Changes of thyroid hormone levels in the progression of coronary arteriosclerosis

The study concerned changes in the levels of thyroid hormones (T3, T4) and their proportional relations in the serum of peripheral venous blood of patients with ischemic heart disease (IHD) with reference to severity of coronary and myocardial insufficiency and clinical symptoms. Thyroid hormones (TH) were examined in patients with stenosing atherosclerosis of the coronary arteries with incipient angina pectoris (IAP), acute myocardial infarction (AMI), chronic IHD before and after MI and postinfarction myocardial dysfunction (PIMD) depending on severity of coronary atherosclerosis. The findings were compared to hemodynamic and metabolic myocardial parameters, severity of coronary atherosclerosis assessed at coronaroangiography. It is shown that TH concentrations depend on efficiency of coronary circulation and characteristics of myocardial metabolism. IHD patients have isometric TH levels before MI, conversion of T4 into T3 being inhibited. After MI and development of PIMD at the compensation stage T4 and T3 levels lowered under control levels. This reflects intensity and pattern of metabolic processes in the myocardium. In intact myocardial function T4/T3 in the above patients was above the control levels because of high concentration of serum T4. In development of acute coronary syndrome the level of T3 fell while that of T4 went up due to suppression of its deiodination.     

Circulating activated protein C is reduced in young survivors of myocardial infarction and inversely correlates with the severity of coronary lesions.

BACKGROUND: Cardiovascular risk factors for myocardial infarction (MI) are less frequent in younger than in older MI survivors. Therefore, the thrombotic component of MI may play a more important role at a young age. As activated protein C (APC) provides systemic anticoagulant and anti-inflammatory protection, a low plasma APC level may be an arterial thrombotic risk factor. AIM: To determine whether there is an association between reduced APC levels and early MI and severe coronary lesions. METHODS: APC was measured in 231 young MI survivors and 231 controls. RESULTS: Low APC levels were significantly associated with MI. Compared with the fourth quartile, the odds ratio (OR) for APC values in the first quartile was 3.7 [95% confidence interval (CI) = 2.1-6.4], and 3.2 (1.5-7.0) after adjustment for cardiovascular risk factors. Moreover, each decrease of 0.43 ng mL(-1) (1 SD) in APC increased the OR 1.7 times (1.4-2.2), and 1.5 times (1.2-1.9) after adjustment for cardiovascular risk factors. Low APC levels were also associated with the number of coronary arteries affected and with the severity of coronary lesions (P < 0.001). CONCLUSIONS: There is a significant association between low circulating APC levels and both early MI and the extent and severity of coronary atherosclerosis, which might be related to the anticoagulant and anti-inflammatory properties of APC.     

Brain natriuretic peptide in patients with ST segment elevation myocardial infarction. Prognostic significance

AIM: To study changes in the level of brain natriuretic peptide (BNP) in patients with ST segment elevation myocardial infarction (MI) to assess prognostic value of this marker and validity of its use as a criterion of therapy effects. MATERIAL AND METHODS: The trial enrolled 217 patients (102 males and 15 females, mean age 63.96 +/- 0.73 years) admitted to hospital on MI day 1. Plasmic level of BNP (Nt-proBNP) was measured 1, 7, 21 days, 8 weeks and 6 months after MI. RESULTS: The severity of chronic cardiac failure (CCF) correlated with peptide content in the blood: it was by 46.6% higher in patients with chronic heart failure (CHF) functional class (FC) IV than in those with CHF FC I (p = 0.047), in FC III by 27.5% higher (p = 0.003) and in FCII--by 13.1% (p = 0.485). Initially high levels of BNP correlated with early development of CHF (R2 = 0.9058), with hospital lethality (in the deceased--1040.0 +/- 65.8 fmol/ml, in the survivors--461.4 +/- 26.2 fmol/ml, r = 0.35, p < 0.001) and overall lethality. A more pronounced decrease in the peptide level was seen in patients after 3 week intake of beta-adrenoblocker esmolol than in those who did not take it (by 125.2 vs 74.1 fmol/ml, respectively, p < 0.05). By BNP level, efficacy of perindopril vs captopris was studied (group 1 and group 2, respectively), in patients with ejection fraction under 40%. Initially, BNP levels were elevated and did not differ among the groups. On MI week 8 there was a decrease in the level of BNP by 25.4% (p = 0.004), 19.1% (p = 0.06) in groups 1 and 2, respectively. Six months after MI patients of group 1 had normal levels of BNP (up to 269.6 +/- 18.3 fmol/l). CONCLUSION: Measurements of BNP levels are useful for prediction of poor prognosis in MI patients and evaluating efficacy of the treatment.     

Rapid and reversible alterations in thyroid function tests in dehydrated patients

Dehydration commonly leads to hypovolemia and hemoconcentration. Changes in thyroid hormone-binding proteins secondary to hemoconcentration profoundly affect total serum thyroid hormone concentrations. The authors sought to determine the acute effects of mild to moderate dehydration on thyroid hormone levels/thyroid function tests and its reversibility upon rehydration. Total thyroxine, total triiodothyronine, free thyroxine, and the free-thyroxine index decreased significantly after hydration, in parallel with the decrease in extra cellular fluid volume status markers. Triiodothyronine-resin uptake increased after hydration. Thyrotropin levels decreased by 8% after hydration. Hypovolemia leads to simultaneous alterations in extracellular fluid volume markers and thyroid hormone serum concentrations that reverse rapidly upon rehydration. This constitutes, by itself, a distinct and new clinical entity.     

癫痫患者甲状腺激素水平及抗癲痫药物对其影响的研究

目的:研究癫痫患者甲状腺激素水平和抗癫痫药物对甲状腺激素水平的影响以及与抗癫痫效果之间的关系。方法:测定确诊的45例未服用过抗癫痫药物的癫痫患者的血清甲状腺激素水平并与30例健康对照组进行比较。再经卡马西平、苯妥英钠、丙戊酸钠三种抗癫痫药物分组单药治疗三月、六月、一年后对甲状腺激素水平的变化及与疗效之间的关系进行现(?)。结果:未服用抗癫痫药物的癫痫患者游离甲状腺素(FT_4)水平显著低于健康对照组,经苯妥英钠、卡(?)西平分别治疗三月、六月、一年后甲状腺激素(T_4)、FT_4、游离三碘甲状腺原氨酸(FT_3)显著低于治疗前水平。经丙戊酸治疗后的不同时间段各甲状腺激素水平与治疗前无显著性差异。甲状腺激素水平的(?)化与抗癫痫效果之间似无相关性。结论:癫痫的反复发作虽不经抗癫痫药物治疗亦存在FT_4水平的降低。苯妥英钠、卡马西平可明显造成癫痫患者的亚临床甲低(T_4、FT_4、FT_3降低)。丙戊酸钠对患者甲状腺激素水平无显著影响。甲状腺激素水平的变化与疗效之间无相关性。     

Interplay of antibody and T cell responses in acute myocardial infarction

This study sought to investigate the interplay between antibody and T cell responses triggered by an acute myocardial infarction (MI) and their possible role in the progress of this disease. Serum samples were collected from two groups of patients, group A (n = 26) within the first week of MI, and group B (n = 28) at 2 weeks and 2 months after MI. Patients in group A were older and had higher prevalence of hypertension and previous attack of MI than patients in group B. The levels of anti-myosin immunoglobulin M and immunoglobulin G antibodies in the serum samples from group A were significantly higher than those in normal control subjects. In group B, the levels of both antibodies were lower than those in group A but remained significantly higher than those in normal control subjects at both 2 weeks and 2 months. The levels of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in the serum samples from group A patients were significantly higher than those in normal control subjects. At 2 weeks after MI (group B), only the level of sVCAM-1, but not that of sICAM-1, was significantly higher than that in normal control subjects, and there were no significant changes in the levels of these two molecules from 2 weeks to 2 months after MI. We conclude that the higher levels of anti-myosin antibodies and adhesion molecules in group A patients as compared with group B patients may be due to higher or more frequent exposures of their immune systems to heart antigens. Furthermore, the immunoglobulin M antibody response during the first week of MI had an inverse relationship with the level of interleukin-2R (sIL-2R), which suggested a possible suppressive or regulatory role of this antibody on the cellular immune response during this time.     

Steroids, sex hormone-binding globulin, homocysteine, selected hormones and markers of lipid and carbohydrate metabolism in patients with severe hypothyroidism and their changes following thyroid hormone supplementation.

Laboratory markers of thyroid function, selected steroid hormones, sex hormone-binding globulin (SHBG), homocysteine, prolactin, major markers of lipid- and glucose metabolism and of insular-growth hormone axes were investigated in fasting sera from 16 female patients with severe hypothyroidism after thyroidectomy because of thyroid cancer. The results obtained in severe hypothyroidism within 5-6 weeks after withdrawal of thyroid substitution therapy before control scintigraphy were compared with those obtained after correction of thyroid function. Elevated levels of homocysteine and prolactin in hypothyroidism significantly decreased after correction, while SHBG concentration increased. Correction of thyroid function led to significant changes of growth hormone and immunoglobulin F1 (decrease and increase, respectively), while insulin and proinsulin increased only insignificantly. Elevated levels of total cholesterol and triglycerides in hypothyroidism were normalized, along with a significant increase in high density lipoprotein (HDL)-cholesterol. As revealed by correlation and factor analyses, different relationships characterizing both states were found in hypothyroidism and after correction of thyroid function. A strong inverse relationship between homocysteine and free thyroid hormones confirms the effect of thyroid hormones on homocysteine metabolism. No such inverse relation was found in euthyroid state, however. Similarly, in hypothyroidism only, dehydroepiandrosterone sulfate correlated positively with immunoglobulin F1 and homocysteine and negatively with thyroid hormones and SHBG.     

Semaphorin 3A attenuates electrical remodeling at infarct border zones in rats after myocardial infarction

Electrical remodeling at infarct border zone has been shown to contribute to the occurrence of ventricular arrhythmias after myocardial infarction (MI). Electrical remodeling is causally associated with sympathetic neural remodeling in MI. Semaphorin 3A (Sema3A), a potent neural chemorepellent for sympathetic axons, has been demonstrated to suppress sympathetic neural remodeling after MI. In the present study, we investigated whether treatment with Sema3A can ameliorate electrical remodeling at infarct border zones using a rat model of MI. Wistar rats underwent sham operation (n = 20), the ligation of left coronary artery (MI group, n = 30), MI with control adenovirus (Ad group, n = 30), and MI with Sema3A adenovirus (Sema3A group, n = 30). Eight weeks after treatment, electrophysiological properties including heart rate variability (HRV), monophasic action potential duration (MAPD) and effective refractory period (ERP) and the expression of arrhythmia-related ion channel proteins including Kv4.2, KChIP2 and Kir2.1 at the infarcted border of the left ventricle were examined. These channel proteins may be required for maintaining normal heart rhythm. Compared with the Ad group, Sema3A significantly increased HRV and shortened MAPD and ERP (all p < 0.05). The expression levels of Kv4.2, KChIP2 and Kir2.1 proteins were significantly decreased in MI group and Ad group, compared to sham control. In contrast, the expression levels of these proteins were restored in Sema3A group, which may represent the molecular basis of the Sema3A-mediated inhibition of electrical remodeling. In conclusion, Sema3A can ameliorate electrical remodeling at infarct border zones after MI.     

Biologic determinants of propranolol disposition: results from 1308 patients in the Beta-Blocker Heart Attack Trial

Our objective was to identify biologic determinants of propranolol serum levels in 1308 patients after myocardial infarction (MI). Patients had had their MI within the previous month. A steady-state propranolol dosage of 40 mg every 8 hours produced a mean trough concentration of 42 ng/ml with extremely great (fiftyfold) interindividual variability. Univariate and multivariate analyses suggested that this variability was the result of many biologic factors. Serum levels were higher in women, in older patients, and in patients receiving concomitant therapy with other antiarrhythmic drugs. Serum levels were also higher in patients with elevated serum creatinine and lactate dehydrogenase levels. Serum levels were lower in black patients than in white patients. Also, serum levels in smokers were lower than those in nonsmokers, but only markedly so in the outpatient setting (6 months after the MI). The influence of sex and race on drug disposition has not previously been reported for beta-blocking drugs. Although a genetic deficiency in the oxidative metabolism of propranolol has been indicated, the frequency distribution of serum propranolol levels did not demonstrate a bimodal distribution for genetically distinct populations.     

Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction

Matrix metalloproteinase-9 (MMP-9) is prominently overexpressed after myocardial infarction (MI). We tested the hypothesis that mice with targeted deletion of MMP9 have less left ventricular (LV) dilation after experimental MI than do sibling wild-type (WT) mice. Animals that survived ligation of the left coronary artery underwent echocardiographic studies after MI; all analyses were performed without knowledge of mouse genotype. By day 8, MMP9 knockout (KO) mice had significantly smaller increases in end-diastolic and end-systolic ventricular dimensions at both midpapillary and apical levels, compared with infarcted WT mice; these differences persisted at 15 days after MI. MMP-9 KO mice had less collagen accumulation in the infarcted area than did WT mice, and they showed enhanced expression of MMP-2, MMP-13, and TIMP-1 and a reduced number of macrophages. We conclude that targeted deletion of the MMP9 gene attenuates LV dilation after experimental MI in mice. The decrease in collagen accumulation and the enhanced expression of other MMPs suggest that MMP-9 plays a prominent role in extracellular matrix remodeling after MI.     

The quantification of ADAMTS4 and 8 expression and selection of reference genes for quantitative real-time PCR analysis in myocardial infarction

Introduction

ADAMTS4 and ADAMTS8 are proteases involved in ECM proteolysis and antiangiogenesis, but little is known about their expression and function in myocardial infarction (MI). We examined ADAMTS4 and ADAMTS8 expression in a rat MI model by quantitative real-time polymerase chain reaction (qPCR) and enzyme linked immunosorbent assay (ELISA). The expressions of glyseraldehyde-3-phosphate dehydrogenase (GAPDH), beta-actin (ACTB), acidic ribosomal phosphoprotein P0 (ARBP), and ribosomal protein L13A (RPL13A) were examined in order to validate the appropriate housekeeping genes after MI.

Methods

Male Wistar rats were subjected to MI, and infarcted myocardial tissue was collected at 3, 6, 12, 24 h, 3, 7, 14 and 21 days after MI. ADAMTS4, ADAMTS8, and the four housekeeping genes were quantified using qPCR and the expression stability of the four housekeeping genes was investigated using GeNorm software. The protein levels of ADAMTS4 were detected using ELISA kits.

Results

The M values of GAPDH, ACTB, ARBP and RPL13A were 0.721, 1.2, 0.812 and 0.812 respectively. GAPDH and ARBP were ranked the most stable genes. ADAMTS4 mRNA increased at 3 h after MI, peaked at 6 h, then decreased rapidly. ADAMTS8 mRNA increased at 6 h, peaked at 24 h, remained high at 3 d, then decreased gradually. The protein levels of ADAMTS4 were significantly increased at 6 h, 12 h, 24 h and 3 d after MI.

Conclusion

The results suggest that GAPDH and ARBP are two appropriate housekeeping genes for the rat MI model. Both ADAMTS4 and ADAMTS8 mRNA levels and ADAMTS4 protein level increased, but they exhibited different expression profiles.     

Short‐term overt hypothyroidism induces discrete diastolic dysfunction in patients treated for differentiated thyroid carcinoma

Background Thyroid hormone has important effects on the cardiovascular system. The consequences of episodes of acute hypothyroidism on cardiac function have been investigated in only a few studies, and their results are inconclusive. Our objective was to investigate the effects of acute hypothyroidism on cardiac function in patients with iatrogenically induced subclinical hyperthyroidism after treatment for differentiated thyroid carcinoma. Material and methods Fourteen patients with a history of differentiated thyroid carcinoma on thyroid‐stimulating hormone (TSH)‐suppressive thyroxine replacement therapy were studied. We assessed cardiac function before, and 1 and 4 weeks after withdrawal of thyroxine substitution. We measured serum levels of free thyroxine, triiodothyronine and TSH and used a new sophisticated Doppler echocardiography technique, tissue Doppler imaging (TDI), to assess detailed and quantitative assessment of systolic and diastolic cardiac function. Echocardiographic parameters in patients were compared to controls. Results Compared to controls, patients had higher left ventricular mass and wall thickness and decreased diastolic function during TSH‐suppressive l ‐thyroxine substitution therapy. Thyroxine withdrawal resulted in a decrease in both early (E) and late (A) diastolic mitral inflow velocities, without impact on E/A ratio. Using TDI, late diastolic velocity (A′) decreased without impact on E′/A′ ratio. Left ventricular dimensions, wall thickness and mass did not change during thyroxine withdrawal. Conclusions Subclinical hyperthyroidism is accompanied by diastolic dysfunction. Subsequent acute hypothyroidism induces only subtle changes in diastolic function.     

Effects of angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade on beta-adrenoceptor signaling in heart failure produced by myocardial Infarction in rabbits: reversal of altered expression of beta-adrenoceptor kinase and G i alpha

Both angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type 1 (AT1) receptor blockers have been demonstrated to improve symptoms and prognosis in heart failure (HF). We compared the effects of ACE inhibition and AT1 receptor blockade on myocardial beta-adrenoceptor desensitization in rabbits with HF established 3 weeks after myocardial infarction (MI) with left circumflex coronary artery ligation. Rabbits with MI were randomized to no treatment, the ACE inhibitor temocapril (0.5 mg/kg/day) or AT1 receptor blocker valsartan (3 mg/kg/day). Echocardiographic examinations showed that, relative to rabbits with untreated MI, rabbits receiving temocapril or valsartan had a limitation of cardiac remodeling and prevention of the development of systolic dysfunction. Circulating plasma norepinephrine levels that were markedly elevated in MI animals were strongly inhibited by temocapril or valsartan therapy. beta-Adrenoceptor density, beta-adrenoceptor proportion showing high-affinity agonist binding, and basal and isoproterenol-stimulated adenylate cyclase activities were significantly reduced in MI rabbits. These defects were similarly reversed by temocapril or valsartan. Importantly, as found in human HF, myocardial protein levels of beta-adrenoceptor kinase 1 and G(i alpha) were significantly elevated in MI rabbits, suggesting that these molecules are contributing to the defects in myocardial beta-adrenoceptor signaling. The expression levels of these molecules were normalized equally by both treatments. The results suggest that pharmacologically different interventions in the renin-angiotensin system can equivalently improve the derangements in the beta-adrenoceptor signaling system in the failing heart. This may be important for the beneficial effects of these agents in HF.     

Effect of pre-incisional versus post-incisional infiltration of lidocaine in patients undergoing thyroid surgery

Besides subjective pain ratings, hormone responses mediated by postoperative pain might result in a negative outcome by affecting recovery or inducing the recurrence of goitre after thyroid surgery. Thus we investigated the effect of early suppression of nociceptive inputs on hormonal responses by local anaesthetic infiltration in 62 patients receiving skin and subcutaneous infiltration of 10 ml lidocaine 1% at the site of incision prior to skin incision (pre-group), or after surgery (post-group), or saline before skin incision in a prospective, double blind, randomised manner. Pain was assessed using a visual analogue scale (VAS in cm) and analgesic rescue medication over 24 hours. Plasma levels of T3, thyroid stimulating hormone (TSH), cortisol, renin and adrenocorticotropic hormone (ACTH) were measured before and after surgery. VAS scores were lower in the pre-group (2.2±0.9 cm) compared with the post-group or the control group (4.0±2.1 cm; 5.4±1.7 cm, respectively; p<0.05). Total amount of rescue medication was higher for the control group than for the pre-group or post-group (p<0.05). Analysis of plasma hormone levels showed for all groups a decrease of T3 levels postoperatively and an increase of TSH-, cortisol-, renin- and ACTH- plasma levels with no difference between the groups.We conclude that pre-incisional infiltration of lidocaine 1% results in a decrease of postoperative pain. This pre-emptive analgesic effect appears not to affect the concomitant release of plasma hormones in patients undergoing thyroid surgery.     

Serum levels of the osteoprotegerin, receptor activator of nuclear factor kappa-B ligand, metalloproteinase-1 (MMP-1) and tissue inhibitors of MMP-1 levels are increased in men 6 months after acute myocardial infarction.

BACKGROUND: Osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANKL) are critical regulators of bone remodeling and RANKL/RANK signaling could also play an important role in the remodeling process of several tissues, such as myocardium. Therefore, we investigated whether the serum concentrations of OPG and RANKL correlate with the serum levels of metalloproteinase-1 (MMP-1), MMP-9 and tissue inhibitors of MMP-1 (TIMP-1), which are known regulators of myocardial healing in acute myocardial infarction (AMI) patients. METHODS: We analyzed blood samples from 51 consecutively hospitalized men with AMI, 12 men with established ischemic heart failure (New York Heart Association category II, NYHA-II) and 12 healthy men age-matched to the NYHA-II patients. Serum levels of MMP-1, MMP-9, TIMP-1, OPG and RANKL were quantified using commercially available ELISA kits. AMI patients were sampled 4 days and 6 months after MI. RESULTS: Our data revealed increased serum levels of OPG, RANKL, MMP-1 and TIMP-1 levels and significant correlations between increased RANKL levels and MMP-1 and TIMP-1 serum levels 6 months after MI. In addition, the ratio OPG/RANKL was very low 6 months after MI, suggesting that the nuclear factor kappa-B signaling is possibly more active 6 months post-MI than it is on day 4 post-MI. CONCLUSIONS: Our data suggest that OPG, RANKL, MMP-1 and TIMP-1 serum levels can be potential mediators of myocardial healing after MI. However, further large studies are needed to confirm the utility of OPG and RANKL as markers of healing after ST elevation in MI.     

标准化甲状腺结节超声培训-考核系统的短期教学效果评估

  目的  评估应用标准化甲状腺结节超声培训-考核系统的短期教学效果。  方法  2017年12月, 面向北京协和医院超声医学科培训学员, 先采用标准化甲状腺结节超声培训-考核系统中的考核系统对学员进行考核, 考察内容为甲状腺结节超声特征识别及恶性风险分级, 然后采用该系统的培训部分对其进行相应培训, 培训后12 h和1个月分别再次采用该系统对所有学员进行考核, 系统自动记录考核得分情况, 比较培训前后得分差异。  结果  共12名学员进入本研究, 既往均接受过甲状腺疾病超声诊断的专业培训。在接受甲状腺结节超声培训后12 h及1个月, 学员考核成绩均较培训前显著提高[(80.7±7.3)分比(69.9±4.0)分, P < 0.01;(78.0±9.2)分比(69.9±4.0)分, P < 0.05], 且培训后12 h甲状腺结节各项超声特征及分级的诊断得分均较培训前显著提高(P < 0.05)。与培训后12 h相比, 培训后1个月学员考核成绩未明显下降(P > 0.05)。  结论  标准化甲状腺结节超声培训-考核系统可在短期内提高学员甲状腺结节超声诊断能力, 为推动甲状腺结节超声诊断的规范化教学提供了新思路。     

不同甲状腺术式对术后甲状腺激素水平的影响研究

目的探讨不同甲状腺术式对术后甲状腺激素水平的影响及临床应用价值。方法回顾性分析本院收治的80例双侧多发甲状腺肿瘤患者的临床资料,其中单纯腺瘤切除术(A组)24例,单侧腺叶切除术+对侧腺瘤切除术(B组)20例,双侧次全切除术(C组)19例,全切除术(D组)17例。比较各组术后甲状腺激素、皮质醇及血钙水平的变化,以及术后6个月超声复查结果。结果与术前相比,B、C组术后1个月的甲状腺激素水平有显著下降,术后3个月恢复正常;D组术后1个月、3个月甲状腺激素水平均显著下降,术后6个月内恢复正常,术后血钙水平短暂下降,但均在2周内恢复。术后6个月,A、B、C组超声复查均有部分阳性病例,而D组未见阳性病例。结论甲状腺全切除术患者术后恢复效果满意,且术后甲状腺激素水平、血钙水平异常均可调整恢复,值得推广。     

计算机辅助诊断系统在甲状腺结节超声诊断中的应用

[摘 要] 目的 评估计算机辅助诊断（Computer-aided Diagnosis ,CAD）系统在甲状腺超声检查中的诊断效能及临床应用价值。方法 选取2018年8月至2019年1月在中南大学湘雅三医院进行甲状腺超声检查并行手术切除的171例患者，共205个甲状腺结节。分别采用CAD及4名不同经验水平的超声医师对205例甲状腺结节的超声图像进行分析并根据美国放射学会（ACR）的TI-RADS指南进行分类，然后对4名不同经验水平的超声医师结合CAD也进行了研究。以手术病理结果为金标准,评估CAD系统在鉴别甲状腺良恶性结节中的诊断效能，以及CAD对不同经验水平的超声医师的影响。结果 CAD系统的使用提高了4名超声医师对甲状腺结节鉴别诊断的敏感性及AUC值(结合CAD系统vs未结合CAD系统:灵敏度：超声医师A, 93.10% vs 87.93%;超声医师B, 90.52% vs 84.48%;超声医师C, 85.34% vs 78.45%;超声医师D, 75.00% vs 66.38%，AUC值：超声医师A, 0.95 vs 0.94;超声医师B, 0.93 vs 0.92;超声医师C, 0.86vs 0.81;超声医师D, 0.86 vs 0.70)，差异均有统计学意义（P均＜0.05）。然而CAD系统的低特异性(73.03%)仅对超声医师C、D有显著性改善(P均＜0.05)。CAD系统对甲状腺恶性肿瘤的诊断敏感性与具有5年经验的超声医师相似，差异无统计学意义（P=1.00），但CAD系统的特异性较低。结论 CAD鉴别诊断甲状腺结节的敏感性较高，但特异性较低。结合CAD可有效提高初级医师甲状腺结节的超声诊断水平，也能提高高年资医师对甲状腺结节鉴别诊断的敏感性。     

Serial changes in the high-frequency ECG during the first year following acute myocardial infarction

BACKGROUND: Previous studies have shown reduced high-frequency QRS components (HF-QRS) after acute myocardial infarction (MI). The purpose of this study was to investigate serial changes in HF-QRS during the first year following acute MI. METHODS: A total of 75 patients were included. Standard- and high-frequency ECGs were recorded on five occasions during the year following the MI (a few days after the MI, after 6 weeks, and after 3, 6 and 12 months). RESULTS: There was a statistically significant increase in HF-QRS during the follow-up year (P = 0.002). There were no significant differences in HF-QRS when comparing either the infarct location or the presence or absence of reperfusive therapy. Large differences in HF-QRS were observed, both intra-individually and inter-individually, during the year. CONCLUSIONS: There was a statistically significant increase in HF-QRS during the year following acute MI.