2017年 · 第45卷第12期

Victor Eisenmenge, an Austrian, was the personal health care provider of Archduke Ferdinand, heir to the throne of Austria-Hungary, known to have been assassinated in 1914, igniting the flames of World War I. But what really made Eisenmanger famous and famous was his 1897 publication in the German journal Clinical Medicine (Zeitschrift für klinische Medizin) published an article entitled "Congenital ventricular septal defect". The article describes a 32-year-old prime-age male construction worker who had cyanosis and dyspnea since childhood and eventually died of hemoptysis, with clubbed fingers and erythrocytosis, cardiac murmur and definite right heart enlargement, with cyanosis and dyspnea aggravated when active. Eisenmanger clinically diagnosed ventricular septal defect based on tremor and murmur in the 3rd and 4th intercostal areas of the left sternum. Post-death autopsy confirmed a 2-2.5 cm defect in the ventricular septum, aorta riding, right ventricle hypertrophy and dilatation, extensive atherosclerosis of the pulmonary artery with thrombosis but no aorta. He believes that the pressure difference between the left and right ventricles of patients leads to left-to-right shunt, insufficient systemic circulation filling, and excessive pulmonary circulation filling leads to pulmonary gas exchange disorder, which is an important cause of cyanosis. Due to the medical conditions at that time, Eisenmanger did not realize the existence of right-to-left reverse shunt in the patient's ventricle and its pathophysiological significance. Instead, he mistakenly believed that the cause of the patient's increased pulmonary circulatory resistance was thrombosis inside the pulmonary artery.

The Chinese Guidelines for Diagnosis and Treatment of Hypertrophic Cardiomyopathy in Adults (hereinafter referred to as the Chinese Guidelines) will be published soon. Due to the low incidence of clinical events in hypertrophic cardiomyopathy, hard, objective clinical consequences [such as heart failure (HF)] often occur after many years, and there are relatively few randomized controlled clinical trials related to hypertrophic cardiomyopathy, such as the 2011 American College of Cardiology Foundation (ACCF) /American Heart Association (AHA) and 2014 European Society of Cardiology (ESC) relevant guidelines^[1,2]Like, China Guide^[3]Many of the recommendations are also derived from expert consensus, meta-analysis, small sample clinical trials and observational studies. The Chinese guidelines do not focus on the etiology and pathophysiology of hypertrophic cardiomyopathy, but closely integrate clinical practice and focus on improving the diagnosis and treatment of hypertrophic cardiomyopathy. Physicians can refer to this guideline to select the optimal treatment plan according to the specific situation of each patient and make clinical decisions that are in the best interest of the patient as much as possible. Like any clinical guidelines, Chinese guidelines cannot replace the independent judgment of doctors, and doctors cannot avoid their responsibilities in the process of diagnosing and dealing with patients. I think the main inspiration of the China guide for us is as follows.

In recent years, infections caused by coagulase negative staphylococcus (CNS) have gradually increased with the increase of the elderly, premature infants, long-term hospitalization and immunodeficiency patients^[1]It has been paid more and more attention in clinical practice. As a kind of CNS, Staphylococcus ludensis is more virulent than other CNS, and can cause endocarditis, osteomyelitis, peritonitis, lymphadenitis, ophthalmitis, skin and soft tissue infection, bloodstream infection, central nervous system infection, bone and joint infection, etc^[2,3,4,5]。 Infectious endocarditis caused by Staphylococcus ludensis is serious, with many complications and high mortality rate^[6,7]Different from other endocarditis caused by CNS, it mainly invades the intrinsic valve, usually causing severe valve damage and growth formation, and the disease progresses more rapidly. Early valve replacement surgery is required while using antibiotics, and the prognosis is poor.

In recent years, cardiovascular specialists have paid more and more attention to hypertrophic cardiomyopathy (HCM), and their understanding at home and abroad has become more in-depth and extensive. European and American medical circles began to standardize the diagnosis and treatment of HCM more than ten years ago. The American College of Cardiology (ACC) and the European Society of Cardiology (ESC) first published the HCM Expert Consensus in 2003^[1]In 2011, the American College of Cardiology Foundation (ACCF) /American Heart Association (AHA) published the first HCM diagnosis and treatment guidelines^[2]In 2014, ESC also issued guidelines for the diagnosis and treatment of HCM^[3]。 In China, in 2007, the Chinese Cardiomyopathy Diagnosis and Treatment Working Group of the Cardiovascular Disease Branch of the Chinese Medical Association issued recommendations for the diagnosis and treatment of cardiomyopathy in China^[4]In 2011, the Chinese Expert Consensus on Ventricular Septal Myocardial Ablation in Hypertrophic Obstructive Cardiomyopathy was published.^[5]。 Based on this, the Cardiovascular Disease Branch of Chinese Medical Association organized the preparation of this guide for professional reference in clinical decision-making.

A 65-year-old male was admitted to the hospital on April 5, 2017 due to "headache after activity for more than 10 days and aggravated for 5 hours". The patient experienced post-activity headache more than 10 days before admission, lasting for several minutes each time, which improved after rest without other discomfort. At the onset of symptoms, my blood pressure was measured at the local county hospital or by myself many times, all of which were around 140/90 mmHg (1 mmHg =0.133 kPa). I did not take vasodilators such as nitrates, did not perform electrocardiogram, and did not treat it. Five hours before admission, the patient experienced a recurrent headache while moving, the pain was severe and persistent without relief, accompanied by profuse sweating, no malignancy and vomiting, no disturbance of consciousness, no disadvantage of limb movement, no slurred speech, no chest tightness and chest pain, no palpitations and shortness of breath. The patient was seen in the emergency department of our hospital and his blood pressure was measured to be 145/90 mmHg. CT angiography of the head showed no obvious abnormalities in cerebral parenchyma and cerebral vessels. ECG showed sinus rhythm, V₁~ V₅The ST segment arch of the lead was elevated dorsally upward by 0.5~1.2 mV (Figure 1）。 Myocardial necrosis markers showed myoglobin (MYO) 399.1 μ g/L, troponin T (cTNT) 0.394 μ g/L, and creatine kinase isoenzyme (CK-MB) 26.34 μ g/L. N-terminal pronatriuretic peptide type B (NT-proBNP) 1 340 ng/L. Echocardiography showed that the inner diameter of each chamber of the heart was normal, the thickness and echo of the interventricular septum and the posterior wall of the left ventricle were normal, the movement of the anterior wall and anterior compartment wall was reduced and uncoordinated, the apex became blunt, and a liquid anechoic area about 3 mm wide was visible on the right ventricular surface of the pericardial cavity. The patient had a history of hypertension for more than 10 years, with the highest blood pressure of 180/100 mmHg. The blood pressure was controlled by oral enalapril tablets at about 140/90 mmHg, and there were no headache symptoms when the normal blood pressure increased. Has a history of diabetes for more than 7 years, and currently takes metformin orally to control blood sugar. Prior history of migraine, peptic ulcer, cerebral hemorrhage and cerebral infarction was denied. Physical examination after admission: body temperature 36.5 ℃, pulse 72 beats/min, breathing 20 beats/min, blood pressure 160/100 mmHg, blood oxygen saturation (SpO₂）95%。 Conscious and fluent in speech. The neck was soft, without resistance, and the jugular vein was not distended. Cardiopulmonary examination showed no obvious abnormalities. Soft abdomen, no tenderness and rebound pain. The limbs move freely, physiological reflexes exist, but pathological reflexes are not elicited. The initial diagnosis was acute anterior ST-segment elevation myocardial infarction, cardiac function grade I (Killip grade), hypertension grade 3 (very high risk) and type 2 diabetes.

Hypertension is a common chronic disease, which is the most important risk factor of cardiovascular diseases in China and one of the main causes of death from cardiovascular diseases in China^[1]。 At the same time, hypertension is also a common psychosomatic disease. Patients with long-term hypertension suffer from both physical and mental torture. Studies have shown that the incidence of hypertension combined with mood disorders is increasing year by year. Mood disorders are not only closely related to the occurrence and development of hypertension, but also affect the effect of drug treatment and prognosis of hypertension. Therefore, in recent years, psychological behavioral intervention treatment has attracted much attention, which can synergistically improve the antihypertensive efficacy of patients with hypertension and mood disorders on the basis of drug treatment and improve the quality of life of patients.

Heart failure (HF), as a common clinical disease, has brought huge economic burden to the country and the people because of its high cost of treatment, high mortality, recurrence of the disease and decline of the quality of life of patients^[1]。 The 2016 European Society of Cardiology guidelines reported that the prevalence of heart failure was 1% to 2%, while the prevalence of people over 70 years old rose to 10%^[2]。 About 20% of patients with heart failure are rehospitalized within 12 months after discharge, and the elderly over 65 years old are at high risk for heart failure rehospitalization. Patients with heart failure not only have a high rate of rehospitalization, but also have a significant impact on their quality of life^[3]。 Although there is evidence that general therapy, drug therapy and mechanical assisted intervention can improve the prognosis of heart failure, it does not reduce the mortality rate of heart failure. Since 1990, several studies have shown that multidisciplinary management can improve the symptoms and reduce the mortality rate of patients with heart failure. Based on these evidences, the 2013 American College of Cardiology Heart Failure Management Guidelines and the 2016 European College of Cardiology Acute and Chronic Heart Failure Guidelines both emphasize the importance of teamwork management^[2,4]In addition, a number of relevant expert consensus also emphasized the importance of team-based management^[5,6]。 The purpose of this article is to discuss the possibility of cooperative management of heart failure team to change the current state of heart failure treatment, and at the same time give the specific plan of its implementation, in order to help the follow-up and treatment of clinical heart failure patients.

There are currently a variety of treatments for vasoobstructive diseases, such as angioplasty, thrombolysis and coronary artery bypass grafting. Although these methods have been established for a long time, they still have their own limitations, especially their inability to regenerate damaged organs. Therefore, there is a need to develop new methods to promote ischemic tissue regeneration, induce new blood vessel growth through the tissue's own potential, and enhance tissue repair. The regeneration and formation of microvessels after myocardial infarction have a significant effect on the recovery of cardiomyocytes and the improvement of cardiac function, especially the role of vascular growth factor is particularly concerned. The growth factors that have been discovered to promote vascular regeneration include vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), hepatocyte growth factor (HGF), insulin-like growth factor (IGF-1), etc. More studies have focused on increasing the level of local vascular growth factor after myocardial infarction. At present, the better results are the use of genetic engineering methods to increase the expression of the factor, and the use of biomaterial methods to implant biomaterials carrying vascular growth factor. In this paper, several angiogrowth factors and their combination with gene technology and biomaterials in the treatment of myocardial infarction are reviewed.

Pin1, a member of peptidyl-prolyl cis-trans isomerase (PPlase), was first discovered and named by Professor Lu Kunping of Harvard Medical School in 1996. It is the only cis-trans isomerase in human body that can recognize phosphorylated serine/threonine-proline (pSer/Thr-Pro) motif^[1]。 The gene encoding Pin1 protein is located at 19p13, consists of 163 amino acids and has a relative molecular weight of 18,000. It contains two domains, WW and PPIase. The WW domain specifically binds to the pSer/Thr-Pro motif of the substrate protein, and the PPIase domain catalyzes the cis-trans isomerization of its peptide bond, thereby changing the conformation of the target protein, regulating the activity, stability, phosphorylation level, subcellular localization and interaction with other proteins, and participating in the regulation of cell cycle, gene transcription and signal transduction^[2]。 Studies have shown that Pin1 dysfunction is closely related to the development of tumors and Alzheimer's disease^[3,4]。 In recent years, studies have found that Pin1 also affects the occurrence of cardiovascular diseases by regulating vascular endothelial function, vascular smooth muscle cell (VSMC) proliferation, myocardial remodeling, cardiac progenitor cell (CPC) aging, glucose and lipid metabolism, and obesity.

pulmonary hypertension (PH) can exist independently as a disease, or it can be a pathophysiological manifestation of many diseases to a certain stage^[1]。 The main manifestations are abnormal proliferation and anti-apoptosis of pulmonary vascular cells, pulmonary vascular remodeling, continuous increase of pulmonary artery pressure, and finally leading to right heart failure and even death^[2]。 MicroRNAs (miRNAs) are a set of highly conserved single-stranded non-coding small nucleotide fragments in eukaryotic cells that negatively regulate target gene expression at the post-transcriptional level. A large number of studies have shown that miRNA is closely related to the proliferation and apoptosis of pulmonary artery smooth muscle cells (PASMC), pulmonary artery endothelial cells (PAEC) and pulmonary artery fibroblasts in the mechanism of PH formation. In this paper, the research progress of miRNA and PH is reviewed.

Coronary artery occlusion leads to myocardial ischemia, which is usually treated with thrombolysis or percutaneous coronary intervention. Myocardial reperfusion will further lead to ischemia-reperfusion injury^[1,2]。 At present, there is still a lack of effective therapeutic measures for myocardial ischemia-reperfusion injury. Studies have confirmed that exosome-mediated intercellular information exchange is widely involved in the pathophysiological process of myocardial ischemia-reperfusion injury, and has potential therapeutic value. This paper reviews the study of exosomes, exosomes in the heart and exosomes from different sources and myocardial ischemia-reperfusion injury.

In recent years, there are 290 million patients with cardiovascular diseases in China, and cardiovascular deaths account for the first cause of death in urban and rural residents, with 44.6% in rural areas and 42.51% in urban areas^[1]。 Chronic heart failure (HF) is the result of multiple factors, which is the terminal stage of most cardiovascular diseases. It is manifested by decreased cardiac pumping function and different degrees of blood stasis in systemic and pulmonary circulation, which seriously affects the quality of life of patients. A large number of studies have shown that myocardial hypertrophy is a common pathophysiological link of heart failure caused by many etiologies, and is an independent risk factor for increased morbidity and mortality of heart failure^[2,3,4]。 In recent years, although important progress has been made in the research of cardiac hypertrophy-related signaling pathways, its mechanism has not been completely defined, and there is no very effective clinical prevention and treatment method. Therefore, the discovery of specific molecules and their corresponding signaling pathways to block myocardial hypertrophy is of great significance to explore the pathogenesis of myocardial hypertrophy and find new drug targets for preventing and treating myocardial hypertrophy.

Read Professor Dong Erdan's article published in the essay column of the editor-in-chief of the 9th issue of the Chinese Journal of Cardiovascular Diseases in 2017-in the name of the Chinese Journal of Cardiovascular Diseases, Professor Dong wrote at the end of the article, "I look forward to the cardiovascular clinic of every hospital and clinic in the motherland, whether in the doctor's office or the lounge, the Chinese Journal of Cardiovascular Diseases can be placed one after another, and doctors or medical students can open the book to read or cover the book to think for a long time". After reading, staring at the bound books of Chinese Journal of Cardiovascular Diseases and some unbound journals that I have personally produced on my bookshelf and desk for decades, I recalled the years when Chinese Journal of Cardiovascular Diseases grew up with me, and my heart surged and my thoughts were abundant, so I couldn't calm down for a long time.