scholarly journals Hyperacute Incidental Late Myocardial Enhancement in Ischemic Stroke using Chest Spectral CT: Relationship with Etiology

2021 ◽  
Author(s):  
Gastón A Rodriguez-Granillo ◽  
Juan J. Cirio ◽  
Celina Ciardi ◽  
Maria L. Caballero ◽  
Lucia A. Fontana ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cardiac Imaging ◽  
Volume Fraction ◽  
Extracellular Volume ◽  
Coronary Calcification ◽  
Extracellular Volume Fraction ◽  
Aortic Plaque ◽  
Stroke Etiology ◽  
Spectral Computed Tomography ◽  
Late Iodine Enhancement

Abstract PurposeHyperacute cardiac imaging of patients with acute ischemic stroke (AIS), though desirable, is impractical. Using delayed-enhancement, low-dose, non-gated, chest spectral computed tomography scans (DESCT), we explored the prevalence and patterns of incidental myocardial late iodine enhancement (LIE) and embolic sources, and the relationship with stroke etiology. MethodsSince July 2020, DESCT was performed after cerebrovascular CT angiography (CTA) among patients with suspected AIS undergoing CT using a dual-layer spectral scanner, without additional contrast administration. Images were analyzed using monoenergetic reconstructions and iodine density maps, and the myocardial extracellular volume fraction (ECV, %) was calculated. ResultsEighty consecutive patients with AIS were included. DESCT identified a cardiac thrombi in 6 patients (7.5%), and a complex aortic plaque in 4 (5%) cases; reclassifying 5 embolic strokes of uncertain source (28% of ESUS) to cardioembolic (CE, n=3) and non-CE (n=2) etiologies. LIE, most commonly ischemic (82%), was identified in 38 (48%) patients. We did not identify significant relationships between AIS etiology and the presence, pattern, and extension of LIE (p>0.05); ECV (p=0.56), severe aortic (p=0.25) or valvular (p=0.26) disease, or the extent of coronary calcification (p=0.39). Patients with evidence of major cardiovascular DESCT findings had higher rate rates of all-cause death at 90 days (42% vs. 19%, p=0.037). ConclusionIn this study, hyperacute cardiac imaging of AIS with DESCT identified a high prevalence of incidental cardiac disease predominantly involving LIE of ischemic etiology and mostly not related to the stroke etiology.

Transmural heterogeneity of diffusion anisotropy in the sheep myocardium characterized by MR diffusion tensor imaging

2007 ◽  
Vol 293 (4) ◽  
pp. H2377-H2384 ◽  
Author(s):  
Yi Jiang ◽  
Julius M. Guccione ◽  
Mark B. Ratcliffe ◽  
Edward W. Hsu
Keyword(s):  
Diffusion Tensor Imaging ◽  
Volume Fraction ◽  
Diffusion Tensor ◽  
Extracellular Volume ◽  
Extracellular Volume Fraction ◽  
Left Ventricular ◽  
Fiber Direction ◽  
Significant Difference ◽  
Mr Diffusion ◽  
Mr Diffusion Tensor Imaging

The orientation of MRI-measured diffusion tensor in the myocardium has been directly correlated to the tissue fiber direction and widely characterized. However, the scalar anisotropy indexes have mostly been assumed to be uniform throughout the myocardial wall. The present study examines the fractional anisotropy (FA) as a function of transmural depth and circumferential and longitudinal locations in the normal sheep cardiac left ventricle. Results indicate that FA remains relatively constant from the epicardium to the midwall and then decreases (25.7%) steadily toward the endocardium. The decrease of FA corresponds to 7.9% and 12.9% increases in the secondary and tertiary diffusion tensor diffusivities, respectively. The transmural location of the FA transition coincides with the location where myocardial fibers run exactly circumferentially. There is also a significant difference in the midwall-endocardium FA slope between the septum and the posterior or lateral left ventricular free wall. These findings are consistent with the cellular microstructure from histological studies of the myocardium and suggest a role for MR diffusion tensor imaging in characterization of not only fiber orientation but, also, other tissue parameters, such as the extracellular volume fraction.

Abstract 17263: Pre-Clinical Left Ventricular Myocardial Remodeling in Patients With Friedreich’s Ataxia: A Cardiac MRI Study

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Karen A Takazaki1 ◽  
Thiago Quinaglia A. C. Silva ◽  
Alberto Martinez ◽  
Tomas Neilan ◽  
Ravi SHAH ◽  
...  
Keyword(s):  
Heart Failure ◽  
Volume Fraction ◽  
Extracellular Volume ◽  
Extracellular Volume Fraction ◽  
Friedreich’S Ataxia ◽  
Left Ventricular ◽  
Friedreich's Ataxia ◽  
Intracellular Water ◽  
Lv Mass ◽  
Burn Out

Background: Heart Failure (HF) is the most common cause of death in Friedreich’s ataxia (FRDA), an inherited mitochondrial disease. Myocardial fibrosis is a well-documented histopathological feature among FRDA patients with HF. Objectives: In this study we will investigate the myocardial extracellular volume fraction (ECV) and intracellular water lifetime (τ ic ), using T1-weighted CMR imaging, in a cohort of patients with FRDA without signs of heart failure. We will also investigate whether myocardial tissue phenotyping by CMR can highlight particular characteristics of LV remodeling in FRDA’s cardiomyopathy, beyond those currently assessed with imaging-based classification of disease severity. Methods: Twenty-six FRDA’s patients (age 26.6±9.3 years, 15 women) without signs of HF, and 10 healthy controls (32.6±7.3 years, 5 women) underwent cardiac magnetic resonance (CMR) studies for assessment of left ventricular (LV) function, myocardial T1, late gadolinium enhancement (LGE), extracellular volume fraction (ECV), and intracellular water-lifetime (τ ic ) as marker of cardiomyocyte size. Neurological decline was determined using the FRDA rating scale (FARS 3). Results: FRDA patients had normal LV ejection fraction (LVEF: 67.66±11.4 vs. 63.9±9.0, P=0.311), larger LV mass index (LVMASSi: 61.03±22.1 vs. 45±4.2g/m 2 , P<0.001), and decreased LV end-diastolic volume index (LVEDVi 53.42±12 vs. 75.7±16.1, P=0.002), compared with controls. ECV and τ ic , were increased in FRDA patients (ECV: 0.36±0.05 vs. 0.25±0.02, P<0.0001; τ ic : 0.13±0.07 vs. 0.06±0.03, P=0.001). ECV was positively associated with LV mass-to-volume ratio (r=0.628, P<0.001). FARS 3 correlated positively with disease duration (r=0.669, P<0.001), and negatively with τ ic , (r=0.478, P=0.039). LVMASSi and cardiomyocyte mass-index [(1–ECV)LVMASSi] declined with age, indicating that LV hypertrophy may transition to a “burn-out” phase with LV atrophy. Conclusions: LV hypertrophy in FRDA reflects an expansion of the myocardial interstitium and an increase in cardiomyocyte size. In contrast, the neurological decline was more likely with decreasing cardiomyocyte size, possibly an early sign of myocardial “burn-out” in FRDA.

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