2018年 · 第46卷第08期

The value of academic research lies in the scientific pursuit of truth and discovery of truth. The free communication of academic information, which is composed of the interconnection and communication between scientific and technological workers, is the lifeline of academic research and academic innovation. Therefore, carrying out high-level, comprehensive and open academic conferences not only provides a good academic innovation environment for scientific and technological workers, but also builds an academic exchange platform that keeps pace with the times for peers to communicate, comment, communicate and gradually form consensus, and plays a positive role in promoting the development of disciplines.

Thromboembolic complications are the main cause of disability and death in atrial fibrillation (AF). Preventing embolic events in patients with AF is an important issue in the treatment of AF. Oral anticoagulants are the most effective methods to prevent thromboembolic complications of AF at present. However, in the era of non-vitamin K antagonist oral anticogulants (NOAC), there is still a significant proportion of patients with atrial fibrillation with anticoagulation indications who do not take oral anticoagulants or have poor compliance. At the end of follow-up in several large randomized controlled studies related to NOAC, the proportion of NOAC discontinuations was greater than 20%. Similarly, retrospective data from the U.S. Business Insurance Database shows that (n=64 661), only 47.5% of patients with atrial fibrillation taking NOAC maintained good compliance at 1-year follow-up (the number of days taken covered more than 80% of the follow-up time)^[1]。 In addition, although NOAC significantly reduces the incidence of severe bleeding complications such as intracranial hemorrhage, it can not be ignored for patients who need to take dual antiplatelet therapy at the same time, have severe renal insufficiency, refractory hypertension, high risk of falls, and previous severe bleeding. Patients with clinical conditions, the bleeding risk of NOAC cannot be ignored. Left atrial appendage occlusion is undoubtedly an important complementary means to prevent embolism in these patients.

Percutaneous left atrial appendage occlusion has been rapidly popularized in some areas in recent years, and controversies about its clinical effect and potential drawbacks have always existed. Intriguingly, the author, as the first surgeon to successfully implement left atrial appendage occlusion in China, is now regarded as a "hinder" of this technology^[1]。 In fact, for one of the few special new therapies in the history of human medical care that permanently removes the normal structure of the human body to indirectly achieve the therapeutic purpose, we only call for strict control of the indications. Therefore, it is necessary to conduct a rational and objective examination of this technology according to relevant research evidence.

Atrial fibrillation (AF) is one of the fastest growing areas of cardiovascular discipline. In recent years, in addition to the updating of therapeutic drugs and therapeutic concepts, the technology is changing with each passing day. Left atrial appendage occlusion has developed rapidly worldwide since its clinical application in 2001, and has been recommended by several international guidelines as an effective alternative to anticoagulant therapy for the prevention of atrial fibrillation stroke. However, this emerging cutting-edge technology has always been questioned since its birth. Is this technology scientific or not? Is it feasible to prevent stroke in atrial fibrillation? This needs to be scientifically analyzed from the perspectives of harm of atrial fibrillation, limitation of anticoagulation therapy of atrial fibrillation, theoretical basis of left atrial appendage occlusion, technical feasibility and value of stroke prevention.

A 33-year-old female complained of "cardiac murmur found for more than 30 years". The patient had excessive sweating, emaciation, history of recurrent pneumonia, no obvious dyspnea, cyanosis of the lips, and could tolerate general physical activity in childhood. After 10 years of age, physical strength began to decrease, slight cyanosis of the lips could be seen after cold or fatigue, and the number of pneumonia infections was significantly reduced; Subsequently, the activity tolerance was further reduced, and shortness of breath occurred after jogging for 100 m. He could only engage in minor physical labor, and he could fall asleep in a lying position at night without obvious discomfort such as holding his breath, coughing, hemoptysis and chest pain. In 2013 (when the patient was 31 years old), he had a cardiac ultrasound examination in Wuhan Asia Heart Hospital and was diagnosed with "giant ventricular septal defect (VSD) and severe pulmonary hypertension (PH)". The doctor suggested that he had lost the indication for surgery and recommended conservative treatment with targeted drugs for pulmonary hypertension.

A 71-year-old male was admitted to the hospital on May 9, 2016 due to "episodic chest tightness for 26 years and fatigue for 1 week". Ectopic heart transplantation was performed 9 years ago for ischemic cardiomyopathy. Three-dimensional CT reconstruction of the heart after admission showed that the recipient's heart was in normal position, and the donor's heart was located on the right side of the recipient's heart and had atrophy (Figure 1）。

A 64-year-old male was admitted to the hospital on 4 January 2017 mainly due to "paroxysmal chest pain for 7 years, 1 month after CPR". The patient began to have chest pain after brisk walking 7 years ago, which could be relieved by 4-5 minutes of rest, and the symptoms could be improved by nitrate treatment. Three months ago, I had a sudden sensation of pharyngeal tightness and sweating during sleep, which lasted for 1 h without relief. I went to a hospital and checked for elevated serum myocardial necrosis markers. I was diagnosed as "coronary heart disease, acute non-ST-segment elevation myocardial infarction". During the visit, ECG monitoring showed ventricular tachycardia (ventricular tachycardia), and it turned to sinus rhythm after electrical cardioversion. After 9 days, coronary angiography showed three-vessel lesions, and a stent was placed in the distal right coronary artery. After discharge, regular drug treatment showed no attack of chest pain. Three weeks after operation, the patient suffered from chest tightness, sweating and transient loss of consciousness during sleep. He went to a hospital. The electrocardiogram showed sinus rhythm, pathological Q wave in Ⅱ, Ⅲ and aVF leads, V₃~ V₆The patient had repeated ventricular tachycardia and ventricular fibrillation (ventricular fibrillation) with depression of the lead ST segment. The ventricular tachycardia was terminated after multiple electric defibrillation and drug therapy. After the treatment, the patient was transferred to our hospital after the hemodynamic stability. History: Hypertension for 18 years, oral bisoprolol 5 mg once daily, nifedipine controlled-release tablets 30 mg twice daily, valsartan 80 mg once daily, blood pressure controlled at 160/80~90 mmHg (1 mmHg =0.133 kPa). Chronic renal insufficiency for 10 years. Two years ago, he underwent arteriovenous fistula of left radial artery-guigao vein and started regular hemodialysis treatment. Hyperlipidemia for 4 years, oral atorvastatin 20 mg once nightly. Physical examination at admission: body temperature 37.1℃, pulse 62 beats/min, breathing 20 beats/min, blood pressure 173/72 mmHg, clear, palpable tremor at left arteriovenous fistula, left jugular vein full, clear breathing sounds in both lungs, small heart boundary, heart rate 62 beats/min, uniform rhythm, grade 2/6 systolic murmur can be heard at the apex of the heart, soft abdomen, no tenderness, and no swelling in both lower limbs. Laboratory tests: Hemoglobin 82 g/L (reference interval 130-175 g/L), hypersensitivity troponin 0.089 μ g/L (reference interval 0-0.024 μ g/L). Echocardiography: left atrial anteroposterior diameter 44 mm, left ventricular end-diastolic diameter 61 mm, left ventricular diastolic function decreased, left ventricular ejection fraction (LVEF) 51%. Venous ultrasound of both upper limbs: The flow velocity of left axillary vein and subclavian vein was significantly higher than that of right axillary vein and subclavian vein.

A 26-year-old male was admitted to the hospital on 13 August 2016 due to "sudden retrosternal pain for 4 h". The patient suffered from sudden retrosternal squeezing pain at 6: 00 am on August 13, 2016, which persisted without relief, accompanied by sweating, chest tightness, shortness of breath, nausea and vomiting, and the vomit was stomach content. He went to the emergency department of our hospital at 10: 00. Physical examination: blood pressure 99/72 mmHg (1 mmHg =0.133 kPa), pulse 122 beats/min. The breathing sounds of both lungs were thick, and no dry or wet rales were heard. The heart rate was 122 beats/min, the heart rhythm was uniform, the heart sounds were normal, and no murmur or additional heart sounds were heard in the auscultation area of each valve. Soft abdomen, no tenderness, no buckle pain in kidney area. There was no edema in both lower limbs. ECG showed sinus tachycardia, V₁~ V₅Lead ST segment elevation, diagnosis of acute extensive anterior wall myocardial infarction (Figure 1）。 At 10:10 a.m., the patient suffered from sudden loss of consciousness and convulsions. ECG monitoring showed ventricular fibrillation. After 200 J asynchronous defibrillation, the patient reverted to sinus rhythm. The patient was in prior health and had no history of hypertension, family history of cardiovascular disease and renal disease. The history of smoking was about 10 years, with an average of 20 cigarettes/d. Emergency laboratory test: blood routine showed platelet count 371×10⁹/L (reference value is 100~300×10⁹/L), white blood cell count 23.51×10⁹/L (reference value is 4.00~10.00×10⁹/L), hemoglobin 181.0 g/L (reference value is 120.0~160.0 g/L), neutrophil percentage 89.8% (reference value is 50.0% ~70.0%); Hypersensitive cardiac troponin I 0.07 ng/L (reference value: 0.01-0.02 ng/L), myoglobin>900 μ g/L (reference value: 23-112 μ g/L), creatine kinase isoenzyme (CK-MB) 27 μ g/L (reference value: 2-7.2 μ g/L); Blood urea 6.10 mmol/L (reference value: 3.20-7.10 mmol/L), creatinine 56.85 μ mol/L (reference value: 58.00-110.00 μ mol/L); Fibrinogen quantification was 4.34 g/L (reference value was 2.00-4.00 g/L), thrombin time was 13.4 s (reference value was 15.8-24.9 s); Potassium ions were 4.80 mmol/L (reference values were 3.50-5.10 mmol/L) and magnesium ions were 0.77 mmol/L (reference values were 0.70-1.00 mmol/L).

The role of dabigatran etexilate as non-vitamin K antagonist oral anticoagulants (NOAC) in stroke prevention in patients with non-valvular atrial fibrillation has been demonstrated in clinical trials and in the real world^[1,2]。 Although the efficacy and safety of dabigatran etexilate are also recognized in the Chinese population^[3]However, when the patient experiences uncontrolled bleeding or needs to undergo emergency surgical treatment, a reversal agent is needed to counteract the effect of anticoagulants. With the approval of idarucizumab in the United States and the European Union, dabigatran etexilate became the first NOAC with a specific reversal agent, marking a new stage of anticoagulant therapy.

Hereditary ventricular arrhythmias are a large class of primary electrocardiac disorders with familial aggregation tendency and clinically manifested as malignant arrhythmias. It is often accompanied by syncope or sudden death with normal heart structure, mainly autosomal dominant inheritance. It mainly includes long QT syndrome (LQTS), Brugada syndrome (BrS), catecholaminergic polymorphic ventricular tachycardia (CPVT), short QT syndrome (SQTS) and early repolarization syndrome (ERS). In recent years, it has been found that there are certain gender differences in the epidemiology, electrophysiological mechanism, clinical characteristics and treatment of hereditary arrhythmias. Differences in sex hormone levels can lead to differences in cardiac electrophysiological parameters in patients of different genders. For example, compared with men, women have faster resting heart rate, longer QT interval, corrected QT interval, ventricular action potential duration and ventricular refractory period, but their PR interval, AH interval, atrial and atrioventricular node refractory period and QRS interval are all shorter. Among all hereditary arrhythmias, sex differences are particularly significant in LQTS and BrS. In this paper, the epidemiology, electrophysiological mechanism, clinical characteristics and gender differences in the treatment of related hereditary arrhythmias are briefly reviewed, so as to seek more effective individualized treatment methods and improve the prognosis of patients in future research.

Cardiovascular and cerebrovascular diseases seriously endanger human health, among which the impairment of vascular function is one of the common mechanisms of many cardiovascular and cerebrovascular diseases. Numerous studies have shown that ion channels are widely involved in the regulation of vascular function^[1]But its specific mechanism is not fully understood. High conductance calcium-activated potassium channel (BK channel) is one of the most important potassium channels in vascular smooth muscle cells^[2]Activation of the BK channel can cause vasodilation^[3]。 In recent years, it has been found that BK channel is structurally coupled with various calcium ion channels and forms a functional complex, which plays an important role in vascular function regulation^[4,5,6,7]。 Based on the introduction of BK channel and calcium channel, the influence of BK channel/calcium channel complex in vascular smooth muscle cells on vascular function and its mechanism are emphasized in this paper, in order to provide ideas for finding new targets for the treatment of cardiovascular and cerebrovascular diseases.

sudden cardiac death (SCD) refers to sudden and unexpected death caused by various cardiac causes; Death occurred within 1 h of onset of symptoms^[1], can occur in all age groups. Compared with patients with severe organic heart disease, although the sudden death rate of the general population is low, the population base is large. The number of SCD in China is more than 540,000 every year, and the prevention task of SCD in the general population is arduous. The age range of SCD in adolescents is 3 to 25 years old^[2]。 Most of the patients had no history of recurrent heart disease; Before the onset of the disease, it is often asymptomatic or the symptoms are mild and easily ignored; Sudden death can occur minutes or less after the onset of symptoms; The first symptom is SCD or cardiogenic syncope, which is easily misdiagnosed (such as epilepsy and other causes of syncope). Juvenile SCD is an interdisciplinary disease, involving cardiology, pediatrics, neurology and even genetics and metabolism. High mortality and low success rate of resuscitation, which seriously threaten the life of adolescents and often bring serious adverse effects to families, schools and society. Most adolescents with SCD can find high-risk groups through screening; Patients and family members with genetic background should be validated, diagnosed early, individualized risk stratified, and prevented and treated early. Clinically, we should avoid simply attributing the cause of sudden death to "overwork" and other triggers, and neglect the diagnosis of the primary disease, especially the screening and treatment of high-risk family members of sudden death related to genetics. Correct evaluation and treatment can bring long-term survival benefits to patients, which is of great significance.

In 2015, I saw such a case in Fuwai Hospital. At first, it had no characteristics from the clinical manifestations, but it was very strange and rare from the heart taken off by transplantation. We consulted domestic and foreign literature and rarely reported it, and through review, pursuit and discussion, we got many useful inspirations. The pathological characteristics and the pathological basis of the clinical manifestations of this case can be seen from the clinical and pathological aspects in turn, and the reason why the clinical manifestation of this case is restrictive cardiomyopathy can be explained from the lesion site. After step-by-step analysis, the source of the disease can be traced down.