2018年 · 第46卷第11期

Numerous pathological and clinical studies have shown that coronary heart disease is a phenotypically complex "broad spectrum" disease ranging from asymptomatic coronary atherosclerotic lesions to sudden cardiac death. In clinical practice, in order to prioritize and treat patients with coronary heart disease with very different manifestations, clinical classification is needed. In 1979, the World Health Organization first classified coronary heart disease into the following types based on clinical symptoms, electrocardiographic findings, and serum enzyme levels: (1) Primary cardiac arrest. (2) Angina pectoris: ① Stress angina pectoris, which is further divided into initial stress angina pectoris, stable stress angina pectoris and worsening stress angina pectoris; ② Spontaneous angina. (3) Myocardial infarction: ① acute myocardial infarction; ② Old myocardial infarction. (4) Heart failure in ischemic heart disease. (5) Arrhythmia. Over the past 40 years, the above classification has had a significant impact on clinical practice in China, but there are obvious defects: (1) the laboratory technology on which the classification relies is obsolete; (2) The pathogenesis, pathological changes, treatment methods and long-term prognosis of different types of coronary heart disease are not involved; (3) Some important clinical types such as unstable angina (UA) are ignored.

stable coronary artery disease (SCAD) is the most common clinical manifestation of coronary artery disease, and there is no accurate epidemiological data of large-scale population in China. According to statistics from the American Academy of Cardiovascular Diseases (ACC) in 2016, the incidence of SCAD is about twice that of myocardial infarction, and it is expected to reach 18% of adults in 2030^[1]However, there are still many gaps in the diagnosis and management of SCAD compared with acute coronary syndrome (ACS). Many cases fail to be correctly diagnosed, with both missed diagnosis and overdiagnosis; Inadequate drug treatment and inadequate application of secondary preventive measures; The revascularization strategy is not standardized enough. China has published "Guidelines for Diagnosis and Treatment of Chronic Stable Angina Pectoris" since 2007^[2]It has not been updated for 11 years, so a new guideline is urgently needed to guide clinical practice. Under such circumstances, the "Chinese Guidelines for the Diagnosis and Treatment of Stable Coronary Heart Disease" (hereinafter referred to as the New Guidelines), organized by experts from the Interventional Cardiology Group, the Atherosclerosis and Coronary Heart Disease Group of the Cardiovascular Disease Branch of the Chinese Medical Association, the Thrombosis Prevention and Treatment Committee of the Cardiovascular Physicians Branch of the Chinese Medical Association and the Editorial Committee of the Chinese Journal of Cardiovascular Diseases, was published in the Chinese Journal of Cardiovascular Diseases^[3]。 It is believed that this guideline will play a positive role in standardizing the diagnosis and treatment of SCAD. The new guide has the following highlights that deserve readers' attention.

With the development of China's economy, the improvement of people's living standard, the change of dietary structure and environmental factors, the incidence of cardiovascular and cerebrovascular diseases is increasing year by year, and it has become the "number one killer" that endangers national health. The key pathological basis of cardiovascular and cerebrovascular diseases such as coronary heart disease, hypertension, stroke and pulmonary hypertension is vascular remodeling caused by imbalance of vascular function and abnormal damage repair^[1]。 Homeostasis is a physiological state in which human basic physiological functions and the composition and characteristics of the internal environment are relatively dynamic and constant. The homeostatic balance of vascular functions is an important basis for the life activities of the body. Vascular remodeling is the active process of changes in vascular structure and function^[2]It is an adaptive process to maintain vascular homeostasis, and it is also a common key pathological link of many important vascular diseases.

With the progress of genetics, more and more patients with genetic diseases obtain effective information for disease diagnosis and precise treatment through genetic testing, and more and more new sequence variations are detected in clinical molecular laboratories. For monogenic diseases represented by long QT syndrome (LQTS), it is of great significance to interpret the clinical significance of mutant sequences hierarchically and clarify the pathogenicity of gene mutations. Organizations such as the American Society for Medical Genetics and Genomics (ACMG) developed a five-level classification standard for disease variants that meet Mendelian genetic characteristics in 2015^[1]This guideline was quickly adopted by the vast majority of genetic screening institutions and applied in clinical practice. Some recent studies still show that even with the application of ACMG guidelines, there is still a large inconsistency in the practice of genetic screening institutions in variant assessment^[2]。

patent foramen ovale (PFO), an open communication between the left and right atrium, is a common congenital structural abnormality of the heart, with PFO present in about 25% of healthy adults. It is generally believed that PFO has no obvious hemodynamic significance and will not cause clinical consequences. Clinicians have been exploring the possible diseases caused by PFO since 1877, when German pathologist Cohnheim first identified cases of stroke death caused by PFO and proposed the concept of paradoxical embolism. PFO can cause venous thrombosis and other embolic substances, such as air, fat, infected growth, etc., to directly enter the arterial system without being filtered by the lungs, thus leading to abnormal embolism. At present, it is believed that the clinical manifestations of PFO-related diseases are diverse, mainly unexplained stroke and migraine, but also transient ischemic attack, recumbent respiratory-orthostatic hypoxemia, unexplained dizziness and syncope, and even non-atherosclerotic myocardial infarction. With the wide application of transcranial Doppler ultrasound and transesophageal echocardiography, it becomes easier to detect PFO. At the same time, with the rapid development of cardiac interventional technology, PFO interventional occlusion has also developed rapidly because of its simple technology, high success rate and low complications. However, which patients with PFO can benefit from occlusion is a real question that neurologists and cardiovascular physicians need to answer together.

With the improvement of people's living standard and the appearance of aging population, the prevalence and mortality of cardiovascular diseases continue to increase^[1]。 In view of the growing population of patients who have become ill and those who are about to become ill, the existing medical level must be improved, but this alone is not enough to guarantee that patients can get high-quality medical services. A nationally representative study found that while the diagnosis and treatment of acute ST-segment elevation myocardial infarction (STEMI) improved, the in-hospital mortality rate of Chinese patients did not improve significantly from 2001 to 2011^[2]。 The reasons may be related to the inadequacy of treatment, treatment delay and improper application of medical measures in the secondary prevention of STEMI in the acute phase and thereafter, and also closely related to the lack of systematic evaluation and effective improvement mechanism. How to evaluate and improve the quality of medical care, improve the output efficiency of national medical and health input, and obtain the best medical outcome is a problem that national health authorities attach great importance to and need to be solved urgently.

The patient, a 75-year-old male, was admitted to the hospital on April 18, 2016 due to "sudden chest tightness and shortness of breath with repeated syncope for 14 h". Recurrent ventricular fibrillation (ventricular fibrillation) was revealed by ECG monitoring in other hospitals 14 hours ago, and "ventricular fibrillation electric storm" was diagnosed, and 39 times of electric defibrillation was performed. Physical examination: pulse 62 beats/min, blood pressure 106/61 mmHg (1 mmHg =0.133 kPa), clear breathing sounds in both lungs, no dry or wet rales; The heart boundary was not large, the heart rate was 62 beats/min, the rhythm was uniform, and no murmur was heard in the auscultation area of each valve; Soft abdomen, no tenderness, unpalpable liver and spleen. Past history: diagnosed as "arrhythmia" more than 20 years ago, the specifics are unknown, and no diagnosis and treatment were given; The history of cerebral infarction was 3 years, and the history of hypertension was 1 year. Deny history of smoking and drinking. Family history: father died of tumor, younger brother died suddenly within 1 h of playing basketball at age 35, and cousin died suddenly during a nap at age 65. Hypersensitivity troponin was 1.229 μ g/L (normal value 0-0.1 μ g/L) on admission; B-type natriuretic peptide 327.81 ng/L (normal value 0~100 ng/L); Electrocardiogram (thoracic lead high-intercostal) showing a quasi-complete right bundle branch block (CRBBB) pattern, V₁Lead J point lift 2 mm, V₂The lead J point was raised by 1 mm (Figure 1）； Echocardiography showed that the intracardiac structure and blood flow were roughly normal, and the left ventricular ejection fraction was 58%; Coronary angiography showed dominant right coronary artery with normal blood vessels and 7-segment muscle bridge of left anterior descending artery; Genetic testing revealed FGF12 c.229-7C>T heterozygous splicing variant (Figure 2）。 Admission diagnosis: ventricular fibrillation electric storm, survival of sudden cardiac death, Brugada syndrome (BrS) likelihood. The patient underwent implantable cardioverter defibrillator (ICD) surgery on 21 Apr 2016 and did not have a recurrent episode of ventricular fibrillation. Because there is no quinidine in China, the patients were given metoprolol succinate 95 mg once/d and amiodarone 200 mg three times/d after ICD. No ventricular arrhythmia occurred within 1 month of medication. On 10 May 2016 (20 d after ICD), the patient voluntarily discontinued metoprolol succinate and amiodarone.

A 46-year-old female was admitted to the hospital on 18 June 2017 due to "episodic chest tightness discomfort for 1 year, aggravated for 1.5 h". The patient developed episodic chest tightness discomfort 1 year ago, which was prone to occur after exertion or emotional agitation, lasting for several minutes, and could be relieved by itself. On December 5, 2016, I went to the doctor due to "chest tightness for 2 h", and the ECG showed ST segment elevation in the inferior wall lead<0.1 mV, creatine kinase (CK) 410 U/L, creatine kinase isoenzyme (CK-MB) 32 U/L, diagnosis of "acute inferior myocardial infarction". Coronary angiography showed no stenosis in the left main, left anterior descending and right coronary arteries, and the left circumflex artery was small, with 95% localized stenosis at the distal end. Percutaneous transluminal coronary angioplasty (PTCA) was performed, with 30% residual stenosis, and double antiplatelet therapy was given postoperatively. After discharge, the patient had excessive diet, anxiety and poor sleep. On February 25, 2017, I saw the doctor again due to "persistent chest tightness for 1 h". When I went to the emergency department, I suffered from ventricular fibrillation. After cardiopulmonary resuscitation, I was treated with mechanical ventilation in the department of critical care medicine. The patient's serum potassium was 2.87 mmol/L, troponin I 0.05 μ g/L (normal value 0-0.05 μ g/L), CK and CK-MB were normal, and ECG Ⅱ, Ⅲ, aVF, V₁~ V₆Transient ST-segment depression of the lead (suggesting spasm of the coronary artery, but not recognized at the time). The patient was diagnosed with "acute coronary syndrome, hypokalemia and ventricular fibrillation". Considering that hypokalemia induced ventricular fibrillation, no coronary angiography was repeated. He was discharged after oral administration of aspirin (100 mg/d), clopidogrel (75 mg/d), atorvastatin (20 mg/d), isosorbide mononitrate (40 mg/d) and metoprolol (25 mg, twice/d), and the hypokalemia was corrected. After discharge, I continued to use the above drugs, and I have been recuperating at home. My anxiety gradually increased, and I experienced transient chest tightness many times. 1.5 h ago, the patient had no obvious trigger to relapse chest tightness, and the symptoms did not relieve within half an hour of onset, so he was admitted to the emergency department. Previous history of hypertension 7 years, no hyperlipidemia, no smoking history. Physical examination: blood pressure 135/80 mmHg (1 mmHg =0.133 kPa); The breathing sounds of both lungs were clear, and there were no dry and wet rales; The heart rate was 56 beats/min, the rhythm was uniform, the heart sound was low and dull, and there was no murmur in the auscultation area of each valve. Electrocardiogram showed inferior wall lead ST segment oblique depression (Figure 1), troponin I, CK, and CK-MB were normal.

The patient, a 46-year-old female, was admitted to hospital on January 27, 2017 due to "chest tightness and shortness of breath for more than 1 month". At the end of November 2016, the patient began to have chest tightness and shortness of breath after exertion, occasionally waking up at night, and his activity tolerance decreased. He climbed 2 floors and had shortness of breath, occasionally palpitations, no chest pain, syncope, no fever, cough and expectoration. He went to the local hospital for treatment, considering "cardiac insufficiency", and was given symptomatic and supportive treatment (specifically unknown). The symptoms were not significantly relieved, so he went to our hospital for further treatment. He was in good health in the past and denied a history of hypertension, coronary heart disease and rheumatic heart disease. Physical examination at admission: pulse 90 beats/min, blood pressure 130/82 mmHg (1 mmHg =0.133 kPa), tall eyebrow arch, hypertrophy of ear, nose and mandible, thickened lips without cyanosis, thickened limbs, thickened interdigital joints, jugular vein distension, coarse breathing sounds in both lungs, wet rales at the base of both lungs, enlarged heart boundary to the left, heart rate 90 beats/min, uniform rhythm, no pathological murmur in auscultation areas of heart valves, and mild depressed edema in both lower limbs. Admission diagnosis: dilated cardiomyopathy, New York Heart Association (NYHA) cardiac function class III; Acromegaly?

non-ischemic cardiomyopathy (NICM) is defined as primary myocardial lesions excluding coronary artery disease and is the most common cause of non-ischemic systolic heart failure (HF)^[1,2]。 The etiology of NICM is complex and the mortality rate is high. It is reported in the literature that about 30% of them die from sudden cardiac death (SCD)^[3]。 implantable cardioverter-defibrillator (ICD) has been shown to be effective in reducing the risk of SCD in patients with NICM heart failure^[4]。 In recent years, the "Golden Triangle" drug therapy concept and the vigorous promotion of cardiac resynchronization device therapy have significantly improved the clinical prognosis of patients with heart failure^[5,6]。 Therefore, for the negative result of ICD implantation in patients with non-ischemic systolic heart failure to reduce all-cause death announced by the DANISH study in 2016, some scholars proposed: Which type of patients are the primary prevention of sudden cardiac death in non-ischemic heart failure? ICD implantation benefits the most^[7,8]。 Therefore, how to define NICM patients with high risk of sudden death and improve the efficiency of ICD in the primary prevention of such patients has been put on the agenda. This article reviews the progress of predictors of SCD in NICM (mainly non-ischemic dilated cardiomyopathy).

Atherothrombotic disease is a general term for a class of chronic arterial diseases, mainly including ischemic heart disease, ischemic stroke and peripheral arterial disease^[1]。 Among them, myocardial infarction and stroke are the leading causes of cardiovascular death in my country, and lower extremity artery and carotid artery atherosclerotic diseases are also common diseases in middle-aged and elderly people, significantly increasing the risk of death^[2]。 Multiple mechanisms are involved in the development of atherothrombotic lesions, among which the common disease process is that on the basis of atherosclerotic plaques, platelets activate, aggregate and form thrombi.

2018 marks the 100th anniversary of the birth of Professor Tao Shouqi. Medical colleagues and academic friends at home and abroad share the deep memory of the respected Professor Tao Shouqi.