Hyperthyroid Heart Research Articles

Anesthetic Management for Urgent Caesarean Section in Patient with Uncontrolled Hyperthyroidism and Severe Mitral Regurgitation

<p><strong>Background :</strong>The prevalence of hyperthyroidism in pregnancy approximately 0.05% to 3% and mostly caused by Graves’ Disease (GD). The prevalence of Hyperthyroid Heart Disease (HHD) in pregnancy is 3.87%. Uncontrolled hyperthyroidism during pregnancy can increase maternal and fetal mortality. We report a case of a pregnant woman with uncontrolled hyperthyroidism and severe mitral regurgitation that underwent cesarean section with spinal anesthesia for delivery.<strong></strong></p><p><strong>Case Illustration :</strong>A 33 years-old patient G4P1A2 visited the Obstetric-Gynecology outpatient clinic at our hospital at 23 weeks of gestation (WoG) due to uncontrolled hyperthyroidism caused by GD that diagnosed 3 years ago and shortness of breath. The echocardiography test obtained severe mitral regurgitation and left atrial dilatation with 58% LVEF. It was decided to maintain the pregnancy till the fetus is viable while still monitoring the patient’s condition. At 32 WoG, the patient came to the ED due to shortness of breath, chest pain, and nausea. Fetal movement and fetal heart rate (FHR) were within normal limits. The patient was given a nasal cannula at 3 liters/minute, extra furosemide 20 mg, and fetal lung maturation with dexamethasone injection. The patient was prepared for termination by cesarean section. Spinal anesthesia was performed in a sitting position using a 27 G spinal needle. Inserted at L 3-4, using a low dose of heavy bupivacaine 0.5% 7.5 mg combined with 25 g fentanyl and 0.1 mg morphine intrathecally. C-section was successfully performed and hemodynamics during surgery was stable, resulting the delivery of a preterm baby who weighed 1.9 kg at birth and the baby was transferred to the NICU for further treatment.<strong></strong></p><p><strong>Conclusion : </strong>Spinal anesthesia with low dose bupivacaine combined with opioids for cesarean section was revealed maternal and neonate safe.</p>

High triiodothyronine levels induce myocardial hypertrophy via BAFF overexpression.

Activated B cells contribute to heart diseases, and inhibition of B‐cell activating factor (BAFF) expression is an effective therapeutic target for heart diseases. Whether activated B cells participate in the development and progression of hyperthyroid heart disease, and what induces B cells activation in hyperthyroidism are unknown. The present study aimed to determine the roles of BAFF overexpression induced by high concentrations of triiodothyronine (T3) in the pathogenesis of hyperthyroid heart disease. Female C57BL/6J mice were subcutaneously injected with T3 for 6 weeks, and BAFF expression was inhibited using shRNA. Protein and mRNA expression of BAFF in mouse heart tissues evaluated via immunohistochemistry, western blotting and polymerase chain reaction (PCR). Proportions of B cells in mouse cardiac tissue lymphocytes were quantified via flow cytometry. Morphology and left ventricle function were assessed using pathological sections and echocardiography, respectively. Here, we demonstrate that compared with the control group, the proportion of myocardial B cells was larger in the T3 group; immunohistochemistry, western blotting and PCR analyses revealed increased protein and mRNA expression levels of TNF‐α and BAFF in heart tissues of the T3 group. Compared with the normal controls group, in the T3 group, the diameter of myocardial cells and some echocardiographic values significantly increased and hypertrophy and structural disorder were noticeable. Our results revealed that elevated levels of circulating T3 can promote the expression of BAFF in myocardial cells and can lead to B‐cell activation, an elevated inflammatory response and ventricular remodelling.

Research Progress of Traditional Chinese and Western Medicine in Hyperthyroid Heart Disease

In recent years, hyperthyroid heart disease has become a condition with high incidence rate and high mortality rate. This paper discusses the pathogenesis, treatment, and influencing factors of hyperthyroid heart disease from two different angles – traditional Chinese medicine and western medicine – in hope to provide a reference basis for the treatment of hyperthyroid heart disease.

CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling

Hyperthyroidism can potentiate arrhythmias and cardiac hypertrophy, whereas Ca2+/calmodulin-dependent kinase II (CaMKII) promotes maladaptive myocardial remodeling. However, it remains unclear whether CaMKII contributes to the progression of hyperthyroid heart disease (HHD). This study demonstrated that CaMKII inhibition can relieve adverse myocardial remodeling and reduce sinus tachycardia, isoproterenol-induced atrial fibrillation, and ventricular arrhythmias in hyperthyroid mice with preserved heart function. Hyperthyroid cardiac hypertrophy was promoted by CaMKII upregulation-induced HDAC4/MEF2a activation. Briefly, CaMKII inhibition benefits HHD management greatly in mice by preventing arrhythmias and maladaptive remodeling.

Association of Plasma Connective Tissue Growth Factor Levels with Hyperthyroid Heart Disease

Hyperthyroid heart disease (HHD) is one of the most severe complications of overt hyperthyroidism and increases the risk of mortality in affected patients. Early identification of patients at a higher risk of developing HHD can improve clinical outcomes through active surveillance and management. Connective tissue growth factor (CTGF), a secreted extracellular protein, plays a significant role in cardiac remodeling and dysfunction. We aimed to investigate the association between plasma CTGF level and the risk of HHD in this study. A total of 142 overt hyperthyroid patients without HHD and 99 patients with HHD were included. The plasma CTGF levels were measured using ELISA kits. Routine clinical medical data and echocardiography parameters were recorded for analysis. The plasma CTGF level was significantly higher in patients with HHD than in those without HHD (P=0.002). The plasma CTGF level was positively correlated with free triiodothyronin, tryrotropin receptor antibody, troponin I and lactate dehydrogenase levels and the left atrium diameters, right atrium diameters, and right ventricular end-diastolic diameters (all P<0.05). Logistic regression analysis showed that quartiles 3 and 4 of plasma CTGF levels were significantly associated with the increased risk of HHD (crude OR: 2.529; 95% CI: 1.188-5.387). However, after adjustment for the potentially confounding variables, quartile 4 alone was significantly associated with the higher risk of HHD relative to quartile 1. Hyperthyroid patients with HHD display higher plasma CTGF levels. Furthermore, CTGF is an independent risk factor for HHD. Therefore, the plasma CTGF level may be a potential biomarker for the risk of HHD.

Valvular Calcific Deposits and Mortality in Peritoneal Dialysis Patients: A Propensity Score-Matched Cohort Analysis

Objective: This study aimed to compare mortality between peritoneal dialysis (PD) patients with and without cardiac valve calcification (CVC). Methods: Patients undergoing PD at the dialysis center of the Second Affiliated Hospital of Soochow University from January 1, 2009, to June 31, 2016, were included and followed through December 31, 2018. The inclusion criteria were (1) age ≥18 years and (2) PD vintage ≥1 month. The exclusion criteria were (1) a history of hemodialysis or renal transplantation before PD; (2) diagnosed congenital heart disease, rheumatic heart disease, or hyperthyroid heart disease; and (3) loss to follow-up. Differences in mortality rates were compared using a Fine-Gray proportional hazards model. Results: A total of 310 patient cases were included in this study, including 237 cases without CVC (non-CVC group). The CVC group included 59 cases with aortic valve calcification (AVC), 6 cases with mitral valve calcification (MVC), and 8 cases of AVC associated with MVC. After propensity score matching, 68 pairs were selected. The multivariate competing risk regression analysis revealed that age (hazard ratio [HR]: 1.06, 95% confidence interval [95% CI]: 1.03–1.10, p < 0.001) and CVC group (HR: 1.83, 95% CI: 1.04–3.20, p < 0.05) were independent risk factors associated with mortality. No significant difference was observed in technique survival between the 2 groups. Conclusion: CVC is an independent risk factor for mortality in PD patients.

Sex impacts cardiac function and the proteome response to thyroid hormone in aged mice

BackgroundSex and age have substantial influence on thyroid function. Sex influences the risk and clinical expression of thyroid disorders (TDs), with age a proposed trigger for the development of TDs. Cardiac function is affected by thyroid hormone levels with gender differences. Accordingly, we investigated the proteomic changes involved in sex based cardiac responses to thyroid dysfunction in elderly mice.MethodsAged (18–20 months) male and female C57BL/6 mice were fed diets to create euthyroid, hypothyroid, or hyperthyroid states. Serial echocardiographs were performed to assess heart function. Proteomic changes in cardiac protein profiles were assessed by 2-D DIGE and LC-MS/MS, and a subset confirmed by immunoblotting.ResultsSerial echocardiographs showed ventricular function remained unchanged regardless of treatment. Heart rate and size increased (hyperthyroid) or decreased (hypothyroid) independent of sex. Pairwise comparison between the six groups identified 55 proteins (≥ 1.5-fold difference and p < 0.1). Compared to same-sex controls 26/55 protein changes were in the female hypothyroid heart, whereas 15/55 protein changes were identified in the male hypothyroid, and male and female hyperthyroid heart. The proteins mapped to oxidative phosphorylation, tissue remodeling and inflammatory response pathways.ConclusionWe identified both predicted and novel proteins with gender specific differential expression in response to thyroid hormone status, providing a catalogue of proteins associated with thyroid dysfunction. Pursuit of these proteins and their involvement in cardiac function will expand our understanding of mechanisms involved in sex-based cardiac response to thyroid dysfunction.

Effect of β-casomorphin-7 on myocardial hypertrophy in hyperthyroidism-induced cardiomyopathy.

The purpose of this study was to investigate the effect of β-casomorphin-7 (β-CM-7) on myocardial hypertrophy (MH) in hyperthyroidism-induced cardiomyopathy in vivo and in vitro. Thirty C56BL/6 mice were randomly divided into three groups: control group, hyperthyroidism group, and β-CM-7 treatment group. An animal model of cardiac hypertrophy of hyperthyroid heart disease (HHD) was constructed by continuous intraperitoneal injection of 100 μg of L-thyroxine (L-Thy) for 28 days, and the serum TT3 and TT4 concentrations were measured. After that, myocardial specimens were collected to measure left and right ventricular MH index, and the myocardial cell structure was observed under hematoxylin and eosin (HE) staining. Thereafter, Masson staining was adopted to determine collagen volume fraction, and hydroxylamine method was used to measure superoxide dismutase (SOD) activity, Meanwhile, DTNB direct method was applied to measure GSH-Px activity, thio-malonylurea method was utilized to measure malondialdehyde (MDA) content, and the level of reactive oxygen species (ROS) was detected by flow cytometry. Finally, the expressions of oxidative stress (OS) and inflammation-related factors in vivo and the nuclear factor-κB (NF-κB) pathway in vitro were detected by Western blot and quantitative real-time polymerase chain reaction (qRT-PCR). Compared with those in control group, TT3 and TT4 were remarkably increased, the structure of myocardial cells was disordered, the interstitial fibrosis and the ventricular MH index were significantly increased, the OS and inflammatory responses were increased, and the NF-κB pathway was activated in the Hyperthyroidism group. In the β-CM-7 group, the content of TT3 and TT4 was decreased, the myocardial cell structure was slightly disturbed, the fibrosis and the ventricular MH index were reduced, OS and inflammatory response were reduced, and the NF-κB pathway was inhibited. β-CM-7 can prevent and treat MH in mice with L-Thy-induced HHD probably through regulating the NF-κB signaling pathway.

Hyperthyroid Heart Disease With Some Comorbidities

Thyroid disease is quite common. The cardiovascular clinical manifestations of hyperthyroidism are palpitation, systolic hypertension, fatigue, or with the basis of existing heart disease, angina or heart failure. In men, the disease is more frequently to develop into congestive heart failure than in women, thus more exploration is needed. This case report discussed a 42-year-old male patient who was admitted to the emergency department due to palpitations, shortness of breath aggravated with activity and lie down position, and alleviated with resting, cough with white sputum, epigastric pain, and constipation since the past 3 days. He was diagnosed with a history of hyperthyroidism and congestive heart disease 1 year ago and routinely consumed propylthiouracil (PTU). He had a history of herniotomy 10 days before admission. The patient did not have a history of hypertension, diabetes mellitus, or hypercholesterolemia. The patient has a smoking habit of up to 3 packs/day since a teenager. The patient was diagnosed with hyperthyroid heart disease (congestive heart failure, atrial fibrillation, and coronary heart disease) with comorbid of electrolyte imbalance, hypoalbuminemia, and thrombocytopenia. The patient was treated in the Intensive Care Unit (ICU) and was given oxygen therapy, crystalloid infusion, antithyroid drug, beta-blocker, diuretics, digitalis, anti-angina, anti-thrombotic, and adjunct therapy. The patient was treated for 8 days in ICU, followed by 2 days in the ward with a good outcome. Early detection and intervention followed by close monitoring is key management for the patient with hyperthyroid heart disease, especially in a male patient, to achieve a better outcome.

Evaluation of the Effects of Schisandra chinensis on the Myocardium of Rats with Hyperthyroid Heart Disease by Using Velocity Vector Imaging Combined with the Estimation of p53 Expression and Calmodulin Activity.

Schisandra chinensis (SC) is reported to improve myocardial ischemia. Velocity vector imaging (VVI) is a noninvasive technique for evaluating myocardial function in humans, while few reported on the application in animals. In this study, we aimed to evaluate the improved effects of SC on the myocardium of Sprague Dawley rats having hyperthyroid heart disease (HHD) using VVI technique. HHD models were established by injecting daily with subcutaneous levothyroxine (0.5 mg/kg). Then, the SC group was administered the aqueous extract of SC (2 g/kg) once daily, while the HHD and control (CON) groups were administered the same amount of distilled water daily. All the rats were provided the same amount of food and water daily, and the intervention was stopped after 28 days. The efficacy of SC in HHD rats was evaluated by ultrasound VVI. The serum total triiodothyronine level, total thyroxine level, N-terminal pro-brain natriuretic peptide expression, p53 expression, and calmodulin (CaM) activity were assessed by western blotting, Hematoxylin-Eosin and Masson staining, and electron microscopy. The results indicated that SC significantly improved the systolic velocity, diastolic velocity, strain, systolic strain rate, and diastolic strain rate of the heart by significantly reducing p53 expression and CaM activity (P < 0.05), improving myocardial fibrosis in HHD rats. Also, VVI can be a valuable tool for the evaluation of myocardial function in HHD rats.

The Association of Autoantibodies in Hyperthyroid Heart Disease Combined with Pulmonary Hypertension.

Hyperthyroidism is a clinical state that results from increased thyroid hormone levels which has a significant impact on cardiac function and structure. Graves' disease is the most common cause of hyperthyroidism in iodine-replete areas. Hyperthyroid heart disease may be associated with pulmonary hypertension in patients who have overt hyperthyroidism. To investigate the association of pulmonary hypertension induced by hyperthyroid heart disease and autoantibody, one hundred and one cases with hyperthyroid heart disease who were consecutively admitted to the inpatient department of endocrinology and metabolism of the Shandong Provincial Hospital between November 2014 and April 2018 were collected and analyzed statistically. According to the Independent samples T-test, variance analysis, chi-square test, Pearson linear correlation analysis, and logistic regression, there was a good correlation between pulmonary artery systolic pressure and thyroid stimulating hormone (TSH) and receptor antibodies (TRAb) (r = 0.264, P=0.025) (OR = 1.037, P=0.029), but there was no significant correlation between the pulmonary artery systolic pressure and other thyroid-related parameters (FT3, FT4, TSH, anti-TPO, and anti-TG). Based on variance analysis, PASP rose as the level of TRAb gets higher. What is more, patients with HHD combined with PH showed a significantly higher serum level of TRAb; moreover, serum TRAb concentration was remarkably correlated with the PASP level. Therefore, TRAb participates in the process of pulmonary hypertension caused by hyperthyroid heart disease.

Hyperthyroid Phase of Hashimoto's Thyroiditis

Hashimoto thyroiditis (chronic autoimmune thyroiditis) is the most common cause of hypothyroidism in iodine-sufficient areas of the world. This condition, however, can sometimes show hyperthyroidism. A 39-year-old femalewas admitted to hospital due to shortness of breath and tremor four hours before hospitalization. There were nausea, chestpain, cold chills, and palpitation. She was diagnosed with Hashimoto's thyroiditis and routinely received tyrosol,propranolol, and dexamethasone. Physical examination showed cervical mass, afebrile, blood pressure of 130/70 mmHg,pulse rate of 110 beats/minute and respiratory rate of 20 breaths/minute. Laboratory examinations showed WBC 7.53 x 109/L, Hb 11.0 g/dL and platelet count of 168 x 109/L. Chest X-Ray: negative for infiltrates. Several laboratory testswere performed, abnormal results were as follows: FT4 level of 2.96 ng/dL (increased), TSH level of 0.003 µIU/mL(decreased), anti-TPO (antithyroid microsomal antibody) level of 306 IU/ml (increased), and IgE level of 213.6 IU/mL(increased). Peripheral blood smear, coagulation test, serum electrolytes, liver function tests, renal function tests, urinalysis,CEA and Ca 125 were within normal limits. Thyroid ultrasound was performed and showed a benign lesion. Fine needleaspiration biopsy showed lymphocytic Hashimoto's thyroiditis. Echocardiography showed hyperthyroid heart disease. Dueto an increase of anti-TPO and FT4 levels, a decrease of TSH levels and lymphocytic thyroiditis from FNAB, this patient wasdiagnosed with a hyperthyroid phase of Hashimoto's thyroiditis. Thyroid function tests and thyroid antibody tests must bemonitored to distinguish between the hyperthyroid and hypothyroid phase of Hashimoto thyroiditis.

HASHIMOTO’S THYROIDITIS HYPERTHYROID STAGE

Preliminary: Hashimoto thyroiditis (chronic autoimmune thyroiditis) is the most common cause of hypothyroidism in iodine- sufficient areas of the world, but can sometimes show hyperthyroidism. Case: A 39-year-old female was referred due to shortness of breath and tremor, four hours before hospitalization. There was nausea, chest pain, cold chills and palpitation. She was diagnosed with Hashimoto’s thyroiditis and routinely received tyrosol, propanolol and dexamethasone. Physical examination: cervical mass, afebrile, blood pressure 130/70 mmHg, pulse rate 110 x/minute and respiratory rate 20 x /minute. Laboratory examinations showed WBC 7.53 x 109/L, Hb 11.0 g/dL and platelet count 168 x 109/L. Chest X-Ray: negative for infiltrates. Several laboratory tests were performed, abnormal results were as follows: FT4 2.96 ng/dL (increased), TSH 0.003 uIU/mL (decreased), anti-TPO (antithyroid microsomal antibody) 306 IU/ml (increased), Ig E 213.6 IU/mL (increased). Peripheral blood smear, coagulation test, serum electrolytes, liver function tests, renal function tests, urinalysis, CEA and Ca 125 were within normal limits. A thyroid ultrasound resulted in a benign lesion. Fine Needle Aspiration Biopsy concluded in lymphocytic Hashimoto’s thyroiditis. Echocardiography showed hyperthyroid heart disease. Discussion: Due to an increase in anti-TPO and FT4, a decrease in TSH and lymphocytic thyroiditis from FNAB, this patient was diagnosed with Hashimoto’s Thyroiditis Hyperthyroid Stage. Conclusion: Thyroid function tests and thyroid antibody tests must be monitored to decide whether it is hyperthyroid or hypothyroid stage of Hashimoto thyroiditis.

Hyperthyroid heart disease in pregnancy: Retrospective analysis of a case series and review of the literature.

BACKGROUNDHyperthyroidism in pregnancy may pose a great threat to maternal and fetal health. The risk of hyperthyroid heart disease (HHD), even heart failure, is significantly elevated in pregnant women.AIMTo investigate the clinical characteristics, prognosis, and therapy of HHD in pregnant women.METHODSWe searched the patient registry data at West China Second University Hospital of Sichuan University in Chengdu, China, following the approval by the Ethics Committee. We retrospectively analyzed the clinical characteristics of pregnant women diagnosed with HHD. The medical records of women with HHD during pregnancy from January 2012 to December 2017 were obtained from the electronic medical records system. All the included patients were followed in outpatient clinics and by telephone interviews until October 2018.RESULTSA total of 155 patients were diagnosed with thyrotoxicosis, of whom six were diagnosed with HHD. Three of them had regular antenatal care. Two patients were complicated with acute heart failure attacks, and one of them had a stillbirth. Both of these patients had a long history of Graves’ disease with poor treatment compliance. Treatments of precipitating factors such as the control of infection could relieve the symptoms and prolong gestation for a better prognosis. Hyperthyroid heart failure could be controlled with aggressive diuretics and management of the coexisting complications. Intense monitoring and timely anti-heart failure treatment were crucial in patients with severe cardiac damage. Our findings indicated the importance of regular antenatal care and treatment adherence in patients with hyperthyroidism.CONCLUSIONThe timely and accurate diagnosis of HHD and the implementation of effective management are important for a better prognosis in pregnant women with HHD. Improvement in patients’ awareness of thyrotoxicosis is needed.

Abstract 265: Thyrotoxic Pericarditis in a Mouse Model of Graves' Disease

Objectives: To investigate the cardiac pathological changes of hyperthyroid heart disease in mice. Methods: A transient model for human Graves’ disease was successfully established in mice using three immunizations with recombinant adenovirus expressing the extracellular A subunit of the human thyrotropin receptor (Ad-TSHR). We induced the hyperthyroid heart mouse model by prolonging the regular injections of Graves’ disease mouse model to nine months. Heart tissues were weighed and stained with hematoxylin-eosin (HE) and MASSON Trichrome staining to check and define the pathological changes. Results: We observed that mice in the Graves’ disease hyperthyroid heart group (GH) showed enhanced cardiac hypertrophy and fibrosis. The HW/BW (ratio of heart weight to body weight) of GH group (5.528±0.4014, n=6) was significantly higher than control group (4.343±0.03913, n=6) (P&lt;0.05). In GH group, 2 of 6 hearts showed typical cor villosum (Image 1). The MASSON Trichrome staining exhibited aggravated cardiac fibrosis on the surface of the heart in GH group. Conclusions: Pericarditis as a complication of thyrotoxicosis has been reported several times in clinical work. This is the first reported case of pericarditis in the mouse model of Graves’ disease, suggesting a possible link between pericarditis and thyrotoxicosis.

Clinical efficacy and safety of traditional Chinese patent medicine for hyperthyroid heart disease: study protocol for a systematic review and meta-analysis.

Hyperthyroid heart disease (HHD), one of the most common complications of hyperthyroidism, is a serious public health problem due to the direct toxic or indirect effects of excessive thyroid hormone on the heart, resulting in high mortality and increasing health care costs. Traditional Chinese patent medicines (TCPMs), developed by combining modernized pharmaceutical technologies with ancient TCM theories, have been widely used in the treatment of HHD. However, the safety and efficacy of TCPMs used in patients with HHD has been uncertain and there has been no standard clinical trial published to confirm this. Thus, we conduct a study to evaluate the safety and efficacy of TCPMs for HHD. The reference lists of randomized controlled trials and 8 electronic databases will be independently and systematically searched by 2 review authors in August 2018. Four English databases [EMBASE, PubMed, National Guideline Clearinghouse (NGC), and Cochrane Central Register of Controlled Trials (CENTRAL)] and 4 Chinese databases [Chinese Biomedical Literature Database (CBM), Chinese National Knowledge Infrastructure [CNKI], Wanfang Database, and VIP Database] will be included. The primary outcomes will be assessed according to the effective rate of treatment, electrocardiogram, and thyroid hormone levels. Data synthesis will be precisely computed using the RevManV5.3 software when a data-analysis is allowed. Methodological quality will be assessed according to Cochrane Handbook. This study will provide a high-quality synthesis of current evidence of TCPMs for HHD from different aspects, including the clinical symptoms, thyroid hormone levels, and ECG changes. The conclusion of this systematic review will provide evidence to prove whether TCPMs are effective therapeutic intervention for patient with HHD.

Method selection and perioperative management of termination of pregnancy during the first and second trimester of pregnancy with severe cardiovascular disease

Objective: To summarize and analyze the methods of termination of pregnancy in the first and second trimester of pregnancy with severe cardiovascular disease. Methods: A retrospective analysis of 27 cases of termination of pregnancy in the first and second trimester of pregnancy in Beijing Anzhen Hospital from January 1, 2016 to December 30, 2017. All of these pregnant women were pregnancy complicated with severe cardiovascular disease in grade Ⅴ pregnancy risk. Results: (1) The age of 27 pregnant women was 22-40 years, gestational age was 6-27 weeks; cardiac function grade before induced labor was: 5 cases of grade Ⅱ, 15 cases of grade Ⅲ, 7 cases of grade Ⅳ. The cardiovascular diseases included ventricular septal defect in 9 cases, simple atrial septal defect in 3 cases, patent ductus arteriosus in 2 cases, tetralogy of Fallot in 2 cases, rheumatic valvular disease in 1 case,arrhythmia-paroxysmal atrial velocity in 2 cases, cardiomyopathy in 2 cases, hypertensive cardiopathy in 2 cases, primary pulmonary hypertension in 1 case, tissue disease complicated with pulmonary hypertension 1 case, hyperthyroid heart disease in 1 case, coronary heart disease in 1 case. Among them, 21 cases were complicated with pulmonary hypertension, and 5 cases with Eisenmenger syndrome. (2) Methods of termination of pregnancy: in 27 cases, eight cases of vacuum curettage, and 2 cases of forceps curettage under general anesthesia without intubation; rivanol intraamniotic induction of labor in 1 case; and hysterotomy delivery in 16 cases (11 cases were treated with continuous epidural anesthesia, 1 case was treated with combined spinal and epidural anesthesia, 4 cases were treated with spinal anesthesia) . (3) After termination of pregnancy, one patient with severe primary pulmonary hypertension at 19 weeks of gestation died on the 1st day postoperative. No significant changes in cardiac function were observed in other patients before and after termination of pregnancy, and all of them survived. Conclusions: In patients with severe cardiovascular disease, termination of pregnancy after pregnancy may result in maternal death even at the second trimester of pregnancy.It is strongly recommended that such patients undergo pre-pregnancy assessment and fertility counseling.If visiting doctor after pregnancy, we should organize a multidisciplinary consultation as soon as possible to assess the risk of continuing pregnancy and give medical advice. If the risk of pregnancy is high, we should terminate the pregnancy as early as possible, after making a suitable treatment plan. During termination of pregnancy, temporary or permanent contraception may be taken if the condition permits.

Size dependent effects of Gold Nanoparticles in ISO-induced Hyperthyroid Rats

In this study, we applied different sizes of gold nanoparticles (Au-NPs) to isoproterenol (ISO)-induced hyperthyroid heart disease rats (HHD rats). Single dose of 5, 40, 100 nm Au-NPs were injected intravenously. Cardiac safety tests were evaluated by cardiac marker enzymes in serum and cardiac accumulation of Au-NPs were measured by ICP-MS. Our results showed that size-dependent cardiac effects of Au-NPs in ISO-induced hyperthyroid rats. 5 nm Au-NPs had some cardiac protective effect but little accumulation in heart, probably due to smaller size Au-NPs can adapt to whole body easily in vivo. Histological analysis and TUNEL staining showed that Au-NPs can induce pathological alterations including cardiac fibrosis, apoptosis in control groups, however they can protect HHD groups from these harmful effects. Furthermore, transmission electron microscopy and western blotting employed on H9C2 cells showed that autophagy presented in Au-NPs treated cells and that Au-NPs can decrease LC3 II turning to LC3 I and decrease APG7 and caspase 12 in the process in HHD groups, while opposite effects on control groups were presented, which could be an adaptive inflammation reacts. As there are few animal studies about using nanoparticles in the treatment of heart disease, our in vivo and in vitro studies would provide valuable information before they can be considered for clinical use in general.

Forensic Analysis of 6 Cases of Sudden Death due to Hyperthyroid Heart Disease

To analyse the cases of sudden death due to hyperthyroid heart disease, and explore the general information of deaths and the forensic pathological characteristics to provide reference evidence for forensic identification of such cases. Six cases of sudden death due to hyperthyroid heart disease between 2001 and 2016 were selected from School of Forensic Medicine, China Medical University. The general information （gender and age）, clinical manifestations, medical history, anatomical and histopathological findings, biochemical parameters and cause of death were analysed retrospectively. Most of the 6 patients had definite history of hyperthyroidism, and they all showed certain degrees of symptoms of cardiovascular disease; had obvious incentive factors of death; histopathological examination of thyroid conformed to the performances of diffuse toxic goiter; with increase of cardiac weight, dilatation of cardiac chambers, myocardial hypertrophy and focal necrosis; postmortem biochemical analyses of pericardial fluid could be used as an additional method for diagnostic of sudden death due to hyperthyroid heart disease. The identification of death due to hyperthyroid heart disease should be based on the clinical history and the results of autopsy, histopathological examination, postmortem toxicology tests. The postmortem biochemical detection of thyroid and cardiac function should be performed if necessary.

Neonatal hyperthyroidism on rat heart: interrelation with nitric oxide and sex.

To clarify the mechanism mediating the effect of hyperthyroidism on cardiac function during the second month of life in rats. Male and female Sprague-Dawley rats were assigned to a control or to a triiodothyronine (T3)-treated group. Treatment of each group was started on the third day after birth. Control rats (Eut) received 0.9 NaCl [0.1ml/100g body weight (BW)] every second day during 60days and T3-treated rats (Hyper) received subcutaneous (SC) T3 injections every second day during 60days. Hyperthyroidism decreased left ventricle volume only in male rats. Female euthyroid rats presented higher atrial nitric oxide synthase (NOS) activity than male rats and hormonal treatment decreased this enzyme's activity in both sexes. Euthyroid male and female rats had similar atrial NOS protein levels, but females had higher caveolin (cav) 3 protein levels. T3 treatment increased this protein only in males. Female rats had lower ventricular NOS activity than male rats; hyperthyroidism increased NOS activity in both sexes but this effect was associated with lower cav 3 protein levels. Hyperthyroidism did not change cav 1 protein levels in both male and female rats. The results of this study demonstrating clinically relevant sex-related differences in the pathophysiology of the hyperthyroid heart have raised new questions regarding the mechanisms responsible for the observed differences. This study suggests that sex-related intrinsic factors such as nitric oxide may modulate the response to hyperthyroidism that leads to cardiovascular dysfunction.