2015年 · 第43卷第01期

The past 2014 can be described as the "guideline year" in the cardiovascular field. In particular, the American College of Cardiology (ACC) and the American Heart Association (AHA) have successively announced the long-awaited new guidelines for dyslipidemia and hypertension since the end of 2013, which has aroused the attention and doubt of China and the whole world, and the academic debate is unprecedentedly active.

The long-awaited results of IMPROVE – IT (improved reduction of outcomes: vytorin efficacy international trial) were announced at the American Heart Association (AHA) Academic Congress in Chicago, USA on November 19, 2014. 1,159 hospitals in 39 countries participated in the study; A total of 18 144 patients ≥50 years old with acute coronary syndrome (ACS) within 10 days of onset were enrolled and randomized to receive simvastatin + cholesterol absorption inhibitor ezetimibe 10 mg/d or simvastatin + placebo; Follow-up was 9 years (median time 6 years); Low-density lipoprotein cholesterol (LDL – C) decreased to 1.4 mmol/L (54 mg/dl) and 1.8 mmol/L (69 mg/dl), respectively, in both groups; The prognostic endpoint in the simvastatin + ezetimibe group was 6.4% less than the relative risk in the simvastatin alone group (P=0.016), an absolute risk reduction of 2%, 1 event reduction per 50 patients treated, a 20% reduction in stroke, a 10% reduction in myocardial infarction, a significant reduction in cardiovascular deaths, and the combination of statin and ezetimibe is safe and does not increase liver and muscle adverse reactions. What are the academic and clinical implications of IMPROVE – IT? What impact will it have on the guidelines?

The international expert consensus on hereditary arrhythmias was first published in the "Updated Definition and Classification of Cardiomyopathy" drafted by the American Heart Association (AHA) in 2006^[1]。 In 2007, the National Heart, Lung and Vascular Institute and the Office of Rare DiseasesCirculationAn expert consensus report on the diagnosis, clinical manifestations, molecular mechanisms and treatment of primary cardiomyopathy caused by gene mutations affecting ion channel function was published in^[2]。 In 2011, the American Heart Rhythm Society/European Heart Rhythm Society released the Expert Consensus on Genetic Testing of Cardiac Ion Channel Disease and Cardiomyopathy^[3]。 In 2013, the American Heart Rhythm Society (HRS) /European Heart Rhythm Society (EHRA) /Asia Pacific Heart Rhythm Society (APHRS) jointly released the Expert Consensus on the Diagnosis and Treatment of Hereditary Primary Arrhythmia Syndrome.^[4]。

From January 2011 to May 2014, 9 cases of coronary artery perforation caused by guidewire occurred during percutaneous coronary intervention in the Heart Center of the First Hospital of Lanzhou University, all of which were treated with gelatin sponge particle embolization. Among them, 7 were males and 2 were females; Age 57-72 years old. There were 4 cases of acute myocardial infarction, 2 cases of unstable angina pectoris and 3 cases of old myocardial infarction combined with unstable angina pectoris. All coronary artery lesions were multi-vessel lesions, and 7 cases of perforated artery were occlusive lesions. Of the 9 cases of coronary artery perforation, hydrophilic coated guidewires were used in 8 cases (3 in Pilot 50 and 5 in Runthrough NS), of which 5 with microcatheter support. All coronary artery perforations were branch or distal small branch perforations, including left anterior descending artery in 3 cases, left circumflex artery in 3 cases and right coronary artery in 3 cases. Ellis classification according to coronary artery perforation^[1]There were 3 cases of type IIIA perforation, 1 case of type IIIB perforation, and 5 cases of type II perforation.

A 70-year-old male was admitted on 10 December 2013 due to intermittent retrosternal pain for 6 months, aggravated for 3 days. Has a history of cerebral infarction for 10 years without obvious sequelae; Smoking history for 50 years, about 25 cigarettes/d; Drinking history 50 years, 2 taels/d. Electrocardiogram after admission showed complete right bundle branch block; Echocardiography showed that the thickness of interventricular septum and left ventricular posterior wall was normal, the pulsation of all segments of left ventricle was generally reduced, and the left ventricular ejection fraction was 43%; Abdominal aortic atherosclerosis by color Doppler ultrasound of large abdominal vessels; Markers of myocardial necrosis: troponin I 0.72 μ g/L, creatine kinase isoenzyme (CK-MB) 5.66 μ g/L; Other tests showed no abnormalities. The admission diagnosis was acute non-ST segment elevation myocardial infarction, cardiac function grade I (Killip grade), and abdominal aortic atherosclerosis.

A 70-year-old female was admitted to the hospital on 12-Apr-2013 due to paroxysmal chest pain for 2 years, aggravated for 2 months. The patient developed precordial pain during activity 2 years ago, lasting 5 to 6 min, and relieved after rest. Two months ago, the onset of the above symptoms was more frequent than before, and it could occur during activity and rest. Previous history of hypertension. Admission physical examination: blood pressure 146/78 mmHg (1 mmHg =0.133 kPa); Clear breathing sounds in both lungs; Heart rate 70 beats/min, rhythm uniform. ECG showed Ⅰ, aVL, V₅and V₆Lead ST segment depression 0.05~0.10 mV. Admission was diagnosed as unstable angina and hypertension. Oral aspirin 300 mg and clopidogrel 300 mg after admission followed by oral aspirin 100 mg/d and clopidogrel 75 mg/d. Coronary angiography showed: left main trunk normal; Diffuse lesion of left anterior descending artery, 60% stenosis in the most severe part; Distal left circumflex artery stenosis was 90%, and proximal blunt artery stenosis was 80%; Multiple lesions of the right coronary artery, with 60% stenosis in the most severe part. It was decided to intervene in the left circumferential branch. After administration of heparin 7 500 U, a 6 F EBU 3.75 guide catheter was delivered to the left coronary artery. A Runthrough NS guidewire (Terumo, Japan) was delivered to the distal end of the left circumflex artery, and the lesion was expanded with a 2.0 mm ×15 mm balloon, and a stent was placed in the left circumflex artery. Postoperative coronary angiography showed myocardial staining (Figure 1), considered coronary artery perforation. Protamine 50 mg of neutralizing heparin was administered with an activated whole blood coagulation time (ACT) of 180 s, and a 1.2 mm ×6 mm balloon was applied to occlude the coronary artery at 4 atm (1 atm =101.325 kPa) for 15 min at the pre-perforation site. Review coronary angiography (Figure 2), no contrast agent exudation was found, and the occlusion was considered successful.

A 77-year-old female was admitted to the hospital for radiofrequency ablation due to "palpitations while speaking for more than 1 year". The patient began to have palpitations when speaking nearly a year ago. After he stopped speaking, the palpitations stopped and gradually worsened. Finally, he could hardly make any speaking movements, and as long as he opened his mouth to pronounce, he had palpitations. Quality of life is severely affected. Treatments such as propafenone and metoprolol have been ineffective. Deny the risk factors of coronary heart disease such as hypertension, diabetes, hyperlipidemia and smoking. Holter electrocardiogram showed speech-induced short bursts of atrial tachycardia (atrial tachycardia). Cardiac ultrasonography showed a left atrial diameter of 35 mm, a left ventricular diameter of 43 mm, and a left ventricular ejection fraction of 57%.

none-ST-segment elevation acute coronary syndrome (NSTE-ACS) includes unstable angina pectoris and non-ST-segment elevation myocardial infarction. According to statistics, it accounts for about 75% of the annual admissions of acute coronary syndrome in the United States, which is much higher than the proportion of ST-segment elevation acute coronary syndrome. NSTE-ACS has acute onset, severe lesions and many complications, but there are no typical electrocardiographic manifestations, and the diagnosis and treatment process is easily delayed. Therefore, how to actively and effectively diagnose and treat NSTE-ACS patients has attracted great attention, and it is one of the fields with the fastest updating of guidelines at present. There are still international controversies on whether interventional therapy should be done and the timing of interventional therapy. This article reviews these issues in conjunction with relevant guidelines published by the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), and the European Society of Cardiology (ESC) in 2011, and evidence-based medical evidence from recent years.

cardiovascular disease (CVD) has one of the highest morbidity and mortality rates in the world^[1]。 Among them, the most common coronary heart disease is a complex disease caused by the combination of many factors. In recent years, the rise of genome wide association study (GWAS) has provided a brand-new means for the study of genetic factors in the development of CAD. In 2007, in just a few weeks, two separate research groups identified the 9p21 segment of chromosome associated with CAD pathogenesis almost simultaneously, making it the earliest genetic risk locus associated with CAD pathogenesis^[2,3]。 The 9p21 segment of chromosome contains a tightly linked disequilibrium haplotype region about 58 kb long, which contains a large number of CAD-related risk single nucleotide polymorphism sites (SNPs). Early studies of GWAS were mainly conducted in the European and American populations, and later their association was found in other ethnic groups such as Asian (including Chinese Han population)^[4,5]), the Middle East and other groups. Interestingly, the 9p21 segment was not significantly associated with cardiovascular disease in African populations, suggesting that risk alleles for this segment may remain in out-of-African populations under selective pressure^[6]。