0.3% higher ECV and 2.6% higher native T1. Among participants with pre-diabetes and diabetes, each 1-SD increment in MA levels was associated with 0.4% and 0.3% higher ECV and 3% and 3.5% higher native T1, respectively (Fig.A) Conclusions: In a community-based setting, measurable MA, independent of age, sex, DM, history of CVD, and other clinical variables, was related to subclinical MF. This association was more significant among participants with preDM, Type2DM, and men. These findings demonstrate that MA, a urine biomarker, may identify participants with high subclinical profibrotic condition. Further studies are warranted to address whether treatment of MA will be associated with lower MF.

Abstract 12034: Diffuse Myocardial Fibrosis, Its Distribution And Relationship To Clinical Outcome And Ventricular Function In Single Ventricles Before And After Fontan: A Cardiac Magnetic Resonance Outcome Study

Introduction: Patients with single ventricle (SV) anatomy are susceptible to myocardial fibrosis as measured by cardiac magnetic resonance (CMR) imaging. This study investigated the association of diffuse myocardial fibrosis prior to Fontan with ventricular function and clinical outcomes after Fontan completion. Methods: Retrospective cohort study of consecutive SV patients who underwent CMR T1 mapping prior to Fontan. Native T1 time and extracellular volume (ECV) of the dominant ventricle and a free wall region of interest (ROI) were measured on CMR pre-Fontan. Longitudinal strain was measured on echocardiography pre- and post-Fontan. Associations between pre-Fontan fibrosis, strain, and clinical outcomes were evaluated using linear and logistic regression. Results: 40 patients were included (table 1). ECV directly correlated to the number of ICU days and post-Fontan strain. The coefficient of variation (CV) of ECV directly correlated to hospital and chest tube days. When limited to single right ventricles (RV), T1 directly correlated to strain pre-Fontan. ECV directly correlated to ICU days as well as strain pre- and post-Fontan. ECV ROI directly correlated to strain post-Fontan. The CV of ECV directly correlated to the number of hospital days (table 2). Conclusions: Myocardial fibrosis prior to Fontan may portend the clinical course after Fontan and should be considered for risk stratification. The CV of ECV is a novel measure of diffuse fibrosis that is associated with clinical outcome. For single RV patients, fibrosis before Fontan is associated with worse ventricular function after. The use of reverse remodeling agents prior to Fontan should be considered.