Dataset Information

Quality assurance of quantitative cardiac T1-mapping in multicenter clinical trials - A T1 phantom program from the hypertrophic cardiomyopathy registry (HCMR) study.

ABSTRACT:

Background

Quantitative cardiovascular magnetic resonance T1-mapping is increasingly used for myocardial tissue characterization. However, the lack of standardization limits direct comparability between centers and wider roll-out for clinical use or trials.

Purpose

To develop a quality assurance (QA) program assuring standardized T1 measurements for clinical use.

Methods

MR phantoms manufactured in 2013 were distributed, including ShMOLLI T1-mapping and reference T1 and T2 protocols. We first studied the T1 and T2 dependency on temperature and phantom aging using phantom datasets from a single site over 4 years. Based on this, we developed a multiparametric QA model, which was then applied to 78 scans from 28 other multi-national sites.

Results

T1 temperature sensitivity followed a second-order polynomial to baseline T1 values (R² > 0.996). Some phantoms showed aging effects, where T1 drifted up to 49% over 40 months. The correlation model based on reference T1 and T2, developed on 1004 dedicated phantom scans, predicted ShMOLLI-T1 with high consistency (coefficient of variation 1.54%), and was robust to temperature variations and phantom aging. Using the 95% confidence interval of the correlation model residuals as the tolerance range, we analyzed 390 ShMOLLI T1-maps and confirmed accurate sequence deployment in 90%(70/78) of QA scans across 28 multiple centers, and categorized the rest with specific remedial actions.

Conclusions

The proposed phantom QA for T1-mapping can assure correct method implementation and protocol adherence, and is robust to temperature variation and phantom aging. This QA program circumvents the need of frequent phantom replacements, and can be readily deployed in multicenter trials.

SUBMITTER: Zhang Q

PROVIDER: S-EPMC7994017 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature

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Publications

Quality assurance of quantitative cardiac T1-mapping in multicenter clinical trials - A T1 phantom program from the hypertrophic cardiomyopathy registry (HCMR) study.

Zhang Qiang Q Werys Konrad K Popescu Iulia A IA Biasiolli Luca L Ntusi Ntobeko A B NAB Desai Milind M Zimmerman Stefan L SL Shah Dipan J DJ Autry Kyle K Kim Bette B Kim Han W HW Jenista Elizabeth R ER Huber Steffen S White James A JA McCann Gerry P GP Mohiddin Saidi A SA Boubertakh Redha R Chiribiri Amedeo A Newby David D Prasad Sanjay S Radjenovic Aleksandra A Dawson Dana D Schulz-Menger Jeanette J Mahrholdt Heiko H Carbone Iacopo I Rimoldi Ornella O Colagrande Stefano S Calistri Linda L Michels Michelle M Hofman Mark B M MBM Anderson Lisa L Broberg Craig C Andrew Flett F Sanz Javier J Bucciarelli-Ducci Chiara C Chow Kelvin K Higgins David D Broadbent David A DA Semple Scott S Hafyane Tarik T Wormleighton Joanne J Salerno Michael M He Taigang T Plein Sven S Kwong Raymond Y RY Jerosch-Herold Michael M Kramer Christopher M CM Neubauer Stefan S Ferreira Vanessa M VM Piechnik Stefan K SK

International journal of cardiology 20210131

<h4>Background</h4>Quantitative cardiovascular magnetic resonance T1-mapping is increasingly used for myocardial tissue characterization. However, the lack of standardization limits direct comparability between centers and wider roll-out for clinical use or trials.<h4>Purpose</h4>To develop a quality assurance (QA) program assuring standardized T1 measurements for clinical use.<h4>Methods</h4>MR phantoms manufactured in 2013 were distributed, including ShMOLLI T1-mapping and reference T1 and T2 ...[more]

PMID: 33535074

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Project description:Background: MRI native T1 mapping and extracellular volume fraction (ECV) are quantitative values that could reflect various myocardial tissue characterization. The role of these parameters in predicting the risk of sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM) is still poorly understood. Aim: This study aims to investigate the ability of native T1 mapping and ECV values to predict major adverse cardiovascular events (MACE) in HCM, and its incremental values over the 2014 European Society of Cardiology (ESC) and enhanced American College of Cardiology/American Heart Association (ACC/AHA) guidelines. Methods: Between July 2016 and October 2020, HCM patients and healthy individuals with sex and age matched who underwent cardiac MRI were prospectively enrolled. The native T1 and ECV parameters were measured. The SCD risk was evaluated by the 2014 ESC guidelines and enhanced ACC/AHA guidelines. MACE included cardiac death, transplantation, heart failure admission, and implantable cardioverter-defibrillator implantation. Results: A total of 203 HCM patients (54.2 ± 14.9 years) and 101 healthy individuals (53.2 ± 14.7 years) were evaluated. During a median follow-up of 15 months, 25 patients (12.3%) had MACE. In multivariate Cox regression analysis, global native T1 mapping (hazard ratio (HR): 1.446; 95% confidence interval (CI): 1.195-1.749; P < 0.001) and non-sustained ventricular tachycardia (NSVT) (HR: 4.949; 95% CI, 2.033-12.047; P < 0.001) were independently associated with MACE. Ten of 86 patients (11.6%) with low SCD risk assessed by the two guidelines had MACE. In this subgroup of patients, multivariate Cox regression analysis showed that global native T1 mapping was independently associated with MACE (HR: 1.532; 95% CI: 1.221-1.922; P < 0.001). In 85 patients with conflicting results assessed by the two guidelines, end-stage systolic dysfunction was independently associated with MACE (HR: 7.942, 95% CI: 1.322-47.707, P = 0.023). In 32 patients with high SCD risk assessed by the two guidelines, NSVT was independently associated with MACE (HR: 9.779, 95% CI: 1.953-48.964, P = 0.006). Conclusion: The global native T1 mapping could provide incremental values and serve as potential supplements to the current guidelines in the prediction of MACE.

Project description:BackgroundThe HCMR (Hypertrophic Cardiomyopathy Registry) is a National Heart, Lung, and Blood Institute-funded, prospective registry of 2,755 patients with hypertrophic cardiomyopathy (HCM) recruited from 44 sites in 6 countries.ObjectivesThe authors sought to improve risk prediction in HCM by incorporating cardiac magnetic resonance (CMR), genetic, and biomarker data.MethodsDemographic and echocardiographic data were collected. Patients underwent CMR including cine imaging, late gadolinium enhancement imaging (LGE) (replacement fibrosis), and T1 mapping for measurement of extracellular volume as a measure of interstitial fibrosis. Blood was drawn for the biomarkers N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin T (cTnT), and genetic analysis.ResultsA total of 2,755 patients were studied. Mean age was 49 ± 11 years, 71% were male, and 17% non-white. Mean ESC (European Society of Cardiology) risk score was 2.48 ± 0.56. Eighteen percent had a resting left ventricular outflow tract (LVOT) gradient ≥30 mm Hg. Thirty-six percent had a sarcomere mutation identified, and 50% had any LGE. Sarcomere mutation-positive patients were more likely to have reverse septal curvature morphology, LGE, and no significant resting LVOT obstruction. Those that were sarcomere mutation negative were more likely to have isolated basal septal hypertrophy, less LGE, and more LVOT obstruction. Interstitial fibrosis was present in segments both with and without LGE. Serum NT-proBNP and cTnT levels correlated with increasing LGE and extracellular volume in a graded fashion.ConclusionsThe HCMR population has characteristics of low-risk HCM. Ninety-three percent had no or only mild functional limitation. Baseline data separated patients broadly into 2 categories. One group was sarcomere mutation positive and more likely had reverse septal curvature morphology, more fibrosis, but less resting obstruction, whereas the other was sarcomere mutation negative and more likely had isolated basal septal hypertrophy with obstruction, but less fibrosis. Further follow-up will allow better understanding of these subgroups and development of an improved risk prediction model incorporating all these markers.

Project description:To determine the utility of cardiac magnetic resonance (MR) T1 mapping for quantification of diffuse myocardial fibrosis compared with the standard of endomyocardial biopsy.This HIPAA-compliant study was approved by the institutional review board. Cardiomyopathy patients were retrospectively identified who had undergone endomyocardial biopsy and cardiac MR at one institution during a 5-year period. Forty-seven patients (53% male; mean age, 46.8 years) had undergone diagnostic cardiac MR and endomyocardial biopsy. Thirteen healthy volunteers (54% male; mean age, 38.1 years) underwent cardiac MR as a reference. Myocardial T1 mapping was performed 10.7 minutes ± 2.7 (standard deviation) after bolus injection of 0.2 mmol/kg gadolinium chelate by using an inversion-recovery Look-Locker sequence on a 1.5-T MR imager. Late gadolinium enhancement was assessed by using gradient-echo inversion-recovery sequences. Cardiac MR results were the consensus of two radiologists who were blinded to histopathologic findings. Endomyocardial biopsy fibrosis was quantitatively measured by using automated image analysis software with digital images of specimens stained with Masson trichrome. Histopathologic findings were reported by two pathologists blinded to cardiac MR findings. Statistical analyses included Mann-Whitney U test, analysis of variance, and linear regression.Median myocardial fibrosis was 8.5% (interquartile range, 5.7-14.4). T1 times were greater in control subjects than in patients without and in patients with evident late gadolinium enhancement (466 msec ± 14, 406 msec ± 59, and 303 msec ± 53, respectively; P < .001). T1 time and histologic fibrosis were inversely correlated (r = -0.57; 95% confidence interval: -0.74, -0.34; P < .0001). The area under the curve for myocardial T1 time to detect fibrosis of greater than 5% was 0.84 at a cutoff of 383 msec.Cardiac MR with T1 mapping can provide noninvasive evidence of diffuse myocardial fibrosis in patients referred for evaluation of cardiomyopathy.

Project description:BackgroundThe term "end stage" has been used to describe hypertrophic cardiomyopathy (HCM) with left ventricular systolic dysfunction (LVSD), defined as occurring when left ventricular ejection fraction is <50%. The prognosis of HCM-LVSD has reportedly been poor, but because of its relative rarity, the natural history remains incompletely characterized.MethodsData from 11 high-volume HCM specialty centers making up the international SHaRe Registry (Sarcomeric Human Cardiomyopathy Registry) were used to describe the natural history of patients with HCM-LVSD. Cox proportional hazards models were used to identify predictors of prognosis and incident development.ResultsFrom a cohort of 6793 patients with HCM, 553 (8%) met the criteria for HCM-LVSD. Overall, 75% of patients with HCM-LVSD experienced clinically relevant events, and 35% met the composite outcome (all-cause death [n=128], cardiac transplantation [n=55], or left ventricular assist device implantation [n=9]). After recognition of HCM-LVSD, the median time to composite outcome was 8.4 years. However, there was substantial individual variation in natural history. Significant predictors of the composite outcome included the presence of multiple pathogenic/likely pathogenic sarcomeric variants (hazard ratio [HR], 5.6 [95% CI, 2.3-13.5]), atrial fibrillation (HR, 2.6 [95% CI, 1.7-3.5]), and left ventricular ejection fraction <35% (HR, 2.0 [95% CI, 1.3-2.8]). The incidence of new HCM-LVSD was ≈7.5% over 15 years. Significant predictors of developing incident HCM-LVSD included greater left ventricular cavity size (HR, 1.1 [95% CI, 1.0-1.3] and wall thickness (HR, 1.3 [95% CI, 1.1-1.4]), left ventricular ejection fraction of 50% to 60% (HR, 1.8 [95% CI, 1.2, 2.8]-2.8 [95% CI, 1.8-4.2]) at baseline evaluation, the presence of late gadolinium enhancement on cardiac magnetic resonance imaging (HR, 2.3 [95% CI, 1.0-4.9]), and the presence of a pathogenic/likely pathogenic sarcomeric variant, particularly in thin filament genes (HR, 1.5 [95% CI, 1.0-2.1] and 2.5 [95% CI, 1.2-5.1], respectively).ConclusionsHCM-LVSD affects ≈8% of patients with HCM. Although the natural history of HCM-LVSD was variable, 75% of patients experienced adverse events, including 35% experiencing a death equivalent an estimated median time of 8.4 years after developing systolic dysfunction. In addition to clinical features, genetic substrate appears to play a role in both prognosis (multiple sarcomeric variants) and the risk for incident development of HCM-LVSD (thin filament variants).

Dataset Information

Quality assurance of quantitative cardiac T1-mapping in multicenter clinical trials - A T1 phantom program from the hypertrophic cardiomyopathy registry (HCMR) study.

Background

Purpose

Methods

Results

Conclusions

Publications

Quality assurance of quantitative cardiac T1-mapping in multicenter clinical trials - A T1 phantom program from the hypertrophic cardiomyopathy registry (HCMR) study.

Similar Datasets

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