2016年 · 第44卷第06期

Recently, a 57-year-old male patient was consulted in a cardiac rehabilitation center. He had a severe chest pain while traveling. After returning home, he went to a local hospital for treatment. Coronary angiography found 90% stenosis of the proximal right coronary artery and 80% stenosis of the middle left anterior descending artery. At that time, the patient was asymptomatic, and the findings of electrocardiogram and echocardiogram were normal. Two hours after returning to the ward after right coronary artery stenting, the patient developed severe chest pain and sweating, and the electrocardiogram showed ST segment elevation in II, III and aVF leads. Another coronary angiography showed that the right coronary artery intima was torn, and the distal end of the right coronary artery stent was completely occluded. Three more stents were placed to open the blood vessel. Patient safe, go back to the ward. After that, no functional evaluation was performed, and the fifth stent was placed in the critical lesion of the left anterior descending artery. After discharge, the patient frequently experienced chest pain attacks, sweating, and even severe chest tightness and chest pain at night. I went to the hospital for a follow-up visit, and the doctor checked and said that there was no problem. I saw that the discharge diagnosis on the medical record was "coronary heart disease, unstable angina pectoris", and there was no mention of acute inferior myocardial infarction caused by interventional operation. Moreover, the second coronary angiography found that the intima tear of the right coronary artery and why three more stents were placed were not informed to the patient and family.

Chronic heart failure (HF) is a severe stage or end-stage manifestation of various types of heart diseases. Although the guidelines recommend that "golden triangle" drug treatment can improve the prognosis of patients, the 5-year mortality rate is still high^[1]。 Therefore, selecting suitable patients for device therapy on the basis of drug therapy is a hot spot of clinical attention at present. cardiac resynchronization therapy (CRT) and implantable cardioverter-defibrillator (ICD) can improve the quality of life of patients with heart failure, reduce the mortality rate and reduce the occurrence of sudden cardiac death, and have become one of the main treatment methods for chronic heart failure. In recent years, a series of clinical studies have further promoted the update of international and domestic guidelines for CRT, consolidating its position as a first-line clinical treatment for heart failure. However, compared with European and American countries, the clinical application of CRT in China is relatively lagging behind, and the implantation rate per million people is still far lower than that in western countries. The reason is not backward technology, but mainly that domestic cardiovascular doctors have insufficient awareness of the benefits of CRT in patients with heart failure, resulting in insufficient understanding of CRT indications. Secondly, the restriction of economic conditions is also an important factor hindering its development. Compared with other cardiac interventional treatments, the proportion of expenses borne by patients is higher. Therefore, combined with China's national conditions and based on the indications recommended in the guidelines, it is the focus of current clinical work to deeply explore patients with heart failure who may benefit more from CRT, and maximize the clinical benefits and health economics benefits.

Heart failure (heart failure) is the final outcome and the main cause of death in most cardiovascular diseases. Although some progress has been made in drug and device treatment, the annual mortality rate of patients with severe heart failure is still as high as 50%, which is similar to that of malignant tumors. Heart failure treatment is still the focus and difficult problem of public health worldwide. A large amount of evidence indicates that there is an imbalance of calcium homeostasis in cardiomyocytes during the pathophysiological process of heart failure, which is closely related to the development of heart failure and its arrhythmia. Early basic research has confirmed the effectiveness of gene-level regulation of intracellular calcium homeostasis imbalance in the treatment of heart failure. With the great breakthrough in safety and myocardial selectivity of adeno-associated virus (AAV) vectors in recent years^[1]The rapid transformation of basic research results into clinical practice has brought hope for the treatment of heart failure, but it is also accompanied by doubts and setbacks. This article will discuss the current status and existing debates and problems of gene therapy strategies for heart failure targeting calcium regulatory protein from basic to clinical.

Clinically, plasma sodium ion concentrations below 135 mmol/L are defined as hyponatremia^[1]It is a common electrolyte disorder in patients with heart failure (heart failure). Hyponatremia occurs in 20% to 30% of patients with acute decompensated heart failure (ADHF)^[2], making the treatment of ADHF more difficult. Study confirms hyponatremia as an independent risk factor for poor prognosis in patients with ADHF and chronic heart failure^[2]It can prolong hospital stay and increase case mortality. Hyponatremia in patients with heart failure can be divided into two categories from the perspective of pathophysiology, true hyponatremia and dilutive hyponatremia. The widespread application of sodium-excreting diuretics brings difficulties to the differential diagnosis of the two. Clinicians first need to identify these two types of hyponatremia, and then adopt different treatment options based on pathophysiology to improve the prognosis. This article focuses on the mechanism and treatment of hyponatremia in patients with heart failure.

Patients with chronic heart failure (CHF) often need to be hospitalized repeatedly due to decompensated cardiac function, which has a huge social and economic burden, and has become one of the serious global health problems^[1]。 Volumetric overload and pulmonary congestion are the main causes of hospitalization in patients with acute decompensated heart failure (ADHF)^[2]。 Fluid retention produces symptoms and signs that prompt hospitalization. Adequate relief of sodium-water retention in CHF patients is an important measure to alleviate symptoms, reduce rehospitalization rate and improve quality of life. Achieving dry body weight is also the basis for the normal efficacy of neuroendocrine hormone antagonists. The therapeutic principle is to adequately remove excess bodily fluid from intra-and extravascular tissue spaces while avoiding further activation of the neuroendocrine system^[3]。 Current CHF management guidelines recommend diuretics as the first-line treatment for ADHF. Diuretic treatment can partially relieve congestion symptoms, but often cannot fully correct fluid retention. About half of patients still have varying degrees of congestion when discharged, which is the main reason for repeated hospitalization due to recurrence of symptoms. The rate of rehospitalization in 3 months is as high as 24% ~31%^[4]。 Extracorporeal ultrafiltration can remove excess body fluid controllably according to the degree of fluid retention of patients, and is an effective method to correct sodium water retention^[5]。 In particular, the progress of ultrafiltration technology in recent 10 years has provided better therapeutic tools for clinic, showed good clinical application prospects, and has become an important supplement or substitute for diuretic treatment of CHF^[6,7]。

A 90-year-old male was admitted to the hospital due to "repeated chest tightness with lower limb edema for more than 2 years, aggravated for 2 days". The patient has a history of hypertension for more than 40 years, with the highest systolic blood pressure of 200 mmHg (1 mmHg =0.133 kPa). Recently, he used nifedipine controlled-release tablets, olmesartan, indapamide and other drugs, and his blood pressure was mostly controlled at 140/60 mmHg level. He has a history of type 2 diabetes for more than 30 years. He regularly uses gliquidone and acarbose. His blood glucose is controlled at 6-8 mmol/L on fasting and 2 hours postprandial, and his glycosylated hemoglobin is 6.5%. Have a history of hypothyroidism for more than 2 years, use levothyroxine regularly, and repeated thyroid function is basically normal. In 2013, he had a history of acute non-ST-segment elevation myocardial infarction, did not undergo coronary angiography, regularly took lipid-lowering, anti-platelet aggregation and other drugs, and did not experience chest tightness, chest pain, palpitations and other discomfort. Since 2012, he has been hospitalized for dyspnea with lower limb edema caused by "cold" many times. After anti-infection, diuresis, antihypertensive treatment, he has improved, and there is no fatigue or dyspnea in daily activities. On 16 January 2014, the patient was admitted to hospital again due to chest tightness with lower limb edema after "cold". Deny the history of hypercholesterolemia, deny the history of smoking and alcohol abuse. Physical examination at admission: body temperature 36.5 ℃, blood pressure 138/58 mmHg, heart rate 66 beats/min, breathing 20 beats/min, weight 67 kg. You can lie down, the jugular vein is full, and the fixed fine wet rales can be heard in the right lower lung. There was no depression or abnormal bulge in the precordial area, the apical beat was located at the midline of the clavicle in the fifth intercostal area of the left chest, no tremor was palpable, the voiced sound boundary of the heart was slightly enlarged to the left, and no pathological murmur was heard in each valve area. Soft abdomen, unpalpable mass, unpalpable subcostal liver and spleen. Depressed edema below the knee joint of both lower limbs, with left side. After admission, blood routine, erythrocyte sedimentation rate, C-reactive protein, thyroid function, liver function, troponin I were roughly normal, B-type natriuretic peptide (BNP) was 362 ng/L, and serum creatinine was 198.6 μ mol/L. Electrocardiogram and chest CT were roughly normal. Ultrasound showed left ventricular ejection fraction of 57%, no effusion in bilateral pleural cavities, and no thrombosis in deep veins of both lower limbs.

Recent studies have shown that the inflammatory-immune response plays an important role in the process of atherosclerosis (AS). The interaction between costimulatory molecule CD137 and its ligand CD137L is a key secondary signal for activating T lymphocytes, and it participates in cellular immune response, immune tolerance and other responses. CD137 is mainly expressed on the surface of activated T lymphocytes, while CD137L is mainly expressed on the surface of antigen presenting cells (APCs), such as monocytes-macrophages, dendritic cells (DCs), etc. The binding of CD137 to CD137L can cause intracellular molecular signal transduction and produce various biological effects. It was found that CD137-CD137L signaling was involved in the occurrence and development of AS plaque. This paper reviewed the research progress of CD137-CD137L signaling in AS plaque.