2015年 · 第43卷第04期

In May 2014, I finally had the opportunity to go back to Kuancheng County, Hebei Province to see where I lived and worked for one year 46 years ago.

In 2014, the field of hypertension has gone through controversies and consensus. This article reviews these controversies and consensus to see what new thinking it has brought us?

Cardiovascular disease is the leading cause of death in our population, accounting for 40% of the total deaths. The data on the prevalence and trend of cardiovascular diseases are of great significance to formulate the strategy of cardiovascular disease prevention and treatment in China and determine the key direction of prevention and treatment. Recent studies have reflected several new characteristics of the epidemic trend of cardiovascular diseases in China, which deserve special attention.

The patient was a 41-year-old female. He was admitted to hospital on December 31, 2012 due to "dizziness, palpitations and amaurosis for half a month". Admission physical examination: body temperature 36.6 ℃, pulse 40 beats/min, blood pressure 102/60 mmHg (1 mmHg =0.133 kPa); The breathing sounds of both lungs were clear, and no dry and wet rales were heard; The void boundary of the heart was not enlarged, the heart rate was 40 beats/min, the rhythm was homogeneous, the cannon sound was audible, no murmur was heard in the auscultation area of each valve, and there was no pericardial friction sound. tumor marker CA199: 164.20 U/ml (normal 0-35.00 U/ml); Blood routine, electrolyte, erythrocyte sedimentation rate, high sensitivity C-reactive protein, myocardial necrosis markers, D-dimer, blood culture, liver and kidney function were all normal. 12-lead ECG showed sinus rhythm, complete atrioventricular block, junctional escape rhythm. The 24-h dynamic electrocardiogram showed sinus rhythm, complete atrioventricular block, borderline escape rhythm, mean ventricular rate 43 beats/min, slowest ventricular rate 20 beats/min (occurrence time 2:40), and fastest ventricular rate 73 beats/min (occurrence time 3:57). Echocardiography (Figure 1) shows that the structure of each chamber of the heart is normal, and a 1.5 cm ×1.0 cm medium echo shadow can be detected between the upper part of the tricuspid septal valve and the coronary sinus in the right atrium, with clear boundaries, homogeneous internal echo and no active part. Cardiac CT (Figure 2) showed that a 1.3 cm ×1.9 cm ×2.8 cm nodular lesion was seen at the base of the atrial septum. Enhanced CT showed that the lesion was relatively low density, and the CT value was 26.6 HU, suggesting neoplastic lesion.

A 46-year-old male was admitted on 7 March 2014 due to "paroxysmal precordial discomfort for 4 months, aggravated for 7 days". The patient experienced dull pain in the precordial area with left shoulder and back discomfort during activity 4 months ago, which could be relieved by stopping activity and was not treated. 7 days ago, there was no obvious inducing symptom aggravation, and there was also an attack at rest, especially when you get up in the morning every day, lasting for more than 10 minutes, and it could be relieved by taking nitroglycerin. The local hospital was admitted to the hospital with "unstable angina" and was given aspirin (100 mg/dose, 1 dose/d), clopidogrel (75 mg/dose, 1 dose/d), metoprolol extended-release tablets (47.5 mg/dose, 1 dose/d), atorvastatin calcium (20 mg/dose, 1 dose/night) orally, and low molecular weight heparin calcium (4 000 U/dose, 2 dose/d) subcutaneously. Coronary angiography showed 90% stenosis of the proximal left circumflex artery, and the interventional treatment failed, so he was transferred to our hospital. 15 years of history of hypertension, 4 years of type 2 diabetes, and more than 20 years of smoking (20 cigarettes/d). Physical examination at admission: blood pressure 140/105 mmHg (1 mmHg =0.133 kPa), heart rate 75 beats/min, and no abnormalities in the rest of the physical examinations. Laboratory tests: blood glucose 7.8 mmol/L, glycosylated hemoglobin 9.2%; Serum cholesterol 2.75 mmol/L, LDL cholesterol 1.62 mmol/L; Troponin I<0.05 μ g/L. Electrocardiogram was normal, chest X-ray and echocardiogram showed no obvious abnormalities. Coronary angiography showed 90% stenosis of the proximal bifurcation of the left circumflex artery, with obvious tortuosity and angle greater than 70°. Interventional therapy was performed 3 days later, using 6 F EBU3.5 guide catheter and BMW guidewire. Because the lesion was tortuous, the guidewire could not reach the distal end of the left circumflex artery through the lesion after repeated operation, so it was placed in the blunt margin branch. After repeated attempts with the Pilot 50 guidewire, it passed through the lesion to the distal end of the left circumflex artery. The 1.5 mm ×15 mm Sprinter balloon was then expanded at 10 atm (1 atm =101.325 kPa) for 10 s and replaced with the 2.5 mm ×15 mm Sprinter The balloon was expanded at 12 atm for 10 s. A 3.0 mm ×16 mm Helios stent was placed (pressurized to 14 atm and released) followed by expansion at 18 atm with a 3.0 mm ×9 mm NC Sprinter balloon. Coronary angiography showed a filling defect in the middle of the stent (Figure 1), repeatedly adjusting the projection angle after angiography, it is not possible to determine whether it is in-stent thrombosis or stent fracture. intravascular ultrasound (IVUS) examination showed the absence of stent wire in the middle section of the stent more than 1/3 of the circumference, which was diagnosed as acute partial stent rupture (Figure 2)。 According to Hinoshi standards^[1]The scaffold fracture type was type I. A 3.0 mm ×10 mm BuMA stent was replaced at the fracture (released after compression to 12 atm) and coronary angiography showed disappearance of the original filling defect (Figure 3), IVUS examination showed that the newly placed stent adhered well and completely covered the original broken stent (Figure 4)。 Continue to take the above medications orally after surgery while controlling blood pressure and blood glucose. Three months after surgery, coronary angiography showed that the stent was intact and well adhered to the wall, without intrastent stenosis, local thrombosis and tumor-like dilatation.

A 23-year-old male was admitted to the hospital in November 2013 due to "repeated chest tightness and shortness of breath for 10 years". Ten years ago, the patient began to have chest tightness, shortness of breath, no chest pain, fever, night sweats and weight loss. The patient had been seen in the local hospital, and the echocardiogram revealed "atrial septal defect", and interventional occlusion was recommended. The patient was not operated for financial reasons. Subsequently, chest tightness and shortness of breath appeared repeatedly, activity tolerance was significantly reduced, and edema of both lower limbs gradually appeared. One year ago, the patient was seen in the local hospital, and the echocardiography revealed "atrial septal defect, Eisenmanger syndrome". Admission physical examination: chronic disease volume; Dilatation of the jugular vein; The breathing sounds of both lungs were coarse, and no dry and wet rales were heard; The boundary of heart turbidity enlarged to the right, the heart rate was 90 beats/min, the rhythm was homogeneous, the second heart sound split could be heard in the auscultation area of pulmonary valve, and no murmur could be heard in the auscultation area of each valve; Soft abdomen, no tenderness and rebound pain; Mild edema of both lower limbs. Electrocardiogram showed complete right bundle branch block. Echocardiography after admission showed a significant enlargement of the right heart and the upper normal limit of the anterior wall of the right ventricle (5 mm); Echo loss of 10 mm in the middle of the atrial septum, bidirectional shunt mainly right to left at the atrial level; Small tricuspid regurgitation; Pulmonary artery systolic pressure was estimated to be 100 mmHg (1 mmHg =0.133 kPa). The size of atrial septal defect did not match the level of pulmonary artery pressure, but no pulmonary venous malformation drainage was detected by multi-section echocardiography. The long axis section of the pulmonary artery shows only the right pulmonary artery branch, and the left pulmonary artery branch is not clear. After cardiovascular multi-slice CT examination, the main trunk of pulmonary artery was significantly widened, and only the right pulmonary artery emerged from the distal end; The left pulmonary artery emanates from the left wall of the ascending aorta 2 cm above the aortic valve; The aortic arch rises left and descends right, and the descending aorta is located on the right side of the spine; No abnormalities were observed in the running and connection of coronary artery and pulmonary vein (Figure 1)。 Thus diagnosed as congenital heart disease: atrial septal defect; The left pulmonary artery abnormality originated in the ascending aorta; Right aortic arch; Eisenmanger's syndrome. The patient was not indicated for surgical treatment and was treated with sildenafil and was followed up outpatiently.

The relationship between physical environment and health is getting more and more attention. Since the 1960s, the relationship between human health and geomagnetic activity parameters has been discussed^[1,2]。 In recent years, it has been found that the occurrence of cardiovascular diseases, especially acute myocardial infarction (AMI), is closely related to the geomagnetic activity induced by space weather events driven by solar activity.

The second plenary working meeting of the 8th editorial committee of Chinese Journal of Cardiovascular Diseases was held in Beijing on December 10, 2014. Jiang Yongmao, president and editor-in-chief of Chinese Medical Journal, Liu Bing, vice president, Hu Dayi, editor-in-chief of this journal, Gao Runlin, honorary editor-in-chief, Huo Yong, Ge Junbo, Han Yaling, Lu Shuzheng, Ma Changsheng, Zhang Yun and Wang Jianan, deputy editors-in-chief, all staff of the editorial department, as well as the editorial board and correspondence editorial board, a total of more than 100 people attended the meeting. The meeting mainly summarized the work, achievements and shortcomings of the magazine since the establishment of the eighth editorial board, and made arrangements and detailed division of labor for the next period of time.

coronary vulnerable plaque is the pathological basis of acute coronary syndrome (ACS). Early recognition of vulnerable plaque and targeted treatment are beneficial to reduce the occurrence of major adverse cardiac events (MACE). Imaging is a reliable method for clinical evaluation of vulnerable plaques. In recent years, with the continuous development of imaging technology, the accuracy of clinical diagnosis of vulnerable plaque has been greatly improved, which provides a more accurate method for early clinical diagnosis and identification of vulnerable plaque in coronary arteries. In this paper, the research status of imaging evaluation methods of vulnerable coronary plaque is systematically described.

Atherosclerosis is a chronic and progressive disease characterized by the accumulation of lipid plaques in the arterial wall, which is the main cause of death and disability^[1]。 In the past, it was believed that with the increase of atherosclerotic lesions, the lumen of the artery narrows, thus causing insufficient blood supply to tissues and organs. However, it has been recently found that there is no obvious relationship between the occurrence of acute coronary syndrome and the severity of coronary artery sclerosis stenosis. The degree of luminal stenosis in most patients with acute coronary syndrome is less than 50%, and these plaques causing mild stenosis are mostly unstable plaques or vulnerable plaques^[2]。 The main characteristics of vulnerable plaques include: large extracellular lipid volume; The fibrous cap is thin and uneven, and the collagen content and smooth muscle cells are few; A large number of chronic inflammatory cells (such as macrophages, T lymphocytes and mast cells, etc.) infiltrate locally, accompanied by angiogenesis; The surface of the plaque may have different degrees of erosion, shedding, cracks and ulcers; In severe cases, the plaque ruptures at the "shoulder" where the fibrous cap is thinnest and the foam cells are most abundant. Plaque rupture with plaque surface thrombosis is the main cause of clinical acute cardiovascular events^[2]。 Different molecular imaging probes can be designed and synthesized for the plaque components of atherosclerotic plaques, especially unstable atherosclerotic plaques, in order to perform in vivo targeted imaging of unstable plaques, analyze the progression degree of plaques, and evaluate the efficacy of anti-atherosclerotic drugs^[3,4]。 magnetic resonance imaging (MRI) has the advantages of high soft tissue resolution, no electromagnetic radiation, high reproducibility, multi-sequence imaging and many types of contrast agents [T1 contrast agent (gadolinium) and T2 contrast agent (nanometer iron oxides such as USPIO and SPIO)], and is the most widely used in molecular imaging of atherosclerosis^[5,6,7]。

rheumatoid arthritis (RA) is a systemic autoimmune disease, mainly chronic inflammatory lesions of synovial joints, and involves organs and tissues such as heart, lungs, nerves and blood. Compared with the general population, RA patients have a higher risk of cardiovascular disease (CVD) morbidity and mortality^[1]。 The increased risk cannot be explained entirely by traditional cardiovascular risk factors, although they do play a part in this. At present, the exact mechanism of RA leading to CVD is still unclear. Inflammation is the most important factor linking RA with CVD, which runs through the whole process of atherosclerosis and strengthens the role of some traditional risk factors. The management of cardiovascular risk in RA should be mandatory, and how to implement it remains to be discussed. This article reviews the epidemiology, pathogenesis, risk assessment and management of RA complicated with CVD.