2015年 · 第43卷第03期

The Beijing CDC released the results of the healthy life expectancy of residents for the first time: the healthy life expectancy of the 18-year-old group in Beijing was 40.17 remaining years, 43.40 remaining years for men and 38.06 remaining years for women. Taking the results of the male group as an example, the life expectancy of men in the 18-year-old group was 62.22 remaining years, the healthy life expectancy was 43.40 remaining years, and the time spent in the state of illness or disability was equivalent to 18.82 years. Women have a longer life expectancy than men, while healthy life expectancy is shorter than men, and women survive longer with illness. The study shows that although people's life expectancy has exceeded 80 years, various factors in their lifetime have caused nearly 20 years of survival with illness, mainly plagued by chronic non-communicable diseases.

In heart failure (heart failure), neuroendocrine activation, especially over-activation of sympathetic nerves, will cause an increase in heart rate. In the past, it was believed that this is the consequence of sympathetic nerve excitement and a marker reflecting the degree of sympathetic nerve excitement. At present, there is evidence that the increase of heart rate in patients with heart failure has a disadvantage, which can directly lead to increased myocardial oxygen consumption, decreased coronary (coronary) blood flow (decreased coronary diastolic blood supply), decreased ventricular fibrillation threshold (more prone to ventricular fibrillation), etc., which will lead to the progression of heart failure, and is the maker of heart failure progression. Therefore, heart rate management has become an important content in the treatment of heart failure.

Heart failure (HF) is the severe and terminal stage of various heart diseases, and it is one of the serious cardiovascular diseases today. In recent years, a number of studies on the "heart rate" of patients with heart failure have been released, making "heart rate control" a hot spot in the treatment of heart failure. Previous studies have shown that increased heart rate is an important factor in promoting the progression of cardiovascular events in patients with coronary heart disease and hypertension. Heart rate control plays an important role in the treatment of coronary heart disease. But in the treatment of heart failure, do all patients need and can strictly control their heart rate? What should be the target value for heart rate control? There is no clear conclusion at present.

Heart failure (HF) has become a major global public health problem due to its high morbidity, mortality and treatment costs. The results of the 2002 multi-center cooperative study on cardiovascular health in China showed that the prevalence of heart failure was 0.9%, and the prevalence of heart failure increased significantly with the increase of age^[1]。 Current treatments to improve the prognosis of patients with heart failure mainly include drug therapy such as angiotensin converting enzyme inhibitor (ACEI), angiotensin II receptor antagonist (ARB), beta-blockers and aldosterone receptor antagonist, as well as implantation of related equipment for treatment^[2]。 However, diuretics have been used in the treatment of heart failure since 1940s, and are still the cornerstone of improving symptoms in the treatment of acute and chronic heart failure, and are the only drugs that can control fluid retention in the treatment of heart failure. Among many drugs to control fluid retention, haptic diuretics are the first choice. Its clinical application can significantly improve the symptoms and signs of pulmonary edema and peripheral edema in most patients in a short time^[2,3]。 At present, flexible adjustment of diuretic administration based on daily body weight changes, close follow-up communication between physicians and patients, and/or monitoring of biological indicators (such as urine output, oxygen saturation, etc.) is a major advance in the treatment of heart failure^[4,5]。 However, there is still a long way to go to prevent the occurrence of fluid retention, especially diuretic resistance is a serious challenge in the treatment of fluid retention in patients with heart failure. Therefore, various therapeutic options to clinically improve fluid retention are still dominated by reducing diuretic resistance.

Hypertension is one of the major public health problems. Although lifestyle control and antihypertensive drugs are very effective in controlling blood pressure and preventing cardiovascular events, about 30% of patients still have blood pressure that fails to meet the standard when they are treated^[1]Increased cardiovascular risk.

A 32-year-old male was admitted to the hospital on 19 November 2013 due to "repeated syncope for more than 8 years, 8 years after implantable cardioverter defibrillator (ICD) implantation". The patient was diagnosed with Brugada syndrome in our hospital 8 years ago due to repeated syncope without obvious inducement. He underwent ICD implantation and took amiodarone 200 mg/d for a long time. During this period, he had 4 discharges. He was added with bisoprolol and gradually increased to 5 mg/d. There was no ventricular fibrillation (ventricular fibrillation) and discharge during the follow-up for several years. In November 2011, the patient underwent ICD (battery capacity 30 J) replacement due to pacing battery depletion, and his condition has been stable with no events at follow-up. On November 7, 2013, the patient experienced electrical discharge during sleep and fainted for about 30 min, accompanied by twitching and cyanosis of limbs. He went to the local hospital and was transferred to our hospital after his condition was stable. ICD program control found that there were multiple records of unsuccessful cardioversion. Has a history of hepatitis B for 10 years and a history of penicillin allergy. Smoking history, 6 cigarettes/d ×15 years.

The patient was a 65-year-old male. He was admitted to the hospital in March 2014 due to "intermittent chest pain for 2 years and worsening for 1 month". Two years ago, I developed chest pain during emotional agitation, radiating to the shoulder and back, accompanied by palpitations, which can be relieved by rest for 15 to 20 minutes. Symptoms attack 1 to 2 times a week, daily activities are not limited, and there is no diagnosis and treatment. One month ago, the frequency of chest pain symptoms increased, about 4 to 6 times a week. The exercise treadmill test result was positive in the outpatient clinic of Peking University Third Hospital, and he was admitted to the hospital with "coronary heart disease and unstable angina pectoris". History of hypertension, diabetes, hyperlipidemia is denied. Physical examination at admission: body temperature 36.3 ℃, pulse 68 beats/min, breathing 18 beats/min, blood pressure 140/80 mmHg (1 mmHg =0.133 kPa). The breathing sounds of both lungs were clear, and dry and wet rales were not heard. The heart boundary was not large, the heart rate was 68 beats/min, the heart rhythm was uniform, and no murmur was heard in the auscultation area of each valve. The abdomen is soft, and the liver and spleen are untouched. Both lower limbs are not swollen.

A 19-year-old male was hospitalized in the Department of Internal Medicine of Zhengzhou People's Hospital on September 10, 2013 due to "2 years of discovery of abnormal electrocardiogram". During the physical examination 2 years ago, the patient found abnormal electrocardiogram, without chest tightness, chest pain, palpitations, dyspnea, fever, cough, expectoration, hemoptysis, nausea, vomiting, abdominal pain, diarrhea, headache, dizziness, tinnitus, and syncope. He had checked myocardial enzymes and myocarditis virus profile many times in other hospitals, and was diagnosed as myocarditis or dilated cardiomyopathy. He was given trimetazidine tablets, coenzyme Q10 capsules and metoprolol sustained-release tablets orally, but there was no systematic diagnosis and treatment. No prior history of hypertension, diabetes, and cerebrovascular disease. Familial genetic history denied.

Cardiac hypertrophy is the cell hypertrophic response of cardiomyocytes to various external stimuli. It can usually be divided into physiological cardiac hypertrophy and pathological cardiac hypertrophy. Pathological myocardial hypertrophy is a change in the structure and function of myocardial cells caused by stress and/or volume overload under pathological conditions, as well as the overstimulation of various growth factors and/or hormones, which is manifested by the enlargement of myocardium along the long axis of cells, the upregulation of the expression of embryonic genes such as atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), β-myosin heavy chain (β-MHC), α-MHC, myocardial sarcoplasmic reticulum Ca^2＋– The expression of functional genes such as ATPase 2a (SERCA2a) is down-regulated, the myocardial contractile function decreases, and the overall mass of the heart increases, accompanied by apoptosis and changes in matrix components (myocardial fibrosis), which ultimately leads to decreased cardiac compliance and circulatory pump function, leading to heart failure, arrhythmia and sudden death^[1]。

Recent studies on molecular and cell biology of cardiovascular diseases have confirmed that the formation of cardiovascular diseases is related to inflammation and autoimmune system, and many cytokines and growth factors are involved in this process as pro-inflammatory mediators. CD4^＋T cells are divided into two different subgroups, Th1 and Th2, according to the pattern of cytokine induction and their biological functions^[1]Th1/Th2 plays an important role in maintaining normal immune status. In recent years, it has been discovered that CD4 present in normal body^＋T cell subsets – T helper 17 cells (Th17) and T regulatory cells (Treg), i.e. Th17/Treg. Its secretion of cytokines is closely related to immune response, inflammatory response, myocardial remodeling and vascular remodeling. Th17/Treg plays an important role in the development of cardiovascular diseases such as coronary atherosclerosis and acute coronary syndrome. This article reviews the research progress of Th17 and Treg in the pathogenesis of cardiovascular diseases.

Cardiac remodeling refers to changes in myocardial structure, including cardiomyocyte hypertrophy, cardiomyocyte loss (e.g. apoptosis and necrosis), proliferation of interstitial cells such as fibroblasts, collagen tissue proliferation, etc. At the same time, cardiac function is also significantly affected, mainly changes in ventricular structure. Ventricular remodeling is often secondary to hypertension, coronary heart disease, primary cardiomyopathy, etc. Ventricular remodeling plays an important role in the development of chronic heart failure.

The most effective treatment for acute ST-segment elevation myocardial infarction (STEMI) is to restore coronary blood flow at the first time, which is commonly known as reperfusion therapy. Reperfusion therapy includes drug therapy (thrombolysis) and percutaneous coronary intervention (PCI). Regardless of the approach taken, its effectiveness depends on the duration of treatment.