Improvement of Myocardial Perfusion Reserve Early After Coronary Intervention: Assessment With Cardiac Magnetic Resonance Imaging. Al-Saadi N, Nagel E, Gross M, et al. J Am Coll Cardiol 2000;36:1557–64

2001 ◽  
Vol 10 (2) ◽  
pp. 33
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Myocardial Perfusion ◽  
Cardiac Magnetic Resonance Imaging ◽  
Myocardial Perfusion Reserve ◽  
Coronary Intervention ◽  
Resonance Imaging ◽  
Perfusion Reserve

Abstract 19008: Is Cold Pressor Cardiac Magnetic Resonance Imaging Testing Useful for Detection of Coronary Endothelial Dysfunction?

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Sherwin Dela Cruz ◽  
Janet Wei ◽  
Chrisandra Shufelt ◽  
Puja Mehta ◽  
Andre Rogatko ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Endothelial Dysfunction ◽  
Cardiac Magnetic Resonance Imaging ◽  
Myocardial Perfusion Reserve ◽  
Cold Pressor ◽  
Resonance Imaging ◽  
Significant Difference ◽  
Coronary Endothelial Dysfunction

Background: Coronary endothelial dysfunction is typically assessed by invasive coronary reactivity testing (CRT) to measure coronary blood flow ([[Unable to Display Character: &#8710;]]CBF) and diameter responses to acetylcholine (Ach). We evaluated if cold pressor testing (CPT) during noninvasive cardiac magnetic resonance imaging (CMRI) measurement of myocardial perfusion reserve index (MPRI) reflects invasive measurements with Ach and CPT in subjects suspected of having endothelial dysfunction. Methods: CRT was performed in 137 symptomatic women using incremental infusions of Ach in the left coronary artery for 3 minutes and with CPT using ice pack on their hand and forearm for 2 minutes. Quantitative coronary angiography was performed 5 mm distal to the Doppler wire positioned in the proximal left anterior descending artery. In 132 women, [[Unable to Display Character: &#8710;]]CBF was calculated from average peak velocity and vessel cross sectional area. Invasive CPT could not be completed on 4 women. All women underwent CPT CMRI (1.5 T) to measure MPRI as a ratio of stress and rest upslopes of the whole myocardium. Five definitions of normal invasive CPT and Ach diameter response (dilation > 0, 5, 10, 15 or 20%) were compared to two abnormal definitions (≤ 0 or - 5%) of endothelial function. Normal [[Unable to Display Character: &#8710;]]CBF was defined as ≤ 50%. We used Wilcoxon Two-Sample statistical test to compare MPRI in each group. Results: CPT MPRI was significantly different in those with normal versus abnormal invasive Ach when Ach diameter response was defined as ≥ 20% or < - 5 % (p=0.04), though not with other thresholds (Table). Conclusion: Noninvasive CPT CMRI may not be useful for detection of endothelial dysfunction in symptomatic women as no significant difference in MPRI was found in those with normal and abnormal invasive CRT. However, there may be a role for CPT MPRI in detecting endothelial dysfunction at higher thresholds of normal diameter response. Additional investigation will evaluate CPT CMRI and cardiovascular outcomes.

Stress Cardiac Magnetic Resonance Imaging

2018 ◽  
pp. 335-343
Author(s):  
Yeonyee E. Yoon ◽  
L. Samuel Wann
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Myocardial Perfusion ◽  
Cardiac Magnetic Resonance Imaging ◽  
Wall Motion ◽  
Scar Tissue ◽  
Resonance Imaging ◽  
Stress Cardiac Magnetic Resonance ◽  
Myocardial Thickening

The chapter Stress Cardiac Magnetic Resonance Imaging reviews how cardiovascular magnetic resonance imaging (CMR) has become a gold standard for evaluating stress induced wall motion abnormalities based on regional endocardial excursion and myocardial thickening. The high spatial and temporal resolution of CMR without limitations imposed by body habitus and acoustic windows allows outstanding visualization of myocardial function. CMR can also be combined with vasodilator stress to perform dynamic first-pass myocardial perfusion imaging. The addition of late gadolinium enhancement allows the accurate of nonviable scar tissue in combination with wall motion and myocardial perfusion assessment. Case studies highlight the opportunity provided by stress CMR.

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.

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