Cardiac Lipids by <sup>1</sup>
H MRS

Szczepaniak, Lidia S.; Smith, Laura G. E.

doi:10.1002/9780470034590.emrstm1453

Cited by 5 publications

(3 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Notice that the (resummed) behavior ∼ (q 2 /µ 2 ) ξ has been also observed when studying the gfp-dependence of fermion propagators through LKF transformations [40,51]. 5 For related studies in the Coulomb gauge, see [47][48][49][50] Evidently, choosing a 0 = 1 and c 1 ≡ c NI = 0.13 ensures that…”

Section: Gluon Propagatormentioning

confidence: 93%

Yang-Mills two-point functions in linear covariant gauges

2015

View full text Add to dashboard Cite

In this work we use two different but complementary approaches in order to study the ghost propagator of a pure SU(3) Yang-Mills theory quantized in the linear covariant gauges, focusing on its dependence on the gauge-fixing parameter $\xi$ in the deep infrared. In particular, we first solve the Schwinger-Dyson equation that governs the dynamics of the ghost propagator, using a set of simplifying approximations, and under the crucial assumption that the gluon propagators for $\xi>0$ are infrared finite, as is the case in the Landau gauge $(\xi=0)$. Then we appeal to the Nielsen identities, and express the derivative of the ghost propagator with respect to $\xi$ in terms of certain auxiliary Green's functions, which are subsequently computed under the same assumptions as before. Within both formalisms we find that for $\xi>0$ the ghost dressing function approaches zero in the deep infrared, in sharp contrast to what happens in the Landau gauge, where it known to saturate at a finite (non-vanishing) value. The Nielsen identities are then extended to the case of the gluon propagator, and the $\xi$-dependence of the corresponding gluon masses is derived using as input the results obtained in the previous steps. The result turns out to be logarithmically divergent in the deep infrared; the compatibility of this behavior with the basic assumption of a finite gluon propagator is discussed, and a specific Ansatz is put forth, which readily reconciles both features.Comment: 28 pages, 10 figure

show abstract

Section: Gluon Propagatormentioning

confidence: 93%

Yang-Mills two-point functions in linear covariant gauges

2015

View full text Add to dashboard Cite

show abstract

“…Myocardial triglyceride content. Myocardial triglyceride content was measured using cardiac 1 H magnetic resonance spectroscopy as described previously (Szczepaniak & Smith, 2007). In short, a single, spectroscopic volume of interest was positioned over the interventricular septum using end-systolic frames of cardiac short axis and pseudo four-chamber cine images.…”

Section: Measurementsmentioning

confidence: 99%

Myocardial steatosis impairs left ventricular diastolic–systolic coupling in healthy humans

Oneglia

Szczepaniak²,

Jaffery

et al. 2023

The Journal of Physiology

View full text Add to dashboard Cite

Mounting evidence suggests that myocardial steatosis contributes to left ventricular diastolic dysfunction, but definitive evidence in humans is lacking due to confounding comorbidities. As such, we utilized a 48‐h food restriction model to acutely increase myocardial triglyceride (mTG) content – measured by 1H magnetic resonance spectroscopy – in 27 young healthy volunteers (13 men/14 women). Forty‐eight hours of fasting caused a more than 3‐fold increase in mTG content (P < 0.001). Diastolic function – defined as early diastolic circumferential strain rate (CSRd) – was unchanged following the 48‐h fasting intervention, but systolic circumferential strain rate was elevated (P < 0.001), indicative of systolic–diastolic uncoupling. Indeed, in a separate control experiment in 10 individuals, administration of low‐dose dobutamine (2 μg/kg/min) caused a similar change in systolic circumferential strain rate as was found during 48 h of food restriction, along with a proportionate increase in CSRd, such that the two metrics remained coupled. Taken together, these data indicate that myocardial steatosis contributes to diastolic dysfunction by impairing diastolic–systolic coupling in healthy adults, and suggest that steatosis may contribute to the progression of heart disease. Key points Preclinical evidence strongly suggests that myocardial lipid accumulation (termed steatosis) is an important mechanism driving heart disease. Definitive evidence in humans is limited due to the confounding influence of multiple underlying comorbidities. Using a 48‐h food restriction model to acutely increase myocardial triglyceride content in young healthy volunteers, we demonstrate an association between myocardial steatosis and left ventricular diastolic dysfunction. These data advance the hypothesis that myocardial steatosis may contribute to diastolic dysfunction and suggest myocardial steatosis as a putative therapeutic target.

show abstract

“…10,11 Proton spectroscopy is another CMR technique that can be used to determine intramyocardial triglyceride (IMTG) content, a measure of altered myocardial bioenergetics and lipotoxicity. [12][13][14] Diffuse myocardial interstitial fibrosis and cardiomyocyte lipotoxicity as measured by MECV and IMTG, respectively, are both considered intermediate HF phenotypes. [15][16][17] Systemic metabolic dysregulation is a major risk factor for HF, one that contributes to altered myocardial energetics.…”

Section: Introductionmentioning

confidence: 99%