小儿心电图T波改变的特点及诊断价值

目的探究小儿心电图T波改变的特点及其临床诊断价值。方法选取我院接收治疗的72例心电图T波改变儿童患者作为观察对象,对其心电图T波改变的病因及特点进行总结分析。结果共同引起小儿心电图T波改变的,有呼吸道感染、心肌炎、心脏功能紊乱。在72例患者中,呼吸道感染引起者13例,占18.05%;中毒引起者4例,占5.56%;呼气频繁引起者7例,占9.72%;心脏功能紊乱引起者32例,占44.44%;β受体功能兴奋引起者7例,占9.72%;心肌炎引起者9例,占12.5%;54例患儿出现早搏现象,占75.0%,其中交界性早搏4例,房性19例,室性31例,他们都是以频发性早搏为主。其中房性57.89%(11/19),室性70.96%(22/31),交界性75.0%(3/4);夜间正常为68.05%(49/72),全天改变为12.50%(9/72),白天改变为19.44%(14/72);以乳酸脱氢酶同工酶(LDI)增高为主的,有56例患者心肌酶谱,占77.78%(56/72),谷草转氨酶(AST)14例,占19.44%(14/72),LDH-L增高22例,占30.56%(22/72),CK-MB增高12例,占16.67%(12/72)。结论当有心电图T波改变出现于儿童中时,需加强儿童心肌酶谱检测,加强对早搏情况、T波改变情况的分析,从而尽早发现病因及早治疗。     

53例急性肺栓塞心电图分析

目的分析和总结肺栓塞时的心电图特点及其在急性肺栓塞的诊断与鉴别诊断中的应用。方法回顾性分析6年来我院确诊的53例急性肺栓塞患者住院期间的心电图表现并对每位患者治疗前后的心电图形进行对比。结果 53例患者中,出现心电图改变者占98.14%,窦性心动过速最多占77.35%,其次是ST-T改变(ST段改变占64.15%,T波改变占62.26%),典型SⅠQⅢTⅢ征者占22.64%,肺型P波占7.55%,完全性或不完全性右束支阻滞的占18.87%,aVR导联出现终末R波占28.30%。经溶栓抗凝治疗后,比对原有心电图上述项目皆发生了动态变化过程。结论心电图对于提示肺栓塞的诊断有一定的临床价值重大意义。     

不典型急性心肌梗死的临床特点及早期识别

目的探究不典型急性心肌梗死的临床特点,以实现临床早期鉴别诊断。方法研究对象为80例不典型急性心肌梗死患者,采用回顾性分析的研究方式归纳总结患者的治疗资料,重点探究其临床特点和早期特异性表现。结果 80例患者中呼吸系统症状占20.00%,循环系统症状占18.75%,消化系统症状占42.50%,神经系统症状占16.25%,2.50%的患者无特征性表现。心电图检查结果中急性非Q波心肌梗死占46.25%,急性Q波性心肌梗死占53.75%。心肌酶谱检查异常升高患者占97.50%。31.25%患者在6h内确诊,47.50%患者在6h~12h确诊,21.25%患者在12h后确诊。经治疗后好转率总有效率为87.50%,总无效率为12.5%,死亡率为7.50%。结论急性心肌梗死患者具有不典型心电图表现,但心肌酶谱检查具有较高的敏感性,临床诊治中可结合进行诊断,以实现早期鉴别诊断,辅助治疗,促进病情预后。     

甲状腺功能亢进性肌病患者的临床特点分析

目的研究甲状腺功能亢进性肌病患者的临床特点。方法回顾性分析1997年1月~2009年5月间甲亢合并周期性麻痹（TPP）患者31例、慢性甲亢性肌病（CTM）患者29例临床资料,并与甲亢患者30例进行比较分析。结果 TPP发病男性居多,甲亢症状及体征低于对照组,TGAb、TMAb滴度明显高于对照组,CTM患者FT3、FT4与对照组相比有显著差异（P〈0.05）。结论早期积极治疗甲亢是治疗甲亢性肌病根本方法。     

急性脑血管病并发脑心综合征68例临床分析

目的探讨急性脑血管病患者脑心综合征的临床特点、发生率和发病机制。方法分析162例急性脑血管病发生脑心综合征的临床资料,观察其心电图、心肌酶谱改变。结果急性脑血管病脑心综合征的发生率为36．9%,心脏损害主要表现为心电图ST—T改变(67．6%)、心律失常(61．8%)、心肌酶谱增高(47．1%)。结论急性脑血管患者心电图的异常改变与预后呈正相关。早期诊断,加强心电监测对指导治疗和改善预后有重要意义。     

致心律失常性右室心肌病的临床特点和心电图分析

目的探讨致心律失常性右室心肌病(arrhythmogenic right ventricular cardiomyopathy,ARVC)的临床特点及心电图表现。方法对本院在2015年1月至2018年1月收治的29例ARVC患者的临床资料进行回顾性分析,观察患者的临床特点及其胸部X线片、心脏超声心动图、心脏MRI和心电图检查结果的特征性表现,重点分析心电图特征。结果 29例患者中,临床特点表现为室性心律失常的占34.48%,右心衰竭占17.24%,无症状型占48.28%,无症状型占比较高(P=0.01);48.28%的患者超声发现右心增大伴三尖瓣反流,48.28%的患者X线片发现右心增大,48.28%的患者心电图检查发现V_1~V_3导联表现出Epsilon波。将V_1~V_3、V_4~V_6导联QRS平均值分别记作QRS_1和QRS_2。所有患者平均QRS_1为(0.13±0.04)s,平均QRS_2为(0.12±0.02)s;QRS_1≥0.13 s的患者占37.93%,QRS_1/QRS_2≥1.2的患者占62.07%。V_1~V_3导联T波倒置者占31.03%。结论 ARVC患者临床主要表现为无症状型及心律失常型。心电图特点是出现Epsilon波与右胸导联QRS波延长。掌握心电图特点为临床提供了ARVC诊断线索,对降低误诊率有一定的价值。     

急性有机磷中毒与心肌损害的临床研究

目的探讨急性有机磷中毒(A0PP)患者心肌酶和心电图变化的规律及临床意义。方法对120例AOPP患者治疗前后的心肌酶和心电图资料进行综合分类分析。结果 120例患者中有异常心电图者107例(占88.3%),心肌酶谱中肌钙蛋白(cTnI)、肌酸激酶同工酶(CK-MB)、血清肌酸激酶(CK)至少有1项异常者106例占(88.3%)。轻、中、重度中毒组间血清中cTnI、CK-MB、CK水平的两两比较均有显著性差异(P0.01);心电图异常改变构成比组间两两比较也有显著性差异(P0.01)。结论在A0PP抢救治疗过程中,应常规动态检查心电图,结合心肌酶结果,及早对心肌行保护性治疗。     

甲状腺功能亢进并发心律失常的临床诊治分析

目的总结分析甲状腺功能亢进(甲亢)并发心律失常的临床表现及预后,探讨甲亢并发心律失常的发病机制、诊断、防治。方法对本院113例甲亢并发心律失常的临床资料进行回顾性分析。结果经治疗,1例甲亢并发窦性心动过速死于住院期间,占0.88%;112例症状均好转或消失,占99.12%。结论甲亢并发的心律失常,窦性心动过速和心房纤颤为主要的并发症,治疗的关键是早日根治甲亢,积极采取抗心律失常治疗。     

急性一氧化碳中毒心脏损害的临床分析

目的 :探讨急性一氧化碳 (CO)中毒对心脏的损害 ,使急性CO中毒患者得到更全面的治疗。方法 :回顾性分析近年来我院收治的急性CO中毒患者的临床表现、心电图及心肌酶改变。结果 :15 8例急性CO中毒患者中 87.3%出现昏迷 ,12 .7%出现心力衰竭 ,随机将其中 6 5例中毒患者作心电图及心肌酶检查 ,发现 5 6例出现心电图改变 ,4 4例出现心肌酶改变。结论 :急性CO中毒不仅对神经系统造成损害 ,对心脏的损害也很严重 ,需要给予相应的治疗。     

消化道大出血合并急性心肌梗死12例临床分析

目的探讨消化道出血合并急性心肌梗死的机制及其临床特点。方法回顾性分析1999年—2007年我院消化道出血合并急性心肌梗死12例患者的临床特点、心电图改变、血清心肌酶学及肌钙蛋白的测定结果。结果消化道出血与急性心肌梗死均为临床危重症,消化道出血合并急性心肌梗死时,病死率明显升高,其发病机制与冠状动脉灌流量减少、血管平滑肌收缩、冠状动脉痉挛、狭窄有关,消化道出血时其急性心肌梗死的表现易被认为由消化道原发病所致,从而被忽视。结论应注意动态观察其心电图、血清心肌酶学、肌钙蛋白的变化。     

Electrocardiographic manifestations in patients with thyrotoxic periodic paralysis

BACKGROUND: Thyrotoxic periodic paralysis (TPP) commonly precedes the overt symptoms and signs of hyperthyroidism and may be misdiagnosed as other causes of paralysis (non-TPP). Because the cardiovascular system is very sensitive to elevation of thyroid hormone, we hypothesize that electrocardiographic manifestations may aid in early diagnosis of TPP. METHODS: We retrospectively identified 54 patients who presented to the emergency department (ED) with hypokalemic paralysis during a 3.5-year period. Thirty-one patients had TPP and 23 patients had non-TPP, including sporadic periodic paralysis, distal renal tubular acidosis, diuretic use, licorice intoxication, primary hyperaldosteronism, and Bartter-like syndrome. Electrocardiograms during attacks were analyzed for rate, rhythm, conduction, PR interval, QRS voltage, ST segment, QT interval, U waves, and T waves. RESULTS: There were no significant differences in age, sex distribution, and plasma K+ concentration between the TPP and non-TPP groups. Plasma phosphate was significantly lower in TPP than non-TPP. Heart rate, PR interval, and QRS voltage were significantly higher in TPP than non-TPP. Forty-five percent of TPP patients had first-degree atrioventricular block compared with 13% in the non-TPP group. There were no significant differences in QT shortening, ST depression, U wave appearance, or T wave flattening between the 2 groups. CONCLUSION: Relatively rapid heart rate, high QRS voltage, and first-degree AV block are important clues suggesting TPP in patients who present with hypokalemia and paralysis.     

Clinical review: Thyrotoxic periodic paralysis: a diagnostic challenge

CONTEXT: The aim of this article was to review the clinical presentation, pathogenesis, and management of thyrotoxic periodic paralysis (TPP). EVIDENCE ACQUISITION: A MEDLINE search was conducted for articles published during the last 40 yr based on the key words thyrotoxic periodic paralysis and hypokalemic periodic paralysis. A total of 281 primary articles and 168 references of the retrieved articles were also reviewed. EVIDENCE SYNTHESIS: TPP is a common complication of hyperthyroidism in Asian men but is increasingly seen in Western countries. Hypokalemia and muscle paralysis results from a sudden intracellular shift of potassium and is not due to potassium deficiency. Clinical features of hyperthyroidism in patients with TPP may be subtle. Immediate potassium supplementation prevents serious cardiopulmonary complications and may hasten the recovery of muscle weakness. Nonselective beta-adrenergic blockers can ameliorate and prevent recurrence of the paralytic attacks. This episodic paralysis will remit with definitive control of hyperthyroidism. Increased sodium-potassium ATPase pump activity and enhanced insulin response in patients with TPP is postulated to contribute to the hypokalemia. The genetic predisposition for TPP is not entirely clear. Association of polymorphisms of the calcium channel alpha1-subunit gene with TPP has been noted. CONCLUSIONS: Due to population mobility, TPP is increasingly common in Western countries. Early diagnosis and prompt treatment prevent life-threatening complications associated with hypokalemia and muscle weakness. Assaying of thyroid function in patients with hypokalemic paralysis distinguishes TPP from other forms of hypokalemic periodic paralysis.     

Thyrotoxic periodic paralysis associated with lactic metabolic acidosis: Case report of an African man and review of literature

BackgroundThyrotoxic periodic paralysis (TPP) is a rare and most often acquired subtype of hypokalemic periodic paralysis. The association of varying degrees of muscle weakness, hyperthyroidism and hypokalemia characterizes it. The treatment requires potassium supplementation, control of hyperthyroidism and prevention measures. It is a frequent disease in Asian men, but much rare in Caucasian or African populations. This is the first report of TPP associated with lactic metabolic acidosis in an African man.Case presentationA 23 year-old African man, native from Morocco, with recurrent episodes of tetraparesis for eleven months, and abdominal pain, was referred for evaluation. Biochemical investigations showed severe hypokalemia associated with hyperthyroidism and lactic metabolic acidosis. His EKG showed signs of hypokalemia such as sinus tachycardia and U waves. After potassium supplementation, neurological recuperation was quick and complete. Thyroid ultrasound identified a hypoechogenic and hypervascularized goiter, associated with high levels of thyroid antibodies, in favor of Grave's disease. With antithyroid drugs and life-style changes, the patient did not have any other attack.Review of literatureIn addition to the case report, this article presents an extended review of literature, from the first large study reporting the diagnosis and incidence of TPP in 1957 to nowadays. Are reported here the latest information concerning epidemiology, clinical manifestations, complementary examinations, management and genetic finding. The lactic acidosis observed initially is exceptional, never described in TPP. TPP is a diagnostic and therapeutic emergency, requiring careful potassium supplementation, in order to avoid the risk of the onset of rebound hyperkalemia, to be maintained until the etiological treatment is effective. Paraclinical assessment with emergency EKG and electromyogram are essential to assess the impact.DiscussionIt is essential in the face of any hypokalaemic periodic paralysis, including in non-Asian subjects, to search hyperthyroidism.ConclusionsThis report demonstrates the importance of thyroid testing in case of acute muscle weakness, even in non-Asian patients in order to diagnose TPP. This is a rare but possible etiology, to be distinguished from the familial form of hypokalemic periodic paralysis. It also questions on the impact of TPP on energetic metabolism, in particular on lactic metabolism.     

Skeletal muscle dihydropyridine-sensitive calcium channel (CACNA1S) gene mutations in chinese patients with hypokalemic periodic paralysis

BACKGROUND: Thyrotoxic periodic paralysis (TPP), familial periodic paralysis (FPP), and sporadic periodic paralysis (SPP) are common causes of hypokalemic periodic paralysis and have similar clinical presentations, thus possibly sharing the identical mutations. METHODS: We analyzed the role of the three known CACNA1S gene mutations (R528H, R1239H, and R1239G) in Chinese patients, including two FPP families, 36 TPP patients, 12 SPP patients, and their relatives. Fifty unrelated healthy subjects were also studied. Genomic DNA was prepared from the peripheral blood of all patients, their family members, and healthy subjects. Mutations of the CACNA1S gene were screened using polymerase chain reaction-based restriction analysis. RESULTS: Two FPP families had the R528H point mutation, but with incomplete penetrance occurring more commonly in men than in women. Only one SPP patient had a de novo mutation (R528H). None of the TPP patients had mutations in the three hot spots. CONCLUSION: Patients with FPP have R528H mutations in the CACNA1S gene. Only a few patients with SPP may share similar mutations with FPP. TPP patients do not carry any of the three known gene mutations.     

Electromyographic (EMG) Study in Thyrotoxic Periodic Paralysis

:Electromyographic (EMG) study in thyrotoxic periodic paralysis. K. Puvanendran, J. S. Cheah and P. K. Wong, Aust. N.Z. J. Med., 1977, 7, pp. 507–510. Thyrotoxic periodic paralysis (TPP) is produced by a different metabolic disorder than familial periodic paralysis.^1,2 In the familial disorder, a myopathic cause is well known, but although electromyography can be used to demonstrate the site of the lesion in TPP, such studies are rare in the medical literature and the results are conflicting. In this report, EMG studies were carried out on eight Chinese patients with thyrotoxic periodic paralysis during the attack and the results compared with studies repeated during a remission. Most cases showed a myopathic pattern during an attack of paralysis which disappeared during remission. The myopathic changes noted were a decrease in duration of muscle action potentials, an increase in po/yphasic potentials, a satisfactory interference pattern with reduced amplitude and a reduced amplitude of the evoked muscle action potential on nerve stimulation. Peripheral nerve function was normal in the cases studied. It is concluded that the weakness in TPP is myopathic and that the peripheral nerve function during paralysis is normal.     

慢性布鲁氏菌病患者203例心电图分析

本文报告了203例慢性布鲁氏菌病患者的心电图,从临床分型、布鲁氏菌素皮试、病程、年龄等几个方面进行了分析,同时与健康组进行了对照。结果表明(1)布鲁氏菌病慢性期可影响心脏而产生心电变化。(2)心电改变共出现17种,其中最多见的为窦缓,右不全、房早及ST-T改变。(3)病情活动可使心电改变增多,其中主要表现为房早,T波低平或倒置以及窦缓。(4)随着病程延长心电改变增多。(5)慢性布鲁氏菌病患者心电改变与皮试强弱无关,与年龄无关。     

短阵房性心动过速后窦性心律的T波增高

目的探讨房性心动过速后窦性搏动T波增高的临床意义.方法分析12导联动态心电图证实的375例房性心动过速患者心动过速发生前后的心电图变化,尤其是T波的改变.结果 375例房性心动速患者中,P波改变14例,R波振幅改变5例（增高1例,降低4例）,ST段压低7例,U波改变2例,T波改变66例（17.6%）.66例T波改变的患者中,46例表现为T波低平或倒置,20例T波振幅增高,包括1例巨大直立T波.结论房性心动过速停止后,窦性心律下,多数患者表现为T波低平或倒置,T波振幅增高相对少见,巨大直立T波罕见,其临床意义尚待探讨.     

HLA and thyrotoxic periodic paralysis in Japanese patients

Periodic paralysis (PP) is a well recognized although rare and peculiar complication of thyrotoxicosis, especially among Chinese and Japanese patients. The susceptibility to autoimmune thyroid disease has recently been reported to be strongly linked to certain immunogenetic factors, and increased frequency of certain HLA antigens has been found in patients with Graves' disease. This study was, therefore, undertaken to determine HLA haplotypes in Japanese men with thyrotoxic periodic paralysis (TPP). HLA typing in 35 TPP patients and 263 normal men and women demonstrated highly significant increases (P less than 0.01) in HLA-A2, Cw3, and DRw8 in the TPP patients. In comparing TPP patients with thyrotoxic men who did not have PP, the frequency of DRw8 antigen was 2.5-fold greater in patients with PP than in those without it (62.8% vs. 28.6%). The data suggest that the HLA-DRw8 gene itself may play a significant role in the susceptibility to TPP among Japanese men.