2018年 · 第46卷第09期

The incidence of coronary heart disease in China is increasing year by year, and percutaneous coronary interventions (PCI) is the main measure in the diagnosis and treatment of coronary heart disease. Currently, the indication for PCI is mainly based on the results of coronary angiography or endovascular imaging (endovascular ultrasound or optical coherence tomography, etc.). However, studies have shown that myocardial ischemia is a key factor in determining the treatment strategy of coronary heart disease. Coronary angiography or endovascular imaging techniques can only evaluate the anatomy of the lesion, but cannot directly reflect the extent of myocardial ischemia. Correct understanding of the dialectical relationship between coronary artery stenosis and myocardial ischemia will help us to make appropriate clinical decisions better and more scientifically.

In 2017, the new U.S. Hypertension Guidelines reduced the diagnostic criteria for hypertension from 140/90 mmHg (1 mmHg =0.133 kPa) to 130/80 mmHg, defining 130~139/80~89 mmHg as Grade 1 hypertension, and ≥140/90 mmHg as Grade 2 hypertension^[1]。 The new European Hypertension Guidelines published in June 2018, although this blood pressure range is still defined as normal high (130~139/85~89 mmHg) or normal blood pressure (120~129/80~84 mm Hg), is not the same as ideal blood pressure (<120/80 mmHg), but the medication and lifestyle recommendations for normal high values are not different from the new U.S. Hypertension Guidelines.

Recently, "homocysteine level is the most accurate independent health indicator" has been widely circulated on the Internet, and at the same time, there is a publishing conference of the translation of "Homocysteine: Cholesterol in a New Era", which has caused controversy in academia and the public for a time. Some scholars believe that hyperhomocysteinemia is the most important independent risk factor for cardiovascular disease and stroke (especially stroke in China).

The "Guidelines for Diagnosis and Treatment of Chronic Stable Angina Pectoris" formulated by a joint committee composed of many experts from the Cardiovascular Branch of Chinese Medical Association in 2007^[1]Fully adopting Chinese population epidemiological and clinical research evidence, combined with foreign research results and guidelines, has played an important guiding role in the prevention and treatment of stable coronary artery disease (SCAD) in China. In the past 10 years, due to the continuous update of evidence-based medicine, the understanding of the pathophysiological mechanism of SCAD, the diagnosis methods and treatment methods of disease have been more deeply understood. Therefore, the Interventional Cardiology Group, Atherosclerosis and Coronary Heart Disease Group of Cardiovascular Disease Branch of Chinese Medical Association, the Thrombosis Prevention and Treatment Professional Committee of Cardiovascular Physicians Branch of Chinese Medical Physicians Association and the Editorial Committee of Chinese Journal of Cardiovascular Diseases organized an expert group to refer to domestic and foreign guidelines on the basis of evidence-based evidence on clinical application of new technologies and new drugs released in recent years^[2,3,4,5]Combined with the actual situation in China, the contents of the 2007 version of the guidelines were updated to provide the basis and principles for the diagnosis and treatment of SCAD patients in China, and to help clinicians make medical decisions.

A 76-year-old male was admitted to the hospital on January 21, 2017 due to "chest tightness and chest pain for 3 h". The patient had sudden chest tightness and chest pain during sleep 3 h ago, accompanied by sweating and nausea, without back pain, amaurosis and syncope. Take 2 capsules of Suxiao Jiuxin Pill by yourself, but the symptoms are not relieved. He had been seen in an external hospital, and his ECG showed V₂~ V₅The leads were oblique depression 0.20 mV, accompanied by high T wave tip. Half an hour later, the patient developed a coma, mandibular breathing, inaccessible aorta, and electrocardiogram showed ventricular fibrillation. Immediately after defibrillation and chest cardiac compression, the patient regained consciousness and was transferred to our hospital. The patient had a history of hypertension for more than 20 years, and his blood pressure was under acceptable control. He has smoked for more than 20 years and has quit smoking for 2 months. Physical examination: body temperature 36.2 ℃, pulse 74 beats/min, breathing 20 beats/min, blood pressure of left upper limb 140/60 mmHg (1 mmHg =0.133 kPa), blood pressure of right upper limb 126/69 mmHg, blood oxygen saturation (SO₂）100%。 Conscious, poor spirits. The breathing sounds of both lungs were thick, and no dry or wet rales were heard. The heart rate was 74 beats/min, the heart rhythm was uniform, and no pathological murmur was heard. Soft abdomen, no tenderness. After admission, the electrocardiogram revealed ST segment elevation of leads Ⅱ, Ⅲ and aVF 0.05 mV, V₂~ V₅Lead ST segment depression 0.5~0.8 mV, T wave high tip (Figure 1）。 Creatine kinase isoenzyme (CK-MB) was 2.0 μ g/L at 7 h of onset (reference value<4.0 μ g/L), 2.6 μ g/L at 11 h of onset (reference<5.0 μ g/L); Troponin I was 50~100 ng/L (reference value<100 ng/L), and 64 ng/L (reference value 0-30 ng/L) at 11 h of onset.

A 14-year-old female was admitted to the hospital on August 26, 2016 due to "chest tightness and shortness of breath with aggravation of cyanosis after activity for 3 years". Patients have weak mobility since childhood, are prone to asthma after activity, and their growth and development lag behind those of children of the same age. Shortness of breath after activity appeared 7 years ago, and the symptoms worsened in the past 3 years and were transferred to our hospital. History of hemoptysis, recurrent pulmonary infection and asthma were denied, and history of chest pain and syncope were denied. Full term natural delivery, denial of HIV and other intrauterine infections and hereditary family history.

Cardiac remodeling is one of the main causes of serious cardiovascular events such as heart failure (HF) and sudden death. Innate immune responses involve complex cascades: pattern recognition receptors (PRRs) encoded by multiple germlines quickly recognize pathogens or damage factors, resulting in increased synthesis and secretion of cytokines, and participate in coordinating host defense responses. The inflammatory response is the body's protective response to a pathogenic signal, usually rapid and specific, and terminates once the signal is released. However, in a state of overactivation or suppression of innate immunity in the body, inflammatory responses can lead to serious consequences, such as cardiac remodeling. In this paper, the role of innate immune signaling molecules in cardiac remodeling in hypertension is reviewed in order to discover more valuable potential therapeutic targets.

coronary atherosclerotic vulnerable plaque is the main cause of acute coronary syndrome (ACS). Traditionally, vulnerable plaque is characterized by large lipid core, thin fibrous cap and massive macrophage infiltration. After rupture, it causes sudden intraluminal thrombosis and causes acute coronary events^[1]。 1994 van der Wal et al.^[2]For the first time, it was found that blood clots can form without rupturing the fibrous cap of the plaque. This type of plaque is called eroded plaque. After that, in 1996 Farb et al.^[3]It was found that approximately 44% of sudden death events due to coronary thrombosis had eroded plaques. Therefore, in 2003 Naghavi et al.^[4,5]The definition of vulnerable plaques was updated and expanded to consider vulnerable plaques that are prone to thrombosis or are at risk of rapidly progressing into accident-causing plaques and can independently trigger ACS. optical coherence tomography (OCT) was used to classify coronary plaques in patients with ACS. There were two main types: ruptured plaques and eroded plaques, among which eroded plaques accounted for 30% ~40%^[6]。 The study found that the proportion of ruptured plaque was higher than that of eroded plaque in patients with ST-segment elevation myocardial infarction, while the proportion of eroded plaque was higher in patients with non-ST-segment elevation myocardial infarction. Recent epidemiological studies have shown that the risk spectrum of ACS is characterized by time-dependent transfer. ST-segment elevation myocardial infarction decreases, while non-ST-segment elevation myocardial infarction increases^[7]。 Although lipid-lowering therapy, especially statin therapy, can thicken the plaque fibrous cap and reduce the volume of the lipid nucleus, thereby stabilizing the plaque with a tendency to rupture, it does not completely reduce the risk^[8]。 In view of the further research on the epidemiology and pathology of ACS, erosion plaque has gradually become a kind of accident plaque that cannot be ignored. Clinical studies have found that the effect of emergency interventional therapy and clinical prognosis of patients with eroded plaque classified by OCT are better than those of patients with ruptured plaque^[9]； EROSION studies have shown^[10]Antithrombotic therapy for patients with eroded plaque can effectively reduce the thrombus area and is expected to avoid stent interventional therapy. Therefore, it is of great significance to study the pathological mechanism of the occurrence and development of erosive plaque and clarify its pathogenesis to guide the accurate diagnosis and treatment of ACS patients and reduce the incidence and mortality of cardiovascular events.

At present, diabetes has become one of the major health problems in the world. The incidence of diabetes and its chronic complications is increasing year by year, which seriously affects human health and socio-economic development. According to statistics from the International Diabetes Federation (IDF) in 2015, there are about 415 million diabetic patients worldwide, and the number of diabetic patients worldwide may exceed 642 million by 2040^[1]。 About 11% of Chinese people have diabetes, including a large proportion of undiagnosed people^[2]。 Chronic complications of diabetes can involve many important organs in the body, such as heart, blood vessels, kidney and nervous system, and diabetic vascular disease is the most common complication and the leading cause of death in diabetic patients^[3,4]。 Clinically, about 70% of diabetic patients die from cardiovascular and cerebrovascular complications such as coronary heart disease and stroke^[5]。 Hyperglycemia caused by diabetes causes metabolic and hemodynamic changes in the body, including the formation of advanced glycation end products (AGE), reactive oxygen species (ROS) production, protein kinase C (PKC) Activation, activation of the polyol pathway and the renin angiotensin system, etc., leading to the characteristic changes of diabetic vasculopathy^[5]。 In addition, vascular calcification is widespread in diabetic patients, resulting in reduced vascular wall elasticity and compliance and an increased risk of clinically adverse cardiovascular events^[6]。 Persistent hyperglycemia and the accumulation of AGE in diabetes mellitus are important causes of diabetic vascular calcification. Therefore, paying attention to AGE and its receptor (RAGE) and its downstream related signal transduction pathways, and clarifying the pathogenesis of diabetic vascular calcification can provide new guidance for the prevention and treatment of diabetic vascular calcification.