楊 梅綜述，周 丹審校(南京醫(yī)科大學(xué)附屬明基醫(yī)院放射科，江蘇 南京 210019)

磁共振成像在糖尿病心肌病心肌評(píng)價(jià)中的進(jìn)展

楊 梅綜述，周 丹審校
(南京醫(yī)科大學(xué)附屬明基醫(yī)院放射科，江蘇 南京 210019)

糖尿病心肌病是引起糖尿病患者心力衰竭的主要原因之一。通過(guò)磁共振結(jié)構(gòu)和功能成像技術(shù)可準(zhǔn)確評(píng)估糖尿病心肌病的病理學(xué)變化，現(xiàn)已應(yīng)用于糖尿病心肌病臨床治療的療效評(píng)估中。評(píng)估糖尿病心肌病的MRI技術(shù)主要包括電影成像、MRS、T1 Mapping等。本文主要對(duì)MRI技術(shù)在糖尿病心肌病心肌評(píng)價(jià)方面的應(yīng)用進(jìn)展進(jìn)行綜述。

糖尿?。恍募〔?；磁共振成像；治療結(jié)果

糖尿病心肌病是一種代謝性疾病，主要表現(xiàn)為糖代謝、脂代謝及能量代謝的異常，高血糖是其發(fā)病機(jī)制的核心[1]。長(zhǎng)期高血糖可導(dǎo)致心肌膠原糖基化，降解減少[2]。此外，由于葡萄糖有氧代謝障礙、心肌能量供應(yīng)不足等一系列不良刺激，最終可引起心肌彌漫性纖維化[3-5]。糖尿病心肌病是獨(dú)立于高血壓、冠狀動(dòng)脈疾病、缺血性心臟病及其他心臟病變的心肌疾病[6-7]，是造成糖尿病患者心力衰竭的主要原因之一[8]。評(píng)價(jià)糖尿病患者心肌損害的影像學(xué)方法主要包括超聲、CT和MRI。隨著近年MR成像技術(shù)的迅速發(fā)展，其在定性和定量評(píng)估心肌病變方面獨(dú)具優(yōu)勢(shì)。MR評(píng)估糖尿病心肌病的方法主要為磁共振電影成像、MRS及T1 Mapping。這三種方法均可準(zhǔn)確評(píng)估糖尿病心肌病的心肌結(jié)構(gòu)和功能的變化，反映心肌代謝情況及心肌纖維化程度，且與組織病理學(xué)具有高度一致性。此外，MRI技術(shù)還具有高度的穩(wěn)定性和可重復(fù)性。本文對(duì)MRI技術(shù)在糖尿病心肌病心肌評(píng)價(jià)中的應(yīng)用進(jìn)展進(jìn)行綜述。

1 糖尿病心肌病MRI心肌評(píng)價(jià)技術(shù)

1.1電影成像 糖尿病心肌病治療前后臨床常用的監(jiān)測(cè)指標(biāo)為左心室結(jié)構(gòu)和功能的改變。左心室結(jié)構(gòu)和功能的變化評(píng)價(jià)指標(biāo)包括左心室質(zhì)量(left ventricular mass， LV mass)、左心室舒張末期容積(left ventricular end-diastolic volume， LVEDV)、左心室收縮末期容積(left ventricular end-systolic volume， LVESV)、左心室舒張?jiān)缙诤屯砥诔溆俾时戎?the ratio of Peak E and Peak A， E/A)、左心室每搏輸出量(stroke volume, SV)、左心室射血分?jǐn)?shù)(left ventricular ejection fraction, LVEF)等。與超聲相比，心臟MR電影成像不基于具體的幾何模型，對(duì)操作者的技術(shù)依賴小，具有較高的可重復(fù)性和較高的空間和時(shí)間分辨率。通過(guò)MR電影成像，可得到高質(zhì)量的左心室時(shí)間—容量關(guān)系圖、二尖瓣流入模式圖以及左心室心肌壁運(yùn)動(dòng)及應(yīng)力圖，能準(zhǔn)確評(píng)估心臟結(jié)構(gòu)及心室舒張和收縮功能[9]。多項(xiàng)研究[10-16]表明，MR電影成像測(cè)定心臟結(jié)構(gòu)和功能具有較高的可重復(fù)性。

1.2MRS 通過(guò)MRS可對(duì)特定原子核及化合物進(jìn)行定量分析，具有無(wú)輻射和無(wú)需示蹤劑的優(yōu)點(diǎn)。由于心肌細(xì)胞內(nèi)脂質(zhì)和心肌細(xì)胞外脂質(zhì)所處的微環(huán)境不同，兩者在1H-MRS上表現(xiàn)為頻率不同的2個(gè)波峰，而共振峰的峰高和面積可反映化合物的濃度[17]。因此，1H-MRS可用于定量分析心肌細(xì)胞內(nèi)脂質(zhì)含量。1H-MRS在測(cè)量心肌脂肪方面可重復(fù)性好。Reingold等[18]應(yīng)用1.5T MR對(duì)體內(nèi)心肌甘油三脂含量進(jìn)行不同時(shí)間點(diǎn)重復(fù)性測(cè)量(2次測(cè)量間隔90天)，結(jié)果顯示2次測(cè)量結(jié)果高度相關(guān)[r=0.987，變異系數(shù)(coefficient of variability， CV)為5%]。van der Meer等[19]對(duì)一組健康人群在不同時(shí)間點(diǎn)進(jìn)行重復(fù)性測(cè)量(2次測(cè)量間隔5 min)，結(jié)果顯示2次測(cè)量結(jié)果的組內(nèi)相關(guān)系數(shù)(intraclass correlation coefficient， ICC)為0.81[95%CI(0.58,0.92)]，CV為17.9%。

1.3T1 Mapping T1 Mapping技術(shù)是基于反轉(zhuǎn)和飽和脈沖激發(fā)，在縱向磁化矢量恢復(fù)的不同時(shí)間采集信號(hào)，可通過(guò)定量分析T1值對(duì)心肌進(jìn)行評(píng)價(jià)。目前應(yīng)用最為廣泛的測(cè)量T1的MR序列為改良的MOLLI(modified look-locker imaging)序列。T1 Mapping包括平掃T1 Mapping及增強(qiáng)后T1 Mapping。平掃T1 Mapping測(cè)量的是整體心肌包括細(xì)胞內(nèi)及細(xì)胞外間質(zhì)的混合信號(hào)，其主要缺點(diǎn)為敏感度低，病變心肌與正常心肌的平掃T1值有較多重疊[20]。增強(qiáng)后T1 Mapping的優(yōu)點(diǎn)為強(qiáng)化后病變心肌的T1值縮短，與正常心肌對(duì)比更加明顯，更易檢出病變；但組織增強(qiáng)后的T1值受較多因素影響，如對(duì)比劑的注射劑量、注射后的延遲時(shí)間和腎臟排泄功能等[21]，均導(dǎo)致定量測(cè)量的精確性和可重復(fù)性下降。

細(xì)胞外容積分?jǐn)?shù)(extracellular volume, ECV)是基于T1 Mapping技術(shù)計(jì)算的一種相對(duì)穩(wěn)定的指標(biāo)，通過(guò)釓對(duì)比劑注射前后分別進(jìn)行T1 Mapping掃描，經(jīng)血細(xì)胞比容校正后獲得。其計(jì)算公式為：心肌ECV=(1-HCT)×(心肌ΔR1/血液ΔR1)；其中ΔR1=1/T1post-1/T1pre，T1pre及T1post分別為對(duì)比劑注射前后的T1值，HCT為對(duì)比劑在血液和心肌細(xì)胞外間隙中的濃度達(dá)到平衡時(shí)的血細(xì)胞比容。ECV避免了對(duì)比劑劑量及腎小球?yàn)V過(guò)率的影響，對(duì)細(xì)胞外基質(zhì)體積的測(cè)量更為準(zhǔn)確，可重復(fù)性更高。ECV可反映未被心肌細(xì)胞占據(jù)的心肌間質(zhì)的體積分?jǐn)?shù)[22]，與膠原纖維的體積分?jǐn)?shù)相關(guān)，在無(wú)水腫、淀粉樣變及其他形式浸潤(rùn)性疾病的情況下，ECV可作為心肌纖維化的生物學(xué)指標(biāo)[23-24]。

T1 Mapping技術(shù)測(cè)量心肌ECV的可重復(fù)性較好。Chin等[25]研究結(jié)果顯示，同一觀察者對(duì)20名健康人重復(fù)測(cè)量ECV的ICC為1.00，2名觀察者重復(fù)測(cè)量ECV的ICC為0.97，間隔7天2次重復(fù)測(cè)量的ICC為0.96。另一項(xiàng)對(duì)中—重度主動(dòng)脈狹窄患者進(jìn)行ECV可重復(fù)性測(cè)量的研究[26]發(fā)現(xiàn)，在測(cè)量ECV方面，同一觀察者重復(fù)測(cè)量的CV為1.83%，2名觀察者重復(fù)測(cè)量的CV為2.31%，間隔7天2次重復(fù)測(cè)量的CV為6.52%。Liu等[27]測(cè)量健康人群與心力衰竭患者增強(qiáng)后12 min和25 min的心肌ECV，結(jié)果顯示2個(gè)時(shí)間點(diǎn)ECV測(cè)量值的r值分別為0.98、0.88，CV分別為2.2%、5.9%。

2 MRI在監(jiān)測(cè)糖尿病心肌病療效中的應(yīng)用

2.1飲食療法 飲食療法是糖尿病的基礎(chǔ)治療方法，長(zhǎng)期限制熱量攝入可減少心肌內(nèi)甘油三脂含量，有效降低血糖，從而改善心功能。而短期限制熱量攝入，可引起心肌內(nèi)甘油三脂的堆積，并伴心功能的下降。Hammer等[28]研究發(fā)現(xiàn)，對(duì)一組2型肥胖糖尿病患者長(zhǎng)期(16周)限制熱量后，患者的空腹血糖、糖化血紅蛋白、血漿游離脂肪酸(plasma free fatty acids， NEFA)、血漿甘油三脂均明顯下降；MRS顯示心肌甘油三脂較治療前下降27%(P=0.019)；電影成像顯示患者的心功能得到改善，主要表現(xiàn)為心輸出量下降18%(P=0.001)、LV mass下降16%(P<0.001)，E/A比率增加15%(P=0.019)。Hammer等[29]的另一項(xiàng)研究顯示，對(duì)2型糖尿病患者短期(3天)限制熱量攝入后，心肌MRS顯示心肌甘油三酯增加48%(P=0.028)，電影成像顯示E峰減速下降19%(P=0.004)、E/A比率下降10%(P=0.002)。

2.2運(yùn)動(dòng)療法 運(yùn)動(dòng)療法是糖尿病治療的重要手段之一。對(duì)糖尿病患者而言，不同的運(yùn)動(dòng)方式及不同的運(yùn)動(dòng)時(shí)間對(duì)心肌脂肪含量及心功能會(huì)產(chǎn)生不同的效果。Jonker等[30]研究發(fā)現(xiàn)，2型糖尿病患者經(jīng)6個(gè)月中等強(qiáng)度的耐力運(yùn)動(dòng)后，MRS顯示心肌甘油三酯含量無(wú)明顯改變[(0.61±0.13)% vs (0.60±0.13)%，P=0.9]，電影成像顯示除LVEF增加2%外，其他心功能指標(biāo)(LV mass、EDV、ESV)及左心室SV與治療前相比均無(wú)明顯變化。Schrauwen-Hinderling等[31]研究報(bào)道，對(duì)2型肥胖糖尿病患者進(jìn)行中等強(qiáng)度的有氧運(yùn)動(dòng)治療12周后，MRS顯示心肌甘油三酯無(wú)明顯變化[(0.80±0.22)% vs (0.95±0.21)%，P=0.15]，但電影成像顯示左心室收縮功能得到改善，表現(xiàn)為ESV減少11%(P=0.004)，LVEF增加10%(P=0.001)。Cassidy等[32]研究發(fā)現(xiàn)，2型糖尿病患者經(jīng)高強(qiáng)度間隔運(yùn)動(dòng)治療12周后，電影成像顯示其左心室結(jié)構(gòu)和舒張、收縮功能均明顯改善，主要表現(xiàn)為L(zhǎng)V mass增加12%(P<0.05)，EDV增加6%(P<0.01)，LVEF增加7%(P<0.05)，左心室舒張?jiān)缙诔溆试黾?4%(P<0.01)。

2.3減肥手術(shù)療法 減肥手術(shù)治療糖尿病是一個(gè)新興的方法，主要通過(guò)減輕體質(zhì)量，從而改變代謝，控制血糖。van Schinkel等[33]監(jiān)測(cè)減肥手術(shù)對(duì)2型肥胖糖尿病患者心肌脂肪含量及心功能的影響，發(fā)現(xiàn)在接受減肥手術(shù)16周后患者糖化血紅蛋白下降13%(P<0.05)，但心肌脂肪含量、左心室舒張和收縮功能均未見(jiàn)明顯改善。

2.4藥物治療 目前治療糖尿病的藥物主要為口服藥物和胰島素。不同藥物具有不同的藥理作用，對(duì)心臟的效應(yīng)也不盡相同。van der Meer等[34]對(duì)78例無(wú)任何心血管疾病的2型糖尿病患者分別采用吡格列酮或二甲雙胍治療24周后進(jìn)行MR成像，發(fā)現(xiàn)2種藥物均未能明顯降低心肌脂肪含量，但應(yīng)用吡格列酮可明顯改善左室舒張功能，表現(xiàn)為EDV增加4%(P=0.045)、E峰減速8%(P=0.034)、左心室SV增加5%(P=0.016)。McGavock等[35]研究結(jié)果顯示，應(yīng)用羅格列酮治療2型糖尿病6個(gè)月后，雖然患者空腹血糖明顯減低[(166±44)mg/dl vs (150±67)mg/dl，P<0.05],但MRI提示心肌甘油三酯含量和心功能均無(wú)明顯改變。Jankovic等[36]研究發(fā)現(xiàn)，2型糖尿病患者通過(guò)短期(10天)胰島素治療后，MRI顯示其心肌甘油三酯增加80%(P=0.008)，LV mass增加13%(P<0.05)，室間隔厚度增加13%(P<0.05)，但左心室舒張和收縮功能均未見(jiàn)明顯改善。Giannetta等[37]監(jiān)測(cè)磷酸二酯酶抑制劑(西地那非)對(duì)糖尿病的效果，發(fā)現(xiàn)2型糖尿病患者服用西地那非3個(gè)月后，電影成像顯示其LVEDV指數(shù)上升6%(P<0.05)，左心室質(zhì)量—容積比率平均下降0.17(P=0.013)，左心室SV增加10%(P<0.05)，LVEF增加4%(P=0.002)。糖尿病患者腎素—血管緊張素—醛固酮系統(tǒng)(renin-angiotensin-aldosteronesystem, RAAS)被激活，升高的血管緊張素Ⅱ(angiotensin Ⅱ， AngⅡ)和醛固酮通過(guò)各自的受體刺激心肌成纖維細(xì)胞增生及膠原代謝改變，最終導(dǎo)致心肌細(xì)胞壞死和心肌纖維化。Wong等[38]對(duì)1 176例2型糖尿病患者用腎素-血管緊張素拮抗劑治療1.3年后，T1 mapping顯示ECV較治療前明顯減小(P=0.028)。

綜上所述，在糖尿病心肌病的臨床治療試驗(yàn)中，評(píng)估不同的心肌指標(biāo)需要不同的MR成像方法。如將心功能作為主要終點(diǎn)事件，則評(píng)估方法以心臟電影成像為主。如將心肌脂肪含量的變化對(duì)心功能的影響作為主要終點(diǎn)事件之一，成像方案中除了心臟電影成像外，還需增加MRS。如需同時(shí)觀察心肌纖維化程度，則需增加T1 Mapping檢查。MRI可動(dòng)態(tài)監(jiān)測(cè)糖尿病心肌病不同治療方式、不同藥物的治療效果。隨著MRI技術(shù)的不斷發(fā)展，其成像速度不斷加快、分辨力不斷提高，必將進(jìn)一步提高對(duì)糖尿病心肌病定性和定量評(píng)估的敏感度和準(zhǔn)確性。

[1] Aneja A, Tang WH, Bansilal S, et al. Diabetic cardiomyopathy: Insights into pathogenesis, diagnostic cllenges, and therapeutic options. Am J Med, 2008,121(9):748-757.

[2] Ng AC, Auger D, Delgado V, et al. Association between diffuse myocardial fibrosis by cardiac magnetic resonance contrast-enhanced T1 mapping and subclinical myocardial dysfunction in diabetic patients: A pilot study. Circ Cardiovasc Imaging, 2012,5(5):51-59.

[3] van Herpen NA, Schrauwen-Hinderling VB. Lipid accumulation in non-adipose tissue and lipotoxicity. Physiol Behav, 2008,94(2):231-241.

[4] Mazumder PK, O'Neill BT, Roberts MW, et al. Impaired cardiac efficiency and increased fatty acid oxidation in insulin-resistant ob/ob mouse hearts. Diabetes, 2004,53(9):2366-2374.

[5] How OJ, Aasum E, Severson DL, et al. Increased myocardial oxygen consumption reduces cardiac efficiency in diabetic mice. Diabetes, 2006,55(2):466-473.

[6] Boudina S, Abel ED. Diabetic cardiomyopathy revisited. Circulation, 2007,115(25):3213-3223.

[7] Owan TE, Hodge DO, Herges RM, et al. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med, 2006,355(3):251-259.

[8] Tang WH. Glycemic control and treatment patterns in patients with heart failure. Curr Cardiol Rep, 2007,9(3):242-247.

[9] Westenberg JJ. CMR for assessment of diastolic function. Curr Cardiovasc Imaging Rep, 2011,4(2):149-158.

[10] Hanneman K, Kino A, Cheng JY, et al. Assessment of the precision and reproducibility of ventricular volume, function, and mass measurements with ferumoxytol-enhanced 4D flow MRI. J Magn Reson Imaging, 2016,44(2):383-392.

[11] Clay S, Alfakih K, Messroghli DR, et al. The reproducibility of left ventricular volume and mass measurements: A comparison between dual-inversion-recovery black-blood sequence and SSFP. Eur Radiol, 2006,16(1):32-37.

[12] Mooij CF, de Wit CJ, Graham DA, et al. Reproducibility of MRI measurements of right ventricular size and function in patients with normal and dilated ventricles. J Magn Reson Imaging, 2008,28(1):67-73.

[13] Luijnenburg SE, Robbers-Visser D, Moelker A, et al. Intra-observer and interobserver variability of biventricular function, volumes and mass in patients with congenital heart disease measured by CMR imaging. Int J Cardiovasc Imaging, 2010,26(1):57-64.

[14] Grothues F, Smith GC, Moon JC, et al. Comparison of interstudy reproducibility of cardiovascular magnetic resonance with two-dimensional echocardiography in normal subjects and in patients with heart failure or left ventricular hypertrophy. Am J Cardiol, 2002,90(1):29-34.

[15] Bellenger N, Francis J, Davies C, et al. Establishment and performance of a magnetic resonance cardiac function clinic. J Cardiovasc Magn Reson, 2000,2(1):15-22.

[16] Hudsmith LE, Petersen SE, Tyler DJ, et al. Determination of cardiac volumes and mass with FLASH and SSFP cine sequences at 1.5 vs. 3 Tesla: A validation study. J Magn Reson Imaging, 2006,24(2):312-318.

[17] Xiao L, Wu EX. Diffusion-weighted magnetic resonance spectroscopy: A novel approach to investigate intramyocellular lipids. Magn Reson Med, 2011,66(4):937-944.

[18] Reingold JS, McGavock JM, Kaka S, et al. Determination of triglyceride in the human myocardium by magnetic resonance spectroscopy: Reproducibility and sensitivity of the method. Am J Physiol Endocrinol Metab, 2005,289(5):E935-E939.

[19] van der Meer RW, Doornbos J, Kozerke S, et al. Metabolic imaging of myocardial triglyceride content: Reproducibility of 1H MR spectroscopy with respiratory navigator gating in volunteers. Radiology, 2007,245(1):251-257.

[20] Abdel-Aty H, Boyé P, Zagrosek A, et al. Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: Comparison of different approaches. J Am Coll Cardiol, 2005,45(11):1815-1822.

[21] Gai N, Turkbey EB, Nazarian S, et al. T1 mapping of the gadolinium-enhanced myocardium: Adjustment for factors affecting interpatient comparison. Magn Reson Med, 2011,65(5):1407-1415.

[22] Ugander M, Oki AJ, Hsu LY, et al. Extracellular volume imaging by magnetic resonance imaging provides insights into overt and sub-clinical myocardial pathology. Eur Heart J, 2012,33(10):1268-1278.

[23] Miller CA, Naish JH, Bishop P, et al. Comprehensive validation of cardiovascular magnetic resonance techniques for the assessment of myocardial extracellular volume. Circ Cardiovasc Imaging, 2013,6(3):373-383.

[24] aus dem Siepen F, Buss SJ, Messroghli D, et al. T1 mapping in dilated cardiomyopathy with cardiac magnetic resonance: Quantification of diffuse myocardial fibrosis and comparison with endomyocardial biopsy. Eur Heart J Cardiovasc Imaging, 2015,16(2):210-216.

[25] Chin CW, Semple S, Malley T, et al. Optimization and comparison of myocardial T1 techniques at 3T in patients with aortic stenosis. Eur Heart J Cardiovasc Imaging, 2014,15(5):556-565.

[26] Singh A, Horsfield MA, Bekele S, et al. Myocardial T1 and extracellular volume fraction measurement in asymptomatic patients with aortic stenosis: Reproducibility and comparison with age-matched controls. Eur Heart J Cardiovasc Imaging, 2015,16(7):763-770.

[27] Liu S, Han J, Nacif MS, et al. Diffuse myocardial fibrosis evaluation using cardiac magnetic resonance T1 mapping: Sample size considerations for clinical trials. J Cardiovasc Magn Reson, 2012, 14(1):72-79.

[28] Hammer S, Snel M, Lamb HJ, et al. Prolonged caloric restriction in obese patients with type 2 diabetes mellitus decreases myocardial triglyceride content and improves myocardial function. J Am Coll Cardiol, 2008,52(12):1006-1012.

[29] Hammer S, van der Meer RW, Lamb HJ, et al. Short-term flexibility of myocardial triglycerides and diastolic function in patients with type 2 diabetes mellitus. Am J Physiol Endocrinol Metab, 2008,295(3):714-718.

[30] Jonker JT, de Mol P, de Vries ST, et al. Exercise and type 2 diabetes mellitus: Changes in tissue-specific fat distribution and cardiac function. Radiology, 2013,269(2):434-442.

[31] Schrauwen-Hinderling VB, Meex RC, Hesselink MK, et al. Cardiac lipid content is unresponsive to a physical activity training intervention in type 2 diabetic patients, despite improved ejection fraction. Cardiovasc Diabetol, 2011,10:47.

[32] Cassidy S, Thoma C, Hallsworth K, et al. High intensity intermittent exercise improves cardiac structure and function and reduces liver fat in patients with type 2 diabetes: A randomised controlled trial. Diabetologia, 2016,59(1):56-66.

[33] van Schinkel LD, Sleddering MA, Lips MA, et al. Effects of bariatric surgery on pericardial ectopic fat depositions and cardiovascular function. Clin Endocrinol (Oxf), 2014,81(5):689-695.

[34] van der Meer RW, Rijzewijk LJ, de Jong HW, et al. Pioglitazone improves cardiac function and alters myocardial substrate metabolism without affecting cardiac triglyceride accumulation and high-energy phosphate metabolism in patients with well-controlled type 2 diabetes mellitus. Circulation, 2009,119(15):2069-2077.

[35] McGavock J, Szczepaniak LS, Ayers CR, et al. The effects of rosiglitazone on myocardial triglyceride content in patients with type 2 diabetes: A randomised, placebo-controlled trial. Diab Vasc Dis Res, 2012,9(2):131-137.

[36] Jankovic D, Winhofer Y, Promintzer-Schifferl M, et al. Effects of insulin therapy on myocardial lipid content and cardiac geometry in patients with type-2 diabetes mellitus. PloS One, 2012,7(12):e50077.

[37] Giannetta E, Isidori AM, Galea N, et al. Chronic inhibition of cGMP phosphodiesterase 5A improves diabetic cardiomyopathy: A randomized, controlled clinical trial using magnetic resonance imaging with myocardial tagging. Circulation, 2012,125(19):2323-2333.

[38] Wong TC, Piehler KM, Kang IA, et al. Myocardial extracellular volume fraction quantified by cardiovascular magnetic resonance is increased in diabetes and associated with mortality and incident heart failure admission. Eur Heart J, 2014,35(10):657-664.

Progresses of MRI in evaluating myocardium of diabetic cardiomyopathy

YANGMei,ZHOUDan*
(DepartmentofRadiology,BenQMedicalCenter,NanjingMedicalUniversity,Nanjing210019,China)

Diabetic cardiomyopathy is one of the major causes of congestive heart failure in patients with diabetes. The histological changes of the diabetic cardiomyopathy can be accurately characterized by MR structure and functional imaging techniques, such as CINE imaging, MRS and T1 Mapping. These cardiac MRI techniques have been used to evaluate the treatment effect of diabetic cardiomyopathy. The progresses of MRI techniques in evaluating myocardium of diabetic cardiomyopathy were reviewed in this article.

Diabetes mellitus; Cardiomyopathy; Magnetic resonance imaging; Treatment outcome

楊梅(1982—)，女，江蘇連云港人，在讀碩士，主治醫(yī)師。研究方向：心血管影像診斷學(xué)。E-mail： mjym2syr@163.com

周丹，南京醫(yī)科大學(xué)附屬明基醫(yī)院放射科，210019。

E-mail： Danny.zhou@benqmedicalcenter.com

2016-10-25

2017-05-25

10.13929/j.1003-3289.201610112

R445.2； R541

A

1003-3289(2017)07-1104-05