2017年 · 第45卷第03期

According to the China Cardiovascular Disease Report 2015, there are nearly 290 million patients with cardiovascular diseases in China, and the mortality rate ranks first among chronic non-communicable diseases (chronic diseases). The importance of clinical research to medical development and prevention and control of chronic diseases is self-evident. Between 2000 and 2011, the cardiovascular mortality rate in the United States experienced an inflection point decline, compared with 2015 published inJAMAAccording to the above research, the innovation of treatment strategies brought by innovative clinical research is one of the important reasons for the decline of cardiovascular mortality in the United States.

"Efficacy and safety evaluation of ivabradine hydrochloride in the treatment of Chinese patients with chronic heart failure: data analysis of SHIFT study China subgroup" published in this issue^[1]It is a very meaningful study of China, and the results deserve attention and provoke deep thought.

In recent years, with the improvement of cancer diagnosis and treatment, especially the advancement of precision medicine under the guidance of genetics and the implementation of targeted therapy and other technologies, the survival time of cancer patients has been continuously extended and the quality of life has been continuously improved^[1,2]。 Many types of tumors gradually persist in the pattern of a chronic disease after treatment. At the same time, research shows that a large number of cancer survivors die from non-tumor causes, and cardiovascular disease is one of the leading causes of death. On the one hand, many tumor treatments themselves are accompanied by potential cardiovascular toxicity, which may affect the prognosis and quality of life of tumor patients. On the other hand, with the extension of human life expectancy, tumors in the elderly on the basis of combined cardiovascular diseases have become a multi-discovery phenomenon, and the interference between the two treatments has become a potential medical problem^[2,3,4,5]。 At the same time, the rapid development of oncology and cardiovascular science makes it difficult for doctors in a single discipline to quickly grasp the treatment progress of the other discipline and the prognostic changes it brings to related diseases, which in turn affects the comprehensive judgment of the rationality of treatment. The mastery of interdisciplinary knowledge is increasingly important for the treatment of such patients. Therefore, tumor cardiology, as a new interdisciplinary discipline, emerged in the era of rapid development of cardiovascular and oncology^[3]。

hypertrophic obstructive cardiomyopathy (HOCM) is characterized by asymmetric myocardial hypertrophy, which often occurs in the sub-aortic region and easily causes obstruction of the left ventricular outflow tract (LVOT). The more severe the obstruction, the more severe the clinical symptoms and the worse the prognosis^[1,2]。 LVOT obstruction is dynamic, and the main goal of treatment is to relieve symptoms. Some patients can improve symptoms such as angina pectoris and dyspnea through drugs, but the available drugs are very limited and subject to many limitations, such as beta blockers, which are contraindicated in sinus bradycardia or atrioventricular block^[1]。 When medical treatment is limited and symptoms are difficult to control, surgical treatment can be considered^[3]。 As early as the 1970s, surgical myectomy (SM) was recognized as the "gold standard" of non-drug treatment.^[4,5]。 In the 1990s, people were keen to treat LVOT obstruction by dual-chamber pacing^[6]However, its effectiveness was not finally confirmed by research. More than 10 years ago, alcohol septal ablation (ASA) began to become a non-pharmacological treatment alternative to SM^[3,7,8]。 This method induces coagulative necrosis of the interventricular septum by selectively injecting ethanol into the septal branch artery through a catheter, thereby alleviating LVOT obstruction and reducing symptoms. A recent domestic report also shows that ASA can improve the symptoms of HOCM patients and have a good long-term prognosis^[9]。 However, there are some anatomical variations in the septal branch artery, which do not always match the obstruction site, thus limiting the effect of ASA to some extent. In addition, if ethanol leaks into non-septal branch arteries, it can cause severe and extensive myocardial necrosis, and the consequences are catastrophic^[8]。

The patient was a 65-year-old female who was admitted to the emergency department on 13-Nov-2015 due to chest pain for 7 h. After admission, the patient's chest pain persisted and could not be relieved, accompanied by profuse sweating and pale complexion. He has a history of "repeated edema of both lower limbs" for more than 4 years. Admission physical examination: blood pressure 128/82 mmHg (1 mmHg =0.133 kPa), heart rate 60 beats/min, homogeneous rhythm, wet rales in both lungs. Emergency ECG showed sinus rhythm, V₁Lead R/S ratio increased, V₁~ V₃Lead T-wave inversion (Figure 1), emergency troponin I 0.62 μ g/L, aspirin 300 mg and clopidogrel 300 mg orally, emergency coronary intervention. Coronary angiography showed massive thrombotic shadows in the middle circumflex branch, distal flow TIMI grade 2, and thrombotic shadows in the proximal middle of the blunt margin branch, distal flow TIMI grade 1 (Figure 2)。 Then, thrombus was repeatedly aspirated in the circumflex branch and the blunt margin branch, and thrombus was visible in the extract. Re-examination of coronary angiography showed that the obstruction of the circumflex branch and the blunt margin branch disappeared, and TIMI grade 3 blood flow was restored (Figure 3)。 Subsequent intracoronary optical coherence tomography (OCT) showed smooth intima, no signs of atherosclerosis, intima tear and thrombosis (Figure 4)。 Acute coronary thromboembolism was diagnosed, and no stent was placed. Antithrombotic and anticoagulant therapy was given. The chest pain of the patient was significantly relieved after operation, and the troponin I was reexamined at 9.67 μ g/L on the second day of admission. On the third day of admission, the patient had recurrent chest pain, which was squeezing, and the troponin I was increased (13.2 μ g/L) after reexamination. After enhanced anticoagulation treatment, the chest pain did not recur.

A 50-year-old female was admitted to the hospital on 15 January 2014 due to "fever and dyspnea for 20 d". Previous history of obstructive hypertrophic cardiomyopathy, denied hypertension, coronary heart disease, aortic stenosis and other diseases. Temperature at admission was 37.8 ℃, blood pressure 120/70 mmHg (1 mmHg =0.133 kPa) and heart rate 86 beats/min. Physical examination revealed apical systolic murmur conduction to the axillary. Electrocardiogram showed sinus rhythm and left deviation of electric axis, and chest radiograph showed cardiothoracic ratio of 0.63. Blood routine showed white blood cells 17.6×10⁹/L, neutrophil ratio 94%, hemoglobin 95 g/L, platelets 127×10⁹/L. C-reactive protein 24.6 mg/L, procalcitonin 6.2 μ g/L, serum creatinine 159 μ mol/L, D-dimer 0.95 mg/L, N-terminal B-type pronatriuretic peptide (NT-proBNP) 5 362 ng/L. Fecal routine and coagulation function were normal. The urine routine contains a small amount of red blood cells and urine protein. Urine culture and three blood cultures were negative.

familial hypercholesterolemia (FH) is an autosomal dominant genetic disease, which is an important public health problem worldwide. The latest evidence shows that the incidence of heterozygous FH is 1/300~1/200, and the incidence of homozygous FH is 1/300,000~1/160,000^[1,2]。 The main characteristics of FH are significantly increased plasma LDL-C levels, and the risk of atherosclerotic cardiovascular disease (ASCVD) is greatly increased. Especially, the risk of early onset coronary heart disease in homozygous patients is increased by 100 times. Myocardial infarction or even death can occur in adolescence; However, the risk of early onset coronary heart disease in heterozygous patients increased by 3 to 13 times^[3]。 Due to the high risk of ASCVD, FH has attracted international attention. Since 2013, international organizations such as the European Atherosclerosis Society and the Cardiovascular Society have issued a number of guidelines for the prevention and treatment of FH^[4,5,6]It is suggested that early diagnosis and early intervention are important strategies to reduce ASCVD mortality.

The incidence of atrial fibrillation (AF) in the general population is 1% to 2%, and the incidence of specific populations will increase by 2 to 3 times in the past 20 to 30 years, and the risk of death in such populations will increase by 2 times^[1,2]。 This specific population mainly includes elderly patients with unreasonably controlled cardiovascular risk factors (such as hypertension) and unreasonably treated cardiovascular diseases (such as coronary heart disease and heart failure). A variety of diseases, such as hypertension, heart failure, diabetes, sleep breathing disorders, and obesity, can contribute to the development of atrial fibrillation. In recent years, studies have found that atrial fibrillation is also related to gastrointestinal dysfunction, especially gastroesophageal reflux disease (GERD) and esophagitis, which increase the risk of atrial fibrillation in patients. Understanding the relationship between acid reflux disease and atrial fibrillation is extremely important to improve the poor prognosis of patients with atrial fibrillation using proton pump inhibitors (PPI), based on the recent study by Linz et al^[3]Published inEuropaceA research paper on the relationship between GERD and atrial fibrillation. This article reviews the relationship between GERD and atrial fibrillation, the underlying mechanisms of triggering atrial fibrillation in GERD patients, and the research progress of using proton pump inhibitors to prevent and treat GRED-related atrial fibrillation.

At present, cardiovascular diseases have become the number one killer of human health, and the pathogenesis and diagnosis and treatment of cardiovascular diseases are extremely important. The mechanism of cardiovascular diseases has been attracting much attention because of its concealment and complexity. 2010 Bollati et al.^[1]An epidemiological investigation on exosome-mediated cardiovascular disease (SPHERE) was initiated to investigate the relationship between exosomes, a paracrine form, and cardiovascular disease. As a result, the relationship between exosomes and cardiovascular diseases officially entered people's field of vision.

Mitochondria is an important place for cardiomyocyte biological oxidation. Besides synthesizing adenosine triphosphate (ATP) through phosphorylation and oxidation of respiratory chain to provide energy for cardiomyocytes, mitochondria are also involved in regulating apoptosis and autophagy of cardiomyocytes^[1]。 Mitochondrial damage leads to the change of cell membrane permeability, oxidative phosphorylation decoupling, and the release of reactive oxygen species (ROS) or apoptotic factors, which promotes cardiomyocyte damage^[1]。 Therefore, timely removal of damaged mitochondria and maintaining the normal structure and number of mitochondria are essential for the normal growth and metabolism of cardiomyocytes. Autophagy is a process of degradation of intracellular material through lysosomes or vesicles. It has been found to degrade everything from soluble proteins to intact organelles, including, of course, mitochondria^[2]。 Mitophagy is a specific autophagy phenomenon that selectively clears damaged or unnecessary mitochondria. Under the action of external stimuli, mitochondria in cardiomyocytes will undergo depolarization and damage. The damaged mitochondria are specifically encapsulated into autophagosomes, fused with lysosomes and completed degradation, which plays an important role in maintaining the normal function and morphology of cells^[3]。 At present, mitochondrial autophagy is a hot topic in the molecular mechanism of organelle-specific autophagy. In this paper, the research progress of the molecular mechanism of mitochondrial autophagy and its role in cardiovascular diseases are reviewed.

milk fat globule epidermal growth factor VIII (MFG-E8) is a mosaic peripheral glycoprotein that adheres to the surface of milk fat globules, also known as lactagglutinin or SED1 (secreted EGF repeats and discoidin domains-containing protein-1)^[1]。 Because MFG-E8 mediates the release of "eat-me" signal between apoptotic cells and phagocytic cells, which can eliminate dead cells in a variety of organs, it is an important factor in controlling the progression of multiple inflammatory diseases and organ remodeling^[2]。 Recent studies have shown that MFG-E8 is a new secretory inflammatory mediator, which can integrate intracellular signals and regulate the pathological progression of many diseases, including cardiovascular metabolic disorders and tumors. MFG-E8 can also mediate the adverse reactions of vascular cells and extracellular matrix under stress stimulation, and affect the progression of hypertension, diabetes and atherosclerosis^[3,4]。 The activation of MFG-E8 signal not only triggers apoptosis of endothelial cells, promotes thrombosis, accelerates endothelial dysfunction, but also promotes the proliferation and invasiveness of smooth muscle cells, the deposition of extracellular matrix and vascular amyloidosis. Therefore, MFG-E8 could be used as a novel vascular aging marker^[2,4]。 This article reviews the study of MFG-E8 in cardiovascular diseases associated with vascular remodeling.