scholarly journals 24 Adenosine stress native T1 mapping demonstrates impaired myocardial perfusion reserve in non-ischemic dilated cardiomyopathy

2019 ◽  
Author(s):  
Zoi Tsoumani ◽  
Chris Miller ◽  
Matthias Schmitt ◽  
Gaetano Nucifora
Keyword(s):  
Myocardial Perfusion ◽  
Dilated Cardiomyopathy ◽  
T1 Mapping ◽  
Myocardial Perfusion Reserve ◽  
Adenosine Stress ◽  
Native T1 ◽  
Perfusion Reserve ◽  
Non Ischemic Dilated Cardiomyopathy

Adenosine stress native T1 mapping demonstrates impaired myocardial perfusion reserve in non-ischemic dilated cardiomyopathy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
G Nucifora ◽  
Z Tsoumani ◽  
C Miller ◽  
M Schmitt
Keyword(s):  
Myocardial Perfusion ◽  
T1 Mapping ◽  
Myocardial Perfusion Reserve ◽  
Adenosine Stress ◽  
Native T1 ◽  
Perfusion Reserve ◽  
Pass Perfusion ◽  
First Pass ◽  
Non Ischemic Dilated Cardiomyopathy ◽  
First Pass Perfusion

Abstract Background Impaired myocardial perfusion reserve has been demonstrated in non-ischemic dilated cardiomyopathy (NIDCM) by positron emission tomography (PET) and adenosine-stress first-pass perfusion cardiac magnetic resonance (CMR) imaging. Adenosine stress native T1 mapping is a novel CMR technique able to assess myocardial perfusion without the use of contrast agents. The aim of the present study was to determine the clinical utility of this novel CMR technique in NIDCM. Methods A total of 20 consecutive patients (mean age 61±12 years, 80% males) with diagnosis of NIDCM who consented to be enrolled in the UHSM CMR registry were included in the present study. CMR at 3T including 1. cine imaging for the assessment of LV volumes, mass and global longitudinal strain (GLS) by tissue-tracking imaging; 2. rest and stress (adenosine 140 mcg/kg/min) MOLLI T1 mapping of mid-ventricular slice for the assessment of rest and stress T1 values and T1 reactivity (ΔT1%); 3. first-pass perfusion imaging for the assessment of myocardial perfusion reserve index (MPRI) and 4. late gadolinium enhancement (LGE) imaging for the assessment of myocardial replacement fibrosis, was performed. Twenty control patients without history of known coronary artery disease and evidence of reversible ischemia or previous myocardial infarct on CMR imaging were included for comparison purposes. Results NIDCM patients had significantly higher native T1 value (1263±47 ms vs. 1234±38 ms, p=0.031), significantly lower ΔT1% (3.2±1.5% vs. 5.7±1.7%, p<0.001, Figure A), significantly lower MPRI (1.32±0.18 vs. 1.67±0.13, p<0.001) and significantly impaired GLS (−10±4% vs. −16±2%, p<0.001) as compared to controls. A significant strong relation between ΔT1% and MPRI (β=0.76, p<0.001, Figure B) and significant moderate relation between ΔT1% and GLS (β=−0.54, p<0.001) were observed. Conclusion T1 reactivity, myocardial perfusion reserve and GLS are significantly reduced in NIDCM patients compared to controls. Adenosine stress T1 mapping holds promise for detection of impaired myocardial perfusion reserve in NIDCM without the requirement for contrast agents. Funding Acknowledgement Type of funding source: None

scholarly journals Molecular Mechanisms of Adenosine Stress T1 Mapping

2021 ◽  
Author(s):  
Soham A. Shah ◽  
Claire E. Reagan ◽  
Brent A. French ◽  
Frederick H. Epstein
Keyword(s):  
Magnetic Resonance Imaging ◽  
Heart Rate ◽  
Magnetic Resonance ◽  
Myocardial Perfusion ◽  
Perfusion Imaging ◽  
T1 Mapping ◽  
Myocardial Perfusion Reserve ◽  
Adenosine Stress ◽  
Resonance Imaging ◽  
Perfusion Reserve

Background: Adenosine stress T1 mapping is an emerging magnetic resonance imaging method to investigate coronary vascular function and myocardial ischemia without application of a contrast agent. Using gene-modified mice and 2 vasodilators, we elucidated and compared the mechanisms of adenosine myocardial perfusion imaging and adenosine T1 mapping. Methods: Wild-type (WT), A 2A AR −/− (adenosine A 2A receptor knockout), A 2B AR −/− (adenosine A 2B receptor knockout), A 3 AR −/− (adenosine A 3 receptor knockout), and eNOS −/− (endothelial nitric oxide synthase knockout) mice underwent rest and stress perfusion magnetic resonance imaging (n=8) and T1 mapping (n=10) using either adenosine, regadenoson (a selective A 2A AR agonist), or saline. Myocardial blood flow and T1 were computed from perfusion imaging and T1 mapping, respectively, at rest and stress to assess myocardial perfusion reserve and T1 reactivity (ΔT1). Changes in heart rate for each stress agent were also calculated. Two-way ANOVA was used to detect differences in each parameter between the different groups of mice. Results: Myocardial perfusion reserve was significantly reduced only in A 2A AR −/− compared to WT mice using adenosine (1.06±0.16 versus 2.03±0.52, P <0.05) and regadenoson (0.98±026 versus 2.13±0.75, P <0.05). In contrast, adenosine ΔT1 was reduced compared with WT mice (3.88±1.58) in both A 2A AR −/− (1.63±1.32, P <0.05) and A 2B AR −/− (1.55±1.35, P <0.05). Furthermore, adenosine ΔT1 was halved in eNOS −/− (1.76±1.46, P <0.05) versus WT mice. Regadenoson ΔT1 was approximately half of adenosine ΔT1 in WT mice (1.97±1.50, P <0.05), and additionally, it was significantly reduced in eNOS −/− mice (−0.22±1.46, P <0.05). Lastly, changes in heart rate was 2× greater using regadenoson versus adenosine in all groups except A 2A AR −/− , where heart rate remained constant. Conclusions: The major findings are that (1) although adenosine myocardial perfusion reserve is mediated through the A 2A receptor, adenosine ΔT1 is mediated through the A 2A and A 2B receptors, (2) adenosine myocardial perfusion reserve is endothelial independent while adenosine ΔT1 is partially endothelial dependent, and (3) ΔT1 mediated through the A 2A receptor is endothelial dependent while ΔT1 mediated through the A 2B receptor is endothelial independent.

Abstract 16976: Derangements in Cardiac Oxidative Metabolism in Humans With Dilated Cardiomyopathy

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Daniel Clark ◽  
Giovanni E Davogustto ◽  
Susan P Bell ◽  
RAVINDER MALLUGARI ◽  
William S Bradham ◽  
...  
Keyword(s):  
Myocardial Perfusion ◽  
Dilated Cardiomyopathy ◽  
Oxidative Metabolism ◽  
Myocardial Perfusion Reserve ◽  
Normal Subjects ◽  
Rate Pressure Product ◽  
Gadolinium Contrast ◽  
Perfusion Reserve ◽  
Demand Rate ◽  
Myocardial Oxidative Metabolism

Introduction: Dilated cardiomyopathy (DCM) is associated with impaired myocardial perfusion reserve and impaired myocardial oxidative metabolism. However, the association between myocardial perfusion reserve and oxidative metabolism, is not fully understood. Hypothesis: Reduced myocardial perfusion reserve is associated with reduced myocardial oxidative metabolism. Methods: Using non-invasive cardiac imaging, we studied 8 DCM patients and 14 normal subjects. Myocardial perfusion reserve index (MPRI) was calculated using cardiac magnetic resonance as the normalized rate of myocardial signal augmentation following gadolinium contrast injection between rest and regadenoson induced stress. Resting oxidative metabolism was calculated as the myocardial mono-exponential decay rate (Kmono) of [ 11 C]acetate by positron emission tomography normalized per unit demand (rate-pressure product, RPP) (Kmono/RPP). Results: MPRI was lower in DCM compared to controls (1.25 ± 0.22 vs 1.59 ± 0.49, p=0.038). Similarly, Kmono/RPP was lower in DCM compared with normal subjects (0.6x10e-3 ± 0.15 x10e-3 vs 1.2x10e-3 ± 0.9x10e-3, p<0.0001). There was a linear relation between Kmono and RPP in normal subjects. However, DCM patients showed no increase in Kmono regardless of RPP (Figure 1A). Kmono/RPP was not significantly related to MPRI in either group (Figure 1B). Conclusions: Patients with DCM exhibit markedly impaired myocardial oxidative metabolism compared to normal subjects. However, this impairment was not quantitatively related to impaired myocardial perfusion reserve. Of the various mechanisms that could explain decrease in oxidative metabolism in DCM, these data suggest that reduced myocardial perfusion is not the principal driver of impaired oxidative metabolism.

Abstract 14783: Relationship Between Native Papillary Muscle T1 Time and Severity of Functional Mitral Regurgitation in Patients With Non-ischemic Dilated Cardiomyopathy

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Shingo Kato ◽  
Sébastien Roujol ◽  
Francesca Delling ◽  
Shadi Akhtari ◽  
Jihye Jang ◽  
...  
Keyword(s):  
Mitral Regurgitation ◽  
Dilated Cardiomyopathy ◽  
Papillary Muscle ◽  
T1 Mapping ◽  
Functional Mitral Regurgitation ◽  
Diffuse Fibrosis ◽  
Regurgitant Fraction ◽  
Native T1 ◽  
Non Ischemic Dilated Cardiomyopathy ◽  
Native T1 Time

Introduction: Functional mitral regurgitation is one of the severe complications of non-ischemic dilated cardiomyopathy (DCM). Non-contrast native T1 mapping has emerged as a non-invasive method to evaluate myocardial fibrosis. Hypothesis: We hypothesized that papillary muscle native T1 time is correlated with severity of functional mitral regurgitation in DCM patients. Methods: Forty DCM patients (55±13 years) and 20 healthy adult control subjects (54±13 years) were studied. Native T1 mapping was performed using a slice interleaved T1 mapping sequence (STONE) which enables acquisition of 5 slices in the short-axis plane within a 90 sec free-breathing scan. We measured papillary muscle diameter, length and shortening. DCM patients were allocated into 2 groups based on the presence or absence of functional mitral regurgitation. Results: Papillary muscle T1 time was significantly elevated in DCM patients with mitral regurgitation (n=22) in comparison to those without mitral regurgitation (n=18) (anterior papillary muscle: 1127±36 msec vs 1063±16 msec, p<0.001; posterior papillary muscle: 1124±30 msec vs 1062±19 msec, p<0.001), but LV T1 time was similar (1129±38 msec vs 1134±58 msec, p=0.93). Multivariate linear regression analysis showed that papillary muscle native T1 time (β=0.109, 95%CI: 0.048-0.170, p=0.001) and tenting height (β=1.334, 95%CI: 0.434-2.234, p=0.005) are significantly correlated with mitral regurgitant fraction. Elevated papillary muscle T1 time was associated with larger diameter, longer length and decreased papillary muscle shortening (all p values <0.05). Conclusions: In DCM, papillary muscle native T1 time is significantly elevated and related to mitral regurgitant fraction. These results suggest that papillary muscle diffuse fibrosis might be associated with severity of mitral regurgitation in this population.

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