Cardiac autonomic neuropathy in patients with diabetes mellitus

Cardiac autonomic neuropathy(CAN)is an often overlooked and common complication of diabetes mellitus.CAN is associated with increased cardiovascular morbidity and mortality.The pathogenesis of CAN is complex and involves a cascade of pathways activated by hyperglycaemia resulting in neuronal ischaemia and cellular death.In addition,autoimmune and genetic factors are involved in the development of CAN.CAN might be subclinical for several years until the patient develops resting tachycardia,exercise intolerance,postural hypotension,cardiac dysfunction and diabetic cardiomyopathy.During its sub-clinical phase,heart rate variability that is influenced by the balance between parasympathetic and sympathetic tones can help in detecting CAN before the disease is symptomatic.Newer imaging techniques(such as scintigraphy)have allowed earlier detection of CAN in the pre-clinical phase and allowed better assessment of the sympathetic nervous system.One of the main difficulties in CAN research is the lack of a universally accepted definition of CAN;however,the Toronto Consensus Panel on Diabetic Neuropathy has recently issued guidance for the diagnosis and staging of CAN,and also proposed screening for CAN in patients with diabetes mellitus.A major challenge,however,is the lack of specific treatment to slow the progression or prevent the development of CAN.Lifestyle changes,improved metabolic control might prevent or slow the progression of CAN.Reversal will require combination of these treatments with new targeted therapeutic approaches.The aim of this article is to review the latest evidence regarding the epidemiology,pathogenesis,manifestations,diagnosis and treatment for CAN.

Alpha-lipoic Acid:Effects on the Beat-to-Beat Vectorcardiographic Parameters in Type 2 Diabetes Mellitus Patients with Cardiac Autonomic Neuropathy

Objective:Relevance of cardiac autonomic neuropathy has not been fully recognized and there is no standardized treatment protocol.Aim:To evaluate the effects of alpha-lipoic acid on the beat-to-beat vectorcardiographic parameters,namely spatial QRS-T angle,QT dispersion(QTd)and corrected QT interval(QTc)in type 2 diabetes mellitus persons with cardiac autonomic neuropathy.Research designs and methods:Our study involved 33 persons with definite stage of cardiac autonomic neuropathy and diabetes mellitus type 2,which were assigned to each of two groups:one took standard antihyperglycaemic treatment(n=15,control group)and the other(n=18)in addition to standard therapy-600 mg of alpha-lipoic acid daily for three months.The analysis of vectorcardiographic parameters was performed.Results:It was found out that alpha-lipoic acid contributed to decrease of the vectorcardiographic parameters,namely QRS-T angle,QTd and QTc.Conclusions:The positive influences of alpha-lipoic acid suggest the usefulness of its prescription to type 2 diabetes mellitus persons with definite stage of cardiac autonomic neuropathy.The efficacy of alpha-lipoic acid is the result of its direct effect on the parameters of vectorcardiography.

Diabetes and cardiac autonomic neuropathy: Clinical manifestations, cardiovascular consequences, diagnosis and treatment

Cardiac autonomic neuropathy(CAN) is a frequent chronic complication of diabetes mellitus with potentially life-threatening outcomes. CAN is caused by the impairment of the autonomic nerve fibers regulating heart rate, cardiac output, myocardial contractility, cardiac electrophysiology and blood vessel constriction anddilatation. It causes a wide range of cardiac disorders, including resting tachycardia, arrhythmias, intraoperative cardiovascular instability, asymptomatic myocardial ischemia and infarction and increased rate of mortality after myocardial infarction. Etiological factors associated with autonomic neuropathy include insufficient glycemic control, a longer period since the onset of diabetes, increased age, female sex and greater body mass index. The most commonly used methods for the diagnosis of CAN are based upon the assessment of heart rate variability(the physiological variation in the time interval between heartbeats), as it is one of the first findings in both clinically asymptomatic and symptomatic patients. Clinical symptoms associated with CAN generally occur late in the disease process and include early fatigue and exhaustion during exercise, orthostatic hypotension, dizziness, presyncope and syncope. Treatment is based on early diagnosis, life style changes, optimization of glycemic control and management of cardiovascular risk factors. Medical therapies, including aldose reductase inhibitors, angiotensin-converting enzyme inhibitors, prostoglandin analogs and alpha-lipoic acid, have been found to be effective in randomized controlled trials. The following article includes the epidemiology, clinical findings and cardiovascular consequences, diagnosis, and approaches to prevention and treatment of CAN.

Cardiovascular autonomic neuropathy in diabetes:Pathophysiology,clinical assessment and implications

Cardiovascular autonomic neuropathy(CAN)is a debilitating condition that mainly occurs in long-standing type 2 diabetes patients but can manifest earlier,even before diabetes is diagnosed.CAN is a microvascular complication that results from lesions of the sympathetic and parasympathetic nerve fibers,which innervate the heart and blood vessels and promote alterations in cardiovascular autonomic control.The entire mechanism is still not elucidated,but several aspects of the pathophysiology of CAN have already been described,such as the production of advanced glycation end products,reactive oxygen species,nuclear factor kappa B,and pro-inflammatory cytokines.This microvascular complication is an important risk factor for silent myocardial ischemia,chronic kidney disease,myocardial dysfunction,major cardiovascular events,cardiac arrhythmias,and sudden death.It has also been suggested that,compared to other traditional cardiovascular risk factors,CAN progression may have a greater impact on cardiovascular disease development.However,CAN might be subclinical for several years,and a late diagnosis increases the mortality risk.The duration of the transition period from the subclinical to clinical stage remains unknown,but the progression of CAN is associated with a poor prognosis.Several tests can be used for CAN diagnosis,such as heart rate variability(HRV),cardiovascular autonomic reflex tests,and myocardial scintigraphy.Currently,it has already been described that CAN could be detected even during the subclinical stage through a reduction in HRV,which is a non-invasive test with a lower operating cost.Therefore,considering that diabetes mellitus is a global epidemic and that diabetic neuropathy is the most common chronic complication of diabetes,the early identification and treatment of CAN could be a key point to mitigate the morbidity and mortality associated with this long-lasting condition.

Cardiac autonomic neuropathy: Risk factors, diagnosis and treatment

Cardiac autonomic neuropathy(CAN)is a serious complication of diabetes mellitus(DM)that is strongly associated with approximately five-fold increased risk of cardiovascular mortality.CAN manifests in a spectrum of things,ranging from resting tachycardia and fixed heart rate(HR)to development of"silent"myocardial infarction.Clinical correlates or risk markers for CAN are age,DM duration,glycemic control,hypertension,and dyslipidemia(DLP),development of other microvascular complications.Established risk factors for CAN are poor glycemic control in type 1 DM and a combination of hypertension,DLP,obesity,and unsatisfactory glycemic control in type 2DM.Symptomatic manifestations of CAN include sinus tachycardia,exercise intolerance,orthostatic hypotension(OH),abnormal blood pressure(BP)regulation,dizziness,presyncope and syncope,intraoperative cardiovascular instability,asymptomatic myocardial ischemia and infarction.Methods of CAN assessment in clinical practice include assessment of symptoms and signs,cardiovascular reflex tests based on HR and BP,short-term electrocardiography(ECG),QT interval prolongation,HR variability(24 h,classic24 h Holter ECG),ambulatory BP monitoring,HR turbulence,baroreflex sensitivity,muscle sympathetic nerve activity,catecholamine assessment and cardiovascular sympathetic tests,heart sympathetic imaging.Although it is common complication,the significance of CAN has not been fully appreciated and there are no unified treatment algorithms for today.Treatment is based on early diagnosis,life style changes,optimization of glycemic control and management of cardiovascular risk factors.Pathogenetic treatment of CAN includes:Balanced diet and physical activity;optimization of glycemic control;treatment of DLP;antioxidants,first of allα-lipoic acid(ALA),aldose reductase inhibitors,acetylL-carnitine;vitamins,first of all fat-soluble vitamin B1;correction of vascular endothelial dysfunction;prevention and treatment of thrombosis;in severe cases-treatment of OH.The promising methods include prescription of prostacyclin analogues,thromboxane A2 blockers and drugs that contribute into strengthening and/or normalization of Na^+,K^+-ATPase(phosphodiesterase inhibitor),ALA,dihomo-γ-linolenic acid(DGLA),ω-3 polyunsaturated fatty acids(ω-3 PUFAs),and the simultaneous prescription of ALA,ω-3 PUFAs and DGLA,but the future investigations are needed.Development of OH is associated with severe or advanced CAN and prescription of nonpharmacological and pharmacological,in the foreground midodrine and fludrocortisone acetate,treatment methods are necessary.

Diabetic cardiac autonomic neuropathy: Do we have any treatment perspectives?

Cardiac autonomic neuropathy(CAN) is a serious and common complication of diabetes mellitus(DM). Despite its relationship to an increased risk of cardiovascular mortality and its association with multiple symptoms and impairments, the significance of CAN has not been fully appreciated. CAN among DM patients is characterized review the latest evidence and own data regarding the treatment and the treatment perspectives for diabetic CAN. Lifestyle modification, intensive glycemic control might prevent development or progression of CAN. Pathogenetic treatment of CAN includes: balanced diet and physical activity; optimization of glycemic control; treatment of dyslipoproteinemia; correction of metabolic abnormalities in myocardium; prevention and treatment of thrombosis; use of aldose reductase inhibitors; dihomo-γ-linolenic acid(DGLA), acetyl-Lcarnitine, antioxidants, first of all α-lipoic acid(α-LA), use of long-chain ω-3 and ω-6 polyunsaturated fatty acids(ω-3 and ω-6 PUFAs), vasodilators, fat-soluble vitamin B1, aminoguanidine; substitutive therapy of growth factors, in severe cases-treatment of orthostatic hypotension. The promising methods include research and use of tools that increase blood flow through the vasa vasorum, including prostacyclin analogues, thromboxane A_2 blockers and drugs that contribute into strengthening and/or normalization of Na^+, K^+-ATPase(phosphodiesterase inhibitor), α-LA, DGLA, ω-3 PUFAs, and the simultaneous prescription of α-LA, ω-3 PUFA and DGLA.

单核细胞Toll样受体和核因子-κB水平与2型糖尿病患者自主神经病变的相关性

目的探讨单核细胞中Toll样受体(TLR)、核因子-κB(NF-κB)表达水平与2型糖尿病(T2DM)患者自主神经病变的相关性。方法选择2021年4月至2022年12月濮阳市人民医院收治的112例T2DM患者为观察组,另选择同期在本院进行体检的50例健康志愿者为对照组。采用反转录聚合酶链反应检测2组受试者血浆单核细胞中TLR2、TLR4、NF-κB表达水平。根据是否并发有自主神经病变将观察组患者分为自主神经病变组(n=46)和无自主神经病变组(n=66),比较2组患者的临床资料,将差异有统计学意义的指标进一步行多因素logistic回归来分析T2DM患者发生自主神经病变的危险因素;采用Spearman相关分析TLR2、TLR4、NF-κB表达水平与T2DM患者发生自主神经病变的相关性。结果观察组患者单核细胞中TLR2、TLR4、NF-κB水平显著高于对照组(P<0.05)。单因素分析结果显示,自主神经病变组与无自主神经病变组患者的年龄、单核细胞/高密度脂蛋白比值(MHR)及胱抑素C、TLR2、TLR4、NF-κB水平比较差异有统计学意义(P<0.05)。多因素logistic回归分析结果显示,MHR、TLR2、TLR4、NF-κB是T2DM患者发生自主神经病变的危险因素(P<0.05)。Spearman相关分析结果显示,TLR2、TLR4、NF-κB水平与T2DM患者发生自主神经病变呈正相关(r=0.825、0.822、0.819,P<0.05)。结论TLR2、TLR4、NF-κB在T2DM患者中表达上调,TLR2、TLR4、NF-κB表达水平与T2DM患者自主神经病变有关。

阿托伐他汀对2型糖尿病合并心脏自主神经病变患者氧化应激反应的影响

目的探讨阿托伐他汀对2型糖尿病(T2DM)合并心脏自主神经病变患者氧化应激反应的影响。方法选取2021年6月至2022年12月南昌大学第四附属医院收治的80例T2DM合并DAN患者作为研究对象,按照随机数字表法分为对照组(40例)与观察组(40例)。两组均行调脂、降压、控糖等对症治疗,对照组口服二甲双胍片,基于此,观察组加用阿托伐他汀。比较两组治疗前、治疗2个月后血糖、血脂[总胆固醇(TC)、三酰甘油(TG)]以及氧化应激指标。结果两组治疗后血糖水平均低于本组治疗前,差异有统计学意义(P<0.05)。治疗后,观察组TG达(3.08±0.49)mmol/L、TC达(5.06±0.71)mmol/L均低于对照组的(3.95±0.61)mmol/L、(6.88±0.85)mmol/L,差异有统计学意义(P<0.05)。观察组治疗后丙二醛(MDA)水平低于对照组,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)均高于对照组,差异有统计学意义(P<0.05)。结论T2DM合并DAN患者普遍存在氧化应激反应,使用阿托伐他汀进行抗氧化治疗利于缓解患者症状,减轻氧化应激反应,改善患者血脂水平,促进康复,值得临床广泛应用。

心脏自主神经病变对于2型糖尿病代谢当量与心率恢复的影响

目的:探讨2型糖尿病(T2DM)合并心脏自主神经病变(CAN)患者在心肺运动试验中最大代谢当量(maxMETs)、心率恢复(HRR)水平及其关系。方法:选取2018年12月—2022年4月于徐州市中心医院心肺康复科行心血管反射试验(CRT)、症状限制性心肺运动试验(CPeT)的79例T2DM患者,根据CRT结果将所有入选T2DM患者分为单纯T2DM组(CAN-组,n=37)与T2DM合并CAN组(CAN+组,n=42)。所有受试者完成心肺运动试验(症状限制性),观察maxMETs及运动终止后1~6min的HRR指标(分别记为HRR1、HRR2、HRR3、HRR4、HRR5、HRR6)。结果:CAN+组maxMETs、HRR1、HRR2、HRR3、HRR4、HRR5、HRR6均低于CAN-组,差异有统计学意义(P<0.05)。所有受试者的maxMETs与HRR1呈正相关性(r=0.455,P<0.05)。结论:HRR1与maxMETs可共同作为T2DM患者康复评定的指标。

2型糖尿病心脏自主神经病变合并视网膜病变和肾病的临床研究

目的:探讨2型糖尿病心脏自主神经病变合并视网膜病变和肾病的患病率及危险因素。方法:选取2022年5月至2023年5月于云南省第一人民医院内分泌科住院的2型糖尿病(type 2 diabetes mellitus,T2DM)患者203例,以心血管反射试验(cardiovascular autonomic reflex tests,CARTs)结合评分判定糖尿病心脏自主神经病变(diabetic cardiac autonomic neuropathy,CAN),按照是否合并糖尿病视网膜病变(diabetic retinopathy,DR)、糖尿病肾脏病变(diabetic kidney disease,DKD)分为单纯CAN组、CAN合并DR组、CAN合并DKD组及CAN合并DR、DKD组,收集所有受试者的临床相关资料。采用SPSS 26.0软件进行统计学分析。结果:①203例T2DM患者中,CAN的患病率为58.62%,CAN合并DR、CAN合并DKD及CAN合并DR、DKD的患病率分别为10.08%、7.56%、10.92%。②在4组中年龄、糖化血红蛋白(glycosylated hemoglobin,HbA1c)、估算肾小球滤过率(estimated glomerular filtration rate,eGFR)、乳酸脱氢酶(lactate dehydrogenase,LDH)、直接胆红素(direct bilirubin,DBIL)、72 h动态血糖葡萄糖在目标范围内时间(72 hours dynamic blood glucose within the target range of time,TIR)等因素差异有统计学意义(P<0.05)。③Logistic回归分析结果:HbA1c(OR=2.948,95%CI=1.015~8.560,P=0.047)、LDH(OR=1.151,95%CI=1.035~1.280,P=0.010)为CAN合并DR、DKD发生发展的促进因素;DBIL(OR=0.057,95%CI=0.005~0.658,P=0.022)、eGFR(OR=0.700,95%CI=0.513~0.955,P=0.025)、TIR(OR=0.877,95%CI=0.775~0.992,P=0.037)、年龄(OR=0.550,95%CI=0.349~0.868,P=0.010)的水平与CAN合并DR、DKD的发生发展相关。结论:较低的eGFR、TIR、DBIL、年龄与CAN合并DR、DKD的发生呈负相关,较高的HbA1c、LDH与CAN合并DR、DKD的发生呈正相关,故在eGFR、TIR、DBIL、年龄相对偏低和(或)HbA1c、LDH相对偏高的糖尿病人群中需更注重CAN合并DR、DKD的筛查。

益气化聚方与硫辛酸治疗2型糖尿病的血糖、代谢及神经病变分析

目的:观察益气化聚方联合硫辛酸对2型糖尿病(T2DM)患者血糖、代谢指标及周围神经病变的影响。方法:选取2020年8月至2022年12月上海中医药大学附属岳阳中西医结合医院收治的T2DM患者120例作为研究对象,采用随机数字表法分为对照组和观察组,每组60例。对照组给予硫辛酸治疗,观察组在对照组基础上加用益气化聚方治疗。比较2组患者在治疗后的临床疗效、血糖变化、代谢相关指标、周围神经病变及治疗期间不良反应发生情况。结果:治疗后,观察组患者治疗总有效率高于对照组,且高低密度脂蛋白胆固醇(HDL-C)水平、总神经运动神经传导速度(MNCV)及感觉神经传导速度(SNCV)评分(正中神经和腓总神经)显著升高,差异有统计学意义(P<0.05),空腹血糖(FPG)、餐后2 h血糖(2 h PG)、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、胰岛素抵抗指数(HOMA-IR)与对照组比较显著降低(P<0.05)。观察组治疗期间出现血小板功能异常2例、脸色苍白1例,对照组治疗期间出现血小板功能异常2例、脸色苍白2例,2组治疗后不良反应发生情况差异无统计学意义。结论:采用益气化聚方联合硫辛酸治疗T2DM可更明显改善周围神经病变,降低血糖,控制血脂,且安全性良好。

甲状腺自身免疫与2型糖尿病心自主神经病变相关性的研究

目的 旨在分析甲状腺自身免疫与2型糖尿病(T2DM)患者心自主神经病变(CAN)之间的相关性,为T2DM患者CAN的预防及治疗提供新思路。方法 选取276例T2DM患者,根据心血管自主神经反射试验结果将研究对象分为CAN (+)组和CAN (-)组。进行24 h动态心电图检查,收集心率变异性参数,采用Spearman相关分析判断甲状腺自身免疫与CAN的相关性,采用二元Logistic回归分析T2DM患者CAN的影响因素。结果 与CAN (-)组患者相比,CAN (+)组患者甲状腺过氧化物酶抗体(TPO-Ab)、甲状腺球蛋白抗体(TgAb)、胰岛素抵抗指数显著升高(P <0.05);TPO-Ab与24 h正常R-R间期标准差(r=-0.148,P=0.014)、24 h每5 min正常R-R间期标准差的平均值(r=-0.152,P=0.011)、24 h相邻R-R间期差值的均方根值(rMSSD,r=-0.317,P <0.001)、24 h相邻正常R-R间期差值>50 ms的心搏数占总心搏数的百分比(pNN50,r=-0.367,P <0.001)、高频(r=-0.353,P <0.001)呈显著负相关关系,与低频/高频(r=0.671,P <0.001)呈显著正相关关系;TgAb与T2DM患者rMSSD (r=-0.257,P <0.001)、pNN50 (r=-0.308,P <0.001)、高频(r=-0.273,P <0.001)呈显著负相关关系,与低频/高频(r=0.551,P <0.001)呈显著正相关关系。二元Logistic回归分析提示TPO-Ab是T2DM患者CAN的独立影响因素。受试者操作特征曲线分析发现TPO-Ab预测CAN的最佳切点值为7.35 U/mL。结论 TPO-Ab可能对T2DM患者CAN的发生、发展具有一定的预测价值,对于TPO-Ab阳性的T2DM患者,有必要定期监测心自主神经功能,预防CAN。

内脏脂肪指数、脂质蓄积指数与糖尿病心脏自主神经病变的相关性研究

目的:分析内脏脂肪指数(VAI)、脂质蓄积指数(LAP)与糖尿病心脏自主神经病变(DCAN)的相关性。方法:选取2型糖尿病病人250例,依据是否发生DCAN分为DCAN组和非DCAN组。比较2组VAI、LAP、Ewing试验参数和相关生化指标水平。2组再依据VAI、LAP四分位数水平分为4个亚组(V1~V4组,L1~L4组),比较各组DCAN的分布情况。应用Spearman相关分析评价VAI、LAP水平与DCAN病人各项Ewing试验参数的相关性,logistic回归分析计算不同VAI、LAP水平病人DCAN的发生风险,ROC曲线分析评估各体脂指标对DCAN的预测诊断价值。结果:250例2型糖尿病病人中,发生DCAN病人158例,未发生DCAN病人92例,DCAN的发生率为63.20%。DCAN组病人年龄、糖尿病病程及腰围、体质量指数、腰身比、腰臀比、VAI、LAP、总胆固醇、三酰甘油、低密度脂蛋白胆固醇水平均明显高于非DCAN组(P<0.01),高密度脂蛋白胆固醇水平明显低于非DCAN组(P<0.01)。随着VAI和LAP四分位水平的增高,DCAN病人的占比不断增大,差异均有统计学意义(P<0.01)。logistic回归分析显示,在调整危险因素后,V4组DCAN的发生风险为约VI组的7.439倍(P<0.05),L4组DCAN的发生风险约为L1组的53.241倍(P<0.01)。Spearman相关分析显示,VAI、LAP与病人Valsalva R-R比值、深呼吸心率差、立卧位心率差均呈负相关关系(P<0.05~P<0.01),与立卧位收缩压差、立卧位舒张压差均呈正相关关系(P<0.05~P<0.01)。ROC曲线分析结果显示,男性和女性病人中,VAI、LAP对DCAN预测的曲线下面积均高于其他指标,且两者在男性病人中的预测曲线下面积高于女性(P<0.05)。结论:DCAN的患病风险与VAI、LAP水平呈正相关关系,随着VAI、LAP水平升高,DCAN的患病风险增高,相较于其他体脂指标VAI、LAP对DCAN的预测能力更佳,且两者在男性中的预测价值更高。

Decreased b-Cell Function is Associated with Cardiovascular Autonomic Neuropathy in Chinese Patients Newly Diagnosed with Type 2 Diabetes

The influence of b-cell function on cardiovascular autonomic neuropathy(CAN), an important diabetesrelated complication, is still unclear. In this study, we aimed to investigate the association between residual b-cell function and CAN in patients newly diagnosed with type 2 diabetes. We enrolled 90 newly-diagnosed type 2 diabetic patients and 37 participants with normal glucose tolerance as controls. The patients were divided into a CAN? group(diabetic patients with CAN, n = 20) and a CAN-group(diabetic patients without CAN, n = 70) according to the standard Ewing battery of tests. Fasting and postprandial plasma glucose, insulin, and C-peptide were measured.Homeostasis model assessment-beta cells(HOMA-B) and HOMA-insulin resistance(IR) were calculated. The prevalence of CAN in this population was 22.2%. Compared with the CAN-group, the CAN? group had significantly lower fasting plasma insulin(6.60 ± 4.39 vs 10.45 ± 7.82 l/L, P = 0.029), fasting C-peptide(0.51 ± 0.20 vs0.82 ± 0.51 nmol/L, P = 0.004), and HOMA-B(21.44 ± 17.06 vs 44.17 ± 38.49, P = 0.002). Fasting C-peptide was correlated with the Valsalva ratio(r = 0.24, P = 0.043) and the 30:15 test(r = 0.26,P = 0.023). Further analysis showed that fasting C-peptide(OR: 0.041, 95% CI 0.003–0.501, P = 0.012) and HOMAB(OR: 0.965, 95% CI 0.934–0.996, P = 0.028) were independently associated with cardiovascular autonomic nerve function in this population. The patients with fasting C-peptide values \ 0.67 nmol/L were more likely to have CAN than those with C-peptide levels C0.67 nmol/L(OR:6.00, 95% CI 1.815–19.830, P = 0.003). A high prevalence of CAN was found in patients with newly-diagnosed type 2 diabetes. Decreased b-cell function was closely associated with CAN in this population.

同型半胱氨酸与2型糖尿病心血管自主神经病变关系的研究进展

心血管自主神经病变(CAN)是2型糖尿病最常见但最易被忽略的并发症之一,其起病隐匿,随病程进展可引起心肌缺血、心律失常甚至心源性猝死等,预后不佳。目前针对CAN治疗还只局限于延缓进展及控制症状。同型半胱氨酸(Hcy)是蛋氨酸代谢的中间产物,研究表明升高的Hcy可通过氧化应激、炎症等多种途径损伤神经系统。本文主要论述Hcy在CAN发生、发展中的可能作用机制,旨在为将来通过降低血浆Hcy来改善CAN提供理论依据。

2型糖尿病患者血清LTB4水平与心血管自主神经病变的关系

目的分析2型糖尿病(T2DM)患者血清白三烯B4(LTB4)水平与心血管自主神经病变(CAN)的关系。方法采用前瞻性队列观察的方法,选择2020年2月至2022年2月该院确诊的T2DM患者共408例作为研究对象,入院根据标准心血管自主神经反射试验(CARTs)分为无CAN组276例和CAN组132例,比较两组患者的临床资料和血生化指标。然后根据LTB4水平中位数分为低LTB4组204例和高LTB4组204例。分析LTB4水平与CARTs参数的相关性。多因素Logistic回归分析筛选CAN的危险因素。最后采用受试者工作特征(ROC)曲线计算LTB4预测CAN的曲线下面积(AUC)。结果CAN组血清LTB4水平明显高于无CAN组,差异有统计学意义(P<0.001)。高LTB4组卧-立收缩压差和CAN发生率比低LTB4组增加,差异有统计学意义(P<0.05),而深呼吸心率差值、Valsalva R-R比值、立-卧心率差值比低LTB4组降低,差异有统计学意义(P<0.05)。Pearson相关结果显示,LTB4与卧-立收缩压差呈正相关(r=0.597,P<0.001),与深呼吸心率差值、Valsalva R-R比值和立-卧心率差值呈负相关(r=-0.502、-0.568、-0.613,P<0.001)。多因素Logistic回归分析显示,LTB4水平升高是CAN发生的独立危险因素(OR=3.265,P<0.001)。ROC曲线计算LTB4水平预测CAN的AUC为0.876(P<0.001)。结论T2DM患者血清LTB4水平升高与CAN发生密切相关,有望成为临床诊断CAN的重要新型标志物。

基于CPET的T2DM伴心脏自主神经病变的心肺适能评估

目的:利用心肺运动试验(CPET)评估2型糖尿病心脏自主神经病变患者(DCAN)心肺适能。方法:筛选我院行CPET检查的DCAN 82例为观察组,同期行CPET检查的健康者78例为对照组。比较两组心肺适能核心指标。结果:观察组VO_(2)peak、AT、METpeak、VO_(2)/HRpeak、WRpeak、运动峰值心率、恢复心率、峰值收缩压、恢复期3min收缩压低于对照组,差异有统计学意义(P<0.05);VE/VCO_(2)、恢复期3min舒张压高于对照组,差异有统计学意义(P<0.05)。结论:DCAN存在心肺适能下降,CPET可精准评估该类患者心肺适能,为下一步制定个体化运动处方奠定基础。

糖尿病性心自主神经、末梢神经病变与糖尿病微血管并发症的关系

目的 观察糖尿病性心自主神经病变和末梢神经病变的患病率及其与其他糖尿病慢性并发症的关系。 方法 利用心自主神经功能检测系统和神经电生理检测仪测定 30 8例糖尿病患者(平均年龄 49岁 ,平均 Hb A1 c9.8% ,平均病程 14年 )的心自主神经功能和肢体的末梢神经传导速度、皮肤痛温觉、振动觉 ,同时检测 2 4h尿白蛋白排泄率和眼底视网膜照相。 结果 糖尿病患者心自主神经病变患病率为 47.1% ,末梢神经病变患病率为 5 4.2 % ,两者呈显著正相关 ,并与病程和糖尿病控制状况呈显著正相关 ,并发糖尿病性神经病变患者并发其他糖尿病慢性并发症的机率增高。 结论 糖尿病性神经病变患病率较高 ,并与糖尿病其他慢性并发症密切相关。

自主神经功能与糖尿病患者左心室功能、心律失常的关系

目的 探讨糖尿病患者自主神经功能与部分心脏合并症之间的关系。方法 采用 2 4小时动态心电图和血压同步监测 10 2例糖尿病患者 ,左心室功能和结构参数用彩色多普勒超声心动图测定。结果 随 SDNN(2 4小时内全部正常 R- R间期的标准差 )降低 ,糖尿病患者的舒张末期二尖瓣口血流频谱 A峰与 E峰峰值流速的比值 (PVA/ PVE)、室间隔厚度 (IVSTd)、左心室后壁厚度 (L VPWTd)、左心室重量指数 (L VMI)均增加 ;二尖瓣前叶活动斜率 (MEF)降低 ,IVSTd/ L VPWTd则无变化 ;严重的心律失常如 L own's≥ 3级的室性心律失常及短阵房速、房颤的发生率也明显增加。上述变化与夜间血压的异常增高相伴随。结论 SDNN低的糖尿病患者心脏受累严重 。

人体生物刺激反馈仪对2型糖尿病患者心血管自主神经病变的筛查及相关危险因素分析

目的探讨人体生物刺激反馈仪(Ezscan)对2型糖尿病患者自主神经病变的检出情况及相关的危险因素。方法回顾性分析上海市长宁区中心医院内分泌科2011年11月—2012年6月收治的2型糖尿病患者98例,采用经典实验和Ezscan检测方法诊断相关患者的心血管神经病变情况。对比两种方法的异常检出率及引起患者发生心血管自主神经病变的危险因素。结果 2型糖尿病心血管自主神经病变的经典实验检出率为45%(44/98),Ezscan检测为50%(49/98),差异无统计学意义(χ2=0.512,P>0.05)。在Ezscan检测中,异常者较正常者的年龄、病程、腰围、体质指数(BMI)、体脂、血压、肌酐、三酰甘油、肱踝脉搏波传导速度及高血压患病率均更高,且差异有统计学意义(P<0.05)。通过Logistic回归分析发现糖尿病心血管自主神经病变的危险因子为:年龄和BMI。结论 Ezscan检测较经典实验的异常检出率无差异,是一种无创性可定量早期诊断及评估糖尿病自主神经病变程度的手段,为临床诊治提供新的依据。