2014年 · 第42卷第03期

In July 2013, I visited Kailuan General Hospital to visit the prevention and treatment of hypertension, which was very inspired and encouraged. Professor Wu Shouling, the project leader, is a graduate student of clinical medicine, but he has been doing clinical epidemiological research and control model exploration of hypertension and related diseases for many years. He has been the president of the General Hospital for many years, and has been able to make great efforts to prevent and control hypertension at the grass-roots level instead of blindly pursuing comparison of gross income. He has personally presided over and successfully completed a large number of high-level and high-quality clinical epidemiological studies.

When it comes to obstructive sleep apnea syndrome (OSAS), many cardiovascular doctors may joke: "Isn't it just snoring during sleep?" In fact, "snoring" accompanied by a large reduction or interruption of oral and nasal airflow is caused by collapse and obstruction of the upper respiratory tract during sleep, and intermittent hypoxemia frequently occurs during sleep, resulting in fragmented sleep.

The epidemiological survey in 2004 showed that the prevalence of atrial fibrillation (AF) in China was about 0.77%^[1]。 According to the population, the number of patients with atrial fibrillation over 30 years old in China is 4.2 million. The prevalence of atrial fibrillation will continue to grow as the population ages. Non-valvular atrial fibrillation generally refers to valvular atrial fibrillation without prosthetic valves or with hemodynamic significance, accounting for the vast majority of patients with atrial fibrillation. Ischemic stroke (stroke) is the most serious complication of atrial fibrillation. Compared with patients without atrial fibrillation, patients with atrial fibrillation have an approximately 5-fold increased risk of stroke, and have a higher disability and fatality rate of atrial fibrillation-related stroke^[2,3]。 Stroke prevention is an important part of comprehensive management of atrial fibrillation.

A 70-year-old male was admitted to the hospital on 30 July 2012 due to "episodic chest pain and chest tightness for half a year, aggravated for 8 h". Eight hours ago, there was sudden suffocation and pain in the precordial area, accompanied by shortness of breath, sweating, nausea and vomiting, which lasted for about 1 hour. 15 years of previous history of hypertension and 40 years of smoking (20 cigarettes/d). ECG showed complete right bundle branch block, V₂~ V₅The ST segment elevation of the lead was 0.2~0.5 mV. Troponin I 18.7 μ g/L, creatine kinase 466 U/L, and creatine kinase isoenzyme (CK – MB) 42.0 μ g/L. Acute ST-segment elevation myocardial infarction was diagnosed. After oral administration of 300 mg of aspirin and 600 mg of clopidogrel, an emergency coronary angiography was performed, and the results showed 100% occlusion of the proximal segment of the left anterior descending artery. The 2.0 mm ×20 mm B. Braun balloon was expanded at 8 to 10 atm (1 atm =101.325 kPa) for 3 s after the Runthrough NS guidewire passed through the occlusive lesion. Braun 3.0 mm ×13 mm Coroflex Please stent (3 s at 12 atm) and B. Braun 2.5 mm ×25 mm stent (3 s at 14 atm) were placed in series, followed by balloon expansion of the stent joint (3 s at 16 atm) with a B. Braun 2.5 mm ×25 mm stent. Coronary angiography showed good stent adhesion, no dissection and thrombosis, and blood flow was grade 3 in myocardial infarction thrombolytic test (TIMI). Postoperatively, oral aspirin (100 mg/dose, once/d), clopidogrel (75 mg/dose, once/d) and low molecular weight heparin calcium (4 100 U/dose, twice/d) were administered.

The child was a 2.5-year-old female, 8.5 kg, who was admitted to the hospital because of "cardiac murmur found for more than 2 years". Nothing special in the past. Admission physical examination: blood pressure of right upper limb 86/40 mmHg (1 mmHg =0.133 kPa), blood pressure of right lower limb 110/60 mmHg; Percutaneous arterial oxygen saturation was 97% in the right upper limb and 97% in the right lower limb; The precordial region was slightly raised, the left margin of the sternum was unpalpable with tremor, and the voiced boundary of the heart was enlarged, P₂Covered by murmur, continuous murmur can be heard in the second intercostal area at the left margin of the sternum, and the conduction is extensive; Smell femoral artery gunshot. Prehospital echocardiography in the diagnosis of congenital heart disease, patent ductus arteriosus (PDA; funnel type, left-to-right shunt). Electrocardiogram showed sinus rhythm, left ventricular hypertrophy. X-ray chest radiograph showed: bilateral lung blood increased, patchy density increased shadow in the right lower lung field shadow, no consolidation in the remaining lung, no tracheal stenosis, and smooth double diaphragm; The posterior segment of the left 3~5 ribs is thin, considering congenital changes; The pulmonary artery segment is flat, and the two heart margins are round and bulging; The cardiothoracic ratio was 0.57.

A 41-year-old female patient began to develop chest pain and discomfort after exertion 7 years ago, which was confined to the chest area and was squeezing-like. It was mostly accompanied by chest tightness and shortness of breath, which lasted for several minutes and could be naturally relieved after rest. Later, the patient went to the First Hospital of Jilin University and was diagnosed with "hypertrophic obstructive cardiomyopathy". The patient experienced dizziness with nausea and vomiting without obvious trigger 1 day ago. He was admitted to the hospital in the emergency department, and his blood pressure was measured at 60/40 mmHg (1 mmHg =0.133 kPa). The above-mentioned discomfort symptoms were significantly improved after vasopressor treatment. Past history: deny history of hypertension, diabetes, no history of liver disease and kidney disease, deny history of long-term heavy smoking and drinking. Physical examination at admission: body temperature 36.5 ℃, pulse 56 beats/min, breathing 16 beats/min, blood pressure 60/40 mmHg, no distension of jugular vein, clear breathing sounds in both lungs, and no obvious dry and wet rales. The heart boundary was normal, the heart rate was 56 beats/min, and a systolic jet-like murmur of grade 3/6 could be heard at the left margin of the sternum. There was no edema in both lower limbs. Admission auxiliary examination: pronatriuretic peptide type B was 10 600.0 ng/L, myocardial injury marker creatine kinase isoenzyme (CK-MB) was 20.90 μ g/L, troponin I was 2.03 μ g/L, and myoglobin was 63.0 μ g/L. ECG: V₄~ V₅Lead T-wave inversion. Cardiac color ultrasound: left atrial anterior-posterior diameter 46 mm, left-right diameter 43 mm, upper-lower diameter 57 mm, right ventricular diameter 21 mm, ventricular septal thickness 22 mm, left ventricular end-diastolic diameter 26 mm, left ventricular posterior wall thickness 18 mm, left ventricular lateral wall basal segment 13 mm, apical segment thickness 10.3 mm, right ventricular wall thickness 9.9 mm. Cardiac function measurement: left ventricular short axis shortening rate (FS) 38%, left ventricular ejection fraction (LVEF) 68%. The left and right ventricular walls were unevenly thickened, mainly in the middle and upper segments of the interventricular septum, with a thicker part of 22 mm. The thickened myocardial echo was enhanced, the pulsation amplitude was weakened, the SAM sign was positive, and the inner diameter of the left ventricular outflow tract was 10.6 mm. Doppler: Maximum flow velocity of left ventricular outflow tract 478 cm/s, pressure step difference (PG) 91 mmHg. There was no obstruction in the right ventricular outflow tract, and the cardiac chamber was almost occluded at the end of systole.

Heart failure (HF) is a clinical syndrome caused by impaired cardiac filling or (and) ejection ability caused by various cardiac structural or functional diseases. It is the end-stage manifestation of various cardiac diseases, and its fatality rate is second only to tumors. It has been established that neuroendocrine factors are involved in the pathogenesis of heart failure, mainly related to mitochondrial damage, matrix remodeling, etc. B-type natriuretic peptide (BNP), as a natural antagonist of renin angiotensin aldosterone system, has been recognized in the diagnosis of heart failure. The value has been recognized and widely used to guide the treatment of heart failure. Heptidin, as a stress product in the body, may become a new heart failure marker that can replace BNP. The protective effect of hydrogen sulfide on cardiovascular disease is relatively clear, but there is no correlation between Heptidin and hydrogen sulfide at present. Studies have confirmed that nitric oxide (NO) can affect the expression of peptides, while hydrogen sulfide interacts with NO. Therefore, the author believes that there may be a correlation between the two in heart failure.

FoxO (forkhead transcription factors of the oclass) is a subset of the forkhead protein family, and the common feature is that it has a conserved DNA binding site, the forkhead box (Fox), in its structure. Since the first discovery of FoxO in 1989, 19 subfamily members, named after A to S, have been identified^[1]。 The FoxO protein specifically binds to the conserved DNA-binding sequence TTGTTAC in the nucleus, and can be associated with some coactivator factors, such as Notch^[2]β-catenin,^[3]And peroxisome proliferator-activated receptor-γ coactivator-1 α (PGC-1 α)^[4]Binding, thereby leading to the transcription of downstream genes, so FoxO has a wide role in maintaining organ development, apoptosis, and regulating immunity^[5]Regulate sugar and lipid metabolism^[6,7], inhibiting tumors^[8,9], oxidative stress^[10]And the senescence of organs^[11]And other processes play an important role.

The peroxisome proliferator-activated receptors (PPAR) family includes three members: PPAR α, PPAR γ, and PPAR β (or δ)^[1], belonging to the ligand-activated steroidal nucleoid receptor superfamily. Vulnerable plaque refers to all atheropathies that are prone to thrombosis and may rapidly progress to sinful plaque, which are mainly characterized by a large lipid pool and a thin fibrous cap, accompanied by a large infiltration of inflammatory cells. It is pointed out that PPAR γ plays an important role in lipid metabolism, inflammatory response, atherosclerosis and other aspects. There are two main ways in which it functions. One is that PPAR γ can bind to retinoid A receptor (RXR) to form a heterodimer after binding to ligand activation, and then bind to the specific DNA sequence on the promoter of the target gene (peroxisome proliferation response element, PREE), resulting in transcriptional activation and regulating the transcription of the target gene. In addition to activating target genes, PPAR γ can also inhibit the transcription of inflammatory response genes in a non-DNA binding manner by interfering with nuclear factor-κ B (NF-κ B), signal transducer and transcription activator (STAT), and activating protein-1 (AP-1) signal transduction pathway^[2]。 Therefore, in-depth research on the role and mechanism of PPAR γ in atherosclerotic vulnerable plaques is crucial to seek the target of stable vulnerable plaques.

Myocardial fibrosis refers to the excessive accumulation of collagen fibers in the normal tissue structure of the myocardium, a significant increase in collagen concentration in the heart tissue, or changes in collagen composition. This pathological change is the inevitable process of the development of various clinical cardiovascular diseases to the terminal stage, and is the main manifestation of cardiac structural remodeling. At present, it is considered that it is closely related to arrhythmia, cardiac dysfunction and even sudden cardiac death. Myocardial fibrosis is characterized by the proliferation of fibroblasts and the deposition of extracellular matrix (ECM). The deposition of ECM causes increased cardiac stiffness and decreased compliance, which affects the normal diastolic and systolic function of the heart. Myocardial fibrosis is a key factor in determining the prognosis of cardiovascular disease. Fibroblasts are the main action cells in the process of myocardial fibrosis. In this study, the origin, differentiation, secretion and the relationship with disease of fibroblasts are summarized.