2016年 · 第44卷第08期

In November 2013, the American College of Cardiology (ACC) and the American Heart Association (AHA) abandoned the traditional system of adult cholesterol education programs in the United States, and hurriedly threw out the seemingly innovative and concise new guidelines on cholesterol-lowering to prevent and control atherosclerotic cardiovascular disease (ASCVD) (hereinafter referred to as the new guidelines), which raised questions from the American Lipid Association, the International Atherosclerosis Society, the European Atherosclerosis Association, the European Society of Cardiology and the Chinese Cholesterol Education Program (CCEP) expert group. The problems of the new guidelines have been systematically explained in a series of previous articles, mostly published in the Chinese Journal of Cardiovascular Diseases, and I will not repeat them here. Eric Topol's latest bestseller, Future Medicine: The Individual Medical Revolution in the Intelligent Age, pointed out sharply: AHA/ACC's statin use guidelines have been formulated in secret until they are officially announced. When asked Dr. Neil Stone, Chairman of the Guidelines Development Committee, why the public had no opportunity to comment on this, he responded "I can't answer that question. But in retrospect, it seems like a good idea, and probably we will do it next time".

Blood vessels are the largest network tissues in the human body, which play a vital role in maintaining life. As early as 2,000 years ago, the Chinese proposed in the Yellow Emperor's Internal Classic that "meridians circulate blood and qi while operating yin and yang". Traditional Chinese medicine regards "bloodline" as the material basis of physiological and psychological activities that people depend on for their survival. All kinds of disharmony of "failure", "clotting" or "occlusion" of blood vessels will lead to the occurrence of disease. In the West, ancient Roman medicine in the 2nd century AD had only just recognized that blood flows like a tide. Arab medicine began to recognize "blood circulation" in the 13th century AD. In 1628, the English scholar Harvey's Treatise on Blood Circulation broke through the confinement of theology and was published. Harvey not only revealed the law of blood circulation movement, but also used modern scientific consciousness and experimental methods to study major physiological problems for the first time in history. After that, modern western medicine was able to start. Improvements in microscopy led to the discovery of capillaries connecting arteries and veins in 1661. In 1835, the prototype of the modern sphygmomanometer was invented, and for the first time, humans could observe blood pressure without incising blood vessels. In 1902, the French scholar Alexis Carrel put forward a series of principles and techniques of vascular anastomosis, and in 1929, the German scholar Werner Forssmann invented cardiovascular catheterography. These two achievements not only won the Nobel Prize in Physiology or Medicine, but also laid the cornerstone of modern vascular disease treatment.

Dietary guidelines are reference books to guide people to eat reasonably and promote health. In order to promote national health and prevent diseases, many countries have formulated and published dietary guidelines for residents, which are constantly updated on the basis of comprehensive evaluation of new findings and evidence in scientific research. The Dietary Guidelines for U.S. Residents are nutritional health guidelines jointly issued by the U.S. Department of Agriculture (USDA) and the Department of Health and Human Services (HHS). They are revised every 5 years by experts in nutrition, medicine, and public health, and apply to all U.S. residents aged 2 years and older. For years, one of the core points of the guidelines has been the recommendation to keep dietary cholesterol intake below 300 mg per day^[1]。 However, in the 2015-2020 Dietary Guidelines for U.S. Residents released on January 7, 2016, the limits on dietary cholesterol intake are no longer set. Why has the United States eased its restrictions on cholesterol intake?

The relationship between triglycerides (TG) and coronary heart disease has been controversial for a long time. The early controversy stems from the existence of a negative correlation between TG and high density lipoprotein cholesterol (HDL-C). Correcting for HDL-C levels may affect the predictive value of TG in assessing the risk of coronary heart disease. The new controversy comes from whether TG should be detected in fasting or non-fasting states, and in which state TG levels are more valuable in predicting the risk of coronary heart disease. Elevated TG levels in plasma mark an increase in chylomicron (CM) and/or very low density lipoprotein (VLDL) particles, which are referred to as triglyceride-rich lipoproteins (TRLs) because they are rich in TG. remnant lipoprotein particles (RLP), the decomposition product of TRL, are considered to have stronger atherogenic effect because of their smaller particle size and relatively rich cholesterol esters. Is it the cholesterol component or the TG component in residual lipoprotein that really increases cardiovascular risk?

In recent years, the prevalence of cardiovascular diseases in China has increased year by year. Besides the aging of the population, the poor prevention and control of cardiovascular disease risk factors is the most important factor. The 2014 Cardiovascular Disease Report shows that there are more than 200 million patients with hypertension and more than 100 million patients with dyslipidemia in China, but the treatment rate of hypertension is about 1/3, while the treatment rate of dyslipidemia is less than 1/3^[1]。 Hypertension and dyslipidemia are often associated. A 2007 epidemiological survey of rural areas in Liaoning Province showed that 51.3% of rural hypertensive patients had combined cholesterol increase^[2]。 CONSIDER study showed that 81.1% of outpatient hypertensive patients in China had dyslipidemia^[3]。 The DYSIS study suggests that about 66% of dyslipidemia patients receiving lipid-lowering therapy are complicated with hypertension^[4]。 The China-Reality study showed that 52% of outpatient dyslipidemia patients had hypertension, but the proportion of statin treatment was 37%, and the compliance rate of low density lipoprotein cholesterol (LDL-C) was only 25.8%^[5]。 It can be seen that there is still huge room for improvement in cholesterol-lowering treatment of hypertensive patients. This consensus expert group reviewed studies on cholesterol-lowering therapy in hypertensive patients and defined specific recommendations for cholesterol-lowering therapeutic strategies in hypertensive patients.

A 26-year-old female was admitted to the hospital on 30 June 2012 due to "intermittent chest tightness and shortness of breath for 2 months". After catching a cold 2 months ago, the patient developed chest tightness and shortness of breath, accompanied by fatigue, palpitations, cough, cough of white sticky phlegm, no fear of cold and night sweats. After anti-inflammatory symptomatic treatment in the local hospital, the fever improved, but both lower limbs gradually edemed. Previous physical health, denied history of tuberculosis and recurrent fever. On admission, the pulse was 120 beats/min, the blood pressure was 90/60 mmHg (1 mmHg =0.133 kPa), the heart turbidity was not large, the auscultation heart rate was 120 beats/min, the rhythm was regular, the respiratory sounds of both lungs were clear, the systolic grade III/6 murmur could be heard in the pulmonary valve area, the systolic grade III/6 murmur could be heard in the right scapular area, the abdomen was flat and soft, the liver and spleen were not enlarged, and the lower limbs were mildly swollen. Auxiliary examination showed erythrocyte sedimentation rate of 35 mm/h (normal<20 mm/h), N-terminal B-type pronatriuretic peptide (NT-proBNP) 1 700 ng/L. Arterial blood gas indicates arterial oxygen partial pressure (PaO₂) 74 mmHg, partial pressure of arterial blood carbon dioxide (PaCO₂) 31 mmHg. The indicators reflecting autoimmunity were all within the normal range. T lymphocyte spot test was negative. Electrocardiogram showed sinus tachycardia with low, flat, inverted T wave. Cardiac color ultrasound showed right heart enlargement, slightly increased pulmonary artery pressure, abnormal movement of ventricular septum, mild tricuspid regurgitation, and minor effusion in pericardial cavity. Pulmonary CT angiography (CTA) showed multiple stenosis of the right pulmonary artery trunk, right upper and lower pulmonary arteries and unclear display of the left lower pulmonary artery, among which the branch wall of the right lower pulmonary artery was annularly thickened, which was caused by inflammatory lesions of pulmonary vasculature or its secondary post-thrombotic changes. The density of the root and branch of the left inferior pulmonary artery is reduced, and it is likely to be inflammatory lesions or organized thrombosis; Scattered inflammation in both lungs, among which there is a small possibility of tuberculosis in the lower lobe of the right lung (Figure 1)。 The results of pulmonary perfusion ventilation showed that the blood flow perfusion of both lungs was impaired, and the multiple blood flow perfusion and ventilation imaging of both lungs were mismatched, which was considered to be related to arterial stenosis. The ventilation function of the dorsal and lateral basal segments of the lower lobe of the right lung was impaired, and there was no abnormality in the remaining blood vessels. Pulmonary artery, celiac artery and common iliac artery angiography showed absence of right upper and left lower pulmonary arteries, and moderate stenosis of right lower pulmonary artery, which was considered as Takayasu arteritis change in combination with clinical consideration. Ductus arteriosus examination showed inflammatory changes in Takayasu arteries. Color ultrasound of both lower limbs and cervical arteries and veins showed no abnormalities. The clinical diagnosis was "Takayasu arteritis pulmonary artery type, pulmonary hypertension". Anticoagulation, prednisone and cyclophosphamide were given to treat Takayasu arteritis, and bergamaglandin sodium was given to treat pulmonary hypertension. The symptoms were relieved and the hospital was discharged.

A 52-year-old male was admitted to the hospital on October 8, 2015 due to "paroxysmal chest tightness and chest pain for 2 years, aggravated for 1 week". The patient developed paroxysmal chest tightness and chest pain without obvious trigger 2 years ago. The pain was located in the right upper abdomen and behind the sternum, lasting for about half an hour, accompanied by sweating and perioral numbness. The attack was accompanied by increased blood pressure, with the highest blood pressure being 150/95 mmHg (1 mmHg =0.133 kPa). After taking "Suxiao Jiuxin Pill and antihypertensive drugs", the above symptoms gradually alleviated. In the past 1 week, the above symptoms occurred frequently, without nausea, vomiting, acid reflux and anorexia. CT angiography of coronary arteries was performed in a local hospital, which showed "about 40% coronary artery stenosis" (details unknown). Has a history of diabetes for more than 10 years in the past, and regularly applies insulin therapy, and has better blood sugar control; History of hypertension for 2 years, intermittent oral administration of "telmisartan" to reduce blood pressure, blood pressure increased when the above symptoms onset, and blood pressure was in the normal range after the symptoms were relieved; History of superficial gastritis 4 years. Deny history of smoking and drinking.

Between October 2010 and June 2014, 11 patients with acute aortic syndrome misdiagnosed as acute coronary syndrome were admitted to China-Japan Friendship Hospital. Among them, there were 9 males and 2 females; Age (56.4±11.8) years. The basic clinical data of the patient are presented inTable 1。

familial hypercholesterolemia (FH) is an autosomal dominant genetic disease, which is a high risk group for early onset coronary heart disease. At present, research shows that the global prevalence of heterozygous FH is 1/500~1/200, but the diagnosis and treatment rate of this disease is still very low worldwide. The concentration of low density lipoprotein cholesterol (LDL-C) in FH patients is greatly increased, and the LDL-C in heterozygous FH patients is usually>4.9 mmol/L. Coronary heart disease can occur in young and middle-aged people. Patients with homozygous FH develop coronary heart disease in childhood or adolescence due to LDL-C>13 mmol/L. At present, FH has been defined as a Grade I type I genetic disease by the Centers for Disease Control of Public Health Genetics in the United States, suggesting that early identification of FH indicator cases and then screening of their family members is very important.

Brugada syndrome (BrS) is an autosomal dominant primary electrocardiac disorder, mainly manifested by V₁~ V₃Lead (or superior/inferior intercostal) ST segment elevation with a fatal ventricular tachyarrhythmia episode causing recurrent syncope, cardiac arrest, and even sudden cardiac death (SCD). Since BrS was proposed by the Brugada brothers in 1992, the research related to BrS has been a difficult point in the field of arrhythmia, and its basic mechanism research and clinical diagnosis and treatment standards have attracted much attention from peers. In view of ethnic differences, this paper briefly summarizes the epidemiological data, genetic basis and related clinical characteristics of BrS in China.

autophagy is an important degradation system in cells, which can use lysosomes to degrade damaged organelles, proteins and other intracellular components through the action of autophagy-associated gene (ATG), thus promoting the regeneration of intracellular substances and energy and maintaining cellular homeostasis^[1]。 For a long time, autophagy has been thought to play a protective role in atherosclerosis (AS), but recent studies have shown that autophagy has two sides in the occurrence and development of AS^[2]。

acute coronary syndrome (ACS) is a critical disease with high mortality and disability rates, including acute ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation acute coronary syndrome (NSTE-ACS). The onset of ACS is acute, and patients are often accompanied by severe chest pain, as well as a series of psychological reactions such as anxiety, nervousness and fear. ACS guidelines recommend morphine as a routine treatment for chest pain^[1,2,3,4]Early intravenous morphine not only has analgesic and sedative effects, but also reduces myocardial oxygen consumption^[5]Improve myocardial ischemia. The pathophysiological mechanism of ACS is the rupture or erosion of coronary atherosclerotic plaque, secondary to complete or incomplete thrombosis, in which platelet activation plays a very important role, and rapid and potent antiplatelet therapy is the key to its treatment. The new ACS guidelines recommend immediate P2Y regardless of early intervention₁₂Receptor antagonist combined with aspirin dual antiplatelet therapy^[6,1,2]。 Therefore, concomitant use of morphine and P2Y is often present in the treatment of ACS patients₁₂Conditions of receptor antagonists. However, little attention has been paid to the existence of drug-drug interactions between these two drugs. A recent CRUSADE study found that patients with NSTE-ACS who used morphine analgesia had a higher mortality rate than those who did not^[7]Therefore, the safety of morphine in patients with ACS and the relationship between morphine and P2Y₁₂There is widespread concern about the presence of drug-drug interactions between receptor antagonists.