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Background and purpose Magnetic resonance imaging quantitative T2* mapping has shown reliable identification of thrombus red blood cell content in vitro. The thrombus composition has been in vivo, associated with outcomes after endovascular therapy for acute ischemic stroke. We aim to analyze the red blood cell content of thrombi retrieved from patients with large vessel occlusions in relation to the thrombus-T2* relaxation time in magnetic resonance imaging. Material and methods Consecutive acute ischemic stroke patients treated by endovascular therapy were scanned with an magnetic resonance imaging quantitative T2* mapping sequence. Quantitative histologic evaluations of red blood cell content were performed. A linear regression assessed the association between vascular risk factors, comorbidities, antithrombotic drugs intake, baseline National Institutes of Health Stroke Scale (NIHSS), intravenous thrombolysis before endovascular therapy, time between onset and groin puncture, patient's outcome at 3 months, magnetic resonance imaging quantitative T2* mapping results, and the red blood cell content of thrombi. The correlation between the mean thrombus-T2* relaxation time and red blood cell content was assessed by calculating the Pearson correlation coefficient. Results Among 31 thrombi, 16 were “Fibrin rich” and 15 “red blood cell dominant.” The median red blood cell content was 39 (range, 0–90; interquartile range, 37). The median (interquartile range) thrombus-T2* relaxation time was shorter in “red blood cell dominant” thrombi (21, interquartile range 6) than in “Fibrin rich” thrombi (24, interquartile range 7), without significant difference ( p = 0.15), as shown in the Box plot. An inverse correlation between thrombus-T2* relaxation time and red blood cell content was found, with a correlation coefficient of −0.41 (95% CI, −0.67 to −0.08, p = 0.02). Conclusion Our study shows that a shorter thrombus-T2* relaxation time is related to a higher red blood cell content within in vivo thrombi.

Aortic wall 18F-fluorodeoxyglucose (FDG)-uptake does not allow differentiation of aortitis from atheroma, which is problematic in clinical practice for diagnosing large vessel vasculitis giant-cell arteritis (GCA) in elderly patients. The purpose of this study was to compare the FDG uptake characteristics of GCA aortitis and aortic atheroma using positron emission tomography/FDG computed tomography (FDG-PET/CT). This study compared FDG aortic uptake between patients with GCA aortitis and patients with aortic atheroma; previously defined by contrast enhanced CT. Visual grading according to standardized FDG-PET/CT interpretation criteria and semi-quantitative analyses (maximum standardized uptake value (SUVmax), delta SUV (∆SUV), target to background ratios (TBR)) of FDG aortic uptake were conducted. The aorta was divided into 5 segments for analysis. 29 GCA aortitis and 66 aortic atheroma patients were included. A grade 3 FDG uptake of the aortic wall was identified for 23 (79.3%) GCA aortitis patients and none in the atheroma patient group (p max, ∆SUV and TBRs) were significantly higher in the aortitis group. ∆SUV was the feature with the largest differential between aortitis and aortic atheroma. In this study, GCA aortitis could be distinguished from an aortic atheroma by the presence of an aortic wall FDG uptake grade 3, an FDG uptake of the 5 aortic segments, and FDG uptake of the peripheral arteries.

Background: Mitral valve prolapse (MVP) is a frequent disease that can be complicated by mitral regurgitation (MR), heart failure, arterial embolism, rhythm disorders, and death. Left ventricular (LV) replacement myocardial fibrosis, a marker of maladaptive remodeling, has been described in patients with MVP, but the implications of this finding remain scarcely explored. We aimed at assessing the prevalence, pathophysiological and prognostic significance of LV replacement myocardial fibrosis through late gadolinium enhancement (LGE) by cardiac magnetic resonance in patients with MVP. Methods: Four hundred patients (53±15 years of age, 55% male) with MVP (trace to severe MR by echocardiography) from 2 centers, who underwent a comprehensive echocardiography and LGE cardiac magnetic resonance, were included. Correlates of replacement myocardial fibrosis (LGE+), influence of MR degree, and ventricular arrhythmia were assessed. The primary outcome was a composite of cardiovascular events (cardiac death, heart failure, new-onset atrial fibrillation, arterial embolism, and life-threatening ventricular arrhythmia). Results: Replacement myocardial fibrosis (LGE+) was observed in 110 patients (28%; 91 with myocardial wall including 71 with basal inferolateral wall, 29 with papillary muscle). LGE+ prevalence was 13% in trace-mild MR, 28% in moderate MR, and 37% in severe MR, and was associated with specific features of mitral valve apparatus, more dilated LV and more frequent ventricular arrhythmias (45% versus 26%, P P =0.009) and moderate-severe MR (odds ratio, 2.28 [95% CI, 1.21–4.31], P =0.011). LGE+ was associated with worse 4-year cardiovascular event–free survival (49.6±11.7 in LGE+ versus 73.3±6.5% in LGE–, P P =0.002) were associated with poor outcome. Conclusions: LV replacement myocardial fibrosis is frequent in patients with MVP; is associated with mitral valve apparatus alteration, more dilated LV, MR grade, and ventricular arrhythmia; and is independently associated with cardiovascular events. These findings suggest an MVP-related myocardial disease. Last, cardiac magnetic resonance provides additional information to echocardiography in MVP.

Funding Acknowledgements Type of funding sources: None. Background Lamin A/C cardiomyopathy (CM) is an inherited disease due to LMNA gene mutation with particular phenotype that associates conduction disorders, frequent atrial fibrillation and life-threatening ventricular arrhythmias, with normal or altered ventricular systolic function. Cardiac magnetic resonance (CMR) studies suggest frequent late gadolinium enhancement (LGE) involving septal mid-myocardium. Aims To assess the added value of CMR to conventional clinical features of Lamin A/C CM for the prediction of a positive LMNA gene testing. Methods We performed a retrospective monocentric study in all index patients referred for genetic testing for a clinical suspicion of Lamin A/C CM. Clinical, ECG and imaging data including CMR at time of genetic testing in patients with a positive test (LMNA+) and patients without (LMNA-) were compared. The diagnostic performances of relevant parameters for the prediction of a positive LMNA gene testing were analyzed in several logistic regression models. Results 90 patients were included (55 LMNA+, 35 LMNA-).49% had significant left ventricular (LV) dilatation on echocardiography,57% had a LV ejection fraction (LVEF) Conclusion CMR, particularly septal mid-myocardium LGE, carries good diagnostic accuracy to predict a positive LMNA gene testing in clinically suspected Lamin A/C CM with increased specificity when added to conventional red flags. Abstract Figure. Logistic regression models performances

Introduction Left ventricular (LV) replacement myocardial fibrosis has been described in MVP. We aimed at assessing the prevalence, pathophysiological and prognostic significance of LV replacement myocardial fibrosis through late gadolinium enhancement (LGE) by cardiac magnetic resonance (CMR) in MVP Method Four hundred patients (53 ± 15 years, 55% male) with MVP underwent echocardiography and CMR. Correlates of replacement myocardial fibrosis (LGE + ), influence of MR degree, and ventricular arrhythmia were assessed. The primary outcome was a composite of cardiovascular events. Results LGE+ was observed in 110 patients (28%; 91 myocardial wall including 71 basal inferolateral wall, 29 papillary muscle). LGE+ prevalence was 13% in trace-mild MR, 28% in moderate and 37% in severe MR, and was associated with specific features of mitral valve apparatus, more dilated LV and more frequent ventricular arrhythmias (45 vs. 26%, P Fig. 1 ). Conclusion LV replacement myocardial fibrosis is frequent in patients with MVP, is associated with mitral valve apparatus alteration, more dilated LV, MR grade, ventricular arrhythmia, and is independently associated with cardiovascular events. These findings suggest a MVP-related myocardial disease. Finally, CMR provides additional information to echocardiography in MVP.

Introduction Structural valve degeneration (SVD) of surgical bioprostheses (BP) is increasingly diagnosed. We aimed to reappraise aortic BP SVD mode, determinants, effect of treatment and outcome. Method A total of 262 SVD patients (78 ± 9 years, 53.4% males) were enrolled. The mode and determinants of SVD were investigated by echocardiography, surgical and macroscopic evaluation. Mortality and the effect of treatment were assessed. Results The predominant mode of SVD was stenosis (58%). The annualized rate of increase in mean gradient was 4.6 ± 3.2 mmHg/year in stenotic SVD. In multivariable analysis, predictive factors of an earlier SVD were age (P 3000 (HR 2.22, P = 0.004). Conclusion The rate of SVD progression is 4 to 5 mmHg/year on average. BP type and post-operative hemodynamic are predictors of faster SVD. NoCalcif accounts for > 15% of SVD. Leaflet fibrosis is a component of SVD. Redo-surgery and VinV are associated with a better outcome, independently of failure mode, and should be considered in most SVD patients.

Secondary mitral regurgitation (MR) is frequent valvular heart disease and conveys worse prognostic. Therapeutic surgical or percutaneous options are available in the context of severe symptomatic secondary MR, but the best approach to treat these patients remains unclear, given the lack of clear clinical evidence of benefit. A comprehensive evaluation of the mitral valve apparatus and the left ventricle (LV) has the ability to clearly define and characterize the disease, and thus determine the best option for the patient to improve its clinical outcomes, as well as quality of life and symptoms. The current report reviews the mitral valve (MV) anatomy, the underlying mechanisms associated with secondary MR, the related therapeutic options available, and finally the usefulness of a multimodality imaging approach for the planning of surgical or percutaneous mitral valve intervention.

Background Structural valve degeneration (SVD) remains the main complication of aortic bioprosthesis. The study aimed to evaluate SVD mode, outcome and effect of treatment. Methods Patients with presumed aortic SVD by echocardiography in our institution between January 2010 and December 2016 were included. All-cause mortality, cardiovascular morbidity, and effect of treatment were assessed. Results After exclusion of 4 patients with others causes of increased gradients, 220 patients were analyzed (78 ± 9 years, 52% men). Regurgitant SVD (n = 94, 43%) occurred later than stenotic (n = 126, 57%) SVD (9.2 ± 3.7 vs. 7.9 ± 3.0 years; P = 0.003). Patients with a regurgitant SVD were more symptomatic, had a larger bioprosthesis, and were more often referred to invasive management. Exclusive medical care (Med) was retained in 67 patients, redo-surgery in 89 and VinV in 64. Macroscopic examination of explanted bioprostheses (n = 71) demonstrated severe calcifications in 56.3%, mainly in stenotic SVD (71 vs. 42%, P = 0.02), and leaflet tear in 28%. Overall survival at 35 months was significantly associated with the type of management (VinV: 85.3 ± 4.9%, redo-surgery 86.7 ± 3.8%, Med 60.1 ± 7.7%, P Conclusion Structural valve degeneration remains a matter of concern. Regurgitant SVD occurs later than stenotic SVD which is characterized by a more severe calcification process. Redo-surgery and VinV are associated with a better outcome, independently of failure mode, and should be considered in most SVD patients. Although VinV was proposed to older and higher-risk patients, its effect on overall survival was comparable to redo-surgery in multivariable analysis.

BACKGROUND AND PURPOSE: The susceptibility vessel sign on MR imaging has been reported to indicate acute occlusion from erythrocyte-rich thrombus. The purpose of this study was to evaluate the influence of the susceptibility vessel sign seen on MR imaging before treatment on the clinical outcome after mechanical thrombectomy for anterior circulation acute stroke. MATERIALS AND METHODS: We retrospectively included 73 consecutive patients who were treated for anterior circulation acute stroke by mechanical thrombectomy from December 2009 to September 2013. Each patient underwent MR imaging before mechanical thrombectomy. The presence (susceptibility vessel sign+) or absence of the susceptibility vessel sign (susceptibility vessel sign−) was recorded. Mechanical thrombectomy was performed either alone or in association with IV tPA according to the site and time after occlusion. Good functional outcome was defined by an mRS ≤2 at 3 months in susceptibility vessel sign+ and susceptibility vessel sign− groups. Patient clinical characteristics, initial NIHSS score and ASPECTS, site of occlusion, time between onset to groin puncture, TICI after mechanical thrombectomy, NIHSS score at day 1, and spontaneous hyperattenuation on CT at day 1 were also analyzed. RESULTS: Fifty-three patients with susceptibility vessel sign+ and 20 with susceptibility vessel sign− were included in our study. mRS ≤2 at 3 months occurred in 65% patients in the susceptibility vessel sign+ group and 26% in the susceptibility vessel sign− group ( P = .004). On multivariate analysis, the susceptibility vessel sign was the only parameter before treatment that could predict mRS ≤2 at 3 months (OR, 8.7; 95% CI, 1.1–69.4; P = .04). CONCLUSIONS: Our study strongly suggests that the susceptibility vessel sign on MR imaging before treatment is predictive of favorable clinical outcome for patients presenting with anterior circulation acute stroke and treated with mechanical thrombectomy.

Introduction Outflow tract obstruction is thought to be involved in left ventricular (LV) remodeling in sarcomeric hypertrophic cardiomyopathy (HCM). Objective To determine the influence of obstruction to biological parameters of remodeling and global longitudinal strain (GLS) in HCM. Material and methods Patients with HCM who accepted to participate to this study were included. Transthoracic echocardiography at rest and exercise with GLS measurement was carried out. Blood was sampled before and early after exercise. Patients were divided into 3 groups according to the presence of an obstruction at rest (OHCM), effort (Latent obstruction: LOHCM) or none (HCM). Results We included 40 HCM patients, 7 OHCM, 19 LOHCM and 14 NOHCM. Troponin-T and NTproBNP levels at rest were significantly higher in OHCM compared to NOHCM (19.5 ± 10 vs 10 ± 5.8 ng/L, P = 0.017 and 1184 ± 389 vs 520 ± 388 ng/L, P = 0.005). Troponin-T and NTproBNP levels at rest were correlated with the outflow tract peak gradient ( r = 0.49, P = 0.001 and r = 0.41, P = 0.005, respectively) and with the alteration of GLS ( r = 0.51, P = 0.001 and r = 0.46, P = 0.003, respectively). GLS at rest was significantly more altered in OHCM. After exercise ST2, IL6, GDF15, Troponin-T and NTproBNP increased significantly in OHCM + LOHCM while only NTproBNP increased in NOHCM. In multivariate analysis, postexercise Troponin-T ( β = 0.57, P Fig. 1 ). Conclusion In HCM, biological parameters of remodeling are correlated to obstruction and GLS. GLS is itself correlated with the outflow peak gradient. Exercise in obstructive forms of HCM induces a significant increase in multiple biological parameters of remodeling. Troponin-T level is a strong predictor of GLS alteration both at rest and exercise.

Introduction The link between acute myocarditis (AM) and familial cardiomyopathies (CM) remains unclear. Purpose To assess the clinical significance of AM in families with CM. Methods We describe the pedigree of 6 families with at least one case of AM and a familial history of CM or sudden death (SD). AM was defined as an infarct-like clinical presentation with normal coronary arteries and myocardial inflammation (MI) documented by cardiac magnetic resonance (CMR), or as an autopsy proven AM. Results In family 1 to 5, genetic testing was triggered by the association of a documented case of AM with an index case of CM or early SD. In this setting, all genetic testing revealed a mutation in the desmoplakin (DSP) gene. In family 1, patient II.1 (15 y.o) was diagnosed with AM 6 months after his 12 y.o sister's SD. In family 2, patient II.4 (17 y.o) was diagnosed with AM. His mother had a DCM, with a CMR revealing the presence of MI. In family 3, patient IV.3 (22 y.o) died suddenly from an AM, attested by post-mortem autopsy. Her aunt had a DCM. In family 4, patient II.4 (41 y.o) had an AM, progressing toward a DCM. Her mother had died suddenly at the age of 39, and her niece had a DCM. In family 5, patient V.16 (9 y.o) presented 4 recurrent episodes of AM. Her cousin's mother had a DCM. In family 6, patient IV.3 had 3 episodes of AM, his father had previously been diagnosed with an arrythmogenic right ventricular cardiomyopathy (ARVC) with a desmoglein 2 (DSG2) mutation ( Table 1 , Fig 1). Conclusion AM is strongly associated to desmosomal mutations when a familial history of cardiomyopathy is present, particularly in DSP gene. In these families, DCM phenotype and SD are frequent, and a notable proportion of isolated LGE suggestive of myocardial fibrosis is present in asymptomatic relatives. These results highlight the need for a comprehensive familial screening in case of AM.