Response to thyrotrophin-releasing hormone in atrial dysrhythmias.

Seventy-eight clinically euthyroid patients with atrial dysrhythmias, either established or paroxysmal, and sixty-three patients in sinus rhythm with coronary disease were screened for hyperthyroidism using thyroid function tests including the thyroid-stimulating hormone (TSH) response to thyrotrophin-releasing hormone (TRH). All had normal levels of serum thyroxine (T4) apart from three with dysrhythmias who were found to have hyperthyroidism. Twenty per cent of patients with atrial dysrhythmias and 10% of those in sinus rhythm had exaggerated TSH response to TRH. Thirty-six per cent of patients with an exaggerated response of TSH to TRH had significant titres of thyroid auto-antibodies compared with 15% with positive antibodies in those with normal TSH response to TRH. Auto-immune thyroid disease may be more closely related to heart disease than has previously been recognized. Rapid atrial dysrhythmias may occur in the presence of a normal serum thyroxine, high levels of TSH and positive thyroid antibodies.     

A sensitive immunoradiometric assay for serum thyroid stimulating hormone: a replacement for the thyrotrophin releasing hormone test?

The value as a thyroid function test of a new, rapid, and highly sensitive immunoradiometric assay for thyroid stimulating hormone (TSH) was assessed in 188 consecutive new patients with suspected hyperthyroidism. The diagnosis was made on clinical grounds and on the basis of serum total triiodothyronine and thyroxine concentrations and the response of TSH to thyrotrophin releasing hormone (TRH) as measured by radioimmunoassay. In all except one patient the basal TSH concentration by immunoradiometric assay predicted the response of TSH by radioimmunoassay to TRH, an undetectable value being recorded in patients with a subnormal response and a measurable value in those with a normal test result. This clear relation was not observed for basal TSH concentrations as measured by radioimmunoassay. In a series of 39 hospital inpatients with acute or chronic non-thyroidal illness, of whom 11 had low concentrations of total thyroxine or triiodothyronine, or both, basal TSH concentrations were detectable by both radioimmunoassay and immunoradiometric assay in all cases and were associated with normal responses to TRH. The immunoradiometric assay for TSH, which is commercially available, may therefore obviate the need for the more time consuming TRH test and simplify the approach to thyroid function testing in patients with suspected hyperthyroidism.     

Atrial fibrillation and hyperthyroidism: a new look at their relationship and therapy with lidoflazine

Various kinds of dysrhythmias are found in association with hyperthyroidism but especially atrial fibrillation. The causal relationship of chronic atrial fibrillation and the endocrine disorder is controversial, as is its therapeutic management. Six patients with this particular combination of disorders were treated with lidoflazine: a new anti-anginal drug with anti-arrhythmic activity. All six patients returned to sinus rhythm on lidoflazine treatment although still hyperthyroid and remained in sinus rhythm during the follow up period ranging from 5 to 14 months. This occurred independently of antithyroid treatment. Some evidence is put forward that dysrhythmias and most commonly chronic atrial fibrillation are triggered off by hyperthyroidism or other disorders but that they are maintained by permanent cardiac damage due to arteriosclerosis, hypertension, coronary heart disease or rheumatic valve disease.     

丙基硫氧嘧啶联合不同剂量普萘洛尔治疗甲亢合并房颤的临床疗效与安全性研究

目的：探讨丙基硫氧嘧啶联合不同剂量普萘洛尔治疗甲亢合并房颤的临床疗效及安全性。方法：112例初治甲亢合并房颤患者在丙基硫氧嘧啶基础治疗上被分为：低剂量组（n=57,普萘洛尔10mg 3次/日口服）,高剂量组（n=57,普萘洛尔30mg 3次/日口服）。观察患者治疗前后FT3、FT4、TSH、LVEF、血压、心率变化,并随访3个月期间不良临床事件发生情况。结果：治疗两周后两组患者FT3、FT4、心率和血压均较治疗前下降显著（均P〈0.05）,TSH较治疗前明显升高（P〈0.05）。高剂量组的LVEF较治疗前明显升高（P〈0.05）,FT3较低剂量组下降明显（P〈0.05）。随访3月两组间不良临床事件无统计学差异（P〉0.05）,但高剂量组的窦性心律转复率更高（P〈0.05）。结论：与低剂量相比,高剂量普萘洛尔治疗甲亢合并房颤能进一步缓解甲亢病情,促进窦性心律转复,改善心功能。     

Graves' ophthalmopathy and subclinical hypothyroidism: diagnostic value of the thyrotropin releasing hormone test.

Five patients with Graves' ophthalmopathy and no previously documented clinical or laboratory evidence of hyperthyroidism were studied. Their serum levels of thyroxine and triiodothyronine (T3) and their T3 uptake were normal. Although the baseline serum level of thyrotropin (TSH) was normal in two patients, it was increased on the other three, and when TSH releasing hormone (TRH) was administered the T3 response was impaired in three patients and the TSH response was exaggerated in all five. These findings facilitated the diagnosis of subclinical hypothyroidism and distinguished the patients from those with Graves' ophthalmopathy and normal thyroid function or subclinical hyperthyroidism. Thyroid antibodies were detected in the serum of four of the five patients, suggesting the coexistence of chronic autoimmune thyroiditis; this disorder could account in part for the subclinical hypothyroidism, which was even present in the two patients in whom thyroid-stimulating immunoglobulin was found in the serum. These observations indicate the value of a TRH stimulation test in detecting subclinical hypothyroidism in patients with Graves' ophthalmopathy who appear from clinical and routine laboratory studies to have normal thyroid function but could have normal function or subclinical hyperthyroidism.     

甲状腺功能亢进性心脏病47例的临床分析

目的:研究与分析甲状腺功能亢进性心脏病的临床特点,探讨临床对其的防治措施。方法:对我院2009年5月～2010年5月收治的47例甲状腺功能亢进性心脏病患者的临床资料进行回顾性分析。结果:47例甲状腺功能亢进性心脏病临床表现主要为心律失常,占80.9%;心电图检查以心房颤动最为常见,共29例,占61.7%:临床误诊18例,占38.3%;经治疗后,43例患者的甲亢病情明显缓解,死亡4例。29例心房颤动中恢复窦性心律者20例。结论:甲状腺功能亢进性心脏病的诊治关键在于早期诊断、对症治疗及对甲亢进行有效的控制。     

Hyperthyroidism due to inappropriate TSH secretion with associated hyperprolactinaemia--a case report and review of the literature.

A patient with inappropriate thyrotrophin (TSH) secretion is described. She initially presented with classical hyperthyroidism during pregnancy, responded to propylthiouracil and, subsequently, had a normal delivery. Hyperthyroidism persisted and 7.5 months later a subtotal thyroidectomy was performed. After a further 16 months, mild symptoms of hyperthyroidism recurred. She again responded to propylthiouracil, but developed galactorrhoea. At that stage, it was noted that she had persistently elevated circulating TSH in the presence of elevated T4 and T3 levels. Her symptomatology was mild, although objective indices of thyroid activity, including pulse rate, BMR, sex hormone binding globulin and cholesterol, were indicative of hyperthyroidism. CT scan and tomography of the sella were normal. She had a markedly exaggerated TSH response to thyrotrophin releasing hormone (TRH). Basal TSH and responsiveness to TRH was suppressed by high dose dexamethasone. The TSH response to TRH was partially suppressed by exogenous T3, but there was no effect on basal TSH levels. TSH also decreased slightly with L-dopa and bromocriptine. Circulating TSH rose markedly during methimazole administration. TSH alpha and beta subunits were elevated and appropriate for the high TSH. In addition, both subunits increased following TRH. The patient had basal hyperprolactinaemia with an impaired prolactin (PRL) response to TRH and metoclopramide. PRL suppressed with L-dopa and bromocriptine. The remaining anterior pituitary function was intact. Most of the laboratory findings argue against the presence of a TSH producing pituitary tumour and the most likely cause for inappropriate TSH secretion in this patient is selective resistance of the thyrotroph to thyroid hormones. A mild element of peripheral resistance might also be present. The hyperprolactinaemia could be related to lactotroph resistance to thyroid hormone. The complexities of treatment in this patient are stressed. Therapy was initially attempted with low dose dexamethasone, but this had no effect. T3 treatment produced an exacerbation of her symptomatology and did not influence basal TSH, thyroid hormones, or 131I uptake. Bromocriptine administration for 11 months partially suppressed basal TSH without influencing T3 and there was an increase in T4. Methimazole did decrease her T4 and T3, but TSH and PRL rose to even greater levels. Her hyperthyroidism was eventually controlled with an ablative dose of 131I. Thyroid hormone will be given in an attempt to suppress her TSH.     

Graves' disease and atrial fibrillation: the case for even higher doses of therapeutic iodine-131

Seventy five consecutive patients with Graves' disease complicated by atrial fibrillation were given a large single therapeutic dose of 600 MBq (16.2 mCi) iodine-131 in an effort to control their hyperthyroidism rapidly and thus restore sinus rhythm. Patients were initially followed up every three months after treatment and then at yearly intervals. The mean period of follow up was 3.1 years. A total of 44 of the patients became hypothyroid and 31 euthyroid, and 33 (75%) and 14 (45%) of these patients, respectively, reverted to sinus rhythm (p less than 0.01). Of the 33 who became hypothyroid and reverted to sinus rhythm, 30 had developed the hypothyroidism within six months after treatment. These results are a strong case for increasing the dose of radioiodine in patients with Graves' disease complicated by atrial fibrillation in an effort to speed the onset of thyroid failure and thus maximise the rate of reversion to sinus rhythm.     

Thyrotropin-and prolactin--secreting pituitary tumor dissociated hormonal response to bromocriptine

A 41-year-old male with recurrent hyperthyroidism resulting from pituitary tumor was studied. Because of recurrent hyperthyroidism, he had been treated with propylthiouracil for four years and had been operated. At the time of high serum thyroid hormone (T4: 20 micrograms/dl; T3:502 ng/dl), there was also elevated basal serum TSH level (55 microU/ml) which could not be suppressed by exogenous thyroid hormone administration. In addition, the serum TSH showed blunt response to intravenous TRH infusion. An elevated serum prolactin level was also observed (111 ng/ml). After bromocriptine administration (2.5 mg daily), the suppressibility of serum TSH level was found better than that of prolactin level. The existence of a TSH- and PRL-secreting pituitary tumor in this patient exhibited a dissociated hormonal response to low doses of dopaminergic agents.     

小剂量多巴胺和胺碘酮治疗老年食管癌患者术后心房颤动疗效观察

目的研究小剂量多巴胺和胺碘酮治疗老年食管癌切除术后心房颤动的治疗效果。方法选择2010年8月至2011年7月解放军第371中心医院心胸外科食管癌术后并发快速型心房颤动老年患者26例,采用小剂量多巴胺和(或)胺碘酮治疗。结果发生快速型心房颤动后72 h内经治疗26例均转为窦性心律,其中单独使用多巴胺治疗9例,多巴胺联合胺碘酮治疗17例。所有患者在心房颤动心律转为窦性心律后继续使用小剂量多巴胺维持,心率呈逐渐下降趋势,并恢复到术前心率水平,血流动力学稳定。结论采用早期、短疗程应用小剂量多巴胺支持心脏功能和(或)胺碘酮抗心律失常可有效治疗食管癌术后快速型心房颤动。     

甲状腺激素与收缩功能下降的心力衰竭患者房颤发生率的相关性研究

目的研究甲状腺激素对收缩功能下降的慢性心力衰竭患者房颤发生率的影响及相关的机制。方法入选181例收缩功能下降的慢性心力衰竭患者,入院后24 h内记录患者病史,测定血清游离甲状腺素（FT4）、游离三碘甲状腺原氨酸（FT3）、促甲状腺激素（TSH）、低密度脂蛋白（LDL）水平;并行十二导心电图及超声心动图检查,根据是否并发房颤分为房颤组和窦律组,分析影响心衰患者发生房颤的相关因素。结果 181例心衰患者中并发房颤102例（56.35%）,房颤组与窦律组的FT4水（15.04±3.26）pmol/L比（13.27±2.61）pmol/L,P〈0.001的差异有统计学意义,两组FT3水平差异（4.02±0.61）pmol/L比（4.26±1.14）pmol/L,P=0.078无统计学意义;FT4水平与左心房内径无明显相关性（r=0.105,P=0.160）,FT3水平与年龄呈负相关（r=-0.286,P〈0.001）;FT4水平、左心房内径、年龄、心衰持续时间与心衰患者房颤发生率相关。结论高FT4水平可能增加了收缩功能下降的慢性心力衰竭患者发生房颤的风险。     

原发性高血压发生心房颤动的危险因素

目的探讨原发性高血压发生心房颤动的危险因素。方法306例符合纳入标准的单纯性原发性高血压病人整群随访5年,由专科医师进行降压治疗的同时记录随访结果。终检标准:心房颤动。影响心房颤动事件的因素用Cox风险比例模型鉴定。结果5年中,发生心房颤动86例(28.1%),平均年发生率5.6%,Cox回归分析显示年龄(HR=1.095,p=0.024)、左室重量指数(HR=1.137,p=0.000)、左房内径(HR=1.232,p=0.000)是原发性高血压发生心房颤动的独立预报因子。结论年龄、左室重量指数、左房内径是原发性高血压发生心房颤动的危险因素。     

球囊二尖瓣扩张术后心房纤颤复律的临床研究

目的探讨二尖瓣狭窄合并心房纤颤患者在球囊二尖瓣扩张后,转复心房纤颤的临床效果及影响心房纤颤转复后窦性心律维持的相关因素.方法 206例二尖瓣狭窄合并心房纤颤患者在球囊扩张术后,采用口服胺碘酮及电复律治疗心房纤颤,对复律成功的患者给予小剂量胺碘酮维持窦性心律并随访1年.结果服用胺碘酮者58例,17例转复成功(29.3%);189例行电转复,178例转复成功(94.2%),电转复成功率明显高于胺碘酮转复(P＜0.01).心房纤颤复发组与保持窦性心律组相比,左心房内径明显扩大(P＜0.01),心房纤颤持续时间明显长(P＜0.01),中度二尖瓣关闭不全人数的比率明显高(P＜0.05).随访1年,有45例患者心房纤颤复发.影响心房纤颤转复后维持窦性心律的相关因素有左心房内径扩大、心房纤颤持续时间长及明显的二尖瓣关闭不全.结论对左心房内径明显扩大、心房纤颤持续时间过长及有明显的二尖瓣关闭不全的患者,在选择心房纤颤转复时应慎重.     

放射性核素碘治疗甲状腺功能亢进性心脏病重要血浆因子水平的变化

目的观察甲状腺功能亢进性心脏病(甲亢性心脏病)患者接受放射性核素碘(131I)治疗前后血白细胞介素1(IL-1)、肿瘤坏死因子α(TNF-α)、内皮素水平的变化,探讨甲亢性心脏病与IL-1、TNF-α、内皮素的关系。方法选取2008年9月至2011年12月经新乡医学院第一附属医院收治126例甲状腺功能亢进患者为单纯甲亢组,另选取同期的甲亢性心脏病患者172例为甲亢性心脏病组。应用酶联免疫吸附法测定131I治疗甲亢性心脏病前后血IL-1、TNF-α、内皮素的水平,并观察甲状腺激素水平及超声心动参数左心室收缩末期内径(LVESD)、左心室舒张末期内径(LVEDD)及左心室射血分数(LVEF)的变化。结果甲亢性心脏病脏病组患者治疗131I治疗前后血内皮素、TNF-α及IL-1均显著高于单纯甲亢组;甲亢性心脏病组患者131I治疗后血内皮素、TNF-α、IL-1、血清游离三碘甲腺原氨酸及血清游离甲状腺素显著下降,而TSH水平增高(P<0.05)。治疗后与治疗前比较,患者LVESD、LVEDD及LVEF的差异均有统计学意义(P<0.05)。结论 131I可能参与了IL-1、TNF-α、内皮素的生成调节,甲亢性心脏病患者的心功能和甲状腺功能的改善与上述因子水平变化有密切联系。     

β型甲状腺激素抵抗综合征患者临床特点分析

背景　β型甲状腺激素抵抗综合征（RTHβ）属于罕见内分泌疾病,临床极易误诊、误治。目的　总结RTHβ患者的临床特点,为临床医师了解本病提供帮助。方法　选取2013-2016年于中国医科大学附属第一医院内分泌与代谢病科诊断为RTHβ的患者6例。回顾性分析6例RTHβ患者的临床资料,包括性别、诊断年龄、发病年龄、家族史、主诉、心电图检查结果、甲状腺触诊结果、甲状腺超声检查结果、甲状腺核素静态显像结果、甲状腺功能指标〔游离三碘甲腺原氨酸（FT3）、游离甲状腺素（FT4）、促甲状腺激素（TSH）〕、促甲状腺素受体抗体（TRAb）、性激素结合蛋白（SHBG）、血清铁蛋白、脂代谢指标、骨代谢指标、骨密度、基因测序情况等。结果　6例RTHβ患者的诊断年龄均高于发病年龄,患者在确诊RTHβ之前均被误诊为甲状腺功能亢进症,长期服用抗甲状腺药物治疗。患者主诉均存在心悸、多汗,3例伴心房颤动。6例患者甲状腺核素静态显像均显示甲状腺双叶摄取率增高。5例RTHβ患者甲状腺超声显示有甲状腺肿大,4例显示多发结节。6例RTHβ患者血清FT3、FT4水平升高,TSH水平在参考范围,且TRAb均为阴性;血清SHBG和血清铁蛋白均在参考范围;甲状腺激素受体（TR）β基因测序均存在点突变。结论　RTHβ的临床表现存在高度异质性,临床诊断时需注意与甲状腺功能亢进症和甲状腺功能减退症区分,同时注意并非所有的RTHβ患者能检测出TRβ基因突变。对于高度怀疑为RTHβ的患者,可以采用促甲状腺素释放激素（TRH）兴奋试验、左旋-三碘甲腺原氨酸（L-T3）抑制试验或TRH兴奋试验联合L-T3抑制试验进行临床诊断。     

胺碘酮联合培哚普利对初发性心房颤动复律后窦性心律维持的影响

观察静脉注射胺碘酮对初发性心房颤动伴快心室反应的转复效果以及口服胺碘酮联合培哚普利对心房颤动转复后远期窦性心律的维持。将89例患者随即分为胺碘酮组(n=48例)和胺碘酮加培哚普利组(n=41例)。观察静注胺碘酮对房颤终止的效果。48小时内转复率70.8%。胺碘酮加培哚普利组对房颤复律后窦性心律的维持,左房内径缩小均明显优于胺碘酮组(P<0.05)。结论胺碘酮联合培哚普利对初发性房颤复律后窦性心律的维持优于胺碘酮组,对左房扩大的延缓及心功能改善均有一定作用。     

Normal thyrotrophin response to intravenous thyrotrophin releasing hormone administration: the best index of optimal L-thyroxine therapy in primary hypothyroidism

Normalization of basal thyrotrophin (TSH) level is used as the endpoint in L-thyroxine (L-T4) therapy of primary hypothyroidism. However, several reports have questioned the reliability of this index because of seasonal variation of TSH. Therefore, we studied 85 consecutive patients with primary hypothyroidism over a period of 3.5 y. In these patients, TSH response (delta TSH) to intravenous thyrotrophin releasing hormone (TRH) administration was examined when basal TSH was normalized with L-T4 therapy. Eight patients showed a blunted response (delta TSH less than 5 microU), whereas 27 patients demonstrated an exaggerated response (delta TSH greater than 25 microU). Thus, 42% of patients were apparently on inappropriate L-T4 dosage. These abnormal TSH responses normalized on adjusting the L-T4 dosage alone; prolonged therapy with the same dose failed to normalize TSH responses. Minor seasonal variations of basal TSH were observed in 30% of patients. However, TSH response to TRH remained normal. Hence, no adjustment of L-thyroxine dose was required. This study, therefore, demonstrates that normalization of TSH response to TRH administration rather than basal TSH may be the best index of adequate L-thyroxine therapy in primary hypothyroidism.     

P波离散度对甲亢患者并发房性心律失常的预测价值

目的:探讨体表心电图P波离散度(P-wave dispersion,Pd)对甲亢患者合并房性心律失常及房颤的预测价值。方法:选择103例甲亢患者进行24小时动态心电图检查及常规十二导心电图检查。根据是否合并房性心律失常的情况分为4组:A组(对照组)即单纯甲亢无房性心律失常组;B组为房早组,C组为短阵房速组;D组为阵发性房颤组。在为窦性心律时,依据常规十二导心电图测量P波时限,计算P波最大时限(Pmax),P波最小时限(Pmin)及Pd。结果:A、B两组Pmax、Pd比较均无显著差异(P>0.05),C、D组与A组Pmax、Pd比较差异有统计学意义(P<0.05);Pmax≥110ms预测房颤敏感性80%,特异性80%,阳性预测值77%;Pd≥40ms预测房颤敏感性84%,特异性83%,阳性预测值81%;Pmax≥110ms及Pd≥40ms合并预测房颤敏感性72%,特异性90%,阳性预测值88%。结论:Pmax、Pd可预测甲亢患者阵发性房颤发生,Pmax与Pd结合预测房颤的特异性和准确性更高。     

ELISA方法检测慢性心房颤动患者心房肌中SK2蛋白的表达

目的探讨慢性心房颤动患者与窦性心律患者心房组织SK2蛋白表达水平的差异。方法将22例接受体外循环手术患者常规切除的右心耳组织作为研究对象,根据心房颤动的定义将标本分为2组:窦性心律组(n=12)、心房颤动心律组(n=10),提取患者心房组织的总蛋白,采用二辛可宁酸(BCA)方法检测总蛋白浓度,应用酶联免疫吸附测定(ELISA)检测心房组织SK2蛋白水平。结果每孔上样量总蛋白为0.1mg的条件下,窦性心律组患者心房组织SK2蛋白浓度为(1.13±0.12)ng/mL,心房颤动心律组患者心房组织SK2蛋白浓度为(3.98±0.48)ng/mL,两组比较,差异有统计学意义(P<0.05)。结论慢性心房颤动患者心房肌组织SK2蛋白的表达水平明显高于窦性心律患者。     

冠心病合并房颤患者的甲状腺激素水平变化及其机制探讨

目的分析冠心病合并房颤患者的甲状腺激素水平的变化及其相关机制。方法选取冠心病患者150例,其中单纯冠心病患者80例(CAHD组),冠心病合并房颤者70例(CAHD+AF组),随机选取同期到院接受体检的健康者50例作为对照组。入院时,对两组患者进行血生化、颈动脉粥样硬化情况和甲状腺激素测定或评估。两组间计量资料比较采用t检验,计数资料比较采用2检验。结果与对照组比较,CAHD组和CAHD+AF组甲状腺激素水平、血脂、凝血功能及动脉粥样硬化厚度均明显升高。其中CAHD+AF和CAHD两组间FT4、TSH、血脂水平、凝血功和动脉粥样硬化程度均存在显著性差异(P<0.05),而两组间TT3、TT4和FT3水平差异无统计学意义(P>0.05)。结论资料显示,FT4和TSH水平的下降可诱导血脂水平上升、凝血功能增强、动脉粥样硬化加重,容易诱发冠心病合并房颤的高危现象的发生。 更多还原