The Future of Cardiovascular Imaging
The Future of Cardiovascular Imaging
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DOI：
10.1161/circulationaha.116.023511
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发表时间：
2016-06-21
期刊：
影响因子：
37.8
通讯作者：
Davidoff, Ravin
中科院分区：
文献类型：
--
作者：
Di Carli, Marcelo F.;Geva, Tal;Davidoff, Ravin
临床上，适应性右室肥厚的特征是保留相对正常的心输出量、射血分数、右室充盈压力和运动能力。病理上，这种形式的右室重构表现为向心性肥厚，伴有轻微的扩张和纤维化。相比之下，适应性不良的右室肥厚的特点是心输出量和射血分数降低，与右室充盈压升高和运动能力降低有关。不适应表型的病理相关性包括偏心性右室肥大和扩张，以及纤维化增加。先进的心脏成像和有创血流动力学测量在已知或可疑的PAH患者的诊断和风险分层中发挥着关键作用。先进的成像工具还为不同疾病表型的潜在病理生物学提供了独特的定量见解，从而为早期诊断和监测对新疗法的反应提供了机会。超声心动图，特别是三维(3D)成像和心脏磁共振(CMR)成像可以准确评估PAH患者的右室重构和功能2(图1)。CMR是测量RV功能、质量和体积的黄金标准。3 CMR测量具有高度的重复性，并允许在临床试验中连续跟踪RV重塑和功能。PAH的共同特征包括右室肥厚和质量增加并伴有心肌细胞萎缩，4这通常与室间隔变平和左弓，以及舒张期功能障碍有关。随着时间的推移，失代偿期患者逐渐出现右室收缩功能障碍，伴随射血分数降低和扩张。将应变成像与斑点跟踪超声心动图、CMR标记或特征跟踪结合使用，可提供早期识别收缩功能减退的机会。超声心动图和CMR对右室重构和功能的许多非侵入性测量都与临床风险相关，这增强了在治疗试验中使用它们作为替代终点的相关性。1，2定量成像也有助于描绘PAH中适应性不良的RV重构的潜在分子指纹。5例如，右室缺血，在放射性核素显像6-9上表现为胸痛和心肌灌注减少，并增加了葡萄糖利用率，6、8、10反映了由于血管生成减少、11毛细血管稀疏、12和严重肥大时冠脉灌注压可能降低而导致的右室血流灌注的慢性减少(图1)。也有一致的证据表明，在适应性不良的RV重塑中，线粒体氧化减少，5导致许多代谢变化，包括增加对非氧化糖酵解的依赖，这可以通过正电子发射断层扫描(PET)成像来量化。事实上，从氧化代谢到低效糖酵解过程的转变导致RV心肌细胞葡萄糖通量的代偿性上调。6、8、10在PAH的肺血管中可以看到类似的从葡萄糖氧化向糖酵解的转变。这与脂肪酸代谢的明显增加有关，特别是在严重的肺动脉压升高和右室功能障碍的情况下。然而，与脂肪酸相比，人们对葡萄糖代谢的依赖程度相对更高。最后，纤维化增加是适应性不良的RV重构的病理标志。晚期Gd增强(LGE)15和潜在的较新的cmr T1标测技术16可以提供…的定量测量
Clinically, adaptive RV hypertrophy is characterized by preservation of relatively normal cardiac output, ejection fraction, RV filling pressure, and exercise capacity. Pathologically, this form of RV remodeling shows concentric hypertrophy with minimal dilatation and fibrosis. In contrast, maladaptive RV hypertrophy is characterized by a reduced cardiac output and ejection fraction, associated with elevation of RV filling pressure and reduced exercise capacity. The pathological correlates of the maladaptive phenotype include eccentric RV hypertrophy and dilatation, and increased fibrosis. Advanced cardiac imaging along with invasive hemodynamic measurements play a key role in diagnosis and risk stratification of patients with known or suspected PAH. Advanced imaging tools also offer unique quantitative insights into the underlying pathobiology of the different disease phenotypes and, in so doing, provide opportunities for early diagnosis and for monitoring response to novel therapies. RV remodeling and function in PAH patients can be accurately assessed with echocardiography, 1 especially 3-dimensional (3D) imaging, and cardiac magnetic resonance (CMR) imaging2 (Figure 1). CMR is the gold standard for measuring RV function, mass, and volumes. 3 CMR measurements are highly reproducible, and permit serial tracking of RV remodeling and function in clinical trials. The common features found in PAH include RV hypertrophy and increased mass with concomitant cardiomyocyte atrophy, 4 which are often associated with interventricular septal flattening and leftward bowing, and diastolic dysfunction, as well. Over time, gradual RV systolic dysfunction with reduced ejection fraction and dilatation develops in decompensated patients. The use of strain imaging with speckle-tracking echocardiography, CMR tagging, or feature tracking provides opportunities for early recognition of decreased systolic function. Many noninvasive measurements of RV remodeling and function with both echocardiography and CMR are associated with clinical risk, which enhances the relevance of their use as surrogate end points in the context of treatment trials. 1, 2 Quantitative imaging can also help delineate underlying molecular fingerprints of maladaptive RV remodeling in PAH. 5 For example, RV ischemia, as evidenced by chest pain and reduced myocardial perfusion on radionuclide imaging6–9 and increased glucose utilization, 6, 8, 10 reflects chronic reduction in RV perfusion resulting from decreased angiogenesis, 11 capillary rarefaction, 12 and potentially decreased coronary perfusion pressure in the setting of severe hypertrophy13 (Figure 1). There is also consistent evidence that mitochondrial oxidation in maladaptive RV remodeling is reduced, 5 resulting in a number of metabolic changes including an increased reliance on nonoxidative glycolysis, which can be quantified by positron emission tomography (PET) imaging. Indeed, the shift from oxidative metabolism to the less efficient process of glycolysis results in a compensatory upregulation of glucose flux in RV myocytes. 6, 8, 10 A similar shift to glycolysis away from glucose oxidation is seen in the pulmonary vessels of PAH. This correlates with an apparent increase in fatty acid metabolism, especially in the setting of severely elevated pulmonary pressure and RV dysfunction. 14 However, there is a relatively increased reliance on glucose metabolism in comparison with fatty acids. Finally, increased fibrosis is a pathological hallmark of maladaptive RV remodeling. Late gadolinium enhancement (LGE) 15 and potentially newer T1 mapping techniques16 with CMR can provide a quantitative measure of …