2018年 · 第46卷第02期

In February, 1945, Roosevelt, Churchill and Stalin, the Big Three of World War II, left a historic group photo in the beautiful Black Sea port city of Yalta. Churchill and Stalin, who sat on both sides, were proud of the spring breeze, while Roosevelt, who was located in the center, looked haggard. At that time, few people knew that Roosevelt was seriously ill. In 1935, Roosevelt was 53 years old, blood pressure 136/78 mmHg (1 mmHg =0.133 kPa); By 1944-1945, blood pressure reached 180-230/110-126 mmHg, and chronic heart failure and renal failure occurred; During the Yalta conference, blood pressure reached 260/150 mmHg. Roosevelt's treatment included phenobarbital, a low-salt diet, a low-fat diet, and digitalis. Two months after the Yalta Conference, on April 12, 1945, Roosevelt died of a cerebral hemorrhage at the age of 63. Eight years after the Yalta Conference, Stalin died at the age of 74 of cerebral hemorrhage complicated by hypertension. Twenty years after the Yalta Conference, Churchill died of a stroke, having suffered 10 strokes before that, at the age of 91. These three giants joined forces to defeat the most vicious fascist in the world, but died of a common enemy: stroke complicated by high blood pressure. What is puzzling is that none of these three heads of state has received antihypertensive treatment. Why is this? To answer this question, we must open the archives of hypertension research that lasted hundreds of years.

With the aging of population and the acceleration of urbanization, the prevalence of cardiovascular disease risk factors is obvious, resulting in the continuous increase of the incidence of cardiovascular diseases^[1]。 It is estimated that there were about 422.7 million patients with cardiovascular disease worldwide in 2015^[2]While the number of cardiovascular diseases in China is as high as 290 million^[1]。 Cardiovascular disease is the main cause of death in Chinese residents, which is higher than tumor and other diseases. Dyslipidemia, hypertension, smoking, diabetes, overweight/obesity are the main risk factors of cardiovascular disease^[1]。 Numerous studies have confirmed that low density lipoprotein cholesterol (LDL-C) plays an important role in the pathogenesis of cardiovascular disease, and elevated LDL-C levels increase the risk of cardiovascular disease^[3]Conversely, the risk is reduced^[4]。 Important studies released in recent years further support the importance of long-term intensive lipid-lowering and LDL-C level reduction in the prevention of high-risk groups of cardiovascular diseases^[5,6]It suggests that intensive lipid lowering seems to be an important strategy to help reduce the risk of high-risk groups of cardiovascular diseases in China and promote the arrival of the "inflection point" of cardiovascular-related disease mortality.

The residual risk of cardiovascular disease usually refers to the fact that low density lipoprotein-cholesterol (LDL-C) has reached the standard after the current standard prevention and treatment measures, and blood pressure and blood glucose have been controlled. However, the risk of cardiovascular disease onset and events still exists, and the residual risk cannot be eliminated. Therefore, it is of great significance to further reduce the events of arteriosclerotic cardiovascular disease (ASCVD) by continuously discovering cardiovascular residual risks and actively intervening and managing them while controlling traditional risk factors. Increased levels of lipoprotein (a) [Lp (a)] have recently been considered to be not only an independent risk factor but also a residual risk for ASCVD. This paper describes the role, pathogenic mechanism, residual risk and treatment progress of Lp (a) in ASCVD, aiming to provide new ideas for further reducing the events of ASCVD.

Aortic aneurysm refers to the tumor-like dilatation of the aorta, exceeding 50% of the normal blood vessel diameter. When the blood flow breaks through the intima and tears the blood vessel wall into the middle layer, an aortic dissection aneurysm is formed. Although the incidence of aortic aneurysm is not as good as that of common cardiovascular diseases such as hypertension and coronary heart disease, its early symptoms are insidious and its clinical manifestations are complicated. Once dissection is formed, it is easy to rupture, and the mortality rate after rupture is>80%. It is an extremely dangerous disease. Aortic aneurysm can be divided into thoracic aortic aneurysm and abdominal aortic aneurysm according to the location of occurrence. The occurrence of thoracic aortic aneurysm is more closely related to genetics, and aortic dissection mostly occurs in the thoracic aorta. There are relatively mature animal models of abdominal aortic aneurysm. angiotensin Ⅱ (Ang Ⅱ) administered to mice with knockout apolipoprotein E (ApoE) or low-density lipoprotein (LDL) receptor by sustained-release pump for 4 to 6 weeks can induce the formation of abdominal aortic aneurysm, which occurs in the abdominal aorta above the renal artery. Abdominal aortic aneurysm models can also be established in rats and mice by infusing elastase or applying calcium chloride to the abdominal aorta below the renal artery. These models have been widely used in the research of pathogenesis and treatment of abdominal aortic aneurysm. The establishment of animal models of thoracic aortic aneurysm and dissection has been an important problem in the field.

Classical familial hypercholesterolemia (FH) is an autosomal (co) dominant genetic disease. Its main clinical manifestations are significantly increased serum low density lipoprotein-cholesterol (LDL-C) levels, and skin/tendon xanthomas^[1]。 Patients with FH have a significantly higher risk of early-onset arteriosclerotic cardiovascular disease, while early screening and early medical treatment can improve the survival rate of patients with FH. At present, FH has been widely concerned by the international community, and relevant diagnosis and treatment expert consensus or guidelines have been issued one after another, but the diagnosis and treatment rate of FH are still seriously insufficient. According to the characteristics of dyslipidemia in Chinese patients, with reference to domestic and foreign clinical research evidence and relevant guidelines consensus, the Atherosclerosis and Coronary Heart Disease Group of Cardiovascular Disease Branch of Chinese Medical Association and the Editorial Committee of Chinese Journal of Cardiovascular Diseases organized and formulated this consensus, aiming at improving the ability of Chinese clinicians to find FH patients, promote the early diagnosis and treatment of FH, and standardize the clinical management of FH.

A 49-year-old female was admitted to the hospital on November 6, 2015 due to recurrent respiratory tract infections and dyspnea after exertion. Echocardiography suggested severe pulmonary valve regurgitation with right heart enlargement after Fallot tetralogy correction. The patient was diagnosed as a congenital heart disease with tetralogy of Fallot at the age of 18 and underwent surgical correction. The postoperative condition was stable. Admission examination: at rest, the percutaneous oxygen saturation was 98%, the heart rhythm was uniform, and the systolic and diastolic murmur of grade 2/6 was heard between the costs of the left margin of the sternum 2 and 3. Chest enhanced CT confirmed the absence of stenosis and other vascular malformations in the peripheral pulmonary artery branches, and the diameter of the pulmonary annulus was 25 mm. Cardiac MRI showed right ventricular end-diastolic volume (right ventricular end-diastolic volume, RVEDV) 156.9 ml/m²End-systolic volume (right ventricular end-systolic volume, RVESV) 98 ml/m²Right ventricular ejection fraction (right ventricular ejection fraction, RVEF) 47%. Therefore, the diagnosis was severe pulmonary valve regurgitation and right ventricular dysfunction after Fallot tetralogy. The World Health Organization (WHO) cardiac function classification was Ⅱ ~ Ⅲ, which met the indications for percutaneous pulmonary valve implantation. Interventional treatment was given after signing the informed consent form. The process went smoothly, and a domestic nickel-titanium alloy self-expanding stent valve (trade name: Venus P valve) was implanted, with a diameter of 26 mm and a length of 25 mm. Immediately after surgery, pulmonary reflux changed from moderate to severe before surgery to disappearing (Figure 1), no intervention-related complications, and the patient was discharged after 3 d. Regular follow-up is recommended after discharge and oral aspirin is given.

Platelets are a class of tiny anucleated cells that play an important role in hemostasis and inflammatory response. Platelet cells have long been considered by researchers to be the residue of megakaryocytes, which, although unnucleated, contain all the components necessary to accomplish signal-dependent translation^[1,2,3]。 Studies have revealed that circulating platelets bind to the site of vascular injury through receptor recognition exposed subendothelial tissue, thus binding receptors and releasing platelet microsomes recognition activation platelets^[1]。 The secretion of platelet microsomes under pathophysiological conditions can increase the response effect of thrombosis, thus helping to regulate thrombosis. The study found that platelets contain about 9 500 transcripts and many different types of small molecule RNA, with the highest content of microRNA (miRNA), accounting for 80% of the small molecule RNA content of platelets^[4]。 Among them, platelet microsomes are rich in miRNAs, which act as transport carriers for these miRNAs in the circulation and mediate their involvement in regulating the function of recipient cells.

Worldwide, the prevalence and mortality of cardiovascular diseases are increasing year by year, which has become a major public health problem. Cardiovascular disease is a collective term for a series of diseases which are composed of genetic factors, environmental factors and the combined action of both, but its specific pathogenesis is still not fully understood. In recent years, more than 50 diseases, including obesity, diabetes, cancer, autism, etc., have been linked to gut microbiological imbalances^[1,2,3]And the relationship between intestinal microecology and cardiovascular diseases is gradually attracting people's attention. The imbalance of intestinal microecology leads to the disorder of bacterial flora structure and disrupts the basic metabolic process of host, thus inducing the occurrence and development of cardiovascular diseases such as coronary heart disease, hypertension and heart failure^[4,5,6]。 At the same time, in the process of understanding this relationship, people also put forward new strategies for cardiovascular disease prevention and treatment^[7,8]。 The correlation between intestinal microecology and cardiovascular diseases is reviewed.

Sarcopenia refers to a progressive, extensive loss of skeletal muscle mass and hypofunction. Old age, skeletal muscle disuse, nutritional deficiency, systemic chronic inflammation, anabolic disorders, etc. are closely related to the occurrence and development of sarcopenia. Cardiovascular diseases and sarcopenia can coexist, which further decreases the exercise tolerance and quality of life of patients, and increases the mortality rate. China's aging speed is accelerating, and the number of patients with cardiovascular diseases and sarcopenia is rising. The resulting health problems such as the loss of labor force and mobility of the elderly deserve attention.