Myocardial metabolic improvement prior to electrocardiographic or volumetric changes of the right ventricle in pulmonary arterial hypertension
Myocardial metabolic improvement prior to electrocardiographic or volumetric changes of the right ventricle in pulmonary arterial hypertension
复制标题
肺动脉高压患者心电图或右心室容积变化之前心肌代谢改善
DOI：
10.1007/s12350-016-0769-8
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发表时间：
2018
期刊：
影响因子：
2.4
通讯作者：
Fukumoto Y
中科院分区：
文献类型：
--
作者：
Nakamura T;Tahara N,Tahara A;Yamagishi SI;Honda A;Igata S;Nitta Y;Bekki M;Nakamura T;Sugiyama Y;Sun J;Takeuchi M;Shimizu M;Yamazaki H;Fukami K;Fukumoto Y
一名26岁男性，有哮喘病史，因劳力性呼吸困难加重而转诊至本院。心电图显示胸前导联右偏，右室肥厚，R波高，ST段压低(图1A)。经胸超声心动图(TTE)显示右室增大伴室间隔向左移位(图1B)和三尖瓣返流，估计收缩压为75毫米汞柱。心导管检查证实为肺动脉高压，肺动脉压81/32(平均50)mm Hg，平均肺动脉嵌压8 mm Hg，心脏指数2.60 L/分/m~2，肺血管阻力8.92Wood单位。患者被归类为特发性PAH，因为其他检查没有发现PAH的原因。18F-脱氧葡萄糖正电子发射断层扫描(FDG-PET)结合计算机断层扫描(CT)显示右室游离壁存在高糖代谢(图1C-E，红色箭头)，提示右室负荷增加。使用Macitentan(每日10 mg)治疗6个月后，患者的肺血流动力学得到改善，PAP降至68/25(平均39)mm Hg，CI升至3.33 L/分钟/m~2，PVR降至5.25Wood单位，且无不良反应。虽然心电图、TTE和CT扫描没有显示右室容量减少或压力超负荷(图1F，G)，但连续FDG-PET/CT扫描显示与血流动力学改善一致的右室心肌明显的代谢改变(图1H-J，白色箭头)。PAH被认为是一种致命性疾病，其特征是PVR进行性增加，导致右室心肌负荷和代谢转移。FDG-PET显像可以直观地显示心肌的葡萄糖代谢，在心电图或容量改变之前显示心肌代谢的改善。糖酵解相关基因和蛋白，如葡萄糖转运蛋白和丙酮酸脱氢酶激酶，被认为在心电图或容量改变之前下调。1、2
A 26-year-old man with a history of bronchial asthma was referred to our hospital due to exacerbation of exertional dyspnea. Electrocardiography (ECG) demonstrated right-axis deviation and right ventricular (RV) hypertrophy with tall R waves and ST segment depression in the inferior and right-sided precordial leads (Figure 1 A). Transthoracic echocardiography (TTE) revealed enlarged RV with interventricular septal displacement toward the left ventricle (Figure 1 B) and tricuspid regurgitation and estimated systolic pressure of 75 mmHg. Cardiac catheterization confirmed the diagnosis of pulmonary arterial hypertension (PAH) with pulmonary arterial pressure (PAP) of 81/32 (mean 50) mmHg, mean pulmonary arterial wedge pressure of 8 mmHg, cardiac index (CI) of 2.60 L/min/m2, and pulmonary vascular resistance (PVR) of 8.92 Wood units. The patient was classified as idiopathic PAH, because other examinations identified no causes of PAH. 18F-Fluorodeoxyglucose-positron emission tomography (FDG-PET) combined with computed tomography (CT) revealed a high glucose metabolism in the RV free wall (Figure 1 C–E, red arrows), indicating increased RV workload. Six-month treatment with Macitentan (10mg daily) improved his pulmonary hemodynamics and lowered the PAP to 68/25 (mean 39) mmHg, increased CI to 3.33 L/min/m2, and lowered PVR to 5.25 Wood units with no adverse effect. Although ECG, TTE, and CT scan did not show a reduction in RV volume or pressure overload (Figure 1 F, G), serial FDG-PET/CT scan demonstrated a marked metabolic shift in the RV myocardium in concordance with the hemodynamic improvement (Figure 1 H–J, white arrows). PAH is considered as a fatal disease characterized by progressive increase in PVR, which leads to workload and metabolic shift in the RV myocardium. The FDG-PET imaging can visualize the myocardial glucose metabolism and demonstrate the improvement of myocardial metabolism prior to electrocardiographic or volumetric changes. Glycolysis-related genes and proteins such as glucose transporter and pyruvate dehydrogenase kinase were considered to be downregulated prior to electrocardiographic or volumetric changes. 1, 2