P2Y12受体基因多态性与PCI术后患者氯吡格雷血小板抑制率的关系

目的探讨P2Y12受体基因多态性与经皮冠状动脉介入术(PCI)术后患者氯吡格雷血小板抑制率的关系。方法回顾性选取2014年6月至2017年6月天府矿务局职工总医院经PCI术治疗的急性冠脉综合征(ACS)患者100例,所有患者均给予75 mg/d氯吡格雷口服治疗,连用5 d,采用聚合酶链式反应-限制性片段长度多态性(PCRRFLP)法检测P2Y12受体基因C34T、G52T多态性,采用血栓弹力仪测定二磷酸腺苷(ADP)诱导的血小板抑制率。结果P2Y12受体基因C34T、G52T的位点基因突变频率分别为15.00%、20.00%,其频率分布符合Hardy-Weinberg平衡。在基因C34T,基因突变患者治疗前后血小板抑制率增加值明显高于未突变患者,差异具有统计学意义(P0.05);在基因G52T,基因突变患者治疗前后血小板抑制率增加值明显低于未突变患者,差异具有统计学意义(P0.05)。结论P2Y12受体基因多态性与PCI术后患者氯吡格雷的血小板抑制率有关,其基因G52T突变可能会降低血小板抑制率,其基因C34T突变可能会增加血小板抑制率。     

血小板膜受体P2Y12基因多态性(C34T和G52T)与冠心病患者介入术后服用氯吡格雷临床预后的相关性研究

目的 探讨血小板膜受体P2Y12 基因多态性(C34T 和G52T)对冠心病患者经皮冠状动脉介入治疗(PCI)术后服用氯吡格雷临床预后的影响.方法 入选2008 年11 月至2009 年11 月收住我院拟行PCI 的冠心病患者268 例,正规服用氯吡格雷12 个月.采用MassARRAY 时间飞行质谱及TaqMan Assay 检测入选患者血小板受体P2Y12 基因C34T 和G52T 两个位点,按基因型对患者进行分组,观察术后1 年间死亡,非致死性心肌梗死、急诊血运重建、支架内血栓形成和心绞痛复发等严重不良心血管事件的发生情况.结果 入选病例按G52T 位点基因型分为H1/H1 型(n ＝195)和H2 携带者(H1/H2 和H2/H2,n ＝73)两组,H1/H1 组双支病变比例高于H2 携带者组(P ＜0.05),两组患者其余临床基本资料均一致,无显著性差异(P ＞0.05).PCI 术后1 年随访期间,两组患者死亡、非致死性心肌梗死、急诊血运重建术等联合终点事件发生率,H2 携带者明显高于H1/H1 组,差异有统计学意义(12.3% vs.5.1%,P ＜0.05).一年累计生存率H2 携带者要低于H1/H1 组(HR ＝2.543,95% CI:1.033 ～6.259,P ＝0.042).两组患者急性心肌梗死、支架内血栓形成、急诊血运重建术和死亡的发生率没有明显统计学差异(P ＞0.05),但H2 携带者心绞痛复发率高于H1/H1 组,有统计学差异(P ＜0.05).入选病例按C34T 位点基因型分为CC 型(n ＝174)和CT/TT 型(n ＝94)两组,两组患者的临床基本资料均匹配(P ＞0.05).PCI 术后1 年随访期间,两组患者联合终点事件发生率和一年累计生存率均无统计学差异(P ＞0.05).结论 血小板膜受体P2Y12 基因H2 携带者可能是中国冠心病患者介入治疗后服用氯吡格雷临床预后的主要影响因素之一,而C34T 位点多态性和介入治疗后服用氯吡格雷临床预后无明显相关性.     

急性缺血性脑卒中患者CYP2C19基因分型与 临床预后的相关性分析

目的:探讨急性缺血性脑卒中患者CYP2C19基因分型与临床预后的相关性。方法:选取应用氯吡格雷治疗的急性缺血性脑卒中患者156例,进行CYP2C19*2和CYP2C19*3基因型检测,根据检测结果分为野生型组(GG)和突变型组(GA/AA)。对比2组的血小板抑制率、氯吡格雷疗效及临床预后情况。结果:野生型组患者的平均血小板抑制率为(42.42±2.74)%,突变型组为(32.41±2.69)%,突变型组的平均血小板抑制率低于野生型组(P0.05)。突变型组的氯吡格雷抵抗发生率为26.32%,显著高于野生型组的1.25%(P0.05)。突变型组的预后不良发生率高于野生型组,卒中复发率及心脑血管不良事件总发生率也高于野生型组(P0.05)。与野生型组相比,突变型组患者随访期间累积无再发心脑血管不良事件的生存率明显更低(P0.05)。结论:急性缺血性脑卒中患者的CYP2C19基因分型与血小板抑制率、临床预后密切相关,携带CYP2C19突变型基因型的患者,血小板抑制率更低,氯吡格雷敏感性越差,预后不良风险越高。     

CYP2C19基因多态性与氯吡格雷抵抗的研究进展

阿司匹林联合氯吡格雷是冠状动脉支架植入术后常规的抗血小板治疗方案。然而,近年来的研究显示接受上述治疗的部分患者血小板的抑制率较低,即氯吡格雷抵抗,与冠脉支架植入术后支架内血栓事件的发生存在因果关系。而导致氯吡格雷抵抗的原因复杂,研究表明CYP2C19基因多态性与其明显相关,对高危人群进行CYP2C19基因多态性检测有利于识别氯吡格雷抵抗,并及时增加氯吡格雷剂量或更换新型血小板P2Y12受体拮抗剂,可降低术后支架内血栓的发生。     

CYP2C19、PON1基因多态性与氯吡格雷在ACS行PCI术后血小板抑制功能的关联分析

目的探讨CYP2C19、PON1基因多态性与氯吡格雷在急性冠脉综合征(ACS)行经皮冠状动脉介入治疗(PCI)术后血小板抑制功能的相关性。方法回顾性分析2016年6月至2017年5月该院ACS行PCI患者636例,按使用抗血小板药物分为氯吡格雷组(491例)和替格瑞洛组(145例)。采用荧光检测仪检测CYP2C19*2、CYP2C19*3、CYP2C19*17、ABCB1、PON1基因;血栓弹力图仪(TEG)检测服药24h后血小板抑制功能,采用t检验和方差分析比较各组血小板抑制率的差异,逻辑回归分析基因型与抗血小板反应性的关联。结果基因型分析显示CYP2C19功能缺失型等位基因*2、*3至少1个单核苷酸多态性(SNP)位点突变率分别为55.6%和7.2%,功能增强型等位基因*17的突变率为0.6%。ABCB1与PON1基因位点突变率基本相同,分别为60.5%和59.4%。TEG检测二磷酸腺苷(ADP)诱导的血小板抑制率:替格瑞洛组较氯吡格雷组高,差异有统计学意义(t=5.75,P0.05),其中比较两组快代谢型ADP抑制率差异无统计学意义(t=1.92,P0.05),而中间代谢型与慢代谢型差异有统计学意义(t=5.06,P0.05;t=2.03,P0.05)。逻辑回归分析患者基本临床信息与替格瑞洛组基因多态性对药物ADP诱导血小板反应性的影响均无统计学意义(P0.05),而氯吡格雷组携带1个CYP2C19功能缺失型等位基因与ABCB1基因对反应性的影响也均无统计学意义(P0.05),携带两个CYP2C19功能缺失型等位基因或至少携带1个PON1突变基因对预测低反应性风险差异有统计学意义(OR:6.622,95%CI:2.283~19.210,P0.05;OR:2.620,95%CI:1.074~6.393,P=0.034;OR:3.503,95%CI:1.104~11.113,P=0.033)。结论对于ACS行PCI的患者,检测CYP2C19功能缺失型等位基因与PON1基因对预测氯吡格雷抗血小板低反应性风险具有重要意义。     

骨保护素基因rs2073617T/C、rs2073618G/C多态性在东南沿海地区汉族人群中分布及与急性冠状动脉综合征相关性研究

目的 探讨骨保护素(OPG)基因启动子rs2073617T/C和第一外显子rs2073618G/C位点基因多态性在福建地区汉族人群中的分布及与急性冠状动脉综合征(ACS)的相关性.方法 纳入720例福建地区无血缘关系的汉族人为研究对象,分成ACS 360例(ACS组)和对照组360例(对照组),采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)技术,对OPG基因rs2073617T/C和rs2073618G/C多态性位点进行基因型分型,同时采用DNA测序对酶切产物进行鉴定.结果 (1)在福建地区汉族人群中,OPG基因rs2073617T/C多态性位点存在TC、TT、CC三种基因型;rs2073618G/C多态性位点也存在GG、GC、CC三种基因型.(2)对ACS组与正常对照组OPG基因rs2073617T/C、rs2073618G/C基因型及等位基因频率分布进行比较均无统计学差异(P均>0.05).(3)ACS组患者单支病变、双支病变及三支以上病变组之间比较OPG基因rs2073617T/C、rs2073618G/C各基因型差异无统计学意义(P均>0.05).结论 福建地区汉族人群OPG rs2073617T/C、rs2073618G/C位点基因多态性与ACS发生无明确相关性.     

冠心病合并高血压患者CYP2C19基因多态性与氯吡格雷抵抗的研究

目的研究冠心病合并高血压患者CYP2C19基因多态性及不同基因型与氯吡格雷抵抗(CR)的关系。方法纳入确诊冠心病患者104例,分为合并高血压组及不合并高血压组,入院治疗上均予以氯吡格雷75 mg联合阿司匹林100 mg抗血小板治疗,留取患者静脉血标本,通过基因芯片法测定CYP2C19基因型,检测入院后次日以及服药5 d血小板聚集率,观察合并高血压组及不合并高血压CYP2C19不同基因型分布及两组氯吡格雷抵抗情况。结果冠心病合并高血压与不合并高血压患者相比,氯吡格雷CYP2C19代谢基因型在两组中分布差异无统计学意义(P=0.135),且两组CR的发生率差异无统计学意义。对CYP2C19基因多态性进行分组,结果发现慢代谢型组及中等代谢型组较快代谢型氯吡格雷抵抗的发生率增高(P0.05),且慢代谢发生CR率显著增高。冠心病合并高血压患者logistic多元回归分析提示CYP2C19基因是CR发生的独立预测因子。结论冠心病患者CYP2C19基因多态性及CR发生率与是否合并高血压无关,但CR和CYP2C19基因多态性显著相关。     

荧光PCR检测CYP2C19基因分型与氯吡格雷临床疗效的相关性研究

目的通过分析CYP2C19基因型与ADP抑制率之间的关系,探讨CYP2C19基因分型与氯吡格雷抗凝治疗效果的关系。方法选取急性冠脉综合征（ACS）并成功接受经皮冠状动脉介入治疗术（PCI）的患者55例,收集患者EDTA抗凝静脉血提取血液基因组DNA,用实时荧光PCR方法分析CYP2C19基因型,测定每名患者ADP抑制率,用统计学方法分析CYP2C19不同基因型患者ADP抑制率的差异。结果所有入组患者根据基因型不同分为快代谢组占49.09%（27/55）,中等代谢组占38.19%（21/55）,慢代谢组占12.73%（7/55）。三组ADP抑制率比较,两两相比差异均有统计学意义（P〈0.01）。结论 CYP2C19基因多态性与氯吡格雷抵抗存在关联,快代谢型患者PCI术后服用氯吡格雷疗效好于携带基因突变的患者,慢代谢型患者PCI术后服用氯吡格雷疗效差。     

脑卒中患者CYP2C19基因多态性与氯吡格雷临床疗效研究

目的:探讨武汉地区部分脑卒中患者氯吡格雷代谢相关CYP2C19基因多态性与氯吡格雷临床疗效的关系。方法:选取武汉大学人民医院神经内科收治的脑卒中患者292例,采用光比浊法检测患者服用氯吡格雷前后的血小板聚集率,计算其血小板抑制率;采用基因芯片法测定患者的CYP2C19基因(*1,*2和*3),并将患者按照基因检测结果分为不同代谢类型:快代谢型(*1/*1),中间代谢型(*1/*2和*1/*3)及慢代谢型(*2/*2,*2/*3和*3/*3)。采用统计学方法分析CYP2C19不同代谢类型患者血小板抑制率的差异。结果:根据CYP2C19基因多态性位点进行代谢分型,快代谢型占37.33%,中间代谢型占46.92%,慢代谢型占15.75%。3种代谢类型患者服用氯吡格雷前后的血小板抑制率分别为(54.39±18.93)%,(30.02±21.53)%及(10.34±3.83)%,3种代谢型患者之间血小板抑制率比较均有统计学意义,其中快代谢型患者显著高于中间代谢型和慢代谢型患者(P<0.05)。结论:脑卒中患者中CYP2C19*2、*3基因变异者使用氯吡格雷抗凝的疗效较差,测定CYP2C19基因型对于脑卒中患者使用氯吡格雷治疗可能具有重要的指导意义。     

MALDI-TOFMS在氯吡格雷基因多态性检测中的应用

目的探讨基因多态性与氯吡格雷个体化用药的相关性及基质辅助激光解析电离飞行时间质谱(MALDI-TOF MS)在氯吡格雷基因多态性检测中的应用价值。方法选取2015-2017年武警重庆总队医院住院的急性冠状动脉综合征(ACS)及拟进行经皮冠状动脉介入术(PCI)的患者160例,在氯吡格雷抗血小板治疗后第5天测定血小板聚集率;同时采用MALDI-TOF MS技术检测CYP2C19*2*、CYP2C19*3、CYP2C19*4、CYP2C19*5、CYP2C19*17和ABCBI、PON1、CES1基因多态性。结果根据血小板最大聚集率(MAR)将研究对象分为氯吡格雷抵抗(CR)组(n=75)和非氯吡格雷抵抗(NCR)组(n=85)。160份样本等位基因检出率为100%,两组均未发现CYP2C19*4、CYP2C19*5、CYP2C19*17突变;携带CYP2C19*2等位基因A及CYP2C19*1/*2、CYP2C19*1/*3、CYP2C19*2/*2、CYP2C19*2/*3代谢型发生氯吡格雷抵抗的风险较高,携带ABCB1等位基因A的GA、AA代谢型发生氯吡格雷抵抗风险较高,携带PON1等位基因T的CT、TT代谢型发生氯吡格雷抵抗的风险较高,携带CES1等位基因T的CT、TT代谢型发生氯吡格雷抵抗的风险较低,差异均有统计学意义(P0.05);携带CYP2C19*3等位基因A发生氯吡格雷抵抗风险较高,CYP2C19*3/*3型发生氯吡格雷的风险较低,差异均无统计学意义(P0.05)。结论 CYP2C19*2、ABCBI、PON1基因突变增加氯吡格雷抵抗的风险,CES1基因突变降低氯吡格雷抵抗风险;MALDI-TOF MS具有准确性高、检测通量大、速度快、成本低等特点,适用于氯吡格雷基因多态性检测,指导临床个体化用药。     

The nucleic acids of T2, T4, and T6 bacteriophages

The deoxyribonucleic acids of the wild type strains of the T₂, T₄, and T₆ bacteriophages have been shown to contain glucose as an integral part of the molecule; the amount of hexose present in each nucleic acid differs. A study of the acid degradation products of the three nucleic acids has revealed that in each instance glucose is linked to the apurinic acid component. In the case of the T₆ nucleic acid it was found that two molecules of glucose are linked to hydroxymethylcytidylic acid. The other mononucleotides contained no glucose. From the results which have been presented here, and from data presented by others, it can be concluded that the three viral nucleic acids differ in that they contain different proportions of free and glucose-substituted hydroxymethylcytidylic acids.     

1.5T及3.0T MR T2 mapping技术定量鉴别子宫良恶性肿瘤

目的对比不同场强下子宫正常结构及常见良恶性肿瘤的T2值,观察T2 mapping技术量化鉴别良恶性肿瘤的效能。方法对比73例子宫肿瘤患者(82个病灶)及34名健康妇女的1.5T及3.0T常规MRI和T2 mapping图像,测量不同TE值下正常子宫组织及良恶性肿瘤信号强度,采用Matlab平台拟合信号,计算并比较T2值;绘制受试者工作特征(ROC)曲线,评价T2值鉴别良恶性肿瘤的效能。结果1.5T MRI子宫正常结构及良恶性肿瘤的T2值均显著高于3.0T(P均<0.05)。1.5T及3.0T MRI子宫良性肿瘤T2值均显著低于恶性肿瘤(P均<0.05)。1.5T及3.0T MRI鉴别良恶性肿瘤的曲线下面积(AUC)分别为0.967和0.999,差异无统计学意义(P>0.05);截断值为93.24 ms和79.28 ms时,敏感度均为100%,特异度分别为96.36%和98.18%。结论T2 mapping技术可定量鉴别正常子宫组织及子宫良恶性肿瘤。     

创伤后T细胞功能与抑制性T细胞及反抑制T细胞活性变化的关系

目的：研究创伤后Ｔ细胞功能与抑制性Ｔ细胞（Ｔｓ）及反抑制Ｔ细胞（Ｔｃｓ）活性变化的关系。方法：利用小鼠截肢伤模型，观察Ｔ细胞功能的变化，并测定Ｔｓ细胞对正常Ｔ细胞功能的抑制活性以及Ｔｃｓ细胞对Ｔｓ细胞的反抑制活性变化。结果：创伤小鼠脾细胞的Ｔ淋巴细胞转化活性降低，辅助性Ｔ细胞（Ｔｈ）、Ｔｃｓ细胞数目一过性减少，Ｔｓ细胞数目一过性增多；创伤后Ｔｓ细胞对正常Ｔ淋巴细胞转化、白细胞介素２（ＩＬ２）生成、ＩＬ２受体α（ＩＬ２Ｒα）表达、ＩＬ２ｍＲＮＡ及ＩＬ２ＲαｍＲＮＡ水平的抑制作用明显增强，而Ｔｃｓ细胞对Ｔｓ细胞的反抑制活性明显减弱；Ｔｓ细胞抑制率及Ｔｃｓ细胞反抑制率变化与Ｔ淋巴细胞转化活性降低均密切相关；去除创伤小鼠脾细胞中Ｔｓ细胞，则可明显提高Ｔ淋巴细胞转化活性、ＩＬ２生成及ＩＬ２Ｒα表达；正常Ｔｃｓ细胞对伤后Ｔｓ细胞抑制作用具有一定的逆转效应。结论：创伤后Ｔｓ细胞活性增强、Ｔｃｓ细胞反抑制活性减弱可能均介导了创伤后Ｔ细胞功能的受抑过程     

3.0T MR T1及T2 mapping评价肩关节软骨退变

目的 观察3.0T MR T1及T2 mapping在肩关节软骨退变中的应用价值。方法 对30例肩关节疼痛患者（患者组，34肩）和30名正常人（正常组）采用3.0T MR仪行肩关节常规、T1及T2 mapping序列扫描，按国际软骨修复协会（ICRS）分级标准对肩关节软骨分级，分别测量其外、中、内带T1及T2 mapping值；比较组间各指标差异，分析T1及T2 mapping值与ICRS分级及年龄的相关性。结果 患者组34肩中，24肩（24/34，70.59%）关节软骨分级ICRSⅠ~Ⅱ级（轻度退变亚组），10肩（10/34，29.41%）Ⅲ~Ⅳ级（重度退变亚组）；正常组30肩关节软骨分级均为ICRS 0级。患者组肩关节软骨T1及T2 mapping值均高于正常组（P均<0.05）；其中重度退变亚组T1 mapping值高于轻度退变亚组及正常组（P均<0.05），轻度退变亚组与正常组间差异无统计学意义（P>0.05）。肩关节软骨外、中、内带T1 mapping值与ICRS分级均呈低度正相关（r=0.282、0.449、0.343，P均<0.05）；T2 mapping值与ICRS分级均呈明显正相关（r=0.635、0.739、0.746，P均<0.05）。随软骨退变程度加重，T1及T2 mapping值呈上升趋势（P均<0.05）。肩关节软骨ICRS分级与年龄呈明显正相关（r=0.678，P<0.05）；T1及T2 mapping值与年龄均呈低度正相关（r=0.393、0.438，P均<0.05）。结论 T1及T2 mapping值可量化肩关节软骨退变，并与年龄相关；T1及T2 mapping序列可作为常规MR评估肩关节软骨退变的重要补充。     

Calibration of myocardial T2 and T1 against iron concentration

Background

The assessment of myocardial iron using T2* cardiovascular magnetic resonance (CMR) has been validated and calibrated, and is in clinical use. However, there is very limited data assessing the relaxation parameters T1 and T2 for measurement of human myocardial iron.

Methods

Twelve hearts were examined from transfusion-dependent patients: 11 with end-stage heart failure, either following death (n = 7) or cardiac transplantation (n = 4), and 1 heart from a patient who died from a stroke with no cardiac iron loading. Ex-vivo R1 and R2 measurements (R1 = 1/T1 and R2 = 1/T2) at 1.5 Tesla were compared with myocardial iron concentration measured using inductively coupled plasma atomic emission spectroscopy.

Results

From a single myocardial slice in formalin which was repeatedly examined, a modest decrease in T2 was observed with time, from mean (±SD) 23.7 ± 0.93 ms at baseline (13 days after death and formalin fixation) to 18.5 ± 1.41 ms at day 566 (p < 0.001). Raw T2 values were therefore adjusted to correct for this fall over time. Myocardial R2 was correlated with iron concentration [Fe] (R² 0.566, p < 0.001), but the correlation was stronger between LnR2 and Ln[Fe] (R² 0.790, p < 0.001). The relation was [Fe] = 5081•(T2)^-2.22 between T2 (ms) and myocardial iron (mg/g dry weight). Analysis of T1 proved challenging with a dichotomous distribution of T1, with very short T1 (mean 72.3 ± 25.8 ms) that was independent of iron concentration in all hearts stored in formalin for greater than 12 months. In the remaining hearts stored for <10 weeks prior to scanning, LnR1 and iron concentration were correlated but with marked scatter (R² 0.517, p < 0.001). A linear relationship was present between T1 and T2 in the hearts stored for a short period (R² 0.657, p < 0.001).

Conclusion

Myocardial T2 correlates well with myocardial iron concentration, which raises the possibility that T2 may provide additive information to T2* for patients with myocardial siderosis. However, ex-vivo T1 measurements are less reliable due to the severe chemical effects of formalin on T1 shortening, and therefore T1 calibration may only be practical from in-vivo human studies.     

Clonal heterogeneity in the requirement for T3, T4, and T8 molecules in human cytolytic T lymphocyte function

In an attempt to define the requirement of T8, T4, and T3 surface molecules in functional interactions occurring between human cytolytic T lymphocytes (CTL) and specific target cells, we have analyzed a large number of CTL clones derived from primary mixed lymphocyte culture (MLC) T cell populations for their susceptibility to inhibition by monoclonal antibodies (mAb) directed against these surface antigens. In most experiments, MLC T cells were stained with B9.4 (anti-T8) or OKT4 (anti-T4) mAb, separated into positive and negative cells using a fluorescence-activated cell sorter (FACS) and cloned under limiting conditions. While the lytic activity of the majority of T8+ CTL clones was inhibited by B9.4 mAb, approximately 15% of these clones were unaffected even in the presence of excess antibody. Flow cytofluorometric analysis of T8 antigen in individual clones did not show any correlation between the amount of T8 antigen expressed, the magnitude of cytolytic activity and the susceptibility (or lack thereof) to inhibition by B9.4 mAb. Of the 16 T4+ CTL clones analyzed, 7 were resistant to inhibition by OKT4 mAb even at doses 10-fold higher than that sufficient for complete inhibition of susceptible clones. Again, no correlation was found between the amount of T4 antigen expressed and the susceptibility to inhibition by the corresponding antibody. The same sets of T8+ and T4+ CTL clones were also analyzed for their susceptibility to inhibition by OKT3 mAb. Although all of the clones expressed the T3 surface antigen, only 15/23 T8+ clones and 9/14 T4+ clones were inhibited by anti-T3 mAb. To further document this clonal heterogeneity, we selected two T3+ T4- T8+ CTL clones that had no concomitant NK-like activity. One clone was resistant to inhibition by OKT3 mAb, whereas the other was highly susceptible. Incubation with OKT3 mAb resulted in modulation of the T3 molecules in both clones. Following modulation, however, the cytolytic activity of the resistant clones was unaffected, whereas the lytic activity of the susceptible clone was abrogated. These results thus indicate extensive clonal heterogeneity in the requirement for T3, T4, and T8 molecules in CTL function. Moreover, it appears that T3 molecules are not always physically and functionally linked to CTL receptor structures.     

Comparison of physiological noise at 1.5 T, 3 T and 7 T and optimization of fMRI acquisition parameters

Previous studies have shown that under some conditions, noise fluctuations in an fMRI time-course are dominated by physiological modulations of the image intensity with secondary contributions from thermal image noise and that these two sources scale differently with signal intensity, susceptibility weighting (TE) and field strength. The SNR of the fMRI time-course was found to be near its asymptotic limit for moderate spatial resolution measurements at 3 T with only marginal gains expected from acquisition at higher field strengths. In this study, we investigate the amplitude of image intensity fluctuations in the fMRI time-course at magnetic field strengths of 1.5 T, 3 T, and 7 T as a function of image resolution, flip angle and TE. The time-course SNR was a similar function of the image SNR regardless of whether the image SNR was modulated by flip angle, image resolution, or field strength. For spatial resolutions typical of those currently used in fMRI (e.g., 3 x 3 x 3 mm(3)), increases in image SNR obtained from 7 T acquisition produced only modest increases in time-course SNR. At this spatial resolution, the ratio of physiological noise to thermal image noise was 0.61, 0.89, and 2.23 for 1.5 T, 3 T, and 7 T. At a resolution of 1 x 1 x 3 mm(3), however, the physiological to thermal noise ratio was 0.34, 0.57, and 0.91 for 1.5 T, 3 T and 7 T for TE near T2*. Thus, by reducing the signal strength using higher image resolution, the ratio of physiologic to image noise could be reduced to a regime where increased sensitivity afforded by higher field strength still translated to improved SNR in the fMRI time-series.     

T1 mapping and T2 mapping at 3T for quantifying the area-at-risk in reperfused STEMI patients

Background

Whether T1-mapping cardiovascular magnetic resonance (CMR) can accurately quantify the area-at-risk (AAR) as delineated by T2 mapping and assess myocardial salvage at 3T in reperfused ST-segment elevation myocardial infarction (STEMI) patients is not known and was investigated in this study.

Methods

18 STEMI patients underwent CMR at 3T (Siemens Bio-graph mMR) at a median of 5 (4–6) days post primary percutaneous coronary intervention using native T1 (MOLLI) and T2 mapping (WIP #699; Siemens Healthcare, UK). Matching short-axis T1 and T2 maps covering the entire left ventricle (LV) were assessed by two independent observers using manual, Otsu and 2 standard deviation thresholds. Inter- and intra-observer variability, correlation and agreement between the T1 and T2 mapping techniques on a per-slice and per patient basis were assessed.

Results

A total of 125 matching T1 and T2 mapping short-axis slices were available for analysis from 18 patients. The acquisition times were identical for the T1 maps and T2 maps. 18 slices were excluded due to suboptimal image quality. Both mapping sequences were equally prone to susceptibility artifacts in the lateral wall and were equally likely to be affected by microvascular obstruction requiring manual correction. The Otsu thresholding technique performed best in terms of inter- and intra-observer variability for both T1 and T2 mapping CMR. The mean myocardial infarct size was 18.8 ± 9.4 % of the LV. There was no difference in either the mean AAR (32.3 ± 11.5 % of the LV versus 31.6 ± 11.2 % of the LV, P = 0.25) or myocardial salvage index (0.40 ± 0.26 versus 0.39 ± 0.27, P = 0.20) between the T1 and T2 mapping techniques. On a per-slice analysis, there was an excellent correlation between T1 mapping and T2 mapping in the quantification of the AAR with an R² of 0.95 (P < 0.001), with no bias (mean ± 2SD: bias 0.0 ± 9.6 %). On a per-patient analysis, the correlation and agreement remained excellent with no bias (R² 0.95, P < 0.0001, bias 0.7 ± 5.1 %).

Conclusions

T1 mapping CMR at 3T performed as well as T2 mapping in quantifying the AAR and assessing myocardial salvage in reperfused STEMI patients, thereby providing an alternative CMR measure of the the AAR.