Myocardial blood flow is the dominant factor influencing cardiac magnetic resonance adenosine stress T2.
Myocardial blood flow is the dominant factor influencing cardiac magnetic resonance adenosine stress T2.
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DOI：
10.1002/nbm.4643
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发表时间：
2022-03
影响因子：
2.9
通讯作者：
Ghugre NR
中科院分区：
文献类型：
--
作者：
Weyers JJ;Ramanan V;Javed A;Barry J;Larsen M;Nayak K;Wright GA;Ghugre NR
通过比较静息和充血负荷时的血流动力学，负荷成像可识别缺血心肌。充血影响心肌的多个血流动力学参数，包括心肌血流量（MBF）、心肌血容量（MBV）和静脉血氧水平（PvO 2）。心脏T2对这些变化敏感，因此是应力成像的一种有前途的非造影剂选择;然而，对单个血液动力学因素对T2的影响了解甚少，使得T2改变与组织内变化之间的联系变得困难。为了更好地理解这种相互作用，我们进行了T2标测，并在不同剂量的腺苷（0.14-0.56 mg/kg/min）诱导的多个充血应激水平下独立测量了健康猪的各种血流动力学因素。T1映射量化了MBV的变化。用微球评估MBF，用速率压力乘积（RPP）测定氧消耗量。还运行模拟以更好地表征个体对T2的贡献。心肌T2、MBF、耗氧量和MBV在每个腺苷应激水平之间都有不同程度的变化（T2=37.6-41.8 ms; MBF=0.48-1.32 ml/min/g; RPP=6507-4001 bmp*mmHg; MBV的最大百分比变化=1.31%）。多变量分析显示，在充血期间，MBF是对T2的主要影响（显著β值>7）。心肌耗氧量对T2几乎没有影响（β值<0.002）;由于PvO 2受耗氧量和MBF的影响，因此腺苷应激期间T2检测到的PvO 2变化可归因于MBF。不同PvO 2和MBV的模拟证实了PvO 2对T2的影响最大，但MBV在高PvO 2时变得重要。总之，这些数据表明了一个模型，其中在腺苷应激期间，心肌T2主要对MBF的变化做出反应，但在高充血时，MBV也有影响。因此，腺苷应激T2的变化现在可以根据导致它的生理变化来解释，使T2标测成为检测缺血性心肌组织的可行的非造影剂选择。心肌血流量，血容量和血氧水平进行了测量，在不同水平的腺苷应力，以确定其对心肌应力T2的个人影响。血流量成为腺苷应激T2的最有影响力的因素，在高充血时血容量也起作用，而耗氧量的影响最小。这提高了我们对哪些因素直接影响应力T2的理解，并允许更好地解释T2的变化如何对应于心肌生理学的变化。
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; max 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 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. Myocardial blood flow, blood volume, and blood oxygen levels were measured during varying levels of adenosine stress to determine their individual impact on myocardial stress T2. Blood flow emerged as the most influential factor on adenosine stress T2 with blood volume also playing a role at high hyperemia, while oxygen consumption had minimal effect. This improves our understanding of what factors directly affect stress T2, and allows a better interpretation of how changes in T2 correspond to changes in myocardial physiology.
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