2014年 · 第42卷第02期

On August 21st, 2013, I went to Panzhihua City again, and had a discussion with the leadership team and academic leaders of the municipal government, the Health Bureau and Panzhihua Central Hospital, summarizing the reform and development of medical and health undertakings in the past 10 years, which was epitomized by the development of the heart center of the central hospital, and sorting out the development ideas in the next 10 years.

China Heart Failure Diagnosis and Treatment Guidelines 2014 (New Guidelines)^[1]Published in this issue. Since the decision of the cardiovascular branch of Chinese medical association to revise the diagnosis and treatment guidelines of chronic heart failure^[2]It took two and a half years until the final version of the new guidelines was published. The Heart Failure (HF) Group is specifically responsible for the revision and writing of the new guidelines. It has held 10 meetings successively and carefully studied the European Cardiology Association (ESC) published in recent years^[3], the National Institute for Clinical Optimization (NICE), and the American College of Cardiology Foundation (ACCF) and American Heart Association (AHA) Heart Failure Guidelines^[4], comprehensively searched and reviewed relevant literature and new clinical trials at home and abroad, evaluated recommendation categories and evidence levels, and established a drafting group. After the first draft was formed, the opinions of experts and doctors were widely solicited in more than 30 cities and regions across the country, and it was repeatedly revised more than 10 times.

In 1974, Gould and Lipscomb first reported that the blood flow decreased significantly when the diameter of the coronary artery (coronary artery) in dogs was>80% narrowed, but the blood flow decreased significantly when the diameter of the coronary artery was>50% narrowed after ligation with arteriole dilators^[1]。 This experiment gave rise to the concept of coronary flow reserve, which was rapidly translated into clinical concepts: ≥50% of coronary diameter stenosis was hemodynamically significant stenosis and ≥85% was borderline stenosis, which in turn quickly deduced into the concept of ischemic stenosis^[2]。 In the past 40 years, clinical cardiologists generally believe that obstructive coronary artery stenosis is the main mechanism of chronic stable angina pectoris, and coronary heart disease can be diagnosed only if the diameter of coronary artery stenosis is ≥50%. In 2006, the European Society of Cardiology stated in the guidelines for the treatment of stable angina pectoris: "Coronary atherosclerosis is the most common cause of myocardial ischemia, and other rare causes of the absence of obstructive coronary atherosclerosis are not considered in this guideline"^[3]。 However, with the popularization of interventional coronary diagnosis and treatment technology, it was found that many patients with evidence of myocardial ischemia had no obvious abnormalities in coronary angiography, while a considerable number of patients showed severe coronary stenosis or even chronic occlusion but had no evidence of angina pectoris and myocardial ischemia, suggesting that there is no direct correspondence between chronic coronary stenosis and myocardial ischemia^[4]While questioning the traditional idea that chronic stenosis leads to myocardial ischemia.

Heart failure (heart failure for short) is a complex group of clinical syndromes with impaired ventricular filling or ejection capacity due to any abnormalities in heart structure or function. Its main clinical manifestations are dyspnea and asthenia (limited activity tolerance), and fluid retention (pulmonary congestion and peripheral edema). Heart failure is one of the most important cardiovascular diseases, which is the severe and terminal stage of various heart diseases with high incidence.

On November 12, 2013, the American Heart Association (AHA) and the American College of Cardiology (ACC) jointly issued the "Guidelines for the Treatment of Blood Cholesterol to Reduce the Risk of Atherosclerotic Cardiovascular Disease in Adults" (hereinafter referred to as the new guidelines)^[1]。 This guideline has many new highlights, and while passing on the basic idea of lowering cholesterol to prevent and treat atherosclerotic diseases, it also points out the lack of evidence in the current clinical practice concept. Some of its ideas are very different from the previous guidelines and, therefore, give us a lot of thought.

A 29-year-old male was admitted with "pain and numbness in the right lower limb for 6 h". Physical examination: Body temperature 36.8 ℃, pulse 82 beats/min, breathing 19 beats/min, blood pressure 128/76 mmHg (1 mmHg =0.133 kPa). Immobility of the right lower limb, swelling and pain of the lower leg, pale skin, lower skin temperature than the opposite side, tenderness in the inguinal area, palpable weak fluctuations in the femoral artery, unpalpable pulsation of the popliteal artery and dorsal pedis artery; The skin temperature of the left lower limb is acceptable, and the femoral, popliteal and dorsal pedis arteries pulse. The remaining signs were not special. Blood biochemistry: K^＋3.8 mmol/L, Na^＋140 mmol/L, Ca^2＋2.25 mmol/L, urea 4.9 mmol/L, creatinine 55.8 μ mol/L, erythrocyte sedimentation rate 6.9 mm/1 h, alanine aminotransferase 24 U/L, aspartate aminotransferase 35 U/L. Electrocardiogram showed high left ventricular voltage. Color Doppler ultrasound showed solid hypoechoic filling (considering thrombus) in the lower abdominal aorta, right common iliac artery, external iliac artery and femoral artery, and no blood flow through the right popliteal, anterior tibial and posterior tibial arteries. Aortic plain scan and enhanced CT (Figure 1) shows aortic dissection (Stanford type A); Embolus of right common iliac artery, external iliac artery and left internal iliac artery with moderate to severe luminal stenosis. The right lower extremity compartment manometry was performed with a pressure of 35 mmHg. The admission diagnosis was "Stanford type A aortic dissection, right lower limb osteofascial compartment syndrome".

The patient was a 29-year-old male. Hypertension was found during physical examination 11 years ago (the specific value is unknown). After physical examination once a year after work, the upper limb systolic blood pressure was up to 250 mmHg (1 mmHg =0.133 kPa), and it was never treated. In July 2004, he came to the hospital for medical treatment due to headache and dizziness. Physical examination: blood pressure of upper limbs 190/110 mmHg, blood pressure of ankle 90/67 mmHg, facial flushing, burly upper body, thin lower limbs, stronger radial artery pulsation than femoral artery, no cyanosis and clubbing of fingers (toes), no murmur in auscultation area of heart valves, and continuous vascular murmur in chest wall. Percutaneous oxygen saturation (fingers, toes) was 98%. Echocardiography showed: left ventricular hypertrophy, left atrial hypertrophy; Widening of coronary sinuses and widening of pulmonary arteries; Mild aortic valve regurgitation. Ascending and descending aorta angiography (Figure 1) showed that the aortic arch was blind at the opening of the left subclavian artery, the beginning of the descending aorta was blind, the internal thoracic artery was tortuous and dilated, and the intercostal artery was dilated. Simple disruption of the aortic arch type A was diagnosed. Ascending aorta-abdominal aorta prosthetic bypass was performed on 24 July 2004. Upper and lower limb blood pressure improved immediately after revascularization, and invasive blood pressure monitoring of the radial and dorsal pedis arteries showed upper limb systolic blood pressure and ankle systolic blood pressure of 150 mmHg. Postoperative administration of nifedipine controlled-release tablets (30 mg/time, 1 time/d) and

A 29-year-old male was admitted to the hospital on 26 October 2012 due to "intermittent fever for 4 months, cough, expectoration, hemoptysis with wheezing for 1 week". Four months ago, the patient had fever without obvious trigger, and the body temperature reached 39℃, accompanied by chills, headache, limb weakness and anorexia. The fever continued for 3 days, and the body temperature fluctuated from 38℃ to 40℃. During this period, the patient went to a military hospital after sudden irritability and delirium for 2 hours. At that time, the physical examination showed that the body temperature was 37.7℃. The breathing sounds of both lungs were clear, the heart rate was 104 beats/min, the rhythm was uniform, and no murmur was heard in each valve area. Blood routine: white blood cells 8.17×10⁹/L, the proportion of neutrophils was 91.8%, and no abnormalities were observed. He was admitted to the Department of Infectious Diseases with "sepsis and hysteria". After admission, the head CT showed cerebral hemorrhage due to obvious irritability, and the head and neck CTA showed intracranial aneurysm combined with cerebral hemorrhage. After 3 days, the patient was transferred to the neurosurgery department of a tertiary hospital for diagnosis and treatment. The neurosurgery department was admitted to the hospital with "cerebral aneurysm". The specific situation at the time of admission was unknown. After admission, he underwent interventional embolization of left middle cerebral aneurysm. The postoperative body temperature fluctuated by 37℃ ~38℃, and he was given antibiotic treatment (details unknown). He was discharged after 1 week. After discharge, the patient still had intermittent fever, and his body temperature fluctuated from 37℃ to 39℃. He went to the surgical hospital many times, reviewed the head CT many times, and was given anti-inflammatory and cooling treatments. The patient still had fever, and the accompanying symptoms were worse than before. I went to the local county hospital half a month ago. The blood routine showed that the neutrophil ratio was 85%, and there was no abnormality. Lung CT and abdominal ultrasound showed no obvious abnormalities, and electrocardiogram showed sinus tachycardia. After giving symptomatic treatment such as anti-inflammatory and cooling, he was discharged. The patient still had fever, and the symptoms of self-discomfort were aggravated. One week ago, he developed cough, expectoration, hemoptysis, accompanied by wheezing and palpitations, and could not lie down at night. The patient went to Beijing for treatment, went to many major hospitals, and went to the emergency department of our hospital 1 day ago. The body temperature was 38.6 ℃, and the blood routine: white blood cells 10.4×10⁹/L, neutrophils 88.1%, red blood cells 3.98×10¹²/L, hemoglobin 98 g/L, platelets 112×10⁹/L. Sinus tachycardia on electrocardiogram. Chest radiograph revealed right lung infection. For further treatment, he was admitted to the Department of Respiratory Medicine of our hospital. At the time of admission, he smelled systolic murmur in the mitral valve auscultation area, and he was suspected of infectious endocarditis. He was transferred to the Department of Cardiology for further diagnosis and treatment. Past history: A year ago, he was hospitalized in the emergency center for more than 4 months due to traffic accident trauma, and had 5 operations, including exploratory laparotomy, suture repair of mesenteric laceration, suture repair of retroperitoneal rupture, etc. During the physical examination: the heart boundary was not large, and no pathological murmur was heard in the auscultation area of each valve. The echocardiogram was re-examined four times successively, and there was no abnormality in the results, and there was no abnormality in the head CT.

The patient was a 57-year-old female. In late June 2012, there was no obvious trigger for fatigue and anorexia, no fever, shortness of breath, palpitations, no cough and sputum, and no care. In late July, the patient developed severe pain in the left lumbosacral region, accompanied by limited movement of the left lower limb, which persisted without relief, no fever, no joint redness, swelling and pain, no edema, no ecchymosis, petechia, and normal skin color. He had visited local county and municipal hospitals many times. Color ultrasound performed on September 28, 2012 showed: left atrial anterior-posterior diameter 37 mm, left ventricular maximum anterior-posterior diameter at the end of diastole 59 mm, right ventricular anterior-posterior diameter 22 mm, left ventricular ejection fraction 52%, left ventricular enlargement, aortic valve thickening, increased blood flow velocity over the aortic valve (2.5 m/s), aortic valve regurgitation (regurgitation velocity 1.8 m/s), and decreased left ventricular diastolic function. The local hospital did not give a definite diagnosis, and the effect of treatment (specific unknown) was not good. In early October, the patient went to the rheumatology department of a provincial hospital due to the above discomfort. During his hospitalization, the color ultrasound of the heart showed: the anteroposterior diameter of the left atrium was 24 mm, the maximum anteroposterior diameter of the left ventricle at the end of the diastole was 61 mm, the left ventricular ejection fraction was 48%, the left ventricle was enlarged, the ascending aorta was slightly wider, the aortic valve neoplasm may attach (about 17.2 mm long), the partial prolapse of the aortic valve was not excluded, the blood flow velocity of the aortic valve mouth was increased and moderately insufficient, and the left ventricular systolic function was slightly reduced. The diagnosis was "undifferentiated spondyloarthritis, iron deficiency anemia". After that, the symptoms of fatigue and anorexia progressively worsened. On the evening of November 16, 2012, when the patient exerted force to defecate, he suddenly felt shortness of breath, accompanied by palpitations, chest stiffness, and cold sweat. After taking "Suxiao Jiuxin Pill" sublingually for 3~5 minutes, the chest stiffness was relieved, and he did not seek medical treatment. After that, the symptoms of shortness of breath gradually worsened, and I couldn't lie down, accompanied by intermittent cold sweats. I first visited our hospital on November 19th. In the past, in 1983, the patient was treated with blood transfusion in a local hospital due to "anemia". During this period, he suffered from meningitis due to infection, which was cured, and denied other chronic disease history. In April 2012, the patient went to the local dental clinic due to gum swelling and pain. He was diagnosed with "pulpitis" and was treated with pulp deactivation.

The deaths caused by thrombosis in atherothrombosis (AS) account for 28.7% ~52.0% of the total deaths, and are the leading cause of death and disability in the world^[1]。 AS thrombosis refers to the rupture of unstable AS plaques, forming platelet-rich thrombus, resulting in a sharp decline or even complete interruption of blood flow, causing acute myocardial infarction, unstable angina pectoris, cardiogenic death, transient ischemic attack and/or vascular events such AS ischemic stroke and peripheral arterial disease^[2]。 Therefore, platelet adhesion, activation and aggregation under high shear stress in narrowed AS vessels are the basis of arterial thrombosis. This paper reviews the role of platelets in the occurrence and development of AS thrombosis.

canonical transient receptor potential channels (TRPCs) play an important role in the development of many diseases. In recent years, it has been found that TRPC plays an important role in the occurrence and development of hypertension, and is related to the target organ damage of hypertension. It is believed that TRPC-mediated calcium influx causes proliferation of smooth muscle, endothelial cells and activation of monocytes to participate in the pathological process of hypertension. This article reviews the role of TRPC channel in the development of hypertension and its research progress.

On February 28, 2012, the US FDA issued an announcement approving an important revision of the safety information in the statin instructions, warning that statins may increase the risk of new diabetes and worsen blood sugar control. The move has once again brought the debate over statin-related diabetes in the medical community into focus in recent years. Many known clinical studies have pointed out such adverse reactions to statins, but large-scale clinical trials still suggest that statin users have significant benefits in reducing cardiovascular and cerebrovascular events and reducing overall mortality. Correct understanding of this adverse reaction of statins and balancing the risks and benefits of lipid-lowering therapy will help guide future treatment strategies.

Complex ventricular arrhythmias such as ventricular tachycardia (VT) and ventricular fibrillation (VF) are the main causes of death and disability in cardiovascular diseases in modern society. The total number of sudden cardiac death (SCD) in China is about 544,000/year. More than 80% of SCD are caused by malignant ventricular arrhythmias (ventricular tachycardia or ventricular fibrillation), so effective prevention and treatment of ventricular arrhythmias can reduce the incidence of SCD. However, at present, there is a lack of effective prevention and treatment methods, and the drug treatment effect is not good and there are many adverse reactions. Implantable cardioverter defibrillator (ICD) is a palliative treatment, but it is expensive and requires multiple replacements in a lifetime, so its application is limited. In recent years, catheter ablation has made significant progress in the treatment of tachyarrhythmia. However, for complex ventricular arrhythmia, the conventional electrophysiological methods are difficult to map, the success rate of ablation is low, the complications are many, and the operation time and X-ray exposure time are long, so new ablation therapy is urgently needed.