2014年 · 第42卷第01期

The 2011 UN Summit issued a political declaration to address the challenge of non-communicable diseases (NCDs). Then, under the coordination of the World Health Organization, a 25/25 phased target was established, that is, by 2025, premature deaths due to NCD will decrease by 25%. The prevention and control of cardiovascular diseases in place is the top priority to achieve 25/25.

After a long debate, the National Institutes of Health (NIH) -supported Adult Cholesterol Education Program 4 (ATP4) still ended fruitlessly. The American College of Cardiology (ACC) and the American Heart Association (AHA) are in full swing, and soon launched the Guidelines for the Treatment of Blood Cholesterol to Reduce the Risk of Atherosclerotic Cardiovascular Disease (ASCVD) in Adults (hereinafter referred to as the Guidelines), which is very different from its predecessor ATP3 and the recent global recommendations and position statements on dyslipidemia management organized by Professor Grundy, chairman of the International Atherosclerosis Association (IAS) expert group. After the publication of the guidelines, the American Lipid Society, which has been involved in the discussion on the development of the guidelines, issued a statement to withdraw from the guidelines. The guidelines have important defects and can only be used as the starting point and focus for further discussion and modification.

The purpose of formulating psychological prescriptions for cardiovascular patients is to make "double-heart medicine" an integral part of "overall heart prevention and treatment system", based on the disciplinary system of cardiovascular diseases, and carry out necessary and appropriate identification and intervention for cardiovascular diseases that are disturbed by mental and psychological factors or manifested as simple mental and psychological problems similar to cardiac symptoms.

A 70-year-old female was admitted to the hospital on 5 February 2006 for "coronary heart disease, unstable angina pectoris, grade 2 hypertension" and was treated with aspirin, clopidogrel, low molecular weight heparin sodium, isosorbide mononitrate, metoprolol, felodipine, benazepril and fluvastatin. Coronary angiography was performed on the afternoon of February 6th, which showed 70% centripetal tubular stenosis in the proximal segment of the left anterior descending artery, 90% eccentric tubular stenosis in the middle and distal segment of the left circumflex artery, and 90% centripetal tubular stenosis in the anterior posterior trigeminal segment of the right distal coronary artery, with thrombosis. One 3.0 mm ×18 mm Vision stent was placed in the right distal coronary artery and one 3.0 mm ×15 mm Vision stent in the left circumflex artery. Surgery shared UVIDXIAN 370 150 ml. The intraoperative blood pressure was about 120/70 mmHg (1 mmHg =0.133 kPa), and there was no obvious discomfort. The operation ended at 17:00. At 23: 10 on the same day, the patient developed restlessness, misanswering questions, disorientation, and no limb hemiplegia. Physical examination: blood pressure 130/90 mmHg, heart rate 110 beats/min, regular heart rhythm, normal muscle strength of limbs, and negative neuropathological reflex. Emergency blood routine, renal function, electrolytes and blood sugar were all normal, and no abnormalities were found in skull CT. Cerebral hemorrhage and metabolic mental abnormalities were excluded. Multiple intravenous injections of diazepam with poor results. Irritability was reduced after chloral hydrate retention enema and mannitol 125 ml intravenous drip. By the day of February 7th, the patient was still restless, disoriented, increased muscle tone of the limbs on physical examination, and negative neuropathological reflexes. After internal discussion and combined with the consultation opinions of neurology department, considering the contrast agent reaction, diazepam, mannitol and dexamethasone were continued. At 17: 00 on February 7th, the patient's consciousness became clear, and he was basically free of irritability. At night, he was restless again, talking nonsense, and was repeatedly injected intravenously with diazepam. After 2: 00 on February 8th, I gradually fell asleep, and after waking up at 7: 00, I was clear and answered the relevant questions. In the afternoon, there was no abnormality in brain CT. After 18 days of hospitalization, he improved and was discharged. After discharge, he took clopidogrel for 1 year, aspirin, valsartan, nifedipine extended-release tablets and metoprolol for a long time, and his condition was stable.

The patient was a 69-year-old female. Chest pain after activity was admitted for 5 years and aggravated for 1 month. Previous hypertension for 4 years, taking metoprolol (trade name: Betaloc) 50 mg/d. Physical examination: blood pressure 140/80 mmHg (1 mmHg =0.133 kPa), heart rate 60 beats/min, and systolic murmur of grade 3/6 could be heard between the 3 and 4 costs of the left margin of the sternum. Electrocardiogram: normal. Echocardiography (UCG): Left atrial diameter increased (47 mm), interventricular septum (IVS) S-shaped curvature, IVS basal segment 14 mm thick, left ventricular posterior wall 11 mm, left ventricular outflow tract diameter (LVOT) 7 mm, left ventricular outflow tract pressure step (LVOTG) 62.8 mmHg. Left ventricular systolic function was normal [left ventricular ejection fraction (LVEF) 60%] and diastolic function was reduced. Coronary angiography showed 50% ~60% stenosis in the middle segment of the anterior descending artery, the remainder was normal, resting LVOTG 110 mmHg. The first septal branch (S1) was ablated by transcatheter injection of 1.5 ml of anhydrous alcohol under temporary pacemaker protection, and the postoperative resting LVOTG was reduced to 23 mmHg. Reexamination after 1 week UCG: LVOT 12 mm, LVOTG 12.8 mmHg. The patient was given 71.25 mg/d metoprolol sustained-release tablets after operation. After 8 months of outpatient follow-up, the patient's discomfort symptoms were alleviated and the activity tolerance was improved. SeeFigure 1、Figure 2。

A 19-year-old male was admitted to the hospital on April 21, 2011 due to "back pain, chest tightness and holding breath for 2 weeks during activity". The patient was not diagnosed and treated in time when the disease started 2 weeks ago, and then chest tightness occurred every hundred meters after walking, accompanied by holding his breath, which could be relieved by rest. Has a history of nephrotic syndrome for 7 years, has been treated with hormone therapy for a short time, intermittently taking dihydrochlorothiazide and tripterygium wilfordii polyglycosides, and has not regularly monitored renal function; Hypertension history for 7 years, highest blood pressure 170/100 mmHg (1 mmHg =0.133 kPa), regular oral benazepril hydrochloride (10 mg/time, 2 times/d), blood pressure controlled at 130-140/90-100 mmHg; History of dyslipidemia for 7 years, no standardized treatment; No history of diabetes. No tobacco and alcohol addiction, no family history of cardiovascular disease. Admission physical examination: blood pressure 110/70 mmHg; Dry and wet rales were not heard in both lungs; The heart boundary enlarged to the lower left, the heart rate was 65 beats/min, and the rhythm was regular, without murmur and extra heart sounds; Moderate depressed edema of both lower limbs. Auxiliary examination: Troponin I 2.19 μ g/L (normal value 0-0.05 μ g/L); Serum creatine kinase isoenzyme (CK-MB) 32 U/L (normal 0-18 U/L); Total cholesterol 5.19 mmol/L, LDL cholesterol 3.55 mmol/L; Serum creatinine 68 μ mol/L; Serum albumin 29.2 g/L; Urinary protein + + +, urine occult blood + +. On admission, ECG showed sinus rhythm, left axis deviation, left ventricular hypertrophy, lead Ⅱ showed QR type, lead Ⅲ and aVF showed QS type, V_3R~ V_5RThe leads were of QS type. Echocardiography: Left ventricular end-diastolic diameter 54 mm, left ventricular ejection fraction 64%, bilateral atrial enlargement, and reduced myocardial movement in the interventricular septum and middle segment of the inferior wall. After 5 days of treatment with antiplatelet, lipid-lowering, blood pressure lowering, heart rate control drugs, coronary angiography showed 50% ~60% stenosis of the proximal left anterior descending artery, 60% stenosis of the middle left circumflex artery, and 100% occlusion of the proximal right coronary artery (Figure 1）。 Three stents of 3.0 mm ×2.9 mm, 3.5 mm ×2.9 mm, and 3.5 mm ×2.4 mm were placed in series in the right coronary artery, and the results were satisfactory (Figure 2）。 Postoperatively, oral aspirin (0.1 g/d), clopidogrel (75 mg/d), benazepril (10 mg/d), metoprolol (23.75 mg/d), atorvastatin (20 mg/d) were administered. Two days after surgery, the patient was stable and discharged. After six months of follow-up, the patient adhered to drug treatment, blood lipid control reached the standard, and could engage in daily mild to moderate physical activity.

The patient was a 93-year-old male. In 2008, he was hospitalized in our hospital for gout. X-ray chest radiograph showed enlarged heart shadow with a cardiothoracic ratio of 0.62; Electrocardiogram showed sinus rhythm, left ventricular hypertrophy with strain. In 2009, exertion palpitations and shortness of breath occurred. Electrocardiogram showed paroxysmal atrial flutter, incomplete right bundle branch block, left ventricular high voltage, ST-T segment changes; Echocardiography showed secondary foraminal atrial septal defect with interrupted atrial septal echo of about 22 mm, bidirectional atrial level shunt, mainly left-to-right shunt, combined with mild aortic regurgitation, severe mitral regurgitation, and moderate tricuspid regurgitation (Figure 1）。 The condition improved after cardiotonic and diuretic treatment. Since then, his condition has recurred and he has been hospitalized in our hospital many times. During his hospitalization, the electrocardiogram showed paroxysmal atrial fibrillation. Since July 2010, the heart rhythm has changed to persistent atrial fibrillation. In January 2013, the patient developed cough and sputum for 1 week after catching cold, and the exertion shortness of breath was worse than before. He also developed nocturnal paroxysmal dyspnea, sitting breathing, and edema of both lower limbs and was readmitted to hospital. Admission physical examination: blood pressure 105/50 mmHg (1 mmHg =0.133 kPa); Filling of jugular vein, positive hepatic jugular reflux sign; A small amount of wet rales can be heard in both lower lungs; The heart boundary enlarged to the lower left, the heart rate was 65 beats/min, the heart rhythm was absolutely irregular, and the intensity of the first heart sound varied, P₂Hyperactivity and fixed division, grade 2/6 systolic soft blow-like murmur can be heard in the 2nd to 3rd intercostal area of the left sternum, and grade 2/6 systolic blow-like murmur can be heard in the auscultation area of the apex and tricuspid valve; Hepatosplenic subcostal unpalpable; Mild depressed edema of both lower limbs. Echocardiography showed atrial septal defect, and the atrial level remained bidirectional shunt, mainly left-to-right shunt; Left ventricular ejection fraction 56%; The anterior-posterior diameter of the left atrium was 65 mm, the left-right diameter was 57 mm, and the upper-lower diameter was 93 mm; Left ventricular end-diastolic diameter 52 mm, end-systolic diameter 37 mm; Right ventricular diameter 44 mm; The transverse diameter of the right atrium is 72 mm, and the upper and lower diameter are 81 mm; The tricuspid valve developed to severe regurgitation, and continuous Doppler showed a tricuspid regurgitation velocity of 3.2 m/s, a pressure difference of 42 mmHg, and pulmonary systolic pressure estimated from tricuspid regurgitation was 57 mmHg. X-ray chest radiographs showed increased, thickened and blurred texture of both lungs, showing signs of pulmonary congestion, widening of both lung hilums, and general enlargement of the heart shadow, mainly the left heart margin, with a cardiothoracic ratio of 0.79. Abdominal B-mode ultrasound showed that the inner diameter of the right hepatic vein was 22 mm, the hepatic vein was significantly widened, and the liver was congested. The partial pressure of oxygen was 83.5 mmHg and the oxygen saturation was 96.5%. After cardiotonic, diuretic and other treatments, paroxysmal dyspnea, orthostatic breathing and edema of both lower limbs disappeared at night, and shortness of breath improved and was discharged.

Recently, the American Heart Association Foundation, the Heart Association, the Association of Physicians, the Association of Thoracic Surgeons, the Association of Cardiovascular Preventive Care, the Association of Cardiovascular Imaging and Intervention, the Association of Thoracic Surgeons (ACCF/AHA/ACP/AATS/PCNA/SCAI/STS) and the European Society of Cardiology (ESC) respectively published the "Guidelines for the Diagnosis and Treatment of Stable Coronary Heart Disease (also known as Stable Ischemic Heart Disease)" (hereinafter referred to as the New Guidelines), which put forward new recommendations on the diagnosis and treatment norms in this field^[1,2,3,4]。 In order to improve the diagnosis and treatment level of Chinese clinicians in this related field, combining the current situation and existing guidelines in China^[5]To interpret the new guidelines.

The 2013 ESH/ESC Guidelines for the Management of Arterial Hypertension were officially released at the 23rd Annual Conference of the European Society of Hypertension (ESH) in Milan, Italy. The new guidelines have revised a number of contents related to the diagnosis and treatment of hypertension, including antihypertensive goals, antihypertensive treatment initiation timing, drug combination treatment plan, etc., and elaborated on blood pressure measurement, overall cardiovascular risk factor assessment, lifestyle intervention, special population treatment and renal denervation. The final version was published simultaneously in the Journal of Hypertension^[1]European Heart Journal and Blood Pressure. With ESH/ESC Guidelines 2007^[2]In contrast, the highlights of the new guide include the following aspects:

percutaneous coronary intervention (PCI) is an important method in the treatment of coronary artery disease by using catheter technique to relieve coronary artery stenosis and restore myocardial perfusion^[1,2]。 Under the current situation of high incidence of coronary heart disease and rapid development of PCI, it is a question worth exploring how to correctly evaluate or compare the effect of PCI in the treatment of coronary heart disease from the perspective of evidence-based medicine by using a large amount of observational data accumulated in clinical practice^[3,4,5]。

Since Kiemeneij and Laarman^[1]Since the successful implementation of the first case of transradial approach (TRA) coronary intervention in 1993, this technique has been developed rapidly. The advantages of TRA over the transfemoral approach (TFA) are that it can effectively reduce puncture site bleeding complications, reduce hospital stay, and improve the postoperative quality of life of patients. Epidemiological survey showed that TRA coronary intervention accounted for 56.3% of all approaches in China in 2007^[2], while the proportion of TRA abroad is lower^[3,4,5]。 Does TRA benefit compared with other approaches? This article reviews the progress of clinical research in this area.

At present, the diagnosis of coronary heart disease is based on coronary angiography showing luminal stenosis ≥50%. Clinical practice has proved that it is incorrect to decide the treatment plan only according to the degree of stenosis of the lumen. It is also necessary to evaluate the hemodynamic status of the stenotic coronary artery, microvascular and myocardial ischemia, etc. For borderline lesions with moderate coronary stenosis (degree of stenosis<70%), stenosis of the lumen is not necessarily hemodynamically significant, and the risk of coronary heart disease is not necessarily related to the degree of stenosis. More and more evidence shows that the relationship between coronary lumen stenosis and myocardial ischemia is complex, and it is unreliable to judge whether myocardial ischemia exists simply by the degree of stenosis^[1,2]。 fractional flow reserve (FFR) refers to the ratio of the maximum blood flow of a blood vessel in the presence of stenotic lesions in the coronary artery to the maximum blood flow that can be obtained in the absence of stenotic lesions. Converting this to pressure, FFR is the ratio of the pressure at the distal end of the stenosis to the pressure of the normal vessel proximal to the stenosis. FFR>0.75, indicating that the stenosis has no hemodynamic significance, otherwise, it suggests that the stenosis leads to distal blood flow disorder. FFR is currently the gold standard to evaluate whether coronary artery stenosis causes hemodynamic disorders, but it needs to be measured by transcatheter and is an invasive diagnostic method, so it is not easy to popularize. In recent years, with the development of computational fluid dynamics, it has become a reality to obtain FFR values from conventional coronary computed tomography angiography (CCTA) images. fractional flow reserve CT imaging (FFR-CT) is an image based on FFR values obtained after computer post-processing based on conventional CCTA images. Since FFR-CT is not an additional CT scan, the patient does not need to increase the radiation dose; At the same time, adenosine loading is not required, so it has rapidly become a research hotspot in the cardiovascular field.