2018年 · 第46卷第04期

The most fundamental guiding principle of health and wellness in the new era is to realize the great transition from treating diseases as the center to health as the center. Health has become the "theme word" of the future development of medical and health undertakings. People's health is an important symbol of national prosperity and national prosperity. It is the common expectation and unmet huge need of hundreds of millions of people for a better life.

The myocardial bridge is the myocardium covering a segment of the epicardial coronary artery (coronary artery for short), which is a congenital developmental abnormality. How to safely and effectively manage patients with myocardial bridge is a common clinical problem. With the advancement of intracavitary imaging and physiological technology, and the abundance of clinical evidence-based evidence, myocardial bridge has been further understood in recent years^[1,2,3,4,5]This is of great significance for guiding clinical practice.

Antiplatelet therapy can significantly reduce the risk of thrombotic events in patients with coronary heart disease, and it is recommended as Class I for the treatment of acute coronary syndrome (ACS) in domestic and foreign guidelines. However, in clinical practice, the efficacy and safety of antiplatelet therapy show large individual differences. Some special patients with high risk of thrombosis and/or bleeding often have thrombosis and bleeding events when receiving conventional antiplatelet therapy, which leads to clinical decision-making difficulties. Specific guidance is urgently needed. Therefore, initiated by the Thrombosis Prevention and Treatment Professional Committee of Cardiovascular Physicians Branch of Chinese Medical Doctors Association, the Interventional Cardiology Group of Cardiovascular Disease Branch of Chinese Medical Association, and the Editorial Committee of Chinese Journal of Cardiovascular Diseases, this suggestion is formulated according to the clinical research results of anti-platelet therapy for special people with coronary heart disease at home and abroad in recent years, combined with the clinical status of China and the clinical experience of practitioners. This recommendation mainly relates to antiplatelet therapy in 12 special groups, including elderly, thrombolytic therapy, concomitant oral anticoagulants, pulmonary embolism (or venous thromboembolism), cerebrovascular disease, recent history of gastrointestinal bleeding, diabetes, renal insufficiency, gout or hyperuric acid, iron deficiency anemia, low platelet count, coronary artery bypass grafting (CABG) and perioperative period of non-cardiac surgery. It is hoped that the formulation and application of this recommendation can provide guidance for optimizing anti-platelet therapy in clinical special populations.

A 65-year-old male was hospitalized on January 25, 2016 due to "dizziness for 1 d and sudden chest pain for more than 2 h". The patient experienced dizziness without obvious trigger 1 d ago, and sudden crushing pain in the precordial area 2 h ago, which radiated to the back and continued without relief. Recent history of upper respiratory tract infections, fever and diarrhea is denied. No history of hypertension and diabetes. Smoking for more than 40 years, 20 cigarettes/d. Admission physical examination: blood pressure 170/95 mmHg (1 mmHg =0.133 kPa). The heart rate was 75 beats/min, the rhythm was uniform, and no pathological murmur was heard in the auscultation area of each valve area. The breathing sounds of both lungs were clear, and no dry and wet rales were heard. Soft abdomen, no tenderness. The muscle strength and tone of the limbs were normal, and the pathological signs were negative. Admission electrocardiogram (Figure 1) showed sinus rhythm, extensive anterior and inferior wall ST segment elevation (Ⅱ, Ⅲ, aVF leads ST segment elevation 0.1~0.2 mV, V₂~ V₅Lead ST segment elevation 0.1~0.4 mV and high T wave sharpness). Myocardial necrosis markers showed myoglobin 167 µg/L (normal value 0-121 µg/L), troponin I 0.010 µg/L (normal value 0-0.034 µg/L), and creatine kinase isoenzyme (CK-MB) 2.83 µg/L (normal value 0-3.70 µg/L). Large artery enhanced CT (Figure 2) shows a lobulated filling defect at the root of the ascending aorta, the upper lobe size is 1.0 cm ×0.8 cm ×0.6 cm, and the lower lobe size is 0.5 cm ×0.5 cm ×0.2 cm, connected with the aortic wall above the opening of the left coronary artery by a pedicle. Cranial CT (Figure 3) showed right brachiopontine infarction with no signs of intracranial hemorrhage (the infarction was missed in the reading on the day of admission).

A 29-year-old male was admitted for "paroxysmal chest tightness for 25 years, aggravated with precordial pain for 5 days". Five days before admission, there was no obvious trigger for precordial pain, chest tightness and shortness of breath, accompanied by fatigue, headache and dizziness. The patient had intermittent chest tightness and shortness of breath since childhood, hypertension for 1 month, blood pressure up to 220/130 mmHg (1 mmHg =0.133 kPa), oral antihypertensive drugs, self-reported blood pressure control was acceptable. Smoking history for 10 years, with an average of 5 cigarettes/d, drinking history for 10 years, and now abstaining from drinking. Family history of diabetes and cardiovascular disease denied. Physical examination at admission: blood pressure 130/80 mmHg, coarse respiratory sounds in both lungs, no dry and wet rales, grade 3~4 systolic blow-like murmur accompanied by tremor could be heard in the third intercostal area on the left margin of the sternum, apical beat was located in the midline of the clavicle in the fifth intercostal area, and the boundary of heart turbidity was enlarged. The rest of the physical examination was normal. Laboratory tests: blood troponin I 0.016 μ g/L (normal value 0.010~0.023 μ g/L), blood N-terminal B-type pronatriuretic peptide (NT-proBNP) 6 660 μ g/L (normal value 300~900 μ g/L). Admission electrocardiogram (Figure 1): rS wave can be seen in lead Ⅱ and Ⅲ, and S wave in lead Ⅲ is deeper, aVR, V₁The R wave of the lead is abnormally upward, and the P wave is high-pointed, and the V₂~ V₆Lead R wave increment was poor, ST segment arch was elevated upward, suggesting sinus rhythm, right atrial and ventricular hypertrophy, and left anterior branch block. Color echocardiography (Figure 2): Diffuse thickening of the interventricular septum, enhanced echo, asymmetric thickening of the left ventricle, muscular stenosis of the right ventricular outflow tract, with an inner diameter of about 4 mm at the narrowest point, positive SAM sign in systole of the anterior mitral valve, suggesting hypertrophic cardiomyopathy, right ventricular outflow tract stenosis (severe), and left ventricular outflow tract stenosis (mild). Coronary angiography (Figure 3): Poor blood perfusion in the systolic septal branch of the left and right coronary arteries can be seen.

A 57-year-old male was admitted to the hospital in January 2017 with "sudden torn back pain for 6 h". After the onset of the disease, the patient sweated generally, accompanied by abdominal pain, and did not vomit. He had a 15-year history of hypertension, with the highest blood pressure of 210/120 mmHg (1 mmHg =0.133 kPa). He took antihypertensive drugs irregularly, and his blood pressure was usually around 150/95 mmHg. No special examination was performed. Has a history of chronic bronchitis for more than 10 years and a history of smoking for more than 20 years. Physical examination after admission: obese body size, weight 92 kg. The blood pressure of the right upper limb was 163/98 mmHg and the blood pressure of the left upper limb was 138/83 mmHg. Cyanosis of the lips. Wheezing sounds spread from both lungs. The turbidity boundary of the heart was enlarged, and no murmur was heard in the precordial area. Soft abdomen, no tenderness. There was no edema in both lower limbs. CT angiography of the aorta (Figure 1) shows that the right arch of the aorta descends to the right, and the starting order of the branches of the aortic arch is the left common carotid artery, the right common carotid artery, the right subclavian artery and the vagal left subclavian artery; The vagal left subclavian artery originates from Kommerell's diverticulum in the descending arch and bypasses the posterior esophagus; Diverticulum complicated by dissection, maximum diameter (including dissection ) 84.6 mm ×72.2 mm ×41.6 mm; The dissection was reversely torn to the proximal end of the root of the left common carotid artery, and the distal end involved the iliac artery. The true lumen of the superior mesenteric artery was supplied with blood, and the true and false lumens of the rest of the visceral branches of the abdominal aorta were supplied with blood at the same time. Echocardiography showed enlargement of left atrium and left ventricle, abnormal left ventricular posterior wall motion, micro-regurgitation of the aortic valve, and abnormally strong echo strips in the descending aorta. Laboratory tests: liver enzyme profile, urea nitrogen, blood lipids and homocysteine were slightly elevated; D-dimer 4.25 mg/L (reference value 0-0.55 mg/L); Arterial blood gas analysis showed partial pressure of oxygen (PaO₂) 48 mmHg, partial pressure of carbon dioxide (PaCO₂) 55 mmHg. The diagnosis was right descending aortic arch with Kommerell's diverticulum, complicated by reverse tear Stanford A aortic dissection; Essential hypertension grade 3 (very high risk group); Chronic obstructive pulmonary disease, respiratory failure.

A variety of cardiovascular or non-cardiovascular diseases can lead to decreased systolic and diastolic function of the heart. When clinically relevant symptoms and signs appear, they are called cardiac insufficiency or heart failure. Myocardial fibrosis is one of the main pathological bases of cardiac dysfunction, which leads to systolic and diastolic dysfunction due to the decrease of myocardial cells and the increase of ventricular wall stiffness; Fibrotic myocardium can also inhibit oxygen diffusion, further aggravate myocardial ischemia and hypoxia, and also affect the electromechanical coupling between myocardial cells. On the basis of primary (such as myocardial hypertrophy) or secondary (such as myocardial ischemia) lesions of the myocardium, many concomitant diseases (such as diabetes) or abnormal functions of other systems and organs will also affect the dynamics of cardiomyocytes and become non-traditional risk factors for cardiac dysfunction, heart failure and myocardial fibrosis.

3D printing is now widely used in the cardiovascular field^[1,2,3]The personalized simulation model is of great significance for the auxiliary diagnosis, preoperative planning and postoperative evaluation of cardiovascular diseases. However, the clinical needs are not limited to the visualization of cardiovascular anatomy and simple preoperative simulation, but also the effective evaluation of cardiovascular fluid dynamics.

Autophagy is a process that relies on lysosomal pathways to degrade cytoplasmic proteins and organelles. As a conserved evolutionary mechanism, autophagy is associated with various cellular pathways and can affect the survival and function of vascular smooth muscle cells (VSMC). After intercellular and/or extracellular stimulation of VSMC, autophagy is activated to exert a protective effect. However, if autophagy is overactivated, it develops into excessive self-digestion, which undoubtedly adversely affects cell survival. Many previous experiments have investigated the effects of autophagy on different physiopathological stages of VSMC under various stimuli, including proliferation, migration, stromal secretion, contraction or relaxation and differentiation, and these stages run through the whole process of vascular disease occurrence and development. Autophagy defects in VSMCs can lead to atherosclerosis and restenosis, so regulating autophagy is expected to be a new target for the treatment of vascular diseases. This paper reviews the relationship between autophagy and VSMC.

Dear Professor Fang Qi left us, we said goodbye in tears. China's cardiovascular community has lost a highly respected master, the people have lost a good doctor, and I have lost a respectable and relatable mentor like everyone else. In the future, we can no longer consult Dr. Fang when we encounter work problems, but his noble character and contribution to the medical cause will always be remembered in our hearts.

In the early morning of February 5th, 2018, the next day after the beginning of spring, it was still biting wind. In the steep spring cold, more than 1,600 people rushed to Peking Union Medical College Hospital from all over the country just to say goodbye to a doctor. The sorrow and joy in the farewell hall are low. In the documentary playing on a loop, he is still diagnosing and treating patients, and he is still preaching for young doctors. His children and grandchildren are around the same roof for four generations. He is in his prime and high spirits, and he is white as snow and light... He is Dr. Fang Qi, a benevolent medical master, a forward-looking discipline pioneer and leader, and a modest gentleman who is as gentle as jade, round on the outside and square on the inside. He left us before another spring, and although he has many glamorous titles, here, we still call him Doctor Fang, his favorite name and the most accustomed to his younger generations.