Post-contrast T1 Time Research Articles

Magnetic resonance post-contrast T1 mapping in the human atrium: validation and impact on clinical outcome after catheter ablation for atrial fibrillation.

The impact of diffuse atrial fibrosis detected by T1 mapping on the clinical outcome after atrial fibrillation (AF) ablation is unknown. This study aimed to validate and assess the impact of post-contrast cardiac magnetic resonance (CMR) imaging atrial T1 mapping on the clinical outcome after catheter ablation for AF. CMR imaging was performed in 3 groups by using a clinical 1.5-T scanner: controls, patients with paroxysmal AF, and patients with persistent AF. A T1 mapping sequence was used to calculate the post-contrast T1 relaxation time (T1 time) at the interatrial septum as an index of diffuse atrial fibrosis. A subset underwent left atrial endocardial bipolar voltage mapping for electrophysiologic correlation. After AF ablation, patients underwent clinical review and 7-day Holter monitoring at 6-month intervals. One hundred thirty-two patients (20 controls, 71 (63%) patients with paroxysmal AF, and 41 (37%) patients with persistent AF) underwent CMR imaging. Post-contrast atrial T1 time was significantly shorter in AF groups (237 ± 42 ms) than in controls (280 ± 37 ms) (P < .001). Post-contrast atrial T1 time correlated with mean septal voltage (R2 = .48; P < .001) and global left atrial voltage (R(2) = .41; P < .001). A diagnosis of AF, AF duration, and left ventricular end-diastolic volume independently predicted shortened post-contrast atrial T1 time. The single procedure success rate was 74% at 12 ± 5 months postablation. Post-contrast atrial T1 time was the only predictor of arrhythmia recurrence in multivariate analysis (P = .015). A post-contrast atrial T1 time of >230 ms was associated with freedom from AF in 85% relative to 62% with a post-contrast atrial T1 time of <230 ms (P = .01). Post-contrast atrial T1 time as measured using CMR imaging provides an index of atrial fibrosis that correlates with tissue voltage, presence of AF, and clinical outcomes after catheter ablation.

A comprehensive evaluation of myocardial fibrosis in hypertrophic cardiomyopathy with cardiac magnetic resonance imaging: linking genotype with fibrotic phenotype.

In hypertrophic cardiomyopathy (HCM), attempts to associate genotype with phenotype have largely been unsuccessful. More recently, cardiac magnetic resonance (CMR) imaging has enhanced myocardial fibrosis characterization, while next-generation sequencing (NGS) can identify pathogenic HCM mutations. We used CMR and NGS to explore the link between genotype and fibrotic phenotype in HCM. One hundred and thirty-nine patients with HCM and 25 healthy controls underwent CMR to quantify regional myocardial fibrosis with late gadolinium enhancement (LGE) and diffuse myocardial fibrosis with post-contrast T1 mapping. Collagen content of myectomy specimens from nine HCM patients was determined. Fifty-six HCM patients underwent NGS for 65 cardiomyopathy genes, including 36 HCM-associated genes. Post-contrast myocardial T1 time correlated histologically with myocardial collagen content (r = -0.70, P = 0.03). Compared with controls, HCM patients had more LGE (4.6 ± 6.1 vs. 0%, P < 0.001) and lower post-contrast T1 time (483 ± 83 vs. 545 ± 49 ms, P < 0.001). LGE negatively correlated with left-ventricular (LV) ejection fraction and outflow tract obstruction, whereas lower post-contrast T1 time, suggestive of more diffuse myocardial fibrosis, was associated with LV diastolic impairment and dyspnoea. Patients with identifiable HCM mutations had more LGE (7.9 ± 8.6 vs. 3.1 ± 4.3%, P = 0.03), but higher post-contrast T1 time (498 ± 81 vs. 451 ± 70 ms, P = 0.03) than patients without. In HCM, contrast-enhanced CMR with T1 mapping can non-invasively evaluate regional and diffuse patterns of myocardial fibrosis. These patterns of fibrosis occur independently of each other and exhibit distinct clinical associations. HCM patients with recognized genetic mutations have significantly more regional, but less diffuse myocardial fibrosis than those without.

Letter by Barison et al Regarding Article, “Cardiac Magnetic Resonance Postcontrast T1 Time Is Associated With Outcome in Patients With Heart Failure and Preserved Ejection Fraction”

HomeCirculation: Cardiovascular ImagingVol. 7, No. 2Letter by Barison et al Regarding Article, “Cardiac Magnetic Resonance Postcontrast T1 Time Is Associated With Outcome in Patients With Heart Failure and Preserved Ejection Fraction” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Barison et al Regarding Article, “Cardiac Magnetic Resonance Postcontrast T1 Time Is Associated With Outcome in Patients With Heart Failure and Preserved Ejection Fraction” Andrea Barison, Giovanni Donato Aquaro and Pier Giorgio Masci Andrea BarisonAndrea Barison Fondazione Toscana Gabriele Monasterio, Pisa, Italy Search for more papers by this author , Giovanni Donato AquaroGiovanni Donato Aquaro Fondazione Toscana Gabriele Monasterio, Pisa, Italy Search for more papers by this author and Pier Giorgio MasciPier Giorgio Masci Fondazione Toscana Gabriele Monasterio, Pisa, Italy Search for more papers by this author Originally published1 Mar 2014https://doi.org/10.1161/CIRCIMAGING.113.001598Circulation: Cardiovascular Imaging. 2014;7:414To the EditorT1 mapping cardiovascular magnetic resonance (CMR) is achieving growing importance because it allows quantification of diffuse fibrosis not detectable with conventional late gadolinium enhancement technique. Mascherbauer et al1 wrote an elegant article on the diagnostic and prognostic role of postcontrast T1 mapping in patients with heart failure with preserved ejection fraction, a condition of increasing clinical relevance. In particular, they demonstrated that postcontrast T1 mapping values correlated with established clinical, echocardiographic, hemodynamic, and biohumoral markers of disease and independently predicted major events during a 17±13-month follow-up. They used a relatively simple and robust imaging protocol2: a midventricular short axis was acquired 15 minutes after contrast injection (0.1 mmol/kg gadolinium) using a conventional inversion recovery spoiled gradient-echo sequence with multiple inversion times. Although they did not correct for precontrast T1 values or for hematocrit, to derive the extracellular volume fraction, postcontrast T1 values showed excellent correlation with cardiac fibrosis at histology.Overall, this article represents a milestone on the diagnostic and prognostic importance of CMR to study interstitial remodeling in patients with heart failure with preserved ejection fraction, which accounts for approximately 50% of heart failure cases and holds poor prognosis. In these patients, CMR has indeed become the gold standard method to assess not only biventricular, biatrial, and pericardial morphology, biventricular volumes, and systolic function, but also ultrastructural characterization.3,4 Nevertheless, the authors did not provide a comprehensive analysis of myocardial tissue characterization: after excluding patients with ischemic heart disease, amyloidosis, and sarcoidosis, as well as myocardial areas with late gadolinium enhancement, they did not mention the presence and extent of late gadolinium enhancement in the study population as a conventional marker of macroscopic myocardial fibrosis compared with the microscopic fibrosis assessed with postcontrast T1 mapping. Moreover, no data about precontrast signal intensity (on T1 mapping, T2 mapping, or T2-short tau inversion recovery imaging) were presented as conventional markers of myocardial edema and ongoing cell damage. A comparison between these conventional methods of myocardial tissue characterization with the novel postcontrast T1 mapping findings presented in the article would create a more comprehensive picture on the diagnostic and prognostic role of T1 mapping CMR in patients with heart failure.Finally, little is known about gadolinium kinetics in patients with heart failure, which is potentially characterized by marked interstitial expansion and abnormal gadolinium wash-in and wash-out kinetics from both the myocardium and the blood pool. In this article, T1 acquisitions were performed only 15 minutes after bolus, with no serial T1 acquisitions to demonstrate a blood–myocardium steady-state equilibrium or to exclude a pathological gadolinium kinetics.Further studies are required before T1 mapping becomes clinically useful for characterization of the cardiac interstitium and clinical management of patients with heart failure, compared with conventional CMR imaging as well as with other imaging techniques. In particular, future studies are needed to address all potentially relevant parameters (contrast delivery rate, dose, agent, acquisition timing, sequences) known to affect results to improve the sensitivity and reproducibility of the technique across different vendors and different centers.5Andrea Barison, MD, PhDGiovanni Donato Aquaro, MDPier Giorgio Masci, MDFondazione Toscana Gabriele MonasterioPisa, ItalyDisclosuresNone.

Interstitial Fibrosis, Left Ventricular Remodeling, and Myocardial Mechanical Behavior in a Population-Based Multiethnic Cohort

Background— Tagged cardiac magnetic resonance provides detailed information on regional myocardial function and mechanical behavior. T1 mapping by cardiac magnetic resonance allows noninvasive quantification of myocardial extracellular expansion (ECE), which has been related to interstitial fibrosis in previous clinical and subclinical studies. We assessed sex-associated differences in the relation of ECE to left ventricular (LV) remodeling and myocardial systolic and diastolic deformation in a large community-based multiethnic population. Methods and Results— Midventricular midwall peak circumferential shortening and early diastolic strain rate and LV torsion and torsional recoil rate were determined using cardiac magnetic resonance tagging. Midventricular short-axis T1 maps were acquired in the same examination pre- and postcontrast injection using Modified Look-Locker Inversion-Recovery sequence. Multivariable linear regression (estimated regression coefficient, B ) was used to adjust for risk factors and subclinical disease measures. Of 1230 participants, 114 had a visible myocardial scar by late gadolinium enhancement. Participants without a visible myocardial scar (n=1116) had no history of previous clinical events. In the latter group, multivariable linear regression demonstrated that lower postcontrast T1 times, reflecting greater ECE, were associated with lower circumferential shortening ( B =−0.1; P =0.0001), lower LV end-diastolic volume index ( B =0.6; P =0.0001), and lower LV end-diastolic mass index ( B =0.4; P =0.0001). In addition, lower postcontrast T1 times were associated with lower early diastolic strain rate ( B =0.01; P =0.03) in women only and lower LV torsion ( B =0.005; P =0.03) and lower LV ejection fraction (B=0.2, P =0.01) in men only. Conclusions— Greater ECE is associated with reduced LV end-diastolic volume index and LV end-diastolic mass index in a large multiethnic population without history of previous cardiovascular events. In addition, greater ECE is associated with reduced circumferential shortening, lower early diastolic strain rate, and a preserved ejection fraction in women, whereas in men, greater ECE is associated with greater LV dysfunction manifested as reduced circumferential shortening, reduced LV torsion, and reduced ejection fraction.

Long-term outcome of transitory “reversible” complete atrio-ventricular block unrelated to myocardial ischemia

fraction: comorbidities drive myocardial dysfunction and remodeling through coronarymicrovascular endothelial inflammation. J AmColl Cardiol 2013;62:263–71. [15] Sekhri V, Sanal S, DeLorenzo LJ, Aronow WS, Maguire GP. Cardiac sarcoidosis: a comprehensive review. Arch Med Sci 2011;7(4):546–54. [16] Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2009;119(14):e391–479. [17] Baughman RP, Teirstein AS, Judson MA, et al. Clinical characteristics of patients in a case control study of sarcoidosis. Am J Respir Crit Care Med 2001;164:1885–9. [18] Quarta G, Holdright DR, Plant GT, et al. Cardiovascular magnetic resonance in cardiac sarcoidosis with MR conditional pacemaker in situ. J Cardiovasc Magn Reson 2011;13:26. [19] Fang L, Beale A, Ellims AH, et al. Associations between fibrocytes and postcontrast myocardial T1 times in hypertrophic cardiomyopathy. J Am Heart Assoc 2013;2(5): e000270.

Reproducibility of multiple T1 Mapping techniques and to ECV quantification

Background T1 Mapping has emerged as a new marker to quantify myocardial extracellular volume (ECV), which is typically increased in the setting of diffuse fibrosis or infiltrative heart diseases. However the reproducibility of the technique is largely unknown. We sought to identify the interobserver, intraobserver variability of different T1 mapping techniques as well as validation of one technique against the standard technique for ECV quantification. Methods We selected 10 patients with the diagnosis of cardiomyopathy (5 with delayed contrast enhancement and 5 without). The Look-Locker (LL) and Modified Look-Locker both precontrast (MOLLI_Pre) and postcontrast (MOLLI_Post) T1 time were measured by 3 investigators blinded to clinical data at 2 different time points. Interobserver and Intraobserver reproducibility were assessed using 2-way ANOVA approach. The ECV was calculated using pre and post contrast T1 and hematocrit. Results There was a strong correlation between LL T1 and Postcontrast MOLLI(MOLLI_Post) (R2 0.82, p < 0.001) and a modest correlation between MOLLI_post and ECV (R2 = 0.42, p < 0.001). The interobserver and intraobserver variability of the measurements were expressed as standard errors of measurements (SEM) and 95% CI and were summarized in table 1. MOLLI_Post had the lowest intraobserver and intraobserver variability with minimal detectable change in T1 of 13.8 and 26.1 respectively. ECV showed minimal both interobserver and intraobserver variability. Conclusions Both LL and MOLLI are highly reproducible technique. LL was strongly correlated with post-contrast MOLLI which is moderately correlated to ECV. Funding None.

Abstract 18189: Focal Fibrosis and Diffuse Fibrosis Are Predictors of Positive Left Ventricular Remodeling in Patients With Non-Ischemic Cardiomyopathy

Background: Prognostic value of myocardial fibrosis in patients with non-ischemic idiopathic cardiomyopathy (NICM) is not well-defined. We sought to assess the association of focal and diffuse myocardial fibrosis to left ventricular reversed remodeling. Methods: Patients with NICM who underwent cardiac MRI and baseline and subsequent follow-up echocardiographic were included in the study. Post-contrast T1 times were measured using Look-Locker gradient echo, and was adjusted for renal function, body size, gadolinium dose and delayed time after Gadolinium injection. Patients were followed over a median time of 29 months (20,37) to evaluate changes of left ventricular end-systolic volume index (LVESVi) over time. Linear Mixed Model was used to assess the relationship between the LVESVi during follow-up,T1 value, and delayed hyperenhancement (DHE). Results: A total of 103 patients (mean age 51±15 years, 62% male) were included in the analysis. Mean LVEF 32±10%, LVESVi 62±39 ml/m2, and T1 time 415+98. DHE was identified in 45 patients (44%). Age, LVEF and LVESVi in patients with DHE are not statistically different compared to patients without DHE. Patient with DHE were more likely to be male (32 vs 11, p=0.024) and had lower T1 time (381±104 Vs 440±87, p=0.003). Patients with focal DHE (n=45) had higher LVESVi at baseline and during follow-up, compared to the patients with no DHE (Δ= 11.3 ml/m2 SE 8.8 ml/2, p= 0.024) (Figure A). However, post T1 values of the myocardium without DHE were not associated with differences in LVESVi. In patients without DHE (n=58), T1 value &gt; 450 was associated with further reduction in LVESVi at the follow-up (Δ= 24.6 ml/m2 SE 14.6 ml/2, p= 0.048)(Figure B.) Conclusion: Presence of myocardial DHE, but not T1 value, is a marker of LV reversed remodeling in NICM patients. However, diffuse fibrosis predicts LV reversed remodling in patients without DHE.

Cardiac Magnetic Resonance Postcontrast T1 Time Is Associated With Outcome in Patients With Heart Failure and Preserved Ejection Fraction

The underlying pathophysiology of heart failure with preserved ejection fraction (HFPEF) is incompletely understood, but myocardial extracellular matrix accumulation is thought to play a major role. Our aims were to estimate myocardial extracellular matrix using cardiac magnetic resonance T1 mapping and to assess the relationship between pathobiology/pathophysiology and prognosis. Patients with suspected HFPEF (n=100) were enrolled in this prospective, observational study. Confirmatory diagnostic tests, cardiac magnetic resonance imaging including T1 mapping, and invasive hemodynamic assessments were performed at baseline. Sixty-one patients with confirmed HFPEF entered a longitudinal outcome-monitoring phase (mean, 22.9±5.0 months), during which 16 had a cardiac event. Cardiac magnetic resonance T1 time (hazard ratio, 0.99; 95% confidence interval, 0.98-0.99; P=0.046), left atrial area (hazard ratio, 1.08; 95% confidence interval, 1.03-1.13; P<0.01), and pulmonary vascular resistance (hazard ratio, 1.01; 95% confidence interval, 1.00-1.01; P=0.03) were significantly associated with cardiac events. Patients with T1 times below the median (<388.3 ms) were at greater risk of cardiac events than the rest of the group (P<0.01). Extracellular matrix of left ventricular biopsies (n=9), quantified by TissueFAXS technology correlated with T1 time (R=0.98; P<0.01). T1 time also correlated with right ventricular-pulmonary arterial coupling (pulmonary vascular resistance: R=-0.36; P<0.01; right ventricular ejection fraction: R=0.28; P=0.01). In the present preliminary study, cardiac magnetic resonance postcontrast T1 time is associated with prognosis in HFPEF, suggesting postcontrast T1 as possible biomarker for HFPEF.

Diffuse and regional patterns of myocardial fibrosis in hypertrophic cardiomyopathy occur independently of each other and have distinct clinical associations

Purpose: Previously, in hypertrophic cardiomyopathy (HCM), only dense regional fibrosis could be identified by cardiac magnetic resonance (CMR) imaging with late gadolinium enhancement (LGE) sequences. Recently, post-contrast T1 mapping has also enabled quantification of diffuse myocardial fibrosis. We sought to explore relationships between both patterns of myocardial fibrosis and several clinical parameters in a typical cohort of patients with HCM. Methods: We performed contrast-enhanced CMR on 123 patients (67% male, mean age 51±14 years) with documented HCM. Regional myocardial fibrosis was evaluated by LGE sequences, and diffuse fibrosis by post-contrast T1 mapping. Correlations between both patterns of fibrosis and patients' clinical characteristics, CMR-derived LV volumetric data and echocardiographic findings were investigated. Results: LGE consistent with HCM was observed in 88% of patients with a mean quantity of 4.6±6.3% of total LV mass, and mean post-contrast myocardial T1 time was 495±81 ms. LGE extent correlated with LV ejection fraction (r = -0.48, p < 0.01) whereas T1 time did not. Conversely, T1 time correlated with E/e' (r = -0.46, p < 0.01) whereas LGE extent did not. Patients with LV outflow tract obstruction had less LGE (3.1±5.6% vs. 6.9±7.5%, p < 0.05), but similar T1 times. Patients with exertional dyspnoea had shorter T1 times (485±84 ms vs. 521±71 ms, p < 0.05), but similar LGE extent. No relationship was observed between LGE and post-contrast T1 time. Conclusions: In HCM, regional and diffuse patterns of myocardial fibrosis occur independently of each other and exhibit distinct clinical associations. Regional fibrosis is associated with reduced LV systolic function and the absence of LV outflow tract obstruction, whereas diffuse fibrosis is associated with higher LV filling pressures and the presence of exertional dyspnoea.

Letter by Iles and Taylor Regarding Article, “Comprehensive Validation of Cardiovascular Magnetic Resonance Techniques for the Assessment of Myocardial Extracellular Volume”

The study by Miller et al1 evaluated cardiac magnetic resonance (CMR) techniques in the assessment of myocardial extracellular volume (ECV). Two commonly used measures of ECV expansion, namely dynamic-equilibrium CMR and isolated measurement of postcontrast myocardial T1 time, were compared with histological analysis of the explanted hearts of transplant recipients. Both measures proved remarkably similar in their correlation with histology on a within-subject basis, with r values of a similar absolute magnitude (≈0.7). However, when correlation was sought on a between-subject basis, dynamic-equilibrium CMR demonstrated a significant correlation with histology ( r value 0.95; P =0.004), whereas postcontrast T1 time did not ( r value …

Cardiovascular Associations and Prognostic Utility of Abdominal Aortic Calcification on Dual-energy X-ray Absorptiometry in Post-menopausal Women

and tissue composition in patientswith biopsy-proven cirrhosis. Methods and Results: Contrast-enhanced CMR imaging for morphological, functional and tissue characterization was performed on 17 patients with cirrhosis and 21 healthy controls. Cardiac structure and function was assessed with standard cine imaging, with post contrast delayed enhancement and myocardial T1 mapping performed to evaluate regional and diffuse myocardial fibrosis respectively. Compared to controls, patients with cirrhosisdemonstrated lower left ventricular end-diastolic volume (135± 36 versus 171± 43, p< 0.05) and a lower post-contrast T1 time consistent with diffuse myocardial fibrosis (489± 88 versus 547± 136, p< 0.05). There were no differences in other cardiac parameters including left ventricular mass and ejection fraction (p-value insignificant for each comparisons). No patients in either group had evidence of regional fibrosis on post contrast imaging. Conclusion:Compared to controls, patientswith cirrhosis have lower LVEDV and lower post-contrast T1-times consistent with diffuse myocardial fibrosis. However, systolic function and left ventricular mass are preserved. http://dx.doi.org/10.1016/j.hlc.2013.05.400

Diffuse myocardial fibrosis by post-contrast T1-time predicts outcome in heart failure with preserved ejection fraction

Background Diffuse myocardial fibrosis plays a key role in disease progression of heart failure with preserved ejection fraction (HFPEF). Recently it was shown that diffuse myocardial fibrosis is strongly related to post-contrast longitudinal relaxation (T1) time by cardiac magnetic resonance imaging (CMR). The aim of our study was to assess diffuse myocardial fibrosis by CMR T1-mapping in HFPEF patients and test its predictive value.

Acute Left Ventricular Remodeling Following Myocardial Infarction: Coupling of Regional Healing With Remote Extracellular Matrix Expansion

This prospective study aimed to assess regional and temporal patterns of extracellular matrix (ECM) changes post-myocardial infarction (MI). A fundamental process in the development of ischemic left ventricular (LV) dysfunction is LV remodeling, characterized by structural and functional abnormalities throughout the myocardium including the noninfarcted (remote) myocardium and interstitium. Contrast-enhanced cardiac magnetic resonance (CMR) was performed on MI patients acutely (mean: 5 days post-MI, n = 25) and repeated subacutely (mean: 139 days post-MI, n = 21), and was also performed in a separate group of 15 patients with chronic MI (mean: 2,580 days post-MI, n = 15). Twenty volunteers without a history of MI acted as controls. CMR was used to evaluate LV morphology and function, with post-contrast T1 mapping to semiquantitatively assess changes in the ECM. Putative mediators of myocardial inflammation and fibrosis, including macrophage migration inhibitory factor (MIF), were also measured. Age, sex, and diabetic and hypertensive status did not differ between MI groups and controls. Compared with controls, patients early post-acute MI demonstrated reduced LV ejection fraction (50.25 ± 7.29% vs. 66.7 ± 6.2% [controls], p < 0.0001). Myocardium remote to the infarction early post-acute MI, compared with controls, demonstrated reduced systolic thickening (60 ± 5.0% vs. 106 ± 7.6%, p ≤ 0.0002), and lower post-contrast myocardial T1 times suggestive of ECM expansion (437 ± 113 ms vs. 549 ± 119 ms, p = 0.01). In a subgroup analysis between early post-acute MI and controls of similar age and sex, the remote sector post-contrast myocardial T1 times remained significantly shorter post-acute MI compared with controls (420 ± 121 ms vs. 529 ± 113 ms, p = 0.03). Serum levels of MIF inversely correlated with global myocardial T1 time in patients early post-acute MI (r = -0.6, p = 0.01), suggesting a coupling of regional healing with acute LV remodeling. Within a week of acute MI, the remote myocardium exhibits systolic dysfunction and expansion of the ECM, which is coupled with physiological infarct healing. Further prospective studies with larger sample sizes are needed to verify these important findings.

Assessment of cardiac involvement in myotonic muscular dystrophy by T1 mapping on magnetic resonance imaging.

Patients with myotonic muscular dystrophy (DM) are at risk for atrioventricular block and left ventricular (LV) dysfunction. Noninvasive detection of diffuse myocardial fibrosis may improve disease management in this population. To define functional and postcontrast myocardial T1 time cardiac magnetic resonance characteristics in patients with DM. Thirty-three patients with DM (24 with type 1 and 9 with type 2) and 13 healthy volunteers underwent cardiac magnetic resonance for the assessment of LV indices and the evaluation of diffuse myocardial fibrosis by T1 mapping. The association of myocardial T1 time with electrocardiogram abnormalities and LV indices was examined among patients with DM. Patients with DM had lower end-diastolic volume index (68.9 mL/m(2) vs 60.3 mL/m(2); P = .045) and cardiac index (2.7 L/min/m(2) vs 2.33 L/min/m(2); P = .005) and shorter myocardial T1 time (394.5 ms vs 441.4 ms; P < .0001) than did control subjects. Among patients with DM, there was a positive association between higher T1 time and LV mass index (2.2 ms longer per g/m(2); P = .006), LV end-diastolic volume index (1.3 ms longer per mL/m(2); P = .026), filtered QRS duration (1.2 ms longer per unit; P = .005), and low-amplitude (<40 mcV) late-potential duration (0.9 ms longer per unit; P = .01). Using multivariate random effects regression, each 10-ms increase in myocardial T1 time of patients with type 1 DM was independently associated with 1.3-ms increase in longitudinal PR and QRS intervals during follow-up. DM is associated with structural alterations on cardiac magnetic resonance. Postcontrast myocardial T1 time was shorter in patients with DM than in controls, likely reflecting the presence of diffuse myocardial fibrosis.

Diffuse myocardial fibrosis in hypertrophic cardiomyopathy can be identified by cardiovascular magnetic resonance, and is associated with left ventricular diastolic dysfunction.

BackgroundThe presence of myocardial fibrosis is associated with worse clinical outcomes in hypertrophic cardiomyopathy (HCM). Cardiovascular magnetic resonance (CMR) with late gadolinium enhancement (LGE) sequences can detect regional, but not diffuse myocardial fibrosis. Post-contrast T1 mapping is an emerging CMR technique that may enable the non-invasive evaluation of diffuse myocardial fibrosis in HCM. The purpose of this study was to non-invasively detect and quantify diffuse myocardial fibrosis in HCM with CMR and examine its relationship to diastolic performance.MethodsWe performed CMR on 76 patients - 51 with asymmetric septal hypertrophy due to HCM and 25 healthy controls. Left ventricular (LV) morphology, function and distribution of regional myocardial fibrosis were evaluated with cine imaging and LGE. A CMR T1 mapping sequence determined the post-contrast myocardial T1 time as an index of diffuse myocardial fibrosis. Diastolic function was assessed by transthoracic echocardiography.ResultsRegional myocardial fibrosis was observed in 84% of the HCM group. Post-contrast myocardial T1 time was significantly shorter in patients with HCM compared to controls, consistent with diffuse myocardial fibrosis (498 ± 80 ms vs. 561 ± 47 ms, p < 0.001). In HCM patients, post-contrast myocardial T1 time correlated with mean E/e’ (r = −0.48, p < 0.001).ConclusionsPatients with HCM have shorter post-contrast myocardial T1 times, consistent with diffuse myocardial fibrosis, which correlate with estimated LV filling pressure, suggesting a mechanistic link between diffuse myocardial fibrosis and abnormal diastolic function in HCM.

T1 mapping of the myocardium: intra-individual assessment of post-contrast T1 time evolution and extracellular volume fraction at 3T for Gd-DTPA and Gd-BOPTA.

PurposeMyocardial T1 relaxation time (T1 time) and extracellular volume fraction (ECV) are altered in patients with diffuse myocardial fibrosis. The purpose of this study was to perform an intra-individual assessment of normal T1 time and ECV for two different contrast agents.MethodsA modified Look-Locker Inversion Recovery (MOLLI) sequence was acquired at 3 T in 24 healthy subjects (8 men; 28 ± 6 years) at mid-ventricular short axis pre-contrast and every 5 min between 5-45 min after injection of a bolus of 0.15 mmol/kg gadopentetate dimeglumine (Gd-DTPA; Magnevist®) (exam 1) and 0.1 mmol/kg gadobenate dimeglumine (Gd-BOPTA; Multihance®) (exam 2) during two separate scanning sessions. T1 times were measured in myocardium and blood on generated T1 maps. ECVs were calculated as .ResultsMean pre-contrast T1 relaxation times for myocardium and blood were similar for both the first and second CMR exam (p > 0.5). Overall mean post-contrast myocardial T1 time was 15 ± 2 ms (2.5 ± 0.7%) shorter for Gd-DTPA at 0.15 mmol/kg compared to Gd-BOPTA at 0.1 mmol/kg (p < 0.01) while there was no significant difference for T1 time of blood pool (p > 0.05). Between 5 and 45 minutes after contrast injection, mean ECV values increased linearly with time for both contrast agents from 0.27 ± 0.03 to 0.30 ± 0.03 (p < 0.0001). Mean ECV values were slightly higher (by 0.01, p < 0.05) for Gd-DTPA compared to Gd-BOPTA. Inter-individual variation of ECV was higher (CV 8.7% [exam 1, Gd-DTPA] and 9.4% [exam 2, Gd-BOPTA], respectively) compared to variation of pre-contrast myocardial T1 relaxation time (CV 4.5% [exam 1] and 3.0% [exam 2], respectively). ECV with Gd-DTPA was highly correlated to ECV by Gd-BOPTA (r = 0.803; p < 0.0001).ConclusionIn comparison to pre-contrast myocardial T1 relaxation time, variation in ECV values of normal subjects is larger. However, absolute differences in ECV between Gd-DTPA and Gd-BOPTA were small and rank correlation was high. There is a small and linear increase in ECV over time, therefore ideally images should be acquired at the same delay after contrast injection.

The protein binding substance ibuprofen does not affect the T1 time or partition coefficient in contrast-enhanced cardiovascular magnetic resonance.

BackgroundContrast enhanced cardiovascular magnetic resonance (CMR) with T1 mapping enables quantification of diffuse myocardial fibrosis. Various factors, however, can interfere with T1 measurements. The purpose of the current study was to assess the effect of co-medication with a typical protein binding drug (Ibuprofen) on T1 values in vitro and in vivo.Methods50 vials were prepared with different concentrations of gadobenate dimeglumine, Ibuprofen and human serum albumin in physiologic NaCl solution and imaged at 1.5T with a spin echo sequence at multiple TRs to measure T1 values and calculate relaxivities. 10 volunteers (5 men; 31±6.3 years) were imaged at 1.5T. T1 values for myocardium and blood pool were determined for various time points after administration of 0.15mmol/kg gadobenate dimeglumine using a modified look-locker inversion-recovery sequence before and after administration of Ibuprofen over 24 hours. The partition coefficient was calculated as ΔR1myocardium/ΔR1blood, where R1=1/T1.ResultsIn vitro no significant correlation was found between relaxivity and Ibuprofen concentration, neither in absence (r=−0.15, p=0.40) nor in presence of albumin (r=−0.32, p=0.30). In vivo there was no significant difference in post contrast T1 times of myocardium and blood, respectively and also in the partition coefficient between exam 1 and 2 (p>0.05). There was good agreement of the T1 times of myocardium and blood and the partition coefficient, respectively between exam 1 and 2.ConclusionsContrast enhanced T1 mapping is unaffected by co-medication with the protein binding substance Ibuprofen and has an excellent reproducibility.

Myocardial T1 mapping with MRI: Comparison of look‐locker and MOLLI sequences

To evaluate the relationship between "Look-Locker" (LL) and modified Look-Locker Inversion recovery (MOLLI) approaches for T1 mapping of the myocardium. A total of 168 myocardial T1 maps using MOLLI and 165 maps using LL were obtained in human subjects at 1.5 Tesla. The T1 values of the myocardium were calculated before and at five time points after gadolinium administration. All time and heart rate normalizations were done. The T1 values obtained were compared to determine the absolute and bias agreement. The precontrast global T1 values were similar when measured by the LL and by MOLLI technique (mean, 1004.9 ms ± 120.3 versus 1034.1 ms ± 53.1, respectively, P = 0.26). Postcontrast myocardial T1 time from LL was significantly longer than MOLLI from 5 to 25 min (mean difference, LL - MOLLI was +61.8 ± 46.4 ms, P < 0.001). No significant differences in T1 values were noted between long and short axis measurements for either MOLLI or LL. Postcontrast LL and MOLLI showed very good agreement, although LL values are higher than MOLLI. Precontrast T1 values showed good agreement, however LL has greater limits of agreement. Short and long axis planes can reliably assess T1 values.

Assessment of Diffuse Myocardial Fibrosis in Rats Using Small-Animal Look-Locker Inversion Recovery T1 Mapping

The concentration of gadopentetate dimeglumine in myocardium and blood can be assessed from T1 measurements and can be used to calculate the extracellular volume (ECV) of the myocardium. We hypothesized that diffuse myocardial fibrosis in a small-animal model could be quantitatively assessed by measuring myocardial ECV using small-animal Look-Locker inversion recovery T1 mapping. Sprague-Dawley rats (n=10) were subjected to continuous angiotensin-2 (AT2) infusion for 2 weeks via a subcutaneously implanted minipump system. Magnetic resonance imaging (MRI) was performed both before and after AT2 infusion. The MRI protocol included multislice cine imaging and before-and-after contrast small-animal Look-Locker inversion recovery T1 mapping and late gadolinium enhancement imaging. Myocardial ECV was calculated from hematocrit and T1 values of blood and myocardium. During the course of AT2 infusion, the mean±SD systolic blood pressure increased from 122±10.9 to 152±27.5 mm Hg (P=0.003). Normalized heart weight was significantly higher in AT2-treated animals than in control littermates (P=0.033). Cine MRI documented concentric left ventricular hypertrophy. Postcontrast myocardial T1 times were shortened after treatment (median [interquartile range], 712 [63] versus 820 [131] ms; P=0.002). Myocardial ECV increased from 17.2% (4.3%) before to 23.0% (6.2%) after AT2 treatment (P=0.031), which was accompanied by perivascular fibrosis and microscarring on myocardial histological analysis. There was a moderate level of correlation between ECV and collagen volume fraction, as assessed by histological analysis (r=0.69, P=0.013). In a small-animal model of left ventricular hypertrophy, contrast-enhanced T1 mapping can be used to detect diffuse myocardial fibrosis by quantification of myocardial ECV.

Myocardial T1-mapping for early detection of left ventricular myocardial fibrosis in systemic sclerosis

Background Subclinical primary left ventricular (LV) dysfunction is a complication of systemic sclerosis (SSc) related to progressive diffuse myocardial fibrosis. Myocardial T1-mapping has recently been proposed as a cardiac magnetic resonance (CMR) method to quantify interstitial fibrosis early in the disease course whereas late-gadolinium enhancement (LGE) imaging remains normal. Objective We aimed to evaluate whether myocardial T1-mapping could detect subclinical abnormalities in SSc patients with normal standard parameters of LV function and normal LGE imaging. Methods We prospectively studied 37 patients (52±12 years) presenting with SSc with no history of heart disease, no pulmonary hypertension at rest, a normal LV assessed by conventional echocardiography (normal volumes, ejection fraction and wall motion), and no LGE. SSc patients were compared to16 matched controls healthy volunteers (47±7 years old). T1 quantification was performed using a Modified Look-Locker Inversionrecovery (MOLLI) sequence at 1.5T (Siemens) on a LV short axis before, 5min and 15 min after 0.2 mmol/Kg gadolinium injection. Imaging protocol included also standard Cine-SSFP imaging, and LGE imaging. LV diastolic function (mitral inflow pattern) was further assessed using echocardiography. Results A non significant shorter mean T1 time (ms, mean± SEM) was observed in SSc patients compared to controls both at 5 (357±5 vs. 361±6, p=0.65) and 15 (448±5 vs. 456±5, p=0.34) minutes after gadolinium injection. Echocardiography displayed a LV diastolic dysfunction in 47% of SSc patients and in 25% of controls (p=0.04). The SSc patients with a LV diastolic dysfunction had a shorter 15 minutes post-contrast T1 time (ms) than those with a normal diastolic function (431±7 vs. 464±8, p=0.01).