Brain volumetric, regional cortical thickness and radiographic findings in adults with cyanotic congenital heart disease.
Brain volumetric, regional cortical thickness and radiographic findings in adults with cyanotic congenital heart disease.
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DOI：
10.1016/j.nicl.2013.12.011
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发表时间：
2014
影响因子：
4.2
通讯作者：
Celermajer, David S.
中科院分区：
文献类型：
--
作者：
Cordina, Rachael;Grieve, Stuart;Barnett, Michael;Lagopoulos, Jim;Malitz, Nathan;Celermajer, David S.
患有先天性心脏病（CHD）的成人慢性紫绀可能导致大脑结构改变，从而导致神经功能受损。这些变化的程度还没有得到充分的描述。我们假设患有青紫型冠心病的成年人会有广泛的改变，包括脑容量异常、皮质厚度下降和小血管和大血管缺血性改变的负担增加。本文采用定量MRI对10例冠心病慢性紫绀患者（40±4岁）进行了研究，平均血氧饱和度为82±2%。同时评估血液学和生化指标。所有受试者均无重大身体或智力损伤。脑容量结果与从我们的正常受试者数据库中随机选择的年龄和性别匹配的对照组进行比较。10个紫绀型受试者中有5个有皮质腔隙性梗死。白质（WM）高负荷也异常高（Scheltens评分为8±2）。定量MRI显示广泛的广泛性脑白质和灰质（GM）体积损失；氰化受试者总体GM体积减少（630±16 mL vs.对照组696±14 mL， p = 0.01）， WM体积减少（471±10 mL vs. 564±18 mL, p = 0.003）。脑脊液容量增加（35±10 vs 26±5 mL, p = 0.002）。在整个大脑中观察到广泛的局部皮层厚度减少。这些变化包括双侧额叶厚度的减少，包括背外侧前额叶皮层和中央前回、后顶叶和颞中回。尾状核、壳核和丘脑皮层下体积发生变化（所有区域p≤0.005）。皮质GM体积与脑利钠肽（R = - 0.89, p = 0.009）、高敏c反应蛋白（R = - 0.964, p < 0.0001）和不对称二甲基精氨酸（R = - 0.75, p = 0.026）呈负相关，但与氧饱和度、堆积细胞体积和黏度无关。我们提出了第一个全面的大脑结构分析成人慢性神经性紫绀由于先天性心脏病。我们展示了明显的大血管和微血管损伤的证据。紫绀患者表现出脑容量减少的整体证据，以及特定的皮质厚度减少灶。GM体积损失与hsCRP、BNP和ADMA相关，提示炎症、神经激素激活和内皮功能障碍可能在其发病机制中起重要作用。脑大、小血管缺血性损伤负担高。广泛的白质和灰质（GM）体积损失。额叶、顶叶和颞叶内双侧局部皮层厚度减少的区域。
Chronic cyanosis in adults with congenital heart disease (CHD) may cause structural brain changes that could contribute to impaired neurological functioning. The extent of these changes has not been adequately characterized. We hypothesized that adults with cyanotic CHD would have widespread changes including abnormal brain volumetric measures, decreased cortical thickness and an increased burden of small and large vessel ischemic changes. Ten adults with chronic cyanosis from CHD (40 ± 4 years) and mean oxygen saturations of 82 ± 2% were investigated using quantitative MRI. Hematological and biochemical parameters were also assessed. All subjects were free from major physical or intellectual impairment. Brain volumetric results were compared with randomly selected age- and sex-matched controls from our database of normal subjects. Five of 10 cyanotic subjects had cortical lacunar infarcts. The white matter (WM) hyperintensity burden was also abnormally high (Scheltens Scale was 8 ± 2). Quantitative MRI revealed evidence of extensive generalized WM and gray matter (GM) volumetric loss; global GM volume was reduced in cyanosed subjects (630 ± 16 vs. 696 ± 14 mL in controls, p = 0.01) as was global WM volume (471 ± 10 vs. 564 ± 18 mL, p = 0.003). Ventricular cerebrospinal fluid volume was increased (35 ± 10 vs. 26 ± 5 mL, p = 0.002). There were widespread regions of local cortical thickness reduction observed across the brain. These changes included bilateral thickness reductions in the frontal lobe including the dorsolateral prefrontal cortex and precentral gyrus, the posterior parietal lobe and the middle temporal gyrus. Sub-cortical volume changes were observed in the caudate, putamen and in the thalamus (p ≤ 0.005 for all regions). Cortical GM volume negatively correlated with brain natriuretic peptide (R = − 0.89, p = 0.009), high sensitivity C-reactive protein (R = − 0.964, p < 0.0001) and asymmetric dimethylarginine (R = − 0.75, p = 0.026) but not with oxygen saturations, packed cell volume or viscosity. We present the first comprehensive analysis of brain structure in adults with chronic neurocyanosis due to congenital heart disease. We demonstrate clear evidence for marked macro- and microvascular injury. Cyanotic patients show global evidence for reduced brain volume as well as specific foci of cortical thickness reduction. The GM volume loss correlated with hsCRP, BNP and ADMA suggesting that inflammation, neurohormonal activation and endothelial dysfunction may have important roles in its pathogenesis. A high burden of cerebral small and large vessel ischemic injury. Extensive white and gray matter (GM) volumetric loss. Regions of bilateral local cortical thickness reduction within the frontal, parietal and temporal lobes.
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