2016年 · 第44卷第02期

On October 25th, 2015, I successfully helped treat a 44-year-old male patient with acute myocardial infarction on the high-speed train from Luoyang to Zhengzhou with volunteers from the Great Medical Fraternity Volunteer Service Corps of the Capital Volunteer Service Federation. Many people say that this patient is lucky, coinciding with the fact that there are doctors on the train and a team of professional doctors, but this is an accident after all, and most public transportation lacks medical staff. So how can this accident become the norm and more lives be saved?

Thrombosis is an important factor in coronary atherosclerosis and its complications, and it is also the initiator of adverse cardiac events in coronary heart disease, which can often cause serious consequences such as myocardial infarction and even death^[1]。 In the past ten years, clinical research on thrombosis prevention and treatment has been very active at home and abroad, and thrombolytic therapy as an important reperfusion method has also obtained some new research evidence. The focus of research has shifted from treatment to equal emphasis on prevention and treatment. Many new antithrombotic drugs have been developed and marketed one after another. Monitoring the efficacy and safety of antithrombotic therapy is becoming increasingly popular. A large number of randomized controlled clinical studies focus on exploring the best dose, compatibility and course of treatment of antithrombotic therapy, and guide clinical practice through timely updates of guidelines, so that the risk of thrombotic events is significantly reduced. However, due to the different causes of thrombosis, the particularity of hemorrhagic complications of antithrombotic therapy and the complexity of clinical conditions of patients, standard antithrombotic therapy is not suitable for all patients, and thrombolytic therapy is far from receiving its due attention in China. Therefore, paying attention to the use of new evidence from China to guide the individualized treatment of thrombolytic and antithrombotic drugs is the current direction of thrombolytic and antithrombotic treatment of coronary heart disease in China.

percutaneous coronary intervention (PCI) is one of the main methods for the treatment of coronary heart disease at present. More than 1 million people in the United States receive PCI every year, and in China, the number has rapidly risen to more than 500,000/year. Hemorrhage is the most common complication after PCI, which not only increases the incidence of death and major cardiovascular events (MACE) after PCI, but also prolongs the length and cost of hospital stay^[1]。

percutaneous coronary intervention (PCI) and the development of antiplatelet drugs, especially aspirin combined with P2Y₁₂The application of receptor antagonists significantly reduces ischemic events in patients with acute coronary syndrome (ACS) and PCI, but the incidence of bleeding increases correspondingly, resulting in poor prognosis. In recent years, the role of genetic genes in the pathogenesis of patients with high risk of hemorrhage and the prediction level of hemorrhage risk through genetic testing have become the hot research topics at home and abroad. This article focuses on the influence of genetic genes on hemorrhage in patients with double antiplatelet after PCI and its predictive value.

Hemorrhage is one of the serious complications after percutaneous coronary intervention (PCI) in patients with coronary heart disease, and its impact on the poor clinical prognosis is no less than ischemic complications, or even more serious. There are many risk factors related to bleeding after PCI. Besides age, sex, weight, kidney function and other risk factors, the choice and dose of anticoagulants are also factors that cannot be ignored.

With the development of antiplatelet therapy concept and drugs, rational application of antiplatelet drugs is an important measure to improve the prognosis of patients with coronary heart disease. The long-term treatment of stable coronary artery disease (SCAD) aims to improve the blood supply to the coronary artery to relieve ischemic symptoms, and to give antiplatelet therapy in addition to anti-atherosclerotic therapy to reduce thrombotic events and reduce mortality^[1]。 Changes in antiplatelet therapy strategies for SCAD stem from a deeper understanding of the course of atherosclerotic lesions. Atherosclerosis is a systemic and progressive process. There are great differences in the development of atherosclerosis in patients with stable clinical manifestations of coronary heart disease. There are often different atherosclerotic plaques (stable and unstable plaques) in multiple sites, while the occurrence of thrombotic events is unpredictable^[2]Long-term antiplatelet therapy in patients with SCAD is critical. At the same time, antiplatelet therapy is bound to be accompanied by the risk of bleeding. Therefore, different intensities of antithrombotic therapy should be used based on the risk of thrombus and bleeding in different individuals. This consensus draws on European and American guidelines^[1,3,4]And review the research evidence in this field to help clinicians further understand and comprehensively evaluate the benefits and risks of antiplatelet therapy, reasonably choose antiplatelet therapy strategies according to the different characteristics of SCAD patients, better reduce the risk of thrombotic events and bleeding events, and improve patient survival rate.

Coronary heart disease is a common disease with high sudden death rate and serious harm. Standardized management of coronary heart disease is the key to improve prognosis and reduce mortality. Whether drugs or interventional therapy are taken, antiplatelet therapy is the cornerstone of coronary heart disease management. Double antiplatelet, i.e. aspirin combined with a P2Y₁₂Receptor antagonists are the standard treatment for patients with acute coronary syndromes (ACS) and/or percutaneous coronary intervention (PCI). Ticagrelor is a novel potent P2Y₁₂Receptor antagonist, multinational, multicenter, double-blind randomized controlled PLATO study showed that ticagrelor improved the prognosis of patients with ACS further than clopidogrel^[1]Since 2011, it has been recommended as the first-line or first-choice antiplatelet drug for ACS patients by many European and American guidelines^[2,3,4,5]。 Ticagrelor was approved in China in November 2012, although it has been recommended by China's non-ST-elevation acute coronary syndromes (NSTE-ACS) guidelines, PCI guidelines and acute ST-elevation myocardial infarction (ST-elevation myocardial infarction, STEMI) diagnosis and treatment guidelines^[6,7,8]However, the experience in clinical use is relatively insufficient. In order to help the majority of clinical workers in China use ticagrelor reasonably and standardizedly, this expert consensus is specially compiled.

The patient was a 58-year-old male. He was admitted to hospital on September 4, 2014 due to "chest tightness, shortness of breath for 5 years and chest pain for 1 week". In the past 5 years, the patient experienced exertion chest tightness, shortness of breath and precordial discomfort, which was relieved after a few minutes of rest, accompanied by sweating, palpitations, without dizziness, amaurosis and syncope, and was not paid attention and systematic diagnosis and treatment. One week ago, after a full meal, a posterior squeezing pain at the lower end of the sternum occurred, accompanied by profuse sweating and dizziness. The symptoms were slightly relieved after 15 minutes, and the symptoms were completely relieved after 30 minutes without syncope. Prior history of hypertension for 8 years, with a maximum of 220/120 mmHg (1 mmHg =0.133 kPa), long-term oral antihypertensive drugs, and blood pressure controlled at around 160/90 mmHg.

The patient was a 21-year-old female, 58 kg. Because the due date had passed, I went to the local hospital for examination. I heard a continuous murmur at the left margin of the sternum after auscultation. Echocardiography showed rupture of aortic sinus aneurysm. With "pregnancy complicated with heart disease, intrauterine pregnancy 42^＋6Zhou ", came to the emergency department of our hospital on January 6, 2013. He had no previous history of hypertension and diabetes, and did not have regular prenatal check-ups during pregnancy. Physical examination: blood pressure 126/66 mmHg (1 mmHg =0.133 kPa), heart rate 102 beats/min, uniform heart rhythm, and continuous murmur of grade 3/6 could be heard in the intercostal area of 3~4 on the left margin of the sternum. Electrocardiogram showed sinus tachycardia and incomplete right bundle branch block. Echocardiography showed no coronary sinus rupture of the aorta into the right ventricular outflow tract (Figure 1)。 Blood biochemical examination showed procalcitonin 0.309 μ g/L (normal value 0-0.096 μ g/L), alanine aminotransferase (ALT) 172 U/L (normal value 0-40 U/L), aspartate aminotransferase (AST) 93 U/L (normal value 0-40 U/L), D-dimer 2.87 mg/L (normal value 0-0.55 mg/L), and the other results were not abnormal. After consultation with multidisciplinary experts in obstetrics, gynecology, cardiology and cardiac surgery, it is recommended to terminate the pregnancy by cesarean section in emergency department first, and then transfer to the intensive care unit of cardiology department after operation. After the condition is stable, transfer to the cardiac surgery department to complete the cardiac surgery.

With the improvement of people's living standards, the incidence of cardiovascular and cerebrovascular diseases is increasing day by day, and it has become the disease with the highest disability and mortality rate in the world. Its pathogenesis is very complex, involving gene, environment, metabolism and other aspects. aldehyde dehydrogenase (ALDH) 2 is a key enzyme of ethanol metabolism pathway and an important antioxidant stress molecule. Its important functional single nucleotide polymorphism, Glu504Lys polymorphism, located at rs671 site, has an important relationship with the development of cardiovascular and cerebrovascular diseases^[1,2,3]。 A genome-wide association analysis study in 2012 confirmed that the *504Lys allele is a genetic susceptibility gene locus for coronary heart disease^[4]。 ALDH2 is also involved in myocardial protection and neuroprotection. Activation of ALDH2 can reduce myocardial ischemic injury^[5]and cerebral ischemic injury^[6]。 Therefore, further in-depth research on the mechanism of ALDH2 affecting cardiovascular and cerebrovascular diseases will surely help to promote early screening, individualized prevention and the development of new molecular target drugs for people susceptible to cardiovascular and cerebrovascular diseases. Relevant mechanism studies show that the effect of ALDH2 on cardiovascular and cerebrovascular diseases is closely related to its effects on alcohol consumption, aldehydes, inflammation and oxidative stress, blood lipids and blood glucose, and endothelial function. This article will review the relationship between ALDH2 and cardiovascular and cerebrovascular diseases and its influence mechanism at home and abroad.

A large number of epidemiological investigations have shown that exposure to PM2.5 can increase the occurrence of cardiovascular events. However, the specific mechanism of cardiovascular damage caused by PM2.5 is still unclear, and the evaluation system of cardiovascular damage caused by PM2.5 is not perfect. Therefore, this paper summarizes the research progress of molecular mechanism and evaluation index of cardiovascular damage caused by PM2.5 in recent years as follows.

aortic dissection (AD) is a process in which blood flows into the middle layer of cystic degeneration through the intimal tear opening, forms a dissecting hematoma, and gradually expands and dissociates in the middle layer of aorta with the driving of blood flow pressure. The onset of this disease is dangerous, the clinical manifestations are complex and diverse, the early diagnosis is difficult, and the mortality rate is high. In recent years, the incidence rate is on the rise^[1]。 The mortality rate of type A AD (Stanford classification) increased by 1% to 2% per hour in the first 24 hours without treatment, and the mortality rate was close to 50% at one week^[2,3]。 In the clinical study of AD, we found that some patients had another disease that appeared to have no causal relationship with each other at the same time. Further research found that there may be a common pathogenic mechanism between the two. We introduced the concept of "comorbidity" to describe this phenomenon. "Comorbidity" was first proposed by Feinstein in 1970, and has been mainly used in the field of psychiatry until now. The Campbell Dictionary of Psychiatry defines it as the presence or suffering from more than one disease in the same patient^[4]。 In this paper, the comorbidity of AD and its possible co-pathogenic mechanism are expounded.