2016年 · 第44卷第05期

There are hundreds of millions of patients with hypertension, diabetes, obesity, tobacco dependence, etc., and millions of atherosclerotic cardiovascular disease, cancer, and chronic obstructive pulmonary disease. Unhealthy lifestyles and behaviors as their root causes are widespread.

The development of percutaneous coronary intervention (PCI) is changing with each passing day. Since the "China percutaneous coronary intervention Guidelines 2012 (Simplified)"^[1]After the publication, many important clinical trial results were published. The Interventional Cardiology Group of Cardiovascular Disease Branch of Chinese Medical Association, the Thrombosis Prevention and Treatment Professional Committee of Cardiovascular Physicians Branch of Chinese Medical Doctors Association and the Editorial Board of Chinese Journal of Cardiovascular Diseases organized an expert group to collect and systematically analyze the latest clinical studies after 2011, especially the results of large-scale clinical trials in Chinese population. With reference to the latest relevant guidelines issued by American College of Cardiology (ACC), American Heart Association (AHA) and European Society of Cardiology (ESC), combined with China's situation and clinical practice, we systematically reviewed the literature, reached a consensus on current hot issues based on careful discussion, updated the 2012 guidelines, and compiled the "Guidelines for Percutaneous Coronary Intervention in China (2016)" (hereinafter referred to as the 2016 guidelines), which is published in this issue^[2]。

Whether in developed or developing countries, the high incidence rate of vascular diseases is increasingly prominent, and its mortality rate ranks first among all-cause deaths, which seriously threatens human health. According to the statistics of the American Heart Association and the Stroke Association, among all causes of death, 45.6% of cardiovascular diseases were mainly coronary heart disease, and 16.1% were mainly cerebrovascular diseases^[1]。 According to the statistics of the 2014 China Cardiovascular Disease Report, the prevalence rate of cardiovascular diseases in urban and rural areas in China is as high as 20.0%, that is, 1 in every 5 adults suffers from cardiovascular diseases, and the number of discharged patients with cardiovascular and cerebrovascular diseases is 14.3529 million, accounting for 12.24% of the total number of discharged patients in the same period^[2]。

Atrial fibrillation (AF) has common risk factors with heart failure (HF), such as hypertension, coronary heart disease, valvular disease, diabetes, obesity and sleep apnea syndrome. The two are mutually causal. Heart failure can facilitate the occurrence of atrial fibrillation through various ways, such as increased atrial pressure or increased atrial volume load, atrial enlargement, stromal fibrosis, electrophysiological remodeling and activation of renin angiotensin aldosterone system. In atrial fibrillation, loss of atrial systolic function, functional mitral/tricuspid regurgitation, tachycardiac cardiomyopathy and shortened ventricular filling time can lead to the occurrence and development of heart failure. Therefore, atrial fibrillation and heart failure often coexist, and the prevalence of central failure in patients with atrial fibrillation is 34%^[1]The prevalence of atrial fibrillation in patients with heart failure is 9% to 31%^[2,3]。 Compared with heart failure patients with sinus rhythm, these patients had a worse prognosis, with significant increases in length of stay and hospitalization, mortality, and mortality from cardiovascular disease^[4]Is a very serious challenge.

Anatomical and pathological studies confirmed that about 90% of thromboembolus in patients with atrial fibrillation (AF) originated from the left atrial appendage^[1]。 In recent years, percutaneous left atrial appendage occlusion has gradually become one of the mainstream treatment methods for preventing cardiogenic embolism in atrial fibrillation. The 2012 European Society of Cardiology Guidelines gave Class IIB recommendation^[2]The U.S. Food and Drug Administration approved the Watchman left atrial appendage occluder for sale in the United States in March 2015.

Since "Chinese Guidelines for Percutaneous Coronary Intervention 2012 (Simplified)"^[1]Since the update, many clinical evidences have been accumulated in percutaneous coronary intervention (PCI) and related fields. Therefore, the Interventional Cardiology 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 publish the 2009 and 2012 Chinese PCI Guidelines^[1,2]Based on the latest clinical research results, especially the results of large-scale randomized clinical trials in the Chinese population, refer to the latest American College of Cardiology/American Heart Association (ACC/AHA), European Society of Cardiology (ESC) and other organizations^{[3,4,5,6,7,8,9]}Combined with China's national conditions and clinical practice, the hot spots and focus issues in the field of PCI treatment were comprehensively discussed and a consensus was reached, and this guide was compiled on this basis.

The patient was a 53-year-old male. Deny history of hypertension, hyperlipidemia, diabetes, gallbladder stones, do not smoke, and drink a small amount of alcohol. I was depressed because of the loss of my father a week ago. Two hours before the visit, after drinking 100 ml of white wine, there was sudden dull pain in the upper abdomen, followed by persistent dull pain, accompanied by nausea, vomiting a little food residue, no hematemesis, no melena, and no fever. The pain could not be relieved by itself. Considering acute gastric mucosal lesions, metoclopramide hydrochloride 10 mg intramuscular injection and pantoprazole 80 mg intravenous drip were given to treat the pain, but there was still no significant relief. The patient's epigastric pain worsened after about half an hour. Bedside electrocardiogram showed sinus rhythm, normal electric axis, upward elevation of ST segment arch in II, III and aVF leads, lower oblique depression of ST segment in aVL lead, inversion of T wave, V₁The lead T wave is low and flat, V₂~ V₆Lead ST segment depression and T wave inversion. Acute inferior wall myocardial infarction is considered. Aspirin 300 mg and ticagrelor 180 mg orally were administered and immediately followed by emergency coronary intervention. At the same time, liver and kidney function, electrolyte, blood sugar, blood lipid, blood routine and cardiac troponin were urgently checked. Coronary angiography showed no obvious stenosis in the left main trunk, a small amount of atheromatous plaque in the middle of the anterior descending artery, mild irregularity in the wall of the canal, and 20% stenosis; No obvious stenosis of the circumflex artery was observed; A small amount of atheromatous plaque in the distal right corona. Left ventriculography with pigtail catheter showed (Figure 1): The systolic activity at the apex of the left ventricle was significantly weakened, and the systolic activity at the base of the heart was violent and spherical. The results of emergency laboratory examination showed that cardiac troponin I (cTnI) was 0.26 μ g/L (reference value 0-0.04 μ g/L) and creatine kinase isoenzyme (CK-MB) was 14.3 μ g/L (reference value 0.3-4.0 μ g/L). The diagnosis was apical balloon syndrome. The patient was treated in the cardiovascular care unit for 1 week, and his vital signs were closely tested. He was given fructose nutrition myocardial therapy, and the patient was instructed to pay attention to rest and eat light diet. One week later, the cardiac myocardial necrosis markers, cTnI 0.02 μ g/L and CK-MB 1.2 μ g/L were re-examined, and all returned to the normal range; Reexamination of echocardiography showed that the morphology of each chamber of the heart basically returned to normal; Electrocardiogram leads also returned to normal.

A 16-year-old male was admitted to the hospital on 10 June 2015 due to "sudden crushing pain in the precordial area and retrosternal bone for half an hour". The patient's chest pain attack was accompanied by sweating, nausea and vomiting. The vomit was stomach content, without dizziness and amaurosis, and the pain persisted without relief. The patient had no general fever, night sweats, joint pain, precordial pain and intermittent claudication. Emergency electrocardiogram showed acute inferior myocardial infarction, hyperacute phase (Figure 1)。 Emergency laboratory tests: lactate dehydrogenase 502 U/L, troponin I 10 μ g/L, creatine kinase isoenzyme (CK-MB) 299 U/L, B-type diuretic peptide 267 U/L.

A 25-year-old female was admitted to the hospital on 11 March 2015 due to "3 years of heart murmur". Three years ago, a heart murmur was found during a physical examination in a local hospital. There were no palpitations, chest tightness, shortness of breath, cyanosis and squat, and there was no difference in growth and development from peers. Physical examination at admission: pulse 74 beats/min, breathing 20 beats/min, blood pressure 115/80 mmHg (1 mmHg =0.133 kPa); There is no cyanosis of the lips and no filling of the jugular vein; The breathing sounds of both lungs were clear, and no dry and wet rales were heard; There was no bulge in the precordial area, no lift-like beat, systolic tremor palpable in the 3rd to 4th intercostal area of the right margin of the sternum, apical beat located 0.5 cm in the 5th intercostal area of the right clavicular midline, no enlargement of the heart turbidity boundary, heart rate 74 beats/min, uniform rhythm, and rough systolic murmur of grade 3/6 could be heard in the 3rd to 4th intercostal area of the right margin of the sternum; The abdomen is soft, and the liver and spleen are untouched under the costs; There was no edema in both lower limbs. Blood routine: red blood cells 4.25×10¹²/L, hemoglobin 138 g/L. Blood gas analysis: pH 7.39, partial pressure of carbon dioxide (PaCO₂) 40 mmHg, oxygen partial pressure (PaO₂) 97 mmHg, oxygen saturation (SaO₂)96%。 Electrolytes, liver and kidney functions and coagulation functions were normal. Conventional 12-lead ECG showed ECG changes in the mirror dextrocardiac (Figure 1)。 The chest X-ray showed that the heart was located on the right side of the chest cavity, which was a mirror dextrocardiac position. Echocardiography showed specular dextrocardia, ventricular septal defect (perimembranous type, diameter 4.9 mm), left-to-right shunt at ventricular level, left ventricular end-diastolic diameter 49.6 mm, right ventricular end-diastolic diameter 17.2 mm, left ventricular ejection fraction 61%. Abdominal ultrasound showed visceral inversion. The admission diagnosis was mirror dextrocardiac with ventricular septal defect and visceral inversion.

A 56-year-old male was admitted to the hospital on 31 October 2015 due to "sudden chest pain for 9 h". The patient had sudden chest tightness and chest pain after dinner 9 h ago, accompanied by radiating pain in the back and palpitations, which were mild and tolerable, and slightly relieved after rest. At 0: 00 a.m. on October 31st, the patient's chest pain was aggravated and unbearable, accompanied by profuse sweating, no nausea, vomiting, dizziness, amaurosis, abdominal pain, abdominal distension, acid reflux and belching, and went to the emergency department of the local hospital. Electrocardiogram showed: sinus rhythm, ST-T changes in II, III and aVF leads; Troponin I 0.34 μ g/L; Chest CT showed high-density nodules in the upper lobe of the right lung, bronchitis with smaller bullae, bilateral pleural thickening, and high-density shadows in the lower esophagus and lower mediastinum (Figure 1)。 After anti-inflammatory and myocardial protection treatment, the symptoms of chest pain were not relieved. After 2 h, the reexamination of troponin I was 0.59 μ g/L, and the chest pain tended to worsen. Acute myocardial infarction was considered, and it was recommended to be transferred to a hospital for continued diagnosis and treatment.

The American Diabetes Association (ADA) inDiabetes CarePublished "2015 ADA Diabetes Medical Diagnosis and Treatment Standards"^[1]Emphasizing that diabetic patients over 40 years old should routinely receive statin treatment; Diabetic patients aged 40 to 75 should receive moderate or high intensity statin therapy; In addition, all diabetic patients with cardiovascular disease and patients aged 40 to 75 years with any risk factor for cardiovascular disease should receive high-intensity statin therapy. One obvious change in the new ADA guidelines is that statin treatment and intensity for diabetic patients should be determined based on the patient's risk assessment, rather than low density lipoprotein cholesterol (LDL-C) levels^[1,2]。

Aging refers to the degenerative changes such as the decline of body shape, structure and function gradually appearing with the increase of age, and is an independent risk factor for cardiovascular and cerebrovascular diseases. Cellular senescence refers to the arrest of the irreversible growth cycle of cells, along with changes in cell morphology, metabolism, related gene expression and epigenetic regulation^[1]Including increased expression of cell cycle inhibitory regulatory proteins, enhanced aging-related β-galactosidase activity, and aging-related heterochromatin aggregation^[2]。 Telomere shortening as the main mechanism leading to cell replicative senescence^[3]In addition, various cytokines, tumor genes and oxidative stress can also induce cell senescence^[4]。 More and more evidence shows that cellular senescence is involved in the aging process of organism through changes in gene expression^[5]Therefore, the study of cellular senescence may be the basis for the study of aging diseases such as cardiovascular diseases, neurodegenerative diseases, and degenerative bone diseases.

ischemia reperfusion injury (IRI) refers to the phenomenon that the metabolic, functional and structural damage of ischemic tissues and organs is aggravated or even irreversible after blood perfusion is restored after a certain period of time^[1]。 The occurrence of IRI is relatively common, and can occur after myocardial infarction, cerebral infarction, lung and kidney transplantation, so it is of great clinical significance to study the pathophysiology and mechanism of IRI. At present, the two main mechanisms of IRI occurrence are intracellular calcium overload and excessive production of reactive oxygen species (ROS)^[2]So how to reduce intracellular calcium overload plays an important role in reducing IRI. In recent years, the results of cell electrophysiological studies have shown that not only the opening of mitochondrial ATP-sensitive potassium channels can reduce intracellular calcium overload, but also reduce IRI^[3]Moreover, high conductance calcium activates potassium channels (BK_CaChannel) openness can also mitigate IRI^[4], even its IRI-mitigating effect is stronger than that of ATP-sensitive potassium channels^[5]Therefore, this paper mainly reviews BK_CaThe role of channels in IRI and their mechanisms.

In recent years, with the increasing incidence of coronary heart disease, acute myocardial infarction has become one of the emergencies that seriously affect human life. The level of first aid for myocardial infarction is also constantly improving, and the survival time of patients is significantly prolonged. Therefore, the follow-up rehabilitation of patients with myocardial infarction and the assessment of labor force level are increasingly important. However, there is always a lack of a concise grading evaluation system for the extent of myocardial damage caused by one myocardial infarction. The team of Professor He Ben, Department of Cardiology, Renji Hospital affiliated to Shanghai Jiao Tong University School of Medicine originally put forward a new grading standard for heart injury after acute myocardial infarction, which has attracted wide attention from academic circles at home and abroad^[1]。