2017年 · 第45卷第02期

After 2 years of thorough discussion, China issued guidelines for the prevention and treatment of adult dyslipidemia (2016 revised edition). The Chinese expert team fully collected and evaluated my country's clinical research and evidence in recent years, excluded the interference of the guidelines of the American College of Cardiology (ACC) and the American Heart Association (AHA) in November 2013, resisted the influence of the commercial interests of pharmaceutical companies, and reached a good guide that is in line with China's national conditions and keeps pace with the times.

statin therapy is the cornerstone of the prevention and treatment of cardiovascular disease, and it is generally safe and well tolerated. However, a few patients have statin-associated symptoms (SAS) during the treatment, including statin-associated muscle symptoms, diabetes, liver damage, central nervous system symptoms, etc^[1,2]。 The appearance of SAS can lead to the reduction or discontinuation of statin drugs in patients. In addition, overreporting of adverse statin reactions is also one of the main reasons for early discontinuation of statin drugs. The reduction or discontinuation of statin drugs can cause an increase in clinical events of atherosclerotic cardiovascular disease (ASCVD). The potential risks and benefits of statin use have become a common concern of doctors and patients. Therefore, it is of great clinical significance to formulate corresponding management strategies for statin-related adverse reactions in clinic.

Dyslipidemia, especially the elevation of plasma low density lipoprotein cholesterol (LDL-C) levels, is a necessary condition for the development and development of atherosclerosis (AS), and is considered to be the most important pathogenic risk factor^[1]。 Therefore, the detection of blood lipid has guiding significance for the diagnosis and treatment of AS. Because of the long history of fasting blood lipid detection, and the results of various large-scale studies in the past that there is a high correlation between fasting blood lipid and coronary heart disease, people (including patients and doctors) generally accept fasting blood lipid detection, and it is a conventional way to detect fasting blood lipid when seeking medical treatment. At present, there is limited understanding of the necessity of non-fasting lipid measurement and its application in clinical work, and we present a brief review of the progress in this regard.

Statins have good effects on reducing myocardial infarction and related death while lowering blood cholesterol. However, the relationship between lowering cholesterol and reducing stroke risk has been paid attention to and discussed. On the one hand, low density lipoprotein cholesterol (LDL-C) decreased after statin treatment, and the prevention of stroke events was weaker than its preventive effect on coronary heart disease events; On the other hand, the increased risk of hemorrhagic stroke associated with decreased serum cholesterol levels has somewhat weakened the clinical benefit of statins in stroke prevention.

The Chinese Guidelines for the Prevention and Treatment of Dyslipidemia in Adults (2016 Revision) (2016 Blood Lipid Guidelines for short) pointed out straight to the point that the blood lipid level of the Chinese population is gradually increasing, and the overall prevalence of adult dyslipidemia is as high as 40.40%^[1]The objective needs of the revision guidelines are clear, that is, to improve the management level of dyslipidemia in the Chinese population and reduce the malignant increase of atherosclerotic cardiovascular disease (ASCVD)^[2]。 It can be seen that it is particularly important to understand the basic contents and main strategies of blood lipid management.

The American Diabetes Association (ADA) has promulgated the 2016 Medical Diagnosis and Treatment Standards for Diabetes (ADA Guidelines)^[1]The American Association of Endocrinologists (AACE) and the American Society of Endocrinology (ACE) also jointly issued the 2016 Consensus Statement on the Integrated Diabetes Management Program (referred to as the AACE Guidelines)^[2]。 In the two new guidelines, lipid management recommendations for diabetic patients have been greatly improved.

Since the 1960s, more and more research evidence has shown that dyslipidemia is an important risk factor for cardiovascular disease. Among them, low-density lipoprotein cholesterol (LDL-C) accounts for 60% to 70% of total cholesterol. Hypercholesterolemia, which is mainly manifested by increased LDL-C, is a pathogenic risk factor for atherosclerotic cardiovascular disease (ASCVD). Therefore, lipid management has become the main strategy for the prevention and treatment of ASCVD, and all guidelines list LDL-C as the primary target of intervention. Statins become the main intervention drugs to reduce LDL-C because they can inhibit hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase in cholesterol synthetase system, inhibit cholesterol synthesis and promote the clearance of LDL-C in blood. However, at the same time, clinical studies have shown that in some patients who have received the currently recognized intensive lipid lowering and standardized control of blood pressure and blood glucose, although the plasma LDL-C level can be maintained at a low level, there is still a high risk of cardiovascular events, that is, the so-called residual cardiovascular risk. Therefore, the new atherogenic lipoprotein spectrum, also known as the lipid triad, has gradually become a research hotspot in recent years. Lipid triad is a group of lipid abnormalities including increased plasma triglycerides, increased small but dense LDL-C, and decreased high-density lipoprotein cholesterol (HDL-C). Among them, high-density lipoprotein (HDL) is one of the main lipoproteins in plasma. It is composed of a group of lipoproteins with heterogeneous size, density, chemical composition and physiological function, and is mainly synthesized in the liver and small intestine. Because of its complex composition and function, at present, the cholesterol content in HDL is mostly detected, that is, the level of HDL-C is used instead of the level of HDL. One of the main functions of HDL is to participate in the reverse transport of cholesterol, that is, it transports cholesterol from extrahepatic tissues to the liver for recirculation or excretion in the form of cholic acid, which is considered to be the main mechanism of HDL against atherosclerosis.

Dyslipidemia is a common metabolic disease, which is closely related to the development of atherosclerotic cardiovascular disease (ASCVD). The elevated level of low-density lipoprotein cholesterol (LDL-C) is recognized as an independent risk factor for cardiovascular events. Statins have become the cornerstone of the prevention and treatment of ASCVD because they can effectively reduce LDL-C and reduce the incidence of cardiovascular events.

A 40-year-old female was admitted to the hospital on December 9, 2015 due to "sudden chest tightness and chest pain for 2 h". At 3 o'clock in the morning, the patient suddenly developed chest tightness and chest pain, which was pressing pain in the precordial area, about the size of a palm, accompanied by radiating pain in the shoulder, back and left upper arm, accompanied by profuse sweating, no paroxysmal dyspnea, no cough, expectoration and hemoptysis, no nausea, vomiting, no acid reflux, belching, no dizziness, headache, no rotation of vision, no numbness of limbs and unstable walking, no amaurosis, no syncope. ECG showed Ⅱ, Ⅲ, aVF, V in the emergency department of our hospital₂~ V₄Lead ST segment elevation (Figure 1)。 There were no obvious abnormalities in the markers of myocardial necrosis. Chest CT showed widening of the ascending aorta. The patient has been in good health and enjoys exercise. History of coronary heart disease, hypertension, diabetes, dyslipidemia, Kawasaki disease, and rheumatic disease was denied, and there was no history of traumatic surgery. No history of smoking and drinking.

A 58-year-old male was admitted to the hospital on 8 December 2015 mainly for "bilateral hypochondrial pain with shortness of breath after activity for 1 month". One month ago, the patient developed bilateral hypochondrial pain without obvious trigger, aggravated by deep inspiration, dyspnea after going up to 2 floors, no fever or cough. Chest CT performed in the outside hospital showed "inflammatory consolidation in both lungs, localized atelectasis in the left lower lobe, a small amount of pleural effusion on the right side and a small amount of pericardial effusion" (Figure 1), intravenous application of moxifloxacin for 8 days, the patient felt that the symptoms did not improve, and showed soreness in both shoulders and lower limbs, and numbness in the skin on the back of both feet. Visited our hospital 7 days ago, ECG V₄~ V₆Lead ST segment depression, Ⅰ, Ⅱ, V₄~ V₆Lead T-wave inversion (Figure 2)。 Creatine kinase isoenzyme MB (CK-MB) 31 U/L, troponin T 1.4 μ g/L, N-terminal B-type pronatriuretic peptide (NT-proBNP) 4 399 ng/L. He was admitted to our department with "heart failure, acute non-ST segment elevation myocardial infarction (NSTEMI)". Since the onset of the disease, the patient is clear, and his family feels that the patient's speech is reduced, his reaction is slow, he sleeps poorly at night, he has no obvious change in urine and stool, and his body weight has lost 5 kg in the past one month. Past history: A history of allergic rhinitis for 13 years. Fluticasone propionate spray was used regularly 3 years ago, and the control was stable. Bronchial asthma for 13 years, salmeterol and ticasone started 3 years ago with stable control. He has a history of hypertension for 15 years, a history of type 2 diabetes for more than 10 years, smoked for 30 years, 25 cigarettes/d, quit for 11 years, and had no drinking habit. A familial genetic history is denied. Physical examination at admission: body temperature 36.8 ℃, pulse 90 beats/min, breathing 16 beats/min, blood pressure 102/70 mmHg (1 mmHg =0.133 kPa). Clear mind, slow response, poor computing power and near memory. Percussion voices below the 9th intercostal line of the right subscapular angle line were voiced, auscultation breathing sounds were reduced, inspiratory phase wet rales were heard in both lower lungs, and there was no pleural friction sound. Heart boundary enlarged to the left, heart rate 90 beats/min, homogeneous rhythm, powerful heart sound, A₂>P₂No murmurs were heard, no pericardial friction. Abdominal physical examination showed no abnormalities, and both lower limbs may have concave edema in the pretibia. The muscle strength of the limbs was grade V, and the needle sensation in the left calf was slightly worse. Blood routine showed a white blood cell count of 11.8×10⁹/L, hemoglobin 130 g/L, platelet count 251×10⁹/L, 42.4% of eosinophils were significantly increased. Urinary routine showed urinary protein (1+), and no microscopic hematuria was observed.

A 56-year-old female was admitted to the hospital on November 25, 2015 mainly due to "chest tightness and shortness of breath for 4 months". There was a history of diarrhea before the onset of the disease, and the activity endurance decreased progressively. Physical examination at admission: pulse 93 beats/min, body temperature 36.3 ℃, 20 breaths/min, blood pressure 72/55 mmHg (1 mmHg =0.133 kPa). The heart rhythm was uniform, the heart rate was 93 beats/min, no obvious pericardial friction sound was heard, wet rales were heard in both lower lungs, and there was no edema in both lower limbs. Chest X-ray showed blood stasis in both lungs and a significant enlargement of the left ventricle. Echocardiography showed the anterior-posterior diameter of left atrium 41 mm, the transverse diameter of left ventricle 65 mm, and the anterior-posterior diameter of right atrium 26 mm. The estimated pulmonary systolic pressure was 57 mmHg, the left ventricular ejection fraction (LVEF) was 19%, and two abnormal echo masses were seen in the lateral wall of left ventricle, considering mural thrombosis. Coronary CT angiography (CTA) showed no obvious abnormalities.

With the acceleration of social aging, the incidence of valvular heart disease, which is the main cause of degenerative disease, is increasing year by year, among which aortic stenosis and mitral regurgitation are the main ones^[1]。 While the surgical treatment of valvular disease continues to develop and improve, medical interventional treatments such as transcatheter aortic valve implantation (TAVI) and transcatheter mitral valvuloplasty (TMVP) have emerged, which have become effective alternative therapies for patients with surgical contraindications or high-risk valvular disease. At the same time, it also puts forward more accurate requirements for preoperative imaging evaluation. Since 3D printing technology was first applied to the medical industry in the early 1990s^[2]With the advantages of precision replication and integral molding, it has been rapidly popularized in the fields of orthopedics, plastic surgery and vascular surgery. The application in cardiovascular related disciplines, especially in the field of valvular heart disease, is only in rudimentary form. Combined with heart valve disease, this paper expounds the steps, software and hardware foundation, raw materials and clinical application status of 3D printing, and discusses the limitations at this stage and the prospective development direction.

Vascular calcification is widespread, affecting approximately 60% of people over 60 and 80% of people over 80, and was once considered an unregulated end-stage degenerative disease^[1]。 However, with the increase of research evidence, it is gradually clear that vascular calcification is an actively regulated process, is a common adverse event in the process of atherosclerosis, and is an important predictor of death and disability of cardiovascular and cerebrovascular diseases^[2]。 This article reviews the latest progress in the origin and classification of vascular calcification, vascular calcification and plaque outcome, several key nodes in vascular calcification formation, related detection methods and clinical significance, etc., hoping to provide a new diagnosis and treatment perspective for clinical decision-making related to vascular calcification.

frailty refers to the decline of physiological reserves in the neuromuscular, metabolic and immune systems of the elderly, thus reducing the ability of the elderly to resist stress^[1]。 Foreign literature reports that the weighted incidence of frailty in community elderly is 10.7%^[2]； The incidence of frailty in elderly patients with cardiovascular disease ranged from 10% to 60%, depending on the study subject and evaluation method^[3]。 The incidence of frailty in older adults aged ≥65 years undergoing percutaneous coronary intervention (PCI) was 20%^[4,5]The incidence of frailty in elderly patients with coronary heart disease aged ≥70 years and receiving cardiac catheterization was 27%^[4,6]。 Recent clinical studies have shown that frailty is closely related to heart failure, heart surgery or transcatheter aortic valve replacement, subclinical cardiovascular disease, and adverse clinical events in patients with acute coronary syndrome (ACS)^[7]。 This article reviews the concept of frailty and the clinical research that frailty is related to ACS in the elderly.