2018年 · 第46卷第03期

Recently, I participated in the "Leader Conference-2018 Brand Advantage Annual Ceremony" jointly organized by "Health News" and "Good Doctor Online", and deeply felt the enthusiasm and enthusiasm of the industry to participate in health management. A variety of ideas and techniques, involving all areas and levels of disease management. How should we make good use of the technology of our time, solve the health problems faced by our time (such as the so-called "lifestyle diseases") and improve our health level? Both the medical and industrial circles are thinking and exploring this issue. I participated in the final discussion session of the conference, mainly expressing a clinician's view on the application of mobile medicine and smart medicine in the management of chronic non-communicable diseases.

The patient was an 82-year-old male who was admitted to the hospital on 24 February 2017 due to "chest pain for 2 h". The patient suffered from sudden chest pain accompanied by sweating 2 h before admission and came to our emergency department. The electrocardiogram showed that the heart rate was 36 beats/min, the ST segment elevation of extensive anterior wall leads was 0.3~0.4 mV, and the ST segment depression of Ⅱ, Ⅲ and aVF leads was 0.1 mV. The patient was previously in good health. Considering "coronary heart disease, acute anterior wall myocardial infarction", after administration of "aspirin 300 mg, ticagrelor 180 mg, atorvastatin 40 mg, heparin 5 000 IU", coronary angiography was performed directly into the catheter laboratory through the right radial artery, which showed 100% occlusion of the proximal segment of the left anterior descending artery (Figure 1), 70% stenosis in the middle of the left circumflex artery, atherosclerotic plaque in the right coronary artery, and no collateral circulation from the right coronary artery to the left coronary artery. When preparing the emergency percutaneous coronary intervention (PCI) equipment, the patient suddenly lost consciousness and convulsed, and the monitoring showed ventricular fibrillation (VF). Immediately, the patient was given 150 J bidirectional asynchronous electric defibrillation once, and the monitoring showed that the heart rate slowed to 30~40 beats/min. Extracardiac compression and adrenaline static push were given. The patient's respiratory rate slowed down, and the patient was given tracheal intubation and ventilator to assist breathing. After that, the patient had repeated ventricular fibrillation, and was given multiple electric defibrillation, adrenaline static push, and continuous extracardiac compression, but the sinus rhythm could not be maintained. After continuous cardiopulmonary resuscitation for 15 min, the patient did not regain consciousness and could not maintain circulation. After explaining his condition to his family and obtaining informed consent, extracorporeal membrane oxygenation (ECMO) implantation was immediately performed. After about 30 min of cardiopulmonary resuscitation, ECMO implantation was successful. The initial transfer flow rate was 4.2 L/min, oxygen 100%, and oxygen flow rate was 3 L/min. After ECMO implantation, the interventional therapy was continued through the radial artery, and thrombosis aspiration and percutaneous coronary angioplasty (PTCA) were performed in the left anterior descending branch. Postoperative coronary blood flow recovered and reached TIMI grade 2~3 (Figure 2）。 During the intervention, the cardiac rhythm was still ventricular fibrillation rhythm. After the operation, the sinus rhythm was restored with 200 J electric defibrillation again, and frequent premature atrial beats occurred, with intermittent atrial fibrillation (AF) rhythm. intra-aortic balloon pump (IABP) was implanted through the left femoral artery to assist circulation. Both pupils were 3.5 mm in diameter, light reflex was present, and he was in a coma state. Monitoring showed blood pressure 102/60 mmHg (1 mmHg =0.133 kPa), heart rate 98 beats/min, blood oxygen saturation (SPO₂）100%。 Postoperative color echocardiography showing reduced segmental wall motion, left ventricular dysfunction, considering acute anterior wall myocardial infarction, left ventricular ejection fraction (left ventricular ejection fraction, LVEF) 38%. Neurological consultation considered brain cell ischemia and hypoxia for too long, so protective brain cell treatment was given. The patient regained consciousness and spontaneous breathing after 2 days. The ventilator was withdrawn on the 4th day, and the ECMO parameters were gradually downadjusted as the condition improved. ECMO was withdrawn after 10 days, and IABP was withdrawn after 12 days. Return color echocardiography after 20 days showed left ventricular end-diastolic diameter 42 mm and LVEF 45%. After 32 days, the ECG showed that the ST segment of the anterior wall lead dropped significantly, and the condition was stable and the hospital was discharged.

The 81-year-old male was admitted to the hospital on October 14, 2016 due to "sudden palpitations, chest tightness and dizziness for 1 d". Emergency electrocardiogram before admission showed complete atrioventricular block. The patient had a history of hypertension for more than 10 years, up to 180/100 mmHg (1 mmHg =0.133 kPa), oral valsartan (80 mg, once/d), amlodipine (5 mg, once/d); With a history of type 2 diabetes for more than 5 years, he took gliclazide extended-release tablets (30 mg, once a day), and his blood pressure and blood glucose were controlled normally. Physical examination on admission: clear consciousness, pulse 35 beats/min, breathing 18 beats/min, blood pressure 170/80 mmHg, clear breathing sounds in both lungs, no dry and wet rales, heart rate 35 beats/min, arrhythmia, no pathological murmur in each valve auscultation area, and no edema in both lower limbs. Electrocardiogram after admission: complete atrioventricular block. Admission diagnosis: (1) arrhythmia, third-degree atrioventricular block; (2) Grade 3 hypertension (very high risk); (3) Type 2 diabetes.

The patient was a 58-year-old male who was admitted to the hospital on December 5, 2016 due to "chest pain for 3 h". The patient began to develop chest pain without obvious trigger 3 h ago, accompanied by palpitations, no sweating, nausea, vomiting, dyspnea and hemoptysis. Previous history of hypertension, systolic blood pressure up to 160 mmHg (1 mmHg =0.133 kPa), untreated. No history of diabetes, no history of smoking or drinking. The symptoms of chest pain persisted and did not relieve. He came to our hospital for treatment. Physical examination: body temperature 36.4 ℃, pulse 62 beats/min, blood pressure 110/80 mmHg, no positive signs. ECG showed: sinus rhythm, V₂~ V₆The ST segment of the lead reached 0.5 mV oblique depression after the J point, and the T wave was symmetrical at the high tip. The ST segment of the aVR lead was elevated about 1.5 mV, and the ST segment of the lead Ⅰ and Ⅱ was mildly depressed (Figure 1）。 Emergency high-sensitivity troponin I was 0.09 μ g/L (0-0.342 μ g/L). The ECG was re-examined after 110 min only V₂~ V₄The R wave of the leads decreased compared with the previous, and the remainder did not change significantly compared with the previous (Figure 2）。 Initial diagnosis of "acute myocardial infarction", emergency coronary angiography showed: no abnormalities in the left main artery, 100% proximal occlusion of the left anterior descending artery, diffuse atherosclerosis and stenosis of the circumflex artery, 50% middle stenosis, subtotal distal occlusion, 90% proximal stenosis of the blunt margin artery, atherosclerosis of the middle and distal right coronary artery, 80% proximal stenosis of the posterior descending artery, and subtotal distal occlusion. One stent was placed in the left anterior descending artery. Electrocardiogram reexamination 35 d after percutaneous coronary intervention (PCI) showed sinus rhythm, V₁~ V₃The leads showed QS waves, V₄The leads showed qrs waves, V₁~ V₅, Ⅰ, coronary T waves appeared in aVL leads, showing ECG manifestations of extensive anterior wall myocardial infarction (Figure 3）。

A 14-year-old female was admitted to the hospital in November 2015 due to "recurrent syncope for 5 years and recurrence for 4 h". Five years ago, I had sudden syncope after running, which lasted about 1 min and then regained consciousness, accompanied by general fatigue, chest tightness, palpitation, sweating and dizziness. After that, syncope occurred twice, each attack was related to strenuous activity, and intermittent oral administration of "Coenzyme Q10 capsules" and other drugs. Sudden syncope after running 4 h ago, regained consciousness about 1 min later, accompanied by general fatigue, palpitation, chest tightness, dizziness, nausea and vomiting of stomach contents, which was non-jetting, and took 1 capsule of "Suxiao Jiuxin Pill". Previous visit to an outside hospital with blood pressure 90/68 mmHg (1 mmHg =0.133 kPa) and heart rate 105 beats/min. Electrocardiogram showed sinus rhythm, Ⅱ, Ⅲ, aVF and V₂~ V₆ST segment depression was 0.2 mV in the leads, and ST segment elevation was 0.1~0.2 mV in aVR and aVL leads. The diagnosis was "transient syncope to be examined (acute severe myocarditis, cardiogenic shock)", and symptomatic supportive treatment such as pressurization (dopamine) and fluid rehydration (specific usage and dose unknown) was given. After 2 hours, the blood pressure gradually returned to normal (specific value unknown). The patient was previously in good health.

Macrophages in tissues and organs participate in the inflammatory response under pathological conditions, and play an important role in the development of heart diseases and atherosclerosis^[1]。 In the non-pathological state, the presence of macrophages in the heart and their molecular mechanisms to regulate cardiac function, especially the influence on cardiac conduction system, are still unclear. The latest report shows that macrophages reside in the heart tissue, which clearly confirms that they play an important regulatory role in the normal conduction system of the heart^[2]This brings new hope to macrophage-targeted therapy, updates the treatment strategy of cardiac conduction system abnormalities, and optimizes the prevention and treatment measures of arrhythmia.

For a long time, compared with heart failure with reduced ejection fraction (HFrEF), left ventricular ejection fraction (LVEF)<40%] and heart failure with preserved ejection fraction (HFpEF, LVEF ≥50%), heart failure with mid-range ejection fraction (HFmrEF, LVEF 40%-49%) It has not received enough attention in clinical practice. With the deepening of research, the clinical characteristics and prognosis of HFmrEF are increasingly different from those of HFrEF and HFpEF. The 2016 European Society of Cardiology (ESC) Heart Failure Diagnosis and Treatment Guidelines independently propose HFmrEF as a concept different from HFrEF and HFpEF, in order to attract researchers' attention to the pathophysiology, clinical features, treatment and prognosis of HFmrEF^[1]。

High conductivity calcium activates potassium ion channels (large-conductance calcium-activated potassium channels, BK_Ca) is widely distributed on mammalian cell membranes, and plays an important role in regulating physiological processes such as vascular tone, neurotransmitter and hormone release. renin-angiotensin-aldosterone system (RAAS) is an important humoral fluid regulation system in human body, which has the functions of maintaining water and electrolyte balance and regulating blood pressure. Current studies have shown that renin, angiotensin, and aldosterone can affect BK_CA expression and activity and regulate its function. In this paper, RAAS versus BK_CaThis paper summarizes the functions and mechanisms of.

The heart is one of the organs that consume more energy in the human body. The maintenance of its function depends on the continuous production and rational and efficient utilization of adenosine triphosphate (ATP). Disorders in the generation or utilization of energy can lead to the development of a variety of heart diseases. A large number of studies have proved that the metabolic remodeling and energy depletion of the heart are important causes of the occurrence and development of heart diseases^[1]。 In the physiological state, more than 90% of ATP in the adult heart is produced by the oxidative metabolism of fatty acids and sugars, while the energy produced by ketone bodies, lactic acid and amino acids is very little^[2,3]。 However, pathological cardiac remodeling, such as hypertensive heart disease, ischemic cardiomyopathy and diabetic cardiomyopathy, is often accompanied by pathological remodeling of energy metabolism, which is manifested by a significant decrease in the oxidative energy supply efficiency of fatty acids and carbohydrates. At this time, whether other energy substrates can supplement or partially supplement the energy supply required for cardiac contraction and relaxation has not been fully elucidated^[4,5]。 Among them, ketone body metabolism is a hot spot in the research of cardiac metabolic remodeling in recent years. It is of great significance to clarify the pathway of ketone body metabolism in cardiomyocytes, clarify the regularity of ketone body metabolism in the process of pathological remodeling, and clarify the role and mechanism of ketone body metabolism in pathological cardiac remodeling. This paper reviews the effects and mechanisms of ketone metabolism on cardiac diseases.

tetrahydrobipterin (BH4) is an essential cofactor of three kinds of nitric oxide synthase, including endothelial nitric oxide synthase (eNOS), neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS). Under normal physiological conditions, nitric oxide synthase catalyzes L-arginine to generate nitric oxide (NO) under the condition of sufficient BH4; When BH4 is deficient, its catalytic product is a superoxide radical. Because NO has the effects of dilating blood vessels and preventing platelet aggregation, and BH4 directly affects NO level in the body, it is also closely related to cardiovascular system activity. BH4 deficiency may lead to a series of changes in cardiovascular activity such as endothelial dysfunction, hypertension, atherosclerosis, etc. This article reviews BH4 biosynthesis, regulation and its role in cardiovascular diseases.