肺动脉高压病人左右心室心肌灌注储备与右心室功能及肺血流动力学之间的相关性

目的应用腺苷负荷MR心肌灌注成像评价肺动脉高压(PAH)病人右心室(RV)与左心室(LV)间心肌灌注储备与心室功能及肺血流动力学的关系。材料与方法本研究符     

Corrected tetralogy of Fallot: delayed enhancement in right ventricular outflow tract

PURPOSE: To evaluate retrospectively the presence of fibrosis and largest diameter of the right ventricular outflow tract (RVOT) by using delayed enhancement magnetic resonance (MR) imaging in patients who had undergone initial correction for tetralogy of Fallot. MATERIALS AND METHODS: MR imaging was performed in 24 consecutive patients (16 male, eight female; mean age, 25 years; age range, 13-47 years) with corrected tetralogy of Fallot. The study protocol was approved by the local ethics committee, and informed consent was not required. Fifteen minutes after injection of 0.2 mmol/kg gadopentetate dimeglumine, an inversion-recovery turbo field-echo sequence was applied for detection of delayed enhancement. Right ventricular volumes, ejection fraction, and anterior-posterior diameter of the RVOT were calculated. Mann-Whitney nonparametric testing was used to compare measurements of ventricular volume, function, and anterior-posterior diameter of the RVOT in the presence or absence of delayed enhancement. Correlation was tested with Pearson coefficient. RESULTS: Delayed enhancement was seen in 17 patients in the RVOT. During initial surgery, transannular patching was performed in 13 (76%) of 17 patients, RVOT patching in one (6%) of 17 patients, and the Brock procedure in two (12%) of 17 patients. In one patient, the type of initial RVOT repair was unknown. Patients with delayed enhancement in the RVOT, as compared with those without delayed enhancement in the RVOT, had increased RVOT diameter (32 mm +/- 7 [standard deviation] vs 22 mm +/- 3, P < .01), decreased right ventricular ejection fraction (43% +/- 6.3 vs 54% +/- 10, P < .001), and increased end-diastolic volume (175 mL/m2 +/- 42 vs 118 mL/m2 +/- 34, P < .01). The diameter of the RVOT correlated with increased right ventricular end-systolic volume (R = 0.86) and was inversely related to ejection fraction (R = -0.65). CONCLUSION: Delayed enhancement occurs frequently in patients after correction for tetralogy of Fallot. Delayed enhancement in the RVOT was associated with RVOT dilatation, which adversely affects right ventricular hemodynamics.     

组织多普勒超声成像技术评价肺动脉高压患者右室功能的临床应用

目的 应用组织多普勒超声成像技术评价肺动脉高压患者右室收缩功能及舒张功能,研究肺动脉高压患者右室功能的变化.方法 选择90例肺动脉高压患者,根据PH程度分为轻度组、中度组、高度组三个亚组(各30例)和60例正常人作为对照组,测量肺动脉内径,右室前壁厚度,右室腔大小,双平面Simpson法测右室射血分数(RVEF),组织多普勒测量三尖瓣环(前瓣瓣环、后瓣瓣环、隔瓣瓣环)收缩期S波峰值速度(Sm),舒张早期负向E波峰值速度(Em),舒张晚期负向A波峰值速度(Am).结果 肺动脉高压组的右室收缩功能及舒张功能均减低,RVEF、Sm、Em和Em/Am均低于对照组,右室前壁厚度、右室腔大小,Am高于对照组,差异均有显著性意义.结论 肺动脉高压患者右室心肌收缩期峰值速度结合右室RVEF可作为评价右室收缩功能的有效指标,舒张期负向峰值速度Em、Em/Am减低,Am增高可准确的评估右室舒张功能.     

Myocardial delayed contrast enhancement in patients with arterial hypertension: Initial results of cardiac MRI

Purpose

In arterial hypertension left ventricular hypertrophy comprises myocyte hypertrophy, interstitial fibrosis and structural alterations of the coronary microcirculation. MRI enables the detection of myocardial fibrosis, infarction and scar tissue by delayed enhancement (DE) after contrast media application.Aim of this study was to investigate patients with arterial hypertension but without known coronary disease or previous myocardial infarction to detect areas of DE.

Methods and material

Twenty patients with arterial hypertension with clinical symptoms of myocardial ischemia, but without history of myocardial infarction and normal coronary arteries during coronary angiography were investigated on a 1.0 T superconducting magnet (Gyroscan T10-NT, Intera Release 8.0, Philips). Fast gradient-echo cine sequences and T2-weighted STIR-sequences were acquired. Fifteen minutes after injection of Gadobenate dimeglumine inversion recovery gradient-echo sequences were performed for detection of myocardial DE. Presence or absence of DE on MRI was correlated with clinical data and the results of echocardiography and electrocardiography, respectively.

Results

Nine of 20 patients showed DE in the interventricular septum and the anteroseptal left ventricular wall. In 6 patients, DE was localized intramurally and in 3 patients subendocardially. There was a significant correlation between myocardial DE and ST-segment depressions during exercise and between DE and left-ventricular enddiastolic pressure. Patients with intermittent atrial fibrillation showed a myocardial DE more often than patients without atrial fibrillation.

Conclusion

In our series, 45% of patients with arterial hypertension showed DE on cardiac MRI. In this clinical setting, delayed enhancement may be due to coronary microangiopathy. The more intramurally localization of DE, however, rather indicates myocardial interstitial fibrosis.     

Left ventricular postmyocardial infarction remodeling studied by combining MR-tagging with delayed MR contrast enhancement

OBJECTIVES: We sought to monitor the evolution of noninfarcted and infarcted myocardium function in the process of left ventricular (LV) remodeling after a reperfused myocardial infarction. MATERIAL AND METHODS: Pigs (n = 8) were subjected to reperfused infarction. Magnetic resonance imaging (MRI) was performed at 3 days and 8 weeks after infarction. Regional circumferential shortening (Ecc) and principal strain L1 in the infarcted, peri-infarcted, and remote myocardium were evaluated by tagged cine MRI combined with matched late enhancement data (Gadolinium-DOTA-enhanced IR-GRE) Global LV function was evaluated by cine MRI. Animals were euthanized after the second imaging session and tissue samples from the different myocardial regions were obtained for histopathologic study. RESULTS: There was a significant deterioration in Ecc between the 3-day and 8-week studies in the peri-infarcted myocardium at apex (-9.9% +/- 4.5% to -6.5 +/- 3.9; P = 0.046) whereas it remained stable for all other regions at all levels. A trend toward improvement in Ecc existed in the infarcted myocardium when infarction transmurality was less than 50% of the LV wall (-7.5% +/- 0.8% to -12.2% +/- 2.9% P = 0.06). Ecc in infarcted myocardium was significantly inferior (P < 0.002) to that in remote and peri-infarcted myocardium at the apical level (2.7% +/- 2.6% vs. -14.4% +/- 3.3% and -9.9% +/- 4.5%, respectively). Global LV function substantially deteriorated after infarction and was associated with a significant LV dilation. CONCLUSION: These results confirm the hypothesis that scarred myocardium imposes additional functional burden to the peri-infarcted myocardium.     

Response of right ventricular systolic function to exercise stress: Effects of pulmonary vascular resistance on right ventricular systolic function

To elucidate factors influencing responses of right ventricular systolic function to exercise stress, we evaluated the right ventricular ejection fraction and peak ejection rate with two different loading conditions, atrial septal defect and mitral stenosis, at rest and during exercise by means of gated equilibrium blood pool radionuclide ventriculography. In both atrial septal defect and mitral stenosis, strong correlations between changes in the right ventricular ejection fraction with exercise and pulmonary vascular resistance at rest (r = ?0.97, p < 0.001; r = ?0.86, p < 0.0005: respectively) were found. Significant correlations between changes in the right ventricular peak ejection rate with exercise and pulmonary vascular resistance at rest (r = ?0.85, p < 0.05; r = ?0.75, p < 0.01: respectively) were found in atrial septal defect and mitral stenosis. Both the right ventricular ejection fraction and peak ejection rate were lower during exercise than at rest when pulmonary vascular resistance at rest was more than 200 dynes·sec·cm^?5·m² in both atrial septal defect and mitral stenosis. In conclusion, right ventricular systolic function responding to exercise stress was influenced by the pulmonary vascular resistance in both atrial septal defect and mitral stenosis.     

Native myocardial T1 mapping in pulmonary hypertension: correlations with cardiac function and hemodynamics

Objectives

To analyze alterations in left ventricular (LV) myocardial T1 times in patients with pulmonary hypertension (PH) and to investigate their associations with ventricular function, mass, geometry and hemodynamics.

Methods

Fifty-eight patients with suspected PH underwent right heart catheterization (RHC) and 3T cardiac magnetic resonance imaging. Ventricular function, geometry and mass were derived from cine real-time short-axis images. Myocardial T1 maps were acquired by a prototype modified Look-Locker inversion-recovery sequence in short-axis orientations. LV global, segmental and ventricular insertion point (VIP) T1 times were evaluated manually and corrected for blood T1.

Results

Septal, lateral, global and VIP T1 times were significantly higher in PH than in non-PH subjects (septal, 1249?±?58 ms vs. 1186?±?33 ms, p?<?0.0001; lateral, 1190?±?45 ms vs. 1150?±?33 ms, p?=?0.0003; global, 1220?±?52 ms vs. 1171?±?29 ms, p?<?0.0001; VIP, 1298?±?78 ms vs. 1193?±?31 ms, p?<?0.0001). In PH, LV eccentricity index was the strongest linear predictor of VIP T1 (r?=?0.72). Septal, lateral and global T1 showed strong correlations with VIP T1 (r?=?0.81, r?=?0.59 and r?=?0.75, respectively).

Conclusions

In patients with PH, T1 times in VIPs and in the entire LV myocardium are elevated. LV eccentricity strongly correlates with VIP T1 time, which in turn is strongly associated with T1 time changes in the entire LV myocardium.

Key Points

? Native T1 mapping detects left ventricular myocardial alterations in pulmonary hypertension ? In pulmonary hypertension, native T1 times at ventricular insertion points are increased ? These T1 times correlate strongly with left ventricular eccentricity ? In pulmonary hypertension, global and segmental myocardial T1 times are increased ? Global, segmental and ventricular insertion point T1 times are strongly correlated

     

斑点追踪技术评价肺动脉高压患者右心室舒张功能的研究

目的：应用斑点追踪成像技术评价肺动脉高压患者右心室舒张功能,并与常规多普勒超声心动对比研究。方法：肺动脉高压患者31例,正常对照组33例,二维斑点追踪成像技术获得右心室各个节段舒张期纵向应变率及运动速度。结果：右心室游离壁及室间隔各段舒张早期应变率（SRe）有显著性差异（P〈0．05）;右室游离壁及室间隔舒张早期应变率（SRe）平均值与右室游离壁厚度、肺动脉收缩压相关性较好。结论：舒张早期应变率与右室游离壁厚度及肺动脉收缩压相关性较好,二维斑点追踪成像技术为评价肺动脉高压右室舒张功能提供了一种可行的方法。     

组织速度成像同步测定右心室三尖瓣环速度和Tei指数评估肺动脉高压右心室功能

目的:探讨应用定量组织速度成像(QTVI)技术同步测定右室游离壁三尖瓣环运动速度和Tei指数评估肺动脉高压(PAH)患者右室功能的联合应用价值。方法:58例PAH患者和47例健康人入选本研究。常规超声心动图测量右室游离壁厚度,右房、右室舒张末期面积和收缩末期面积(RAEDA,RAESA,RVEDA,RVESA)并计算右室面积变化率;获取入选者标准心尖部右室流入道长轴和四腔观TVI图像,离线分析右室4个壁三尖瓣环处组织速度曲线,测量右室游离壁三尖瓣环处收缩期峰值速度(Sa)、舒张早期峰值速度(Ea)、舒张晚期峰值速度(Aa);依据公式计算右室4个壁瓣环处Tei指数,取其平均值作为右室整体心肌做功指数。结果:与正常人相比,PAH患者具有更厚的右室游离壁,更大的RAEDA、RAESA、RVEDA、RVESA、Tei指数,更高的肺动脉收缩压,更低的右室面积变化率、Sa、Ea、Aa、Ea/Aa。PAH患者右室结构参数(右室游离壁厚度,RAEDA、RAESA、RVEDA、RVESA)与功能参数(Tei指数、Sa、Ea、Aa、Ea/Aa、右室面积变化率)间均具有一定的相关性(r=0.34～0.76,P<0.05～0.001)。PAH患者Sa、Ea、Aa、Ea/Aa、右室面积变化率与Tei指数均有一定的相关性(r=0.39～0.68,P<0.05～0.001)。结论:QTVI技术同步测定三尖瓣环运动指标和Tei指数可更好地评估PAH患者右室功能。     

HGF、c-Met蛋白与左向右分流型肺动脉高压肺血管重构的关系

目的 观察肝细胞生长因子(HGF)、c-Met原癌基因编码产物及Caspase-3在左向右分流型大鼠肺动脉高压(PAH)形成过程中肺动脉内的表达,探讨HGF及c-Met在PAH形成中的作用.方法 4～5周龄SD大鼠80只,随机均分为分流组与对照组,分流组采用套管法行颈总动脉-颈外静脉分流术以建立左向右分流型肺动脉高压模型,对照组行假手术.两组均在术后第4、8、12、16周行肺血流动力学和病理学检查,采用免疫组织化学法检测HGF、c-Met、Caspase-3在肺动脉壁内的表达.结果 分流组术后各时间点肺动脉收缩压(PASP)、肺动脉平均压(mPAP)及肺循环血流量/体循环血流量(Qp/Qs)均明显高于对照组(P<0.01);随时间延长,分流组肺动脉中膜厚度百分比(MT%)及右室肥厚指数(RVHI)明显增高,与对照组比较差异显著(P<0.01);分流组术后8周HGF、c-Met表达明显高于对照组(P<0.01),此后缓慢下降,术后4周Caspase-3表达最高(P<0.01),此后逐渐下降并低于对照组.结论 套管法连接颈总动脉与颈外静脉建立左向右分流型肺动脉高压大鼠模型简易可靠.HGF、c-Met在肺循环高灌注大鼠肺血管中的表达与肺动脉压力变化及肺血管重构有关.PAH形成中Caspase-3表达逐渐降低,可能与肺动脉壁平滑肌细胞增殖有关.     

Magnetic resonance imaging of delayed enhancement in hypertrophic cardiomyopathy: relationship with left ventricular perfusion and contractile function

PURPOSE: The aim of the study was to analyze the relationship between myocardial delayed enhancement, first-pass perfusion, and contractile function in hypertrophic cardiomyopathy (HCM) patients, using MR. METHODS: Fifty-three patients diagnosed with HCM were prospectively examined using a 1.5-T MR unit. Multiphase gradient-echo sequences were performed to study global left ventricular function, wall thickness, and left ventricular mass. Myocardial tissue tagging was conducted to evaluate contractile function. T1-weighted inversion-recovery sequences were obtained at rest to study myocardial contrast enhancement at first pass and delayed enhancement 10 minutes later. RESULTS: Delayed enhancement found in 30 patients (56.6%) was most commonly seen in hypertrophic segments. Nine patients exhibited delayed enhancement in segments with normal wall thickness (<15 mm). Sixteen patients (30.1%) showed first-pass perfusion defects at rest, which were associated with significantly lower stroke volume (P<0.05) and lower cardiac output (P<0.01). The hypokinetic segments found in 16 patients (30.1%) were significantly thicker at end diastole (P<0.01). Delayed enhancement correlated positively with perfusion defects (r=0.5, P<0.01) and hypokinetic segments (r=0.3, P<0.05). CONCLUSION: Delayed myocardial enhancement is most commonly found in hypertrophic segments but also can be seen in segments with normal wall thickness. Perfusion defects at rest and impaired contractile function are related abnormalities with delayed myocardial enhancement. Further studies are necessary to assess the role of myocardial tagging, first-pass perfusion, and delayed enhancement in risk stratification for patients with HCM.