2017年 · 第45卷第09期

After more than 40 years of hard work, Chinese Journal of Cardiovascular Diseases, founded in 1973, has developed into a well-known professional journal in the cardiovascular field in China, with many readers and wide academic influence. Looking back on my growth path, it is inseparable from the cultivation of Chinese Journal of Cardiovascular Diseases. From my relationship in 1990, my first research paper in this journal to my review in June 2016, Chinese Journal of Cardiovascular Diseases has been cultivating and accompanying me for 27 years. From a reader, author to editor, Chinese Journal of Cardiovascular Diseases has become my learning platform and development stage.

hypertrophic cardiomyopathy (HCM) is a primary cardiomyopathy with increased myocardial weight, especially asymmetric, diffuse or segmental left ventricular abnormal hypertrophy as typical changes, which can eventually lead to cardiac pumping dysfunction and electrocardiac disorder. The incidence rate of HCM is about 0.2%, which is one of the important causes of sudden death, heart failure and atrial fibrillation (AF) in adolescents and athletes^[1]。 Atrial fibrillation is the most common persistent arrhythmia in HCM patients. Studies have found that 2% to 3.8% of HCM patients are newly diagnosed with atrial fibrillation every year, which increases the risk of heart failure, stroke/embolism and death in such patients, especially when there is left ventricular outflow tract obstruction^[2]。 Left ventricular filling in HCM patients mainly depends on atrial contraction. Because atrial fibrillation will shorten the left ventricular filling time and impair left ventricular diastolic function, HCM patients have poor tolerance to atrial fibrillation, which leads to frequent hospital admission and decreased quality of life. Therefore, it is very important to do a good job in clinical management of HCM complicated with atrial fibrillation. This article summarizes the epidemiology, risk assessment, prognosis and clinical management of HCM patients with atrial fibrillation.

Sarcoidosis is a multisystemic, granulomatous disease that is common in women aged 25 to 60 years (70%) and rarely in people aged under 15 and over 70 years^[1,2]。 Sarcoidosis is also a worldwide disease, with a prevalence of (4.7-64) /100 000, with the highest prevalence in Japan, northern Europe and black areas in the United States^[2,3]The relevant statistics in China are still unclear. Increasing evidence suggests that sarcoidosis may be caused by the interaction of genes and the environment, that is, the immune response induced by unknown antigens in genetically sensitive individuals^[3]。 The clinical characteristics of cardiac sarcoidosis (CS) depend on the site, extent and activity of the disease. The typical clinical manifestations are conduction block, ventricular arrhythmia and heart failure. About 5% of patients with sarcoidosis have obvious symptoms of cardiac involvement, and 20% to 25% of patients present with asymptomatic cardiac infiltration^[4]。 Earlier studies attributed 85% of sarcoidosis deaths to CS^[5]。 There are also autopsy results that the clinical missed diagnosis rate of patients who eventually died of CS is more than 50%^[6]。 With the increasing prevalence of CS^[7]Its early diagnosis and treatment are particularly important.

Myocarditis refers to the impairment of cardiac function caused by myocardial inflammatory injury caused by various causes, including reduced systolic and diastolic function, and arrhythmias^{[1,2,3,4,5,6]}。 The etiology includes three categories: infection, autoimmune disease and toxin/drug toxicity, among which infection is the main cause of disease, and viruses are the most common pathogens, including enterovirus (especially Coxsackie B virus), adenovirus, cytomegalovirus, Epstein-Barr virus and influenza virus. Clinically, it can be divided into acute phase, subacute phase and chronic phase. The acute phase usually lasts for 3~5 days, mainly caused by virus invasion and replication to damage myocardium; Immune response is the main pathophysiological change in subacute phase; A small number of patients enter the chronic phase, presenting with chronic persistent and sudden aggravation of inflammatory activity, weakened myocardial contractility, myocardial fibrosis, and cardiac enlargement^[4,5,6]。 The clinical manifestations of common acute myocarditis vary greatly. Most of them are manifested as slight chest tightness and palpitations after activity. In severe cases, acute left ventricular failure or even sudden death can occur. Therefore, individualized treatment is needed according to the severity of the disease.

A 66-year-old female was admitted to the hospital on 11 July 2016 due to "sudden syncope for 1 d". The patient experienced dizziness and vision rotation after emotional agitation, followed by loss of consciousness, which lasted for 1 to 2 minutes and recovered spontaneously, and accompanied by fatigue after consciousness. No chest pain, chest tightness and sweating, no radiating pain and palpitations, no limb twitching and incontinence. Previous history of type 2 diabetes for 1 year, control diet, blood sugar control can. History of hypertension, coronary heart disease and cerebrovascular disease is denied. Deny smoking and drinking habits. Admission physical examination: body temperature 36.5 ℃, breathing 17 times/min, pulse 55 times/min, blood pressure 123/66 mmHg (1 mmHg =0.133 kPa), body mass index 22.3 kg/m²。 Conscious. No carotid murmur was heard. The breathing sounds of both lungs were clear, and no dry and wet rales were heard. Percussion heart turbidity sound boundary is not large, heart rate is 55 beats/min, rhythm is uniform, heart sound is strong, P2<A2, no murmur was heard in the auscultation area of each valve. The abdomen is soft, and the liver and spleen are not palpable under the right rib. There was no edema in both lower limbs. Emergency ECG showed Ⅱ, Ⅲ, aVF and V₁~ V₆The lead T wave is deeply collapsed and the QT interval is prolonged (Figure 1)； Troponin I was 0.53 μ g/L, creatine kinase isoenzyme (CK-MB) was 10.1 μ g/L, and N-terminal B-type pronatriuretic peptide (NT-proBNP) was 2 586 ng/L. The initial diagnosis was acute non-ST segment elevation myocardial infarction, and aspirin and clopidogrel were given antiplatelet therapy, atorvastatin calcium tablets were given anticoagulation therapy for lipid reduction, plaque stabilization and low molecular weight heparin.

Heart failure (heart failure) is the terminal stage of many cardiovascular diseases. "China Cardiovascular Disease Report 2013" proposes that the number of cardiovascular diseases in China is on the rise, and cardiovascular deaths account for the first cause of total death among urban and rural residents. Epidemiological studies show that 40% to 60% of patients with heart failure have heart failure with preserved ejection fraction (heart failure with preserved ejection fraction, HFpEF)^[1]Current standard treatment regimens for heart failure can significantly benefit patients with heart failure with reduced ejection fraction (HFrEF), but do not reduce hospitalization and mortality in patients with HFpEF^[2]。 Brouwers et al.^[3]It is expected that HFpEF will become the main type of heart failure globally in the next 10 years.

pulmonary atrerial hypentension (PAH) refers to a hemodynamic and pathophysiological state in which pulmonary artery pressure increases beyond a certain limit, which can cause right heart failure and serious complications, and eventually lead to death. In recent years, based on the research of molecular pathology treatment of PAH, there are three targeted therapeutic pathways, namely nitric oxide pathway, prostacyclin pathway and endothelin pathway. Prostacyclin and its analogs are targeted drugs developed in the early stage for the clinical treatment of PAH. There are four kinds of clinically used epoprostol, treprostinil, iloprost and beraprost sodium. Among them, treprostinil has a long half-life, stable drug structure and convenient use, and is widely used as a first-line treatment and rescue drug. In this paper, the research progress of treprostinil in the treatment of PAH is reviewed.

The American Heart Association (AHA) issued a scientific statement in 2014 that listed depression as a risk factor for poor prognosis in patients with acute coronary syndrome (ACS)^[1]。 The statement pointed out that there is substantial evidence supporting depression after ACS as a risk factor for all-cause and cardiogenic death and composite endpoints including mortality and non-fatal cardiac events. This statement is the first to formally identify psychological variables as risk factors for cardiovascular disease endpoints, which is of historic significance. A large number of studies have found that depression and cardiovascular disease are closely related. So how do the two interact with each other? This article reviews the occurrence of depression and cardiovascular diseases, its influence on existing cardiovascular diseases and its possible mechanisms, as well as the influence of antidepressant therapy on cardiovascular diseases.

Heart failure (HF) is one of the leading causes of death and disability worldwide. In the United States, there were 5.7 million patients with heart failure in 2010, 550,000 new patients were added every year, and 280,000 deaths due to heart failure, resulting in economic losses of more than $40 billion^[1,2]。 In China, the prevalence rate of heart failure is 0.9%, and there are about 4 million patients with central failure in the 35-74 year old population^[3]。 Heart failure is a typical age-related disease^[3,4]China is gradually entering an aging society, and the incidence of heart failure is increasing year by year^[3,5]It has become a major public health problem in our country, bringing a heavy economic burden to society and families.