对心脏良、恶性病变的~（18）F-FDG PET/CT诊断标准及显像前准备方法的初步探讨
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摘要
第一部分18F-FDG PET/CT鉴别诊断心脏良、恶性病变的可行性研究
1.研究目的
1.1通过分析18F-FDG PET/CT用于心脏良、恶性病变鉴别诊断的价值，来探讨18F-FDGPET/CT鉴别诊断心脏病变良、恶性的可行性。
1.2计算18F-FDG PET/CT鉴别心脏病变良、恶性的最佳临界值（SUVmax及SUVmaxLesion/Blood），同时计算单独CT及PET/CT鉴别诊断心脏病变良、恶性的敏感性、特异性、准确性。综合分析，初步制定心脏病变的18F-FDG PET/CT诊断思路。
2.材料与方法
2.1研究对象
29例经病理或临床证实的心脏良、恶性病变进行18F-FDG PET/CT扫描，其中恶性病变17例，良性病变12例。
2.2 18F-FDG PET/CT检查方法
2.2.1检查前准备
29例中24例患者全身显像前禁食12小时以上，5例患者行PET/CT检查前2餐采用低碳水化合物高脂饮食，餐后3～6小时内进行PET/CT扫描。
2.2.2检查方法所有患者均行PET/CT扫描及胸部双期增强扫描。
2.2.3数据分析
测得病灶、心腔（血本底）SUVmax及SUVmax病灶/SUVmax心腔（SUVmaxLesion/Blood），结果用“均数±标准差”表示，并观察病灶的CT特征及与周围组织关系。选取不同SUVmax及SUVmax Lesion/Blood分别计算其作为心脏良、恶性病变的临界值时的诊断价值，以计算出最佳临界SUVmax及SUVmax Lesion/Blood。同时分别计算单独CT及PET/CT诊断心脏良、恶性病变的敏感性、特异性、准确性。
2.2.4统计学方法
所有计量资料均先行正态性检验，采用两独立样本t检验/校正t检验（正态分布）或两独立样本非参数检验（Mann-Whitney U检验）（非正态分布）的方法分别分析SUVmax、SUVmax Lesion/Blood在良、恶性病变之间有无统计学差异（P<0.05，差别有统计学意义）。采用配对x2检验，比较PET/CT及单独CT在诊断准确性上的差异。检验标准：P<0.05，差别有统计学意义。所有统计分析经SPSS13.0统计软件处理。
3.结果
良性病变SUVmax为0.5～7.4，平均为2.26±1.81；恶性病变SUVmax为2.6～21.2，平均为8.37±5.20。SUVmax值在良、恶性病变之间比较采用独立样本t检验，显示差别有高度统计学意义（t = 4.473，P = 0.000），恶性病变的SUVmax值大于良性病变，SUVmax在良、恶性病变两组均数的差值为6.11，差值的95%可信区间为（3.27，8.95）。
良性病变SUVmax Lesion/Blood为1.15±1.06，恶性病变SUVmax Lesion/Blood为4.24±2.02。SUVmax Lesion/Blood值在良、恶性病变之间比较采用独立样本t检验，显示差别有高度统计学意义（t = 4.842，P = 0.000），恶性病变的SUVmax Lesion/Blood值大于良性病变，SUVmax Lesion/Blood在良、恶性病变两组均数的差值为3.09，差值的95%可信区间为（1.78，4.40）。
SUVmax以3.5或SUVmax Lesion/Blood以1.8～2.2为阈值时，诊断价值最高，为PET鉴别心脏病变良、恶性的最佳临界值。
29例心脏病变中，CT平扫及增强单独诊断正确20例，根据最佳临界SUVmax及SUVmax Lesion/Blood同时结合CT平扫及增强图像，即PET/CT诊断正确27例。单独CT及PET/CT鉴别诊断心脏病变良、恶性的敏感性、特异性、准确性分别为64.7%（11/17）、75.0%（9/12）、69.0%（20/29）；100.0%（17/17）、83.3%（10/12）、93.1%（27/29）。CT与PET/CT比较，诊断准确性有统计学差异（P = 0.016）（McNemar检验）。
4.结论
18F-FDG PET/CT可以较为准确地提示病变的位置、形态、大小、范围、附着点、以及肺部、纵膈（大血管、冠状动脉等）、心包、胸腔的受累情况、同时提供病变的代谢活性，从而能够较为敏感、特异、准确地鉴别心脏、心包病变的良、恶性。
1.研究目的
测量禁食组及低碳水化合物高脂组两种不同显像前准备方法的患者心肌摄取18F-FDG程度（SUVmax），比较两种方法的患者心肌SUVmax，制定适合心脏病变的18F-FDG PET/CT显像前准备方法的设定。
2.材料与方法：
2. 1研究对象
30例临床怀疑心脏病变患者显像前通过不同的显像前准备，接着进行18F-FDG PET/CT扫描。
2.2 18F-FDG PET/CT检查方法
2.2.1检查前准备
禁食组：共17例患者，均为PET/CT检查前禁食12小时以上，16小时以内。低碳水化合物高脂组：共13例患者，PET/CT检查前2餐采用低碳水化合物高脂饮食，餐后3～6小时内进行PET/CT扫描。
2.2.2统计学方法
分别测量禁食组与低碳水化合物高脂组两组患者心肌SUVmax及检查前血糖水平。所有数据先行正态分布检验，采用两独立样本t检验/ t’检验（正态分布）或两独立样本非参数检验（Mann-Whitney U检验）（非正态分布）分析SUVmax及血糖值在良性与恶性病变之间有无统计学差异（P<0.05，差别有统计学意义）。
3.结果
禁食组与低碳水化合物高脂组患者的心肌SUVmax分别为2.2～19.3（中位数为3.1）、0.7～3.4（中位数为2.1）。比较两组SUVmax采用Mann-Whitney U检验，显示禁食组SUVmax的平均秩次为20.18，低碳水化合物高脂组SUVmax的平均秩次为9.38，Z = -3.333,P = 0.001，两者之间差别有统计学意义，低碳水化合物高脂组患者心肌SUVmax低于禁食组患者心肌SUVmax。
禁食组血糖水平为3.7～9.0，平均为6.73±1.77；低碳水化合物高脂组的血糖水平为4.2～8.6，平均为5.82±1.05。血糖水平在两组之间比较采用独立样本t检验，显示差别没有统计学意义（t = 1.746，P = 0.092），血糖水平的两组均数的差值为0.52，差值的95%可信区间为（-0.16，1.97）。
4.结论
患者行PET/CT检查前2餐采用低碳水化合物高脂饮食，餐后3～6小时内进行PET/CT扫描能够较为有效的抑制心肌摄取18F-FDG，使心肌的显影程度不影响诊断，为一种较为合理的适合心脏、心包病变的18F-FDG PET/CT显像前准备方法。
1.Objective
1.1 To probe the clinical utilization of Fluorine-18 fluorodeoxyglucose positron emissiontomography CT ( 18F-FDG PET/CT ) in diagnosis of malignant from nonmalignant heart andpericardium lesions, in order to assess the feasibility of 18F-FDG PET-CT for the differentiationof malignancy from benign manifested as heart and pericardium lesions,
1.2 To find out the optimal cut-off value of maximum standard uptake values ( SUVmax ) andSUVmax lesion/blood for diagnosing the heart and pericardium lesions, than calculate thediagnostic sensitivity, specificity, accuracy of CT and PET-CT respectively. To make a 18F-FDGPET/CTdiagnostic criteria for heart and pericardium lesions by comprehensive analysis.
2.Materials and Methods
2.1 Object of study
A total of 29 cases ( malignancy: benign = 17: 12 ) with cardiac and pericardial lesions wereanalyzed in the present study, all of which were pathologically or clinically confirmed.
2.2 FDG-PET/CT scanning
2.2.1 Preparation for examination
2.2.2 Scanning methods
All patients were examined by 18F-FDG PET/CT and enhancement CT scan.
2.2.2 Image analysis
All lesions were evaluated semi-quantitatively using maximum standard uptake values (SUVmax) and SUVmax lesion/blood, and the density of the heart and pericardium lesions andthe relation with surrounding tissues were evaluated. To find out the optimal cut-off value ofmaximum standard uptake values ( SUVmax ) and SUVmax lesion/blood for diagnosing theheart and pericardium lesions, Than calculate the diagnostic sensitivity, specificity, accuracy ofCT and PET-CT respectively.
2.2.3 Statistical Methods
All the measurement data was performed by the Normal Test. The differences of SUVmaxand SUVmax lesion/blood of benign between malignant lesions were analyzed byIndependent-Samples T Test or T’Test ( Normal ), or Mann-Whitney U Test ( Non-normaldistribution ). The statistic difference in sensitivity, specificity, accuracy, positive predictivevalue and negative predictive value of CT and PET/CT were compared by x2 test. Thestatistically significant difference was set at P<0.05. All the statistical analysis was made usingSPSS 13.0 software package.
3.Results
The SUVmax of the benign lesions ranged from 0.5 to 7.4 (mean 2.26±1.82), and theSUVmax of the malignancy ranged from 2.6 to 21.2 (mean 8.37±5.20). The showed significantdifference ( t = 3.473, P = 0.000), the SUVmax Lesion/Blood of malignancy 1.15±1.06 andbenign 4.24±2.02 also prohibited significant difference(t = 4.842, P = 0.000).
The optimal cut-off value of SUVmax is 3.5 and SUVmax Lesion/Blood is 1.8～2.2.
The sensitivity, specificity, accuracy of CT and PET-CT were 64.7% ( 11/17 ), 75.0%( 9/12 ), 69.0% ( 20/29 ) and 100.0% ( 17/17 ), 83.3% ( 10/12 ), 93.1% ( 27/29 ) respectively.There was a significant differenec between CT and PET/CT in accuracy (P = 0.016)(McNemarTest).
4.Conlusion
18F-FDG PET-CT can correctly predict benignity or malignancy of cardiac and pericardiallesions.
1. Objective
Myocardial 18F-FDG uptake in PET scans in patients prepared by the usual fasting protocolmay result in difficulties in interpretation because variable uptake may yield false-positive resultsregarding mediastinal abnormalities. We aimed to analyze, retrospectively, the effect of diet onmyocardial FDG uptake.
2. Materials and Methods
2.1 Object of study
A total of 30 cases with cardiac and pericardial lesions were performed by PET/CT.
2.2 FDG-PET/CT scanning
2.2.1 Preparation for examination
The "fasting" group comprised 17 consecutive patients before a clinical change in thepatient preparation protocol. The "new diet" group comprised 60 consecutive patients after theclinical protocol change who were directed to consume a very high-fat, low-carbohydrate,protein-permitted diet before FDG injection. All patients were given a questionnaire that wasused to verify diet adherence.
2.2.2 Statistical Methods
All the measurement data was performed by the Normal Test. The differences of SUVmaxand the blood glucose level of "fasting" group between The "new diet" group were analyzed byIndependent-Samples T Test or T’Test ( Normal ), or Mann-Whitney U Test ( Non-normaldistribution ). All the statistical analysis was made using SPSS 13.0 software package.
3. Results
The SUVmax of the "fasting" group ranged from 2.2 to 19.3 (median 3.1), and the SUVmaxof the"new diet" group ranged from 0.7 to 3.4 (median 2.1). The showed significant differenceby Mann-Whitney U Test ( Z = -3.333, P = 0.001<0.01),
The blood glucose level of the "fasting" group ranged from 3.7 to 9.0 (mean 6.73±1.77),and the lood glucose level of the"new diet" group ranged from 4.2 to 8.6 (mean 5.82±1.05). Theshowed significant difference by t Test ( t = 1.746，P = 0.092),
4. Conlusion
A very high-fat, low-carbohydrate, protein-permitted diet before FDG injection suppressesmyocardial FDG uptake. This should facilitate definition of mediastinal abnormalities on FDGPET. It is a more reasonable patient preparation protocol for the patients with heart andpericardium lesions.
1.研究目的
1.1通过分析18F-FDG PET/CT用于心脏良、恶性病变鉴别诊断的价值，来探讨18F-FDGPET/CT鉴别诊断心脏病变良、恶性的可行性。
1.2计算18F-FDG PET/CT鉴别心脏病变良、恶性的最佳临界值（SUVmax及SUVmaxLesion/Blood），同时计算单独CT及PET/CT鉴别诊断心脏病变良、恶性的敏感性、特异性、准确性。综合分析，初步制定心脏病变的18F-FDG PET/CT诊断思路。
2.材料与方法
2.1研究对象
29例经病理或临床证实的心脏良、恶性病变进行18F-FDG PET/CT扫描，其中恶性病变17例，良性病变12例。
2.2 18F-FDG PET/CT检查方法
2.2.1检查前准备
29例中24例患者全身显像前禁食12小时以上，5例患者行PET/CT检查前2餐采用低碳水化合物高脂饮食，餐后3～6小时内进行PET/CT扫描。
2.2.2检查方法所有患者均行PET/CT扫描及胸部双期增强扫描。
2.2.3数据分析
测得病灶、心腔（血本底）SUVmax及SUVmax病灶/SUVmax心腔（SUVmaxLesion/Blood），结果用“均数±标准差”表示，并观察病灶的CT特征及与周围组织关系。选取不同SUVmax及SUVmax Lesion/Blood分别计算其作为心脏良、恶性病变的临界值时的诊断价值，以计算出最佳临界SUVmax及SUVmax Lesion/Blood。同时分别计算单独CT及PET/CT诊断心脏良、恶性病变的敏感性、特异性、准确性。
2.2.4统计学方法
所有计量资料均先行正态性检验，采用两独立样本t检验/校正t检验（正态分布）或两独立样本非参数检验（Mann-Whitney U检验）（非正态分布）的方法分别分析SUVmax、SUVmax Lesion/Blood在良、恶性病变之间有无统计学差异（P<0.05，差别有统计学意义）。采用配对x2检验，比较PET/CT及单独CT在诊断准确性上的差异。检验标准：P<0.05，差别有统计学意义。所有统计分析经SPSS13.0统计软件处理。
3.结果
良性病变SUVmax为0.5～7.4，平均为2.26±1.81；恶性病变SUVmax为2.6～21.2，平均为8.37±5.20。SUVmax值在良、恶性病变之间比较采用独立样本t检验，显示差别有高度统计学意义（t = 4.473，P = 0.000），恶性病变的SUVmax值大于良性病变，SUVmax在良、恶性病变两组均数的差值为6.11，差值的95%可信区间为（3.27，8.95）。
良性病变SUVmax Lesion/Blood为1.15±1.06，恶性病变SUVmax Lesion/Blood为4.24±2.02。SUVmax Lesion/Blood值在良、恶性病变之间比较采用独立样本t检验，显示差别有高度统计学意义（t = 4.842，P = 0.000），恶性病变的SUVmax Lesion/Blood值大于良性病变，SUVmax Lesion/Blood在良、恶性病变两组均数的差值为3.09，差值的95%可信区间为（1.78，4.40）。
SUVmax以3.5或SUVmax Lesion/Blood以1.8～2.2为阈值时，诊断价值最高，为PET鉴别心脏病变良、恶性的最佳临界值。
29例心脏病变中，CT平扫及增强单独诊断正确20例，根据最佳临界SUVmax及SUVmax Lesion/Blood同时结合CT平扫及增强图像，即PET/CT诊断正确27例。单独CT及PET/CT鉴别诊断心脏病变良、恶性的敏感性、特异性、准确性分别为64.7%（11/17）、75.0%（9/12）、69.0%（20/29）；100.0%（17/17）、83.3%（10/12）、93.1%（27/29）。CT与PET/CT比较，诊断准确性有统计学差异（P = 0.016）（McNemar检验）。
4.结论
18F-FDG PET/CT可以较为准确地提示病变的位置、形态、大小、范围、附着点、以及肺部、纵膈（大血管、冠状动脉等）、心包、胸腔的受累情况、同时提供病变的代谢活性，从而能够较为敏感、特异、准确地鉴别心脏、心包病变的良、恶性。
1.研究目的
测量禁食组及低碳水化合物高脂组两种不同显像前准备方法的患者心肌摄取18F-FDG程度（SUVmax），比较两种方法的患者心肌SUVmax，制定适合心脏病变的18F-FDG PET/CT显像前准备方法的设定。
2.材料与方法：
2. 1研究对象
30例临床怀疑心脏病变患者显像前通过不同的显像前准备，接着进行18F-FDG PET/CT扫描。
2.2 18F-FDG PET/CT检查方法
2.2.1检查前准备
禁食组：共17例患者，均为PET/CT检查前禁食12小时以上，16小时以内。低碳水化合物高脂组：共13例患者，PET/CT检查前2餐采用低碳水化合物高脂饮食，餐后3～6小时内进行PET/CT扫描。
2.2.2统计学方法
分别测量禁食组与低碳水化合物高脂组两组患者心肌SUVmax及检查前血糖水平。所有数据先行正态分布检验，采用两独立样本t检验/ t’检验（正态分布）或两独立样本非参数检验（Mann-Whitney U检验）（非正态分布）分析SUVmax及血糖值在良性与恶性病变之间有无统计学差异（P<0.05，差别有统计学意义）。
3.结果
禁食组与低碳水化合物高脂组患者的心肌SUVmax分别为2.2～19.3（中位数为3.1）、0.7～3.4（中位数为2.1）。比较两组SUVmax采用Mann-Whitney U检验，显示禁食组SUVmax的平均秩次为20.18，低碳水化合物高脂组SUVmax的平均秩次为9.38，Z = -3.333,P = 0.001，两者之间差别有统计学意义，低碳水化合物高脂组患者心肌SUVmax低于禁食组患者心肌SUVmax。
禁食组血糖水平为3.7～9.0，平均为6.73±1.77；低碳水化合物高脂组的血糖水平为4.2～8.6，平均为5.82±1.05。血糖水平在两组之间比较采用独立样本t检验，显示差别没有统计学意义（t = 1.746，P = 0.092），血糖水平的两组均数的差值为0.52，差值的95%可信区间为（-0.16，1.97）。
4.结论
患者行PET/CT检查前2餐采用低碳水化合物高脂饮食，餐后3～6小时内进行PET/CT扫描能够较为有效的抑制心肌摄取18F-FDG，使心肌的显影程度不影响诊断，为一种较为合理的适合心脏、心包病变的18F-FDG PET/CT显像前准备方法。
1.Objective
1.1 To probe the clinical utilization of Fluorine-18 fluorodeoxyglucose positron emissiontomography CT ( 18F-FDG PET/CT ) in diagnosis of malignant from nonmalignant heart andpericardium lesions, in order to assess the feasibility of 18F-FDG PET-CT for the differentiationof malignancy from benign manifested as heart and pericardium lesions,
1.2 To find out the optimal cut-off value of maximum standard uptake values ( SUVmax ) andSUVmax lesion/blood for diagnosing the heart and pericardium lesions, than calculate thediagnostic sensitivity, specificity, accuracy of CT and PET-CT respectively. To make a 18F-FDGPET/CTdiagnostic criteria for heart and pericardium lesions by comprehensive analysis.
2.Materials and Methods
2.1 Object of study
A total of 29 cases ( malignancy: benign = 17: 12 ) with cardiac and pericardial lesions wereanalyzed in the present study, all of which were pathologically or clinically confirmed.
2.2 FDG-PET/CT scanning
2.2.1 Preparation for examination
2.2.2 Scanning methods
All patients were examined by 18F-FDG PET/CT and enhancement CT scan.
2.2.2 Image analysis
All lesions were evaluated semi-quantitatively using maximum standard uptake values (SUVmax) and SUVmax lesion/blood, and the density of the heart and pericardium lesions andthe relation with surrounding tissues were evaluated. To find out the optimal cut-off value ofmaximum standard uptake values ( SUVmax ) and SUVmax lesion/blood for diagnosing theheart and pericardium lesions, Than calculate the diagnostic sensitivity, specificity, accuracy ofCT and PET-CT respectively.
2.2.3 Statistical Methods
All the measurement data was performed by the Normal Test. The differences of SUVmaxand SUVmax lesion/blood of benign between malignant lesions were analyzed byIndependent-Samples T Test or T’Test ( Normal ), or Mann-Whitney U Test ( Non-normaldistribution ). The statistic difference in sensitivity, specificity, accuracy, positive predictivevalue and negative predictive value of CT and PET/CT were compared by x2 test. Thestatistically significant difference was set at P<0.05. All the statistical analysis was made usingSPSS 13.0 software package.
3.Results
The SUVmax of the benign lesions ranged from 0.5 to 7.4 (mean 2.26±1.82), and theSUVmax of the malignancy ranged from 2.6 to 21.2 (mean 8.37±5.20). The showed significantdifference ( t = 3.473, P = 0.000), the SUVmax Lesion/Blood of malignancy 1.15±1.06 andbenign 4.24±2.02 also prohibited significant difference(t = 4.842, P = 0.000).
The optimal cut-off value of SUVmax is 3.5 and SUVmax Lesion/Blood is 1.8～2.2.
The sensitivity, specificity, accuracy of CT and PET-CT were 64.7% ( 11/17 ), 75.0%( 9/12 ), 69.0% ( 20/29 ) and 100.0% ( 17/17 ), 83.3% ( 10/12 ), 93.1% ( 27/29 ) respectively.There was a significant differenec between CT and PET/CT in accuracy (P = 0.016)(McNemarTest).
4.Conlusion
18F-FDG PET-CT can correctly predict benignity or malignancy of cardiac and pericardiallesions.
1. Objective
Myocardial 18F-FDG uptake in PET scans in patients prepared by the usual fasting protocolmay result in difficulties in interpretation because variable uptake may yield false-positive resultsregarding mediastinal abnormalities. We aimed to analyze, retrospectively, the effect of diet onmyocardial FDG uptake.
2. Materials and Methods
2.1 Object of study
A total of 30 cases with cardiac and pericardial lesions were performed by PET/CT.
2.2 FDG-PET/CT scanning
2.2.1 Preparation for examination
The "fasting" group comprised 17 consecutive patients before a clinical change in thepatient preparation protocol. The "new diet" group comprised 60 consecutive patients after theclinical protocol change who were directed to consume a very high-fat, low-carbohydrate,protein-permitted diet before FDG injection. All patients were given a questionnaire that wasused to verify diet adherence.
2.2.2 Statistical Methods
All the measurement data was performed by the Normal Test. The differences of SUVmaxand the blood glucose level of "fasting" group between The "new diet" group were analyzed byIndependent-Samples T Test or T’Test ( Normal ), or Mann-Whitney U Test ( Non-normaldistribution ). All the statistical analysis was made using SPSS 13.0 software package.
3. Results
The SUVmax of the "fasting" group ranged from 2.2 to 19.3 (median 3.1), and the SUVmaxof the"new diet" group ranged from 0.7 to 3.4 (median 2.1). The showed significant differenceby Mann-Whitney U Test ( Z = -3.333, P = 0.001<0.01),
The blood glucose level of the "fasting" group ranged from 3.7 to 9.0 (mean 6.73±1.77),and the lood glucose level of the"new diet" group ranged from 4.2 to 8.6 (mean 5.82±1.05). Theshowed significant difference by t Test ( t = 1.746，P = 0.092),
4. Conlusion
A very high-fat, low-carbohydrate, protein-permitted diet before FDG injection suppressesmyocardial FDG uptake. This should facilitate definition of mediastinal abnormalities on FDGPET. It is a more reasonable patient preparation protocol for the patients with heart andpericardium lesions.
引文
[1] Burke A, Virmani R. Tumors of the heart and great vessels In: Atlas of tumor pathology. 3rdseries, fasc 16 [J]. Washington, DC: Armed Forces Institute of Pathology, 1996.
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[3] Morphet JA. A 30-year analysis of cardiac neoplasms at autopsy [J]. Can J Cardiol, 2006, 22:80.
[4] Debourdeau P, Gligorov J, Teixeira L, et al. Malignant cardiac tumors [J]. Bull Cancer, 2004,91 (Suppl 3): 136-146.
[5] Butany J, Nair V, Naseemuddin A, et al. Cardiac tumours: diagnosis and management [J].Lancet Oncol, 2005, 6: 219-228.
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[18] Azarine A, Castela S, Mousseaux E. Magnetic resonance imaging diagnosing a leftventricular lipoma in a patient with T wave changes on ECG. Heart, 2005, 91 (7):873.
[19] Zingas AP, Carrera JD, Murray CA 3rd, et al. Lipoma of the myocardium. J Comput AssistTomogr, 1983, 7: 1098-1100.
[20] Conces DJ, Vix VA, Tarver RD. Diagnosis of a myocardial lipoma by using CT. AJR Am JRoentgenol, 1989, 153: 725-726.
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[1] Williams G, Kolodny GM. Suppression of myocardial 18F-FDG uptake by preparing patientswith a high-fat, low-carbohydrate diet [J]. AJR Am J Roentqenol, 2008, 190(2): W151-156.
[2] Randle PJ, Garland PB, Hales CN, et al. The glucose fatty acid cycle: its role in insulinsensitivity and metabolic disturbance of diabetes mellitus [J]. Lancet, 1963, 1: 785-789
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[4] Williams G, Kolodny G. A facile, reproducible method to decrease myocardial FDG uptakein PET studies [abstract]. J Nucl Med. 2006, 47(suppl 1): 273P.
[5] Williams G, Kolodny G. Method for detecting biological active coronary artery disease(CAD) by F18-fluorodeoxyglucose (FDG): positron emission tomography (PET)/computedtomography (CT). Paper presented at: Radiological Society of North America; December 2006,Chicago, Illinois.
[6] Williams G, Kolodny GM. Method for decreasing uptake of 18F-FDG by hypermetabolicbrown adipose tissue on PET. AJR. 2008, 190: 1406-1409.
[7] Wykrzykowska J, Lehman S, Williams G, et al. Imaging of inflamed and vulnerable plaquein coronary arteries with 18F-FDG PET/CT in patients with suppression of myocardial uptakeusing a low-carbohydrate, high-fat preparation. J Nucl Med. 2009, 50 (4): 563-568.
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[1] Burke A, Virmani R. Tumors of the heart and great vessels In: Atlas of tumor pathology. 3rdseries, fasc 16. Washington, DC: Armed Forces Institute of Pathology, 1996.
[2] Grebenc ML, Rosado de Christenson ML, et al. Primary Cardiac and Pericardial Neoplasms:Radiologic-Pathologic Correlation. Radiographics, 2000, 20: 1073-103; quiz 1110-1, 1112.
[3] Beghetti M, Gow RM, Haney I, et al. Pediatric primary benign cardiac tumors: a 15-yearreview. Am Heart J, 1997, 134: 1107-1114.
[4] Morphet JA. A 30-year analysis of cardiac neoplasms at autopsy. Can J Cardiol, 2006, 22:80.
[5] Debourdeau P, Gligorov J, Teixeira L, et al. Malignant cardiac tumors. Bull Cancer, 2004, 91(Suppl 3): 136-146.
[6] Soja J, Szlubowski A, Reifland-Kabata A, et al. Primary tumors of the heart in adults. PolArch Med Wewn, 2003, 109: 557-561.
[7] Butany J, Nair V, Naseemuddin A, et al. Cardiac tumours: diagnosis and management.Lancet Oncol, 2005, 6: 219-228.
[8] Smith DN, Shaffer K, Patz EF. Imaging features of nonmyxomatous primary neoplasms ofthe heart and pericardium. Clin Imaging, 1998; 22:15-22.
[9] Abrams HL, Adams DF, Grant HA. The radiology of tumors of the heart. Radiol Clin NorthAm 1971; 9:299-326.
[10] Davis GD, Kincaid OW, Hallermann FJ. Roentgen aspects of cardiac tumors. SeminRoentgenol 1969; 4:384-394.
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[15] Andreas W, Ingo P, Stefan R, et al. High-Dose dobutamine-atropine stress cardiovascularMR imaging after coronary revascularization in patients with wall motion abnormalities at rest.Radiology, 2004, 233: 210–216.
[16] Warburg O. On the origin of cancer cells. Science, 1956, 123(2): 309-314.
[17] Khorsand A, Graf S, Eidherr H, et al. Gated Cardiac 13N-NH3 PET for Assessment of LeftVentricular Volumes, Mass, and Ejection Fraction: Comparison withElectrocardiography-Gated 18F-FDG PET. J Nucl Med, 2005, 46(12): 2009-2013.
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[22] Pandolfino TL, Cotell S, Katta R. Pigmented vulvar macules as a presenting feature of theCarney complex [J]. Int J Dermatol, 2001, 40(11): 728-730.
[23] Carney JA. The Carney complex. Dermatol Clin, 1995, 13: 19–26.
[24] Burke AP, Virmani R. Cardiac myxoma: a clinicopathologic study. Am J Clin Pathol, 1993,100: 671-680.
[25] Tsuchiya F, Kohno A, Saitoh R, et al. CT findings of atrial myxoma. Radiology, 1984, 151:139-143.
[26] Burke AP, Tazelaar H, Gomez-Roman JJ, et al. Benign tumours of pluripotent mesenchyme.In: Travis WT, Brambilla E, Muller-Hermelink HK, Harris CC, editors. Pathology andgenetics of tumours of the lung, pleura and heart. World Health Organisation Classification oftumours. Lyon: IARC, 2004. p. 260-5.
[27] Kuwashiro T, Toyoda K, Otsubo R, et al. Cardiac papillary fibroelastoma as a cause ofembolic stroke: ultrasound and histopathological characteristics. Intern Med, 2009,48(1):77-80.
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[31] Azarine A, Castela S, Mousseaux E. Magnetic resonance imaging diagnosing a leftventricular lipoma in a patient with T wave changes on ECG. Heart, 2005, 91 (7):873.
[32] Zingas AP, Carrera JD, Murray CA 3rd, et al. Lipoma of the myocardium. J Comput AssistTomogr, 1983, 7: 1098-1100.
[33] Conces DJ, Vix VA, Tarver RD. Diagnosis of a myocardial lipoma by using CT. AJR Am JRoentgenol, 1989, 153: 725-726.
[34] Hananouchi GI, Goff WB. Cardiac lipoma: six-year follow-up with MRI characteristics anda review of the literature. Magn Reson Imaging, 1990, 8: 825-828.
[35] Khadilkar UN, Harish R, Tantry G, et al. Primary cardiac sarcoma. Indian J PatholMicrobiol, 2008, 51 (1): 30-31.
[36] Amonkar GP, Deshpande JR. Cardiac angiosarcoma. Cardiovasc Pathol, 2006, 15: 57-58.
[37] Burke AP, Virmani R. Osteosarcomas of the heart. Am J Surg Pathol, 1991, 15: 289-295.
[38] Laya MB, Mailliard JA, Bewtra C, et al. Malignant fibrous histiocytoma of the heart: a casereport and review of the literature. Cancer, 1987, 59: 1026-1031.
[39] Shanmugam, G. Primary cardiac sarcoma. Eur J Cardiothorac Surg, 2006, 29(6): 925–32.doi: 10.1016/j.ejcts.2006.03.034.
[40] Kaul TK, Fields BL, Kahn DR. Primary malignant pericardial mesothelioma: a case reportand review. J Cardiovasc Surg, 1994, 35: 261-267.
[41] Suman S, Schofield P, Large S. Primary pericardial mesothelimoma presenting aspericardial constriction: a case report. Heart, 2004, 90 (1): e4.
[2] Beghetti M, Gow RM, Haney I, et al. Pediatric primary benign cardiac tumors: a 15-yearreview [J]. Am Heart J, 1997, 134: 1107-1114.
[3] Morphet JA. A 30-year analysis of cardiac neoplasms at autopsy [J]. Can J Cardiol, 2006, 22:80.
[4] Debourdeau P, Gligorov J, Teixeira L, et al. Malignant cardiac tumors [J]. Bull Cancer, 2004,91 (Suppl 3): 136-146.
[5] Butany J, Nair V, Naseemuddin A, et al. Cardiac tumours: diagnosis and management [J].Lancet Oncol, 2005, 6: 219-228.
[6] Smith DN, Shaffer K, Patz EF. Imaging features of nonmyxomatous primary neoplasms ofthe heart and pericardium [J]. Clin Imaging, 1998; 22:15-22.
[7] Abrams HL, Adams DF, Grant HA. The radiology of tumors of the heart [J]. Radiol ClinNorth Am 1971; 9:299-326.
[8] Davis GD, Kincaid OW, Hallermann FJ. Roentgen aspects of cardiac tumors [J]. SeminRoentgenol 1969; 4:384-394.
[9] Andreas W, Ingo P, Stefan R, et al. High-Dose dobutamine-atropine stress cardiovascular MRimaging after coronary revascularization in patients with wall motion abnormalities at rest [J].Radiology, 2004, 233: 210–216.
[10] MuziM, FeremnaS.D, Bumrws, et al. Knetic charaeterization of hexokinase isoenzymesfrom glioma cells: implications for FDG imaging of human brain tumors [J]. Nucl Med Biol,2001, 28: 107-116.
[11] Warburg O. On the origin of cancer cells [J]. Science, 1956, 123(2): 309-314.
[12] Di Chior G, DelaPaz RL, Brooks RA, et al. Glucose utilization of cerebral gliomasmeasured by [18F] fluorodeoxyglucose and positron emission tomography [J]. Neurology,1982, 32: 1323-1329.
[13]黄劲,宋文忠,何作祥.恶性肿瘤细胞葡萄糖转运蛋白与脱氧葡萄糖摄取[J].中华核医学杂志, 2006, 26(3): 190-192.
[14] Pandolfino TL, Cotell S, Katta R. Pigmented vulvar macules as a presenting feature of theCarney complex [J]. Int J Dermatol, 2001, 40(11): 728-730.
[15] Carney JA. The Carney complex. Dermatol Clin, 1995, 13: 19–26.
[16] Burke AP, Virmani R. Cardiac myxoma: a clinicopathologic study. Am J Clin Pathol, 1993,100: 671-680.
[17] Tsuchiya F, Kohno A, Saitoh R, et al. CT findings of atrial myxoma. Radiology, 1984, 151:139-143.
[18] Azarine A, Castela S, Mousseaux E. Magnetic resonance imaging diagnosing a leftventricular lipoma in a patient with T wave changes on ECG. Heart, 2005, 91 (7):873.
[19] Zingas AP, Carrera JD, Murray CA 3rd, et al. Lipoma of the myocardium. J Comput AssistTomogr, 1983, 7: 1098-1100.
[20] Conces DJ, Vix VA, Tarver RD. Diagnosis of a myocardial lipoma by using CT. AJR Am JRoentgenol, 1989, 153: 725-726.
[21] Hananouchi GI, Goff WB. Cardiac lipoma: six-year follow-up with MRI characteristics anda review of the literature. Magn Reson Imaging, 1990, 8: 825-828.
[22] Balasubramanyam A, Waxman M, Kazal HL, Lee MH. Malignant lymphoma of the heart inacquired immune deficiency syndrome. Chest 1986; 90:243-246.
[23] Curtsinger CR, Wilson MJ, Yoneda K. Primary cardiac lymphoma. Cancer 1989;64:521-525.
[24] Holladay AO, Siegel RJ, Schwartz DA. Cardiac malignant lymphoma in acquired immunedeficiency syndrome. Cancer 1992; 70:2203-2207.
[25] Ceresoli GL, Ferreri AJ, Bucci E, Ripa C, Ponzoni M, Villa E. Primary cardiac lymphomain immunocompetent patients. Cancer 1997; 80:1497-1506.
[26] Skorton DJ, ed. Marcus cardiac imaging: a companion to braunwald’s heart disease. 2nd ed.NewYork: Saunders, 1996. 863-871.
[27] Wilhite DB, Quigley RL. Occult cardiac lymphoma presenting with cardiac tamponade[J].Tex Heart Inst J, 2003, 30(1): 62-64.
[28] Leukemic infiltrates of the heart [J]. J Surg Oncol, 2000, 75(3): 203-207.
[29] Khadilkar UN, Harish R, Tantry G, et al. Primary cardiac sarcoma. Indian J PatholMicrobiol, 2008, 51 (1): 30-31.
[30] Amonkar GP, Deshpande JR. Cardiac angiosarcoma. Cardiovasc Pathol, 2006, 15: 57-58.
[31] Burke AP, Virmani R. Osteosarcomas of the heart. Am J Surg Pathol, 1991, 15: 289-295.
[32] Laya MB, Mailliard JA, Bewtra C, et al. Malignant fibrous histiocytoma of the heart: a casereport and review of the literature. Cancer, 1987, 59: 1026-1031.
[33] Shanmugam, G. Primary cardiac sarcoma. Eur J Cardiothorac Surg, 2006, 29(6): 925–32.doi: 10.1016/j.ejcts.2006.03.034.
[34] Beghetti M, Gow RM, Haney I, et al. Pediatric primary benign cardiac tumors: a 15-yearreview. Am Heart J, 1997, 134: 1107-1114.
[35] Vimani R, Farb A, Burke A, eds. Atlas of cardiovascular pathology. Philadelphia: Saunders,1996, 79-92.
[36] Reznek RH. Imaging in the staging of renal cell carcinoma. Eur Radiol, 1996, 6: 120-128.
[37] Heslin MJ, Casper ES, Boland P, et al. Preoperative identification and operativemanagement of intraatrial extension of lung tumors. Ann Thorac Surg, 1998, 65: 544-546.
[38] Roberts WC. Primary and secondary neoplasms of the heart [J]. Am J Cardiol, 1997, 80(5):671-682.
[39] Almeda FQ, Adler S, Rosenson RS. Metastatic tumor infiltration of the pericardiummasquerading as pericardial tamponade [J]. Am J Med, 2001, 111(6): 504-505.
[40] Kaul TK, Fields BL, Kahn DR. Primary malignant pericardial mesothelioma: a case reportand review. J Cardiovasc Surg, 1994, 35: 261-267.
[41] Suman S, Schofield P, Large S. Primary pericardial mesothelimoma presenting aspericardial constriction: a case report. Heart, 2004, 90 (1): e4.
[42] Duhaylongsod FG, Lowe VJ, Patz EJ, et al. Lung tumor growth correlates with glucosemetabolism measured by fluoride-18 fluorodeoxyglucose positron tomography [J]. AnnThorac Surg, 1995, 60 (5): 1348-1352.
[43] Patz EF, Loew VJ, Hoffman JM, et al. Focal pulmonary abnormalities: evaluation with F-18fluorodeoxyglucose PET scanning [J]. Radiology, 1993, 188(2): 487-490.
[44] Patz EF, Lowe VJ, Hoffman JM, et al. Persistent or recurrent bronchogenic carcinoma:detection with PET and 2-[F-18]-2-deoxy-D-glucose[J]. Radiology, 1994, 191(2): 379-381.
[1] Williams G, Kolodny GM. Suppression of myocardial 18F-FDG uptake by preparing patientswith a high-fat, low-carbohydrate diet [J]. AJR Am J Roentqenol, 2008, 190(2): W151-156.
[2] Randle PJ, Garland PB, Hales CN, et al. The glucose fatty acid cycle: its role in insulinsensitivity and metabolic disturbance of diabetes mellitus [J]. Lancet, 1963, 1: 785-789
[3] Frayn KN. The glucose-fatty acid cycle: a physiological perspective [J]. Biochem Soc Trans2003, 31 (Pt 6): 1115-1119
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[5] Williams G, Kolodny G. Method for detecting biological active coronary artery disease(CAD) by F18-fluorodeoxyglucose (FDG): positron emission tomography (PET)/computedtomography (CT). Paper presented at: Radiological Society of North America; December 2006,Chicago, Illinois.
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