Molecular Mechanisms of Adenosine Stress T1 Mapping

Shah, Soham A; Reagan, Claire E; French, Brent A.; Epstein, Frederick H.

doi:10.1161/circimaging.120.011774

Cited by 10 publications

(5 citation statements)

References 45 publications

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“…Although the exact mechanisms behind the ΔT1 response are not fully understood, it is largely mediated by endothelium-dependent mechanisms, while myocardial perfusion reserve is endothelium independent. 4 Our findings support the hypothesis that cardiac endothelial injury may underlie vascular impairment in PACS+POTS. It is recognized as a limitation in the current study that a POTS group without prior COVID-19 was not included.…”

supporting

confidence: 86%

Microvasular Dysfunction and Reduced Cardiac Stress Reactivity in Postural Orthostatic Tachycardia Associated With Postacute COVID-19

Mahdi

Lodin

Reistam

et al. 2023

Circ: Arrhythmia and Electrophysiology

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supporting

confidence: 86%

Microvasular Dysfunction and Reduced Cardiac Stress Reactivity in Postural Orthostatic Tachycardia Associated With Postacute COVID-19

Mahdi

Lodin

Reistam

et al. 2023

Circ: Arrhythmia and Electrophysiology

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“…This likely reflects the timings of the first-pass perfusion acquisitions, which were not performed at peak stress in this study (i.e. acquired at 4 min and 15 min vs. typically 1–2 min in clinical practice) rather than the choice of vasodilator agent, given recent animal studies have shown no significant differences in MBF when comparing adenosine and regadenoson 40 . Our data supports that there are clear differences in stress T1 reactivity between the methods tested, with ShMOLLI demonstrating a significantly greater stress T1 response and effect size.…”

Section: Discussionmentioning

confidence: 98%

Cardiac stress T1-mapping response and extracellular volume stability of MOLLI-based T1-mapping methods

Burrage

Shanmuganathan

Zhang

et al. 2021

Sci Rep

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Stress and rest T1-mapping may assess for myocardial ischemia and extracellular volume (ECV). However, the stress T1 response is method-dependent, and underestimation may lead to misdiagnosis. Further, ECV quantification may be affected by time, as well as the number and dosage of gadolinium (Gd) contrast administered. We compared two commonly available T1-mapping approaches in their stress T1 response and ECV measurement stability. Healthy subjects (n = 10, 50% female, 35 ± 8 years) underwent regadenoson stress CMR (1.5 T) on two separate days. Prototype ShMOLLI 5(1)1(1)1 sequence was used to acquire consecutive mid-ventricular T1-maps at rest, stress and post-Gd contrast to track the T1 time evolution. For comparison, standard MOLLI sequences were used: MOLLI 5(3)3 Low (256 matrix) & High (192 matrix) Heart Rate (HR) to acquire rest and stress T1-maps, and MOLLI 4(1)3(1)2 Low & High HR for post-contrast T1-maps. Stress and rest myocardial blood flow (MBF) maps were acquired after IV Gd contrast (0.05 mmol/kg each). Stress T1 reactivity (delta T1) was defined as the relative percentage increase in native T1 between rest and stress. Myocardial T1 values for delta T1 (dT1) and ECV were calculated. Residuals from the identified time dependencies were used to assess intra-method variability. ShMOLLI achieved a greater stress T1 response compared to MOLLI Low and High HR (peak dT1 = 6.4 ± 1.7% vs. 4.8 ± 1.3% vs. 3.8 ± 1.0%, respectively; both p < 0.0001). ShMOLLI dT1 correlated strongly with stress MBF (r = 0.77, p < 0.001), compared to MOLLI Low HR (r = 0.65, p < 0.01) and MOLLI High HR (r = 0.43, p = 0.07). ShMOLLI ECV was more stable to gadolinium dose with less time drift (0.006–0.04% per minute) than MOLLI variants. Overall, ShMOLLI demonstrated less intra-individual variability than MOLLI variants for stress T1 and ECV quantification. Power calculations indicate up to a fourfold (stress T1) and 7.5-fold (ECV) advantage in sample-size reduction using ShMOLLI. Our results indicate that ShMOLLI correlates strongly with increased MBF during regadenoson stress and achieves a significantly higher stress T1 response, greater effect size, and greater ECV measurement stability compared with the MOLLI variants tested.

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“…This may also account for the continued trends of systemic measurements (BP, HR, RPP) through the 4× adenosine dose, as each organ has differing ratios of each receptor 56 . Additionally, the continued increase in MBV after MBF begins to drop can be explained by the recent findings of Shah et al, who found that adenosine‐induced changes in MBF and MBV are controlled by different adenosine receptors: MBF via the A 2A adenosine receptor, and MBV through both the A 2A and A 2B receptor subtypes 57 . We should also point out that, since the distribution of each adenosine receptor subtype varies from species to species, 56 it is possible that our model may need to be adjusted for stress imaging studies in other species.…”

Section: Discussionmentioning

confidence: 99%

Myocardial blood flow is the dominant factor influencing cardiac magnetic resonance adenosine stress T2

et al. 2021

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Stress imaging identifies ischemic myocardium by comparing hemodynamics during rest and hyperemic stress. Hyperemia affects multiple hemodynamic parameters in myocardium, including myocardial blood flow (MBF), myocardial blood volume (MBV), and venous blood oxygen levels (PvO2). Cardiac T2 is sensitive to these changes and therefore is a promising non‐contrast option for stress imaging; however, the impact of individual hemodynamic factors on T2 is poorly understood, making the connection from altered T2 to changes within the tissue difficult. To better understand this interplay, we performed T2 mapping and measured various hemodynamic factors independently in healthy pigs at multiple levels of hyperemic stress, induced by different doses of adenosine (0.14‐0.56 mg/kg/min). T1 mapping quantified changes in MBV. MBF was assessed with microspheres, and oxygen consumption was determined by the rate pressure product (RPP). Simulations were also run to better characterize individual contributions to T2. Myocardial T2, MBF, oxygen consumption, and MBV all changed to varying extents between each level of adenosine stress (T2 = 37.6‐41.8 ms; MBF = 0.48‐1.32 mL/min/g; RPP = 6507‐4001 bmp*mmHg; maximum percent change in MBV = 1.31%). Multivariable analyses revealed MBF as the dominant influence on T2 during hyperemia (significant β‐values >7). Myocardial oxygen consumption had almost no effect on T2 (β‐values <0.002); since PvO2 is influenced by both oxygen consumption and MBF, PvO2 changes detected by T2 during adenosine stress can be attributed to MBF. Simulations varying PvO2 and MBV confirmed that PvO2 had the strongest influence on T2, but MBV became important at high PvO2. Together, these data suggest a model where, during adenosine stress, myocardial T2 responds predominantly to changes in MBF, but at high hyperemia MBV is also influential. Thus, changes in adenosine stress T2 can now be interpreted in terms of the physiological changes that led to it, enabling T2 mapping to become a viable non‐contrast option to detect ischemic myocardial tissue.

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Molecular Mechanisms of Adenosine Stress T1 Mapping

Cited by 10 publications

References 45 publications

Microvasular Dysfunction and Reduced Cardiac Stress Reactivity in Postural Orthostatic Tachycardia Associated With Postacute COVID-19

Microvasular Dysfunction and Reduced Cardiac Stress Reactivity in Postural Orthostatic Tachycardia Associated With Postacute COVID-19

Cardiac stress T1-mapping response and extracellular volume stability of MOLLI-based T1-mapping methods

Myocardial blood flow is the dominant factor influencing cardiac magnetic resonance adenosine stress T2

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