Hutchinson-Gilford Progeria syndrome (HGPS) is characterized by accelerated aging leading to death in the teen years, usually due to severe coronary and/or carotid disease. The clinical presentation includes stunted growth, alopecia, loss of subcutaneous fat, osteoporosis, and cardiovascular disorders occurring in late childhood and the teen years including hypertension and accelerated vascular aging that precipitates myocardial infarction and cerebrovascular attacks. The disease is a nuclear laminopathy, due to a Lmna gene mutation. The aberrant protein (Progerin) accumulates in and distorts the nuclear envelope. We review the genetic and biochemical mechanism of HGPS; the clinical presentation with special attention to the cardiovascular pathology and complications; current therapeutic developments to address the disease; and the results of the clinical trials attempting to translate basic research insights into therapeutic benefit. An understanding of HGPS may lead to better treatment of other age-related disorders, particularly cardiovascular diseases.

Background: The prevalence of atrial fibrillation (AF) increases with age and is associated with high morbidity and mortality. The main objective of this study is to describe the clinical characteristics and antithrombotic status and the factors that determine antithrombotic use in hospitalized elderly patients with AF. Methods: Data were collected involving patients hospitalized at the First Affiliated Hospital of Shihezi Medical University from June 2015 to September 2017. Results: A total of 621 patients with an average age of 82.4 ± 5.0 years (42.3% females; 91.8% Han) were included. The prevalence of risk factors and cardiovascular disease: hypertension (56.5%), heart failure (38.2%), coronary artery disease (76.8%), and carotid atherosclerosis (21.3%). Among the 621 patients, 35.7% were taking oral anticoagulant therapy (OAT) including warfarin (25.6%) or a novel oral anticoagulant (10.1%), 32.4% of patients were taking oral antiplatelet therapy, and 31.9% received 17 anticoagulant therapy. According to the European Guidelines for AF management, CHA2DS2-VASc score was used for stroke risk stratification. All patients in this study had a score of ≥2; However, the rate of OAT was 35.7%. Follow-up data were available for 97.3% of the patients (n = 604), of which 26.6% of patients (n = 159) were deceased and 16.75% of patients (n = 104) continued to receive anticoagulation treatment. Hospitalized patients older than 80 years with AF showed numerous comorbidities. The percentage of appropriately anticoagulated patients was suboptimal according to CHA2DS2-VASc score, with only 35.7% of those requiring treatment receiving it. Conclusion: The percentage of patients with AF appropriately anticoagulated at the First Affiliated Hospital of Shihezi Medical University is at a substandard level.

Ischemic preconditioning is a protective phenomenon, by which brief ischemic stimuli in a vascular bed are able to counteract the damage from a longer subsequent ischemia. Preconditioning may also confer protection from ischemia to distal tissues and organs. In this case, ischemic preconditioning is known as remote ischemic preconditioning (RIPC). RIPC can be safely and easily reproduced in clinical settings. Indeed, over the past years, its protective actions have been tested in various clinical settings, including cardiac surgery and elective percutaneous coronary interventions. However, translational studies on RIPC have provided conflicting results on reduction of mortality. Recently, studies in humans have investigated the effects of RIPC on coronary circulation, showing that RIPC could have a protective effect on coronaries. This recent area of research may offer innovative insights for designing translational studies on RIPC, unveiling new mechanisms by which RIPC protects the heart. The aims of the present manuscript are to summarize the available clinical evidence on RIPC efficacy for cardioprotection and to review studies assessing the effects of RIPC on coronary circulation in humans.

Chapter 1: Prevalence of Hypertension Cardiovascular disease has become the world's leading cause of death. The total mortality rate of cardiovascular disease in China has increased from 2400/million in 2004-2718/million in 2012.[1,2] Previous studies have shown that hypertension is an important risk factor for cardiovascular and cerebrovascular diseases.[2-4] The results of the Global Burden of Disease Study 2010 showed that the risk factors affecting the global burden of disease in hypertension in the 1990s jumped from fourth to first[4] in China. The prevalence rate of hypertension increased year by year, and the number of patients continues to increase. Although the control status of hypertension has improved, it remains at a low level. Prevention and treatment of hypertension are urgent. The Prevalence and Trend of Hypertension in China Hypertension status quo High blood pressure is defined as the systolic blood pressure exceeding 140 mmHg and/or diastolic pressure 90 mmHg 3 day of the same period without the use of antihypertensive drugs. History of hypertension and antihypertensive drugs are currently being used, although blood pressure is lower than 140/90 mmHg also diagnosed with hypertension.[5] China Nutrition and Health Survey 2002 (CHNS)[6] showed that the hypertension prevalence rate was 18.8% in people 18 years of age and older in China. Nearly 153 million people were suffering from hypertension among whom 20.2% were male and 18% female.[7] The latest report on the status of nutrition and chronic diseases in China (2015) showed that the prevalence rate of hypertension among people 18 years of age and older was 25.2% in 2012 in China.[1] There are notable differences in prevalence of hypertension between different regions, cities and villages, gender, and ages. From the regional distribution, the prevalence rate of hypertension in eastern China is the highest (32.6%), followed by the Northeast (31.8%), with the lowest in the Southwest (20.1%).[8] From the perspective of urban and rural distribution, in people 15 years of age and older, the prevalence rate of hypertension in medium-sized cities was higher than that of rural areas (31.3% >29.7%) in the Heilongjiang Province.[9] In the Beijing area, 18-79 year olds in the city showed a higher prevalence rate of hypertension compared to rural areas (35.6% >34.9%); however, the gap between urban and rural areas has narrowed in recent years.[10] From the perspective of gender and age, in 2012 in the Henan Province hypertension, the prevalence rate was 24.9% in 15-74-year-old people, among them male (26.6%) and women (23.5%). The overall prevalence rate increased with age; however, the prevalence rate of men under 55 years of age was higher than that of women. The prevalence rate of women older than 55 years of age was more than that of men.[11] In 2010, the prevalence rate of hypertension was 22.59% in 17,437 residents over the age of 18 in the south of China, among whom the rate for males (23.36%) was higher than females (21.77%). The overall prevalence rate increased with age; however, the prevalence rate of men between 18 and 49 years of age was higher than that of women, and the prevalence of women older than 50 years of age was greater than men. In addition, with the increase of age, the risk of hypertension among people 18-44 years of age has increased 8.53 times that of people 60 years of age and older.[12] Trend of hypertension prevalence In the past 50 years, China has carried out the four national surveys of hypertension in 1958-1959, 1979-1980, 1991, and 2002, respectively. The results showed that in people 15 years of age and older the prevalence rate of hypertension was 5.1%, 7.7%, 13.6%, and 17.6%[6] [Figure 1]. The results of the CHNS showed that the prevalence of hypertension in China increased from 14.5% in 1991 to nearly 21.4% in 2009, with an absolute increase of 6.9%.[13] The results of a longitudinal cohort study from the 1991 to 2011 Chinese health and nutrition survey also shows that in China the prevalence rate of hypertension increased from 23.4% to 28.6% including changes in men and in elderly patients with the most obvious.[14] The 2015 National Health and Family Planning Commission of the People's Republic of China released data suggesting that in 2012 the country's adult hypertension prevalence rate was 25.2% in people 18 years of age and older.[1]Figure 1:: Prevalence of hypertension in Chinese population aged >15 yearsOn the whole, the prevalence of hypertension in China is higher in men than in women, with the northern region higher than the southern and cities higher than rural areas. However, the gap between urban and rural areas is gradually narrowing. The prevalence of hypertension in China is increasing year by year as suggested by this timeframe. In summary, men, the elderly and rural areas remain the focus of hypertension prevention and control efforts in China. Risk Factors of Hypertension in China Traditional risk factors for hypertension include high sodium and low potassium diets, overweight and obesity, alcohol consumption, mental stress, family history of hypertension, and lack of physical activity. Domestic scholars have shown that smoking, drinking, diabetes, and dyslipidemia increased the risk of hypertension.[12] Recent studies have also been conducted on other risk factors such as air quality (fog and haze) and hypertension. Sodium-potassium intake and hypertension: intake of sodium was positively correlated with blood pressure and prevalence of hypertension, while potassium salt intake was negatively correlated with blood pressure. The results of a survey from 19,519 community residents 35-91 years old in 2008 in Shanghai showed that daily salt intake was <12 g; the prevalence rate of hypertension was 44.11% - higher than that of 12 g; the prevalence rate of hypertension was 54.54%; and the prevalence rate of hypertension increased by 10.43%.[15] According to data reported in the salt reduction and hypertension control project in Shandong Province of 2011, the urinary sodium levels at 24 h in 1948 adults were divided into five groups ranging from low to high. The results showed that residents with the highest salt intake had the highest risk of high blood pressure, an increase of 30% compared with the lowest group.[16] The INTERSALT Study on salt and hypertension analyzed data on 10,079 adults from 32 different countries in 52 populations including 600 Chinese people from Beijing, Nanning, and Tianjin. This study found that the median of 24 h urine sodium increased per 100 mmo1/day, systolic blood pressure increased by a median of 5-7 mmHg, and diastolic blood pressure increased by a median of 2-4 mmHg.[17] The results of the INTERMAP study of salt and blood pressure involving four countries and international collaboration showed that the index reflects the ratio of sodium/potassium intake in 24 h was approximately 6, which was far higher than that western countries 2-3.[18] This partly explains why the prevalence of obesity is much lower in China compared to western countries; however, the prevalence of high blood pressure remains at a higher level Overweight and obesity: A 10-year prospective study of overweight and obesity showed a baseline normal weight cumulative incidence of hypertension was 36.3%. The overweight and obesity cumulative incidence of hypertension were 55.3% and 69.2%, respectively.[19] Data from the 2011-2012 study of 1870 subjects in Ji'nan showed that overweight, obesity, and central obesity were all risk factors for hypertension; however, the effect of obesity on hypertension was the highest[20] Drink wine: The study in Kailuan looked at 32,389 adults without hypertension, after 4 years of follow-up, and daily alcohol consumption (calculated daily alcohol intake) for 0.1-24 g, 25-49 g, 50-99 g, 100-149 g, and over 150 g. The cumulative incidence of hypertension was 25.0%, 28.8%, 30.10%, 37.1%, 40.1%, and 42.5%.[21] With the increase in alcohol consumption, the prevalence of hypertension is also rising. In 2008, a study in Suzhou showed that the prevalence of hypertension increased with the increase in alcohol consumption, as shown in Figure 2[22]Figure 2:: Prevalence of hypertension in different groups of people drinking alcohol in Suzhou in 2008Family history: The prevalence of hypertension was significantly increased with a family history of hypertension. According to a 2008 survey, on the prevalence of family history of hypertension among 19,519 community residents between 35 and 91 years of age in Shanghai, the prevalence rate of hypertension was 51.3%. The rate among residents with no family history of hypertension was 39.0%[15] Air quality (fog and haze): In addition to the above traditional risk factors, the effect of air quality (fog and haze) on the prevalence of hypertension continues to raise concern. Of the 24,845 adults in Northeast China with an average follow-up of 3 years, PM10 increased 19 ug/m, the risk of hypertension increased 1.12 (95% confidence interval [CI] from 1.08 to 1.16); SO2 increased by 20 ug/m, the risk of hypertension increased 1.11 (95% CI 1.04-1.18); O3 increased 22 ug/m, and the risk of hypertension increased by 1.13 (95% CI 1.06-1.20). The results showed that the concentrations of PM10, SO2, and O3 in the air increased, and the risk of hypertension increased.[23] The data on the correlation between PM and hypertension are still unclear. Awareness Rate, Treatment Rate, and Control Rate of Hypertension in China The awareness rate, treatment rate, and control rate of hypertension patients Overall, the control of hypertension in China is still at a low level; however, there has been a trend of improvement. The national hypertension survey in 2002 showed that the awareness rate, treatment rate, treatment control rate, and control rate of hypertension were 30.2%, 24.7%, 25%, and 6.1%, respectively, for people 18 years of age and older.[6] Results from the 13 Province survey of 50,171 people 18 of age and older in 2009-2010 showed that the rates of hypertension awareness, treatment rate, control treatment rate, and control rate were 42.6%, 34.1%, 27.4%, and 9.3%, respectively.[24] The results of the survey in different regions of the country suggested significant differences in the awareness rate, treatment rate, and control rate of hypertension among different populations [Table 1].[10,12,25-28]Table 1: Awareness rate, treatment rate, and control rate of hypertension in different areasThe change trend of awareness rate, treatment rate, and control rate of hypertension The CHNS conducted surveys of awareness, treatment, and control rates of hypertension among people 18 years of age and older in nine provinces in the past 1991 and 2009 years. The results showed an upward trend in the awareness rate, treatment rate, and control rate of hypertension, but still at a low level, as shown in Figure 3.[13]Figure 3:: Prevalence of hypertension in different groups of people drinking alcohol in Suzhou in 2008Another at the age of 35-59 years old adult data analysis results showed that the rates of hypertension awareness, treatment, and control rates were 32.4%, 22.6% from 1992 to 1994 and 2.8% increased to 48.4% in 2004-2005, 38.5%, and 9.5%.[29] Cognition and practice of hypertension awareness and control The HAPPEN study of attitudes and needs on hypertension in China tertiary hospitals published by the European Society of Hypertension showed that 90% of the doctors told patients with hypertension[30] diagnosis and numerical control of blood pressure when it reached the target value, but only 67% the patients know their blood pressure target value, suggesting that the doctor also overestimated the awareness rate on blood pressure in patients with the target value. Doctors think they admissions of patients 70% patients with blood pressure can be achieved, but in fact, according to the blood pressure measurements for 2 weeks, the blood pressure of the patients know, only 31% patients reached target blood pressure. The results showed that in the daily management of hypertension, the Chinese doctors overestimated the target blood pressure awareness rate and the control rate of blood pressure. Current situation and problems The prevalence rate of hypertension in China is still on the rise, and the number of patients is increasing, but the rate of increase has slowed. The prevalence rate of hypertension in people 18 years of age and older in 2012 was 25.2%. Although the awareness rate, treatment rate, and control rate of hypertension in China have been improved, they are still at a low level The main risk factors of hypertension were high salt, overweight, obesity, and excessive drinking The prevalence of hypertension was still high in the north and low in the south There were some differences between the doctors and patients in the cognition and practice of target blood pressure and blood pressure control. Recommendations Improve and strengthen the screening of hypertension, increase the opportunistic screening and screening in public places, improve the awareness of hypertension in the population, all of which are the primary basis for prevention and treatment of hypertension Develop strategies to conform to the local conditions of various regions when providing education and outreach on the harm of high blood pressure and related risk factors, including diet (especially high salt) and the influence of obesity on hypertension, to improve overall public awareness of the dangers of hypertension On the basis of health education, all regions should also be consistent with blood pressure measurement and maintain a dynamic grasp of the prevalence of hypertension. For high-risk areas and vulnerable groups, an integrated detection model to regularly detect the risk factors of hypertension is needed. Chapter 2: Epidemiological Characteristics of Hypertension in China Molecular epidemiological characteristics of hypertension Hypertension is related to heredity. The risk of hypertension in first-degree relatives was 2 times higher than that of the general population. Familial aggregation of hypertension suggests that blood pressure is affected to some extent by genetic factors. The genetic mechanism of hypertension is complex, which is caused by the interaction of multiple genes and environmental factors. Data from twin studies in the Chinese population suggest that genetic factors account for 30%-46%.[31] The linkage and candidate gene association study of the 1990s found at least 150 of primary hypertension and blood pressure variability associated with susceptibility loci, involving the renin-angiotensin system, wake up with solid sympathetic nerve system, endothelin, Lena skin, kallikrein-kinin system, and ion channels of the skin.[32-36] In 2009-2011 study, under the cooperation of China, Japan, Korea, and other East Asian countries, six blood pressure-related susceptibility genes, or regions were identified. The analysis published in 2015 China crowd large-scale, multistage hypertension genome-wide association (GWAS), gene chip were detected in 11,816 cases of individuals, and repeated verification was conducted in 69,146 samples. 19 susceptibility genes associated with blood pressure and hypertension were identified and 4 newly identified four genetic susceptible regions or genes (CACNA1D, CYP21A2, HLA-B, and MED13 L). In the SLC4A7 region, it was found the Chinese population-specific susceptibility locus rs820430. It was confirmed that 14 genetic susceptibility loci previously reported by other countries were associated with blood pressure and hypertension in the Chinese population.[37] The risk score of the 19 genetic variants, with an increased genetic risk score, systolic blood pressure (P = 4.73 * 10-67), and diastolic blood pressure (P = 2.03 * 10-69) significantly increased.[37] GUCY1A3 gene variants are associated with blood pressure in Chinese and European populations. GUCY1A3 gene encoding soluble guanylate cyclase (sGC) is a key enzyme in the NO-cGMP pathway, which has been used in clinical trials for the treatment of pulmonary hypertension and pulmonary The study an important basis for the treatment of hypertension and other cardiovascular diseases with environmental factors affecting blood pressure variability include the intake of sodium and potassium in the showed a different blood pressure to sodium and potassium which are salt and potassium respectively. The results showed that the of blood pressure to sodium and potassium also had genetic The of in the China northern people a low salt high salt, and high salt potassium In this study, they the genetic mechanism of more than genes including renin-angiotensin and and ion and found a number of related genes, such as is a and which are related with salt and/or potassium A genome-wide association analysis found potassium salt susceptible genes or regions identified as and results important for the mechanism of sodium and potassium blood pressure. A follow-up showed an increased risk of high blood pressure with an increasing genetic risk According to the genetic risk score, the patients were divided into four with the lowest the risk of hypertension in the other groups increased by and according to a study on in China. Current status of hypertension in urban Prevalence of hypertension in different urban On the basis of a national survey of hypertension, various cities in the country have also carried out a survey of the prevalence of hypertension, the data of which are shown in 2: Prevalence of hypertension in urban areas of different trend of the prevalence of hypertension in urban The prevalence of hypertension in China increased from in 1991 to in 2009, a trend year by Current situation of hypertension in rural areas Prevalence of hypertension in rural areas the period of there were a number of studies on the prevalence of hypertension in rural areas. The results showed an increase in the prevalence rate of up to [Table Prevalence and control of hypertension in rural areas of prevalence rate of hypertension in the rural population influence of million adults 18 years of age and older in rural population showed that the prevalence rate of male was higher than and the prevalence of the disease was higher in the north than in the prevalence of hypertension in rural areas The prevalence of hypertension in rural areas increased from in to in a upward trend [Figure The prevalence of hypertension in rural areas increased from to Overall, the prevalence of hypertension in rural areas was however, the awareness rate, treatment rate, and control rate were at a low level. With the of the prevalence of hypertension in rural areas increased and the gap between urban and rural areas gradually In addition, rural areas of low awareness of and should more to the of hypertension in rural areas. Current situation of hypertension in areas China is a country different to the differences in genetic and the and epidemiological characteristics of hypertension are and According to the China Nutrition and Health Survey in 2002, and had the highest incidence of hypertension with national prevalence rates of 24.7%, and respectively. were higher than that of the population and the prevalence rate of hypertension among and people was lower than that of the which was 7.7%, In addition, epidemiological survey of Hypertension of the People's of cases over years old in patients with hypertension were found in and in the incidence rate of hypertension were and A survey of adults between and years of age found that the prevalence rates of hypertension among the and were and epidemiological survey of cases of hypertension in adults 50 years of age and older showed that the prevalence of hypertension in the was data analysis showed that the prevalence of hypertension among the same groups in different regions also showed The data showed that the incidence of hypertension among in and was and to the characteristics of areas China, it is to the various of hypertension to and Current and Hypertension is affected by the of genetic factors and environmental factors. factors to some extent the of environmental factors that the of The study found genes related to hypertension and The study found four genetic susceptibility regions or genes and confirmed that the genetic susceptibility loci of 14 previously reported by countries were associated with blood pressure and hypertension in the Chinese population. The interaction between genes and the an important in the and of hypertension in China differences in the prevalence rates of hypertension are between urban and rural areas and different The prevalence rate of hypertension is still higher in the and lower in the The rural prevalence rate is as high as has increased and a trend between urban and rural areas has been Recommendations in to genetic characteristics associated with hypertension have to strategies that for on the conditions of regions, genetic characteristics should be when populations in The in rural areas is and to prevention and control strategies for hypertension. the of the hospitals and rural health a is to use of to improve the level of diagnosis and treatment of hypertension in rural areas to the and associated with various and the and of prevention and treatment of hypertension in areas should be to more the of prevention and treatment of hypertension in the areas of China. Chapter The Disease Burden of Hypertension Hypertension can only the physical health and quality of patients but also to burden on individuals, and the with the According to the Global Burden of Disease Study 2010, million people of hypertension in 2010 in China million male and million The years of hypertension was million million male and million with the years of at million and the years of with at which for of the total According to in the caused by hypertension in 2010 was in population in China, of which was to and was to The Burden of Hypertension The burden of hypertension is defined as to hypertension, which and burden the on hypertension including diagnosis and and including and From the the only include the but also by Chinese patients their drugs in and the of are defined as burden the health to the and caused by hypertension. The health caused by hypertension can be with the model including the of to the or death. The burden can also be by The of is only of the health and it is an burden in a The burden also which be by For the of quality to hypertension, such as and other and the on daily to hypertension, can be defined as or However, it is to the of quality it is related to to In the burden by the patients can be with the of cause by hypertension. burden is in recent In this the burden of hypertension only is in a and the burden is the latest such as population, of hypertension, and index are in all the burden is with the in and the data in published are to in with the index to the burden in to the that there is no on the burden of hypertension in China, all data on burden in this are on the latest samples. the and national the national and the national burden of hypertension are Previous studies were conducted in China on the disease burden and burden of hypertension. The burden of hypertension was by the and of the of Health on the basis of the data from the National Health in and the and of the Health of China. In the total burden of hypertension was which was in the after and The and burden in was and and The National Health data had been and no is on burden on The of hypertension include the of and According to the latest in 2011 in Shandong of with hypertension, the average of and were and respectively. The total were The national index by from the year the average of with hypertension in Shandong Province in was as According to the of health and family in the latest per of Shandong Province was while the national average was and the national index was the national average on hypertension after was In the rate of hypertension was and there were million patients with The of hypertension, which the average per burden by the total number of was have shown that the treatment of hypertension, the average of was there were million patients with hypertension in in China, and the daily Domestic was the of to the of was the treatment of hypertension. have shown that in the average of for of was the average nutrition were The national index was by from to the average for and nutrition in was and respectively. With the population of national hypertension patients at the total and nutrition were and respectively. In the total of and nutrition to the treatment of hypertension was The burden was The of was of the total burden while the of was The of was while the of was The burden of hypertension the of to the disease and the of to death. The of to the disease the average of for year of patients with hypertension by the daily per by the total number of patients with hypertension in China. has shown that the average of to hypertension was In per was With as daily per in as and million patients with hypertension in the of to hypertension was The of to can be as years of by per has shown that the years was years per The population in China in was With the population in and per in the burden to with hypertension in was the the burden in was with 70% to caused by the disease and the other up the and burden the total burden of hypertension in was with for with hypertension. The up of the total In the total of health in China was with the of hypertension up 4 shows the of all of burden by the in including the per burden and the total The national burden of Health of the Prevention and Treatment of Hypertension In a 2015 study, the cardiovascular disease China was to the health of the prevention and treatment of hypertension. The effect of cardiovascular by high blood pressure among adults from the year was in this According to the National the treatment of hypertension and other were and the health was by the years is a index which the effect of health by the quality as as the for have shown according to the all of the patients with be with there be a of 1.11 cardiovascular year of and of and the health increase by all patients with and with hypertension above 2 blood blood pressure without history of be with there be a of cardiovascular year of and of and the health increase by all patients with and with hypertension at and 2 without history of be with there be a of cardiovascular year of and 1.13 of and the health increase by million The are shown in 1:: The effect of on among different population is to to patients and with hypertension over but no is to to patients and with hypertension at and but no Cardiovascular has shown the of different The is to the population of patients from patients with to with hypertension over 2 without history of Although the with the average increase of the increase by which is lower than by the per of It from the of health all patients with and with hypertension at and 2 without history of be with more health can be lower which is a health with high The is to the population of patients to with hypertension at and In this with the average increase of the increase by This is currently in Beijing, Shanghai, and other to be in and health with high This shows that the public health and education with drugs according to the National have of and health in the prevention and treatment of should increase efforts in the screening and prevention of hypertension among patients over 35 years improve the of patients by the of drugs and gradually increase the of patients with hypertension of and Current and The disease burden of hypertension in China in 2010 is as The population caused by hypertension was The of Chinese population caused by hypertension was with the years to at and the at which for of the total Nearly of the were caused by in patients and were caused by In the total on health in China was with the of hypertension at The average was with up up and up 31% The has shown that all patients with be with there be a of 1.11 cardiovascular year of and of and the health increase by all patients with hypertension at and 2 or without history of be with there be a of cardiovascular year of and 1.13 of and the health increase by million The of data on the health of hypertension in China is from the Chinese The health of different on prevention and treatment of hypertension is still There is also no among the of different drugs. health and more to the prevention and treatment of hypertension and other related diseases an and continues treatment of hypertension with or without the of conditions there should be an analysis of different on the prevention and treatment of hypertension and of the differences of to the effect of drugs by the National on the prevention and treatment of should increase efforts in the screening and prevention of hypertension among patients over 35 years improve the of patients by the of and gradually increase the of patients with hypertension of and and of There are no of

Enhanced fibrosis and reactive oxygen species (ROS) generation are two major features of aged heart. Since a loss-of-function mutation of ALDH2 was found in nearly half of East Asian population, we explored the impact of ALDH2 deficiency on the process of aging in the heart. We found that the body weight increased profoundly in aged wild-type (WT) mice but not in ALDH2 knockout (KO) mice. However, the ratio of heart weight to body weight increased significantly only in KO mice. Echocardiographic assessment showed that left ventricular ejection fraction of aged WT mice was significantly decreased, which was further aggravated by ALDH2 deficiency. Further study revealed that the compromised cardiac function of aged KO mice might be resulted from PI3K/Akt pathway-mediated fibrosis formation, as shown by remarkable upregulation of collagen I, transforming growth factor-β, and α-smooth muscle actin expression. Aging-induced ROS generation was quantified by the expression of 4-hydroxy-2-nonenal-adducted proteins, which was notably increased in the myocardium of aged KO mice. Besides, the expression of cleaved caspase-3 and 8-oxoguanine DNA glycosylase also increased significantly in the myocardium of aged KO mice. Further study demonstrated that increased ROS generation stimulated a prominent upregulation of ROS scavenger SOD2 expression in the myocardium of aged WT mice but not in KO mice. Our findings suggest that mitochondrial ALDH2 deficiency accelerates aging in the heart by increasing fibrosis formation and oxidative stress.

OBJECTIVE: To evaluate novel variations in a Chinese family of Han ethnicity, with Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) by the powerful technology of Whole-Exome Sequencing (WES). METHODS: Genomic DNA from representative family members was extracted and processed for WES via standardized methods. The exome sequence data was analyzed by Genome Analysis Toolkit software. Sanger sequencing was performed on DNA from the proband for genotype confirmation and from the other family members for familial co-segregation analysis. RESULTS: A rare single nucleotide variant c.1592T>G (p.Phe531Cys) in exon 10 of DSG2 was identi ed by WES in the affected individuals but not in the healthy control, which was con rmed by Sanger sequencing, suggesting the mutation probably was a causal mutation for the familial disorder of ARVC. CONCLUSION: We identi ed a rare disease-causing mutation of the DSG2 gene associated with familial ARVC. The results might contribute to the early genetic analysis in inherited cardiomyopathies.

Objective: To investigate the genetic basis of a Chinese familial third degree atrioventricular block. MethOds: The clinical data of all family members were collected, including physical examination, electrocardiogram and echocardiography. Exome sequencing was performed for all patients. Results: This family contains 22 members of which 6 are patients. Cardiac symptoms appeared at forty years of age, starting with second degree atrioventricular block eventually developing into third degree atrioventricular block. These 6 patients received permanent pacemaker implantation. The genetic pedigree suggested that the autosomal disorder may not be completely dominant. Compared with normal subjects, 24 different genes were detected in patients with familial atrioventricular block. Conclusion: This family is unambiguously affected by familial atrioventricular block caused by incomplete dominant inheritance of euchromosome, and another genetic mutations that may contribute to it.

Introduction Left ventricular hypertrophy (LVH) is an important manifestation of hypertensive organ damage associated with increased ventricular wall thickness, left ventricle mass, and cardiac remodeling. Neurohumoral and hemodynamic factors play important roles in the development of LVH. The heart is the most vulnerable target organ for hypertension, and >30% of patients with hypertension will undergo LVH. The incidence rate is positively correlated with the severity of hypertension.[1] LVH is an independent risk factor for a number of cardiovascular disorders such as coronary diseases, congestive heart failure, stroke, temporary ischemic heart disease, and sudden death.[2] LVH accompanied with hypertension can increase and the progression of cardiovascular and cerebrovascular diseases, thus, hypertension associated LVH as a contributor to organ damage, should be paid attention to. Asia is a region with a high prevalence of hypertension (20%-30% of the population). The growth rate of the hypertensive population within Asia is higher than in developed countries.[3,4] A Chinese cohort study showed that 64.6% of pre-hypertensive patients developed hypertension 17 years later, with a total mortality rate of 27.9/1000 person/year. The main cause of death was stroke,[5] and hypertension-associated LVH is related to stroke. A higher risk of coronary disease and stroke was found in the Asian populations with increased systolic pressure than in Caucasians.[6] With urbanization, day-to-day stress, obesity, and high-salt/high-fat diets are becoming more prevalent in Asia, and thus an unhealthy lifestyle has become an important risk factor for heart diseases, which is the main cause of hypertension-induced LVH. The dysfunction in cardiac diastole, as well as the rate of symptomatic heart failure, is also increased. A study from Japan reported that >50% of people with high blood pressure having LVH combined with obviously increased cardiovascular events.[7] Effective blood pressure control and regression of LVH significantly decreased the risk of cardiovascular events and death.[8-10] Taking all these into account, health guidelines for the Asian Region all take LVH as an important index for hypertension-induced heart damage, and by consequence, blood pressure control is an important therapeutic strategy for treatment of LVH.[11-13] Because of the importance of LVH in hypertension and cardiovascular diseases, and the insufficient strategy for intervention of LVH, experts in the Asian Region have achieved a consensus regarding diagnosis, classification, and treatment criteria for LVH, as well as clinical guidelines for the diagnosis and management of patients with hypertension combined with LVH (this guideline is only aimed at hypertension-associated hypertension). Epidemiology of Hypertension-Associated Left Ventricular Hypertrophy At present, the diagnosis of LVH for patients with hypertension relies on electrocardiogram (ECG) and echocardiogram (ECHO) readouts. The detectable rate relying on adopted method and the differences are non-ignorable [Table 1].Table 1: Summaries the predictive value, practicability, repeatability and cost effectiveness of electrocardiogram, echocardiogram, and cardiac magnetic resonanceA retrospective analysis of 26 studies shows that the prevalence of ECG-diagnosed LVH (ECG-LVH) is 18.1%-18.9% within hypertensive patients. A sex-based analysis shows that the average prevalence of LVH is 24.2%-24.4% in men and 16.6%-16.8% in women.[14] Under the same diagnostic criteria (Sokolow-Lyon voltage: SV1 + RV5/RV6 ≥3.5 mV), the prevalence of ECG-LVH in Caucasian hypertensives is 8.6%-26.4%.[14] LVH prevalence in Asian hypertensives is also very high. In a Japanese study, the prevalence of ECHO-diagnosed LVH (ECHO-LVH) is as high as 40%.[15] Prevalence of ECHO-LVH in Chinese hypertensive patients varies from 19.2% to 34.3%,[16-18] and a Taiwan study shows that the prevalence of ECHO-LVH is 13%.[19] A retrospective analysis including 30 studies shows that the prevalence of ECG-LVH is 35.6%-40.9% in the hypertensive patients. A sex-based analysis shows that the average prevalence of LVH is 36.3%-43.5% in men and 37.9%-46.2% in women.[1] Under the same diagnostic criteria (Sokolow-Lyon voltage: SV1 + RV5/RV6 ≥3.5 mV), ECG-LVH patients with hypertension Caucasian detection rate is 14.5%-44.8%.[1] In a Japanese study, the prevalence of ECHO-LVH is as high as 58.3%;[7] an Indian study shows that ECHO-LVH is 24.4%.[20] Prevalence of ECHO-LVH in Chinese hypertensive patients varies from 26% to 73.2%,[17,21-23] and women show an obviously higher prevalence of LVH than that of men.[22-24] Mechanisms Driving Hypertension Combined Left Ventricular Hypertrophy and the Harm Mechanisms of hypertension combined left ventricular hypertrophy The development of cardiac hypotrophy can be divided into three stages as follows: progressing period, compensatory stage, and decompensatory stage. Pathological hypotrophy includes eccentric hypotrophy and concentric hypotrophy. In some conditions, eccentric hypotrophy can also be derived from concentric hypotrophy. The mechanisms of hypertension-related LVH have not been completely elucidated; the pathogenic process is related to factors such as (a) hemodynamics, (b) neurohumoral, paracrine, and autocrine secretions in cardiovascular tissue, and (c) genetic background of patients. Both hemodynamic and neurohumoral factors play major roles in the progression of hypertension-related LVH. Hemodynamics factors Systolic phase overload is pressure overload, and diastolic phase overload is volume overload. Hypertensive patients suffer both pressure overload and volume overload. Both of these overloads can increase the volume of cardiac myocytes, enlarge the size of cardiac myocytes and change components of collagen proteins in the extracellular matrix, all of which can finally induce cardiac hypotrophy.[25] Blood pressure is the most important factor for LVH. The Framingham study revealed that left ventricular mass increased by 10.6 g/m2 for male patient and 3.0 g/m2 for female patient per 20 mmHg increases in systolic pressure. The PALEMA study of 2002 enrolled 2050 patients, in which the left ventricular mass is the highest in hypertensive patients without treatment.[26] Neurohumoral factors Neurohumoral factors are the renin-angiotensin-aldosterone system (RAAS), sympathetic nervous, and adrenal system and the endothelin system.[27] In hypertensive patients, the RAAS activity and synthesis of angiotensin II (AngII) and aldosterone are increased. Circulating AngII can efficiently increase blood pressure through vigorously shrinking arterioles, stimulating secretion of aldosterone to increase circulating blood volume, and promoting the release of catecholamine. AngII in local tissue tends to play long term, therapeutic roles. AngII binds with type I receptor, and regulates expression of proto-oncogene and related protein, causing hypotrophy of cardiac myocytes and overexpression of collagen proteins.[28,29] The activity of the sympathetic nervous system for patients with hypertension-related LVH is much higher than that of primary hypertension without LVH.[30] In patients with the active sympathetic system, the concentration of norepinephrine (NE) in circulation is also higher. NE can promote protein expression in cardiac myocytes through activating α1-adrenergic receptor; it can also activate β-adrenergic receptors to enhance the systolic ability of cardiac muscle, increase heart rate as well as the synthesis of glycogen and adenosine phosphate. The increased content of total protein and un-contractile protein in cardiac myocytes leads to cardiac hypotrophy.[31,32] Meanwhile, increased activity of the sympathetic nervous system enhances invasion of inflammatory mediators into the heart, causing cardiac fibrosis, and aggravating cardiac hypotrophy.[33] In summary, neurohumoral factors participate in the formation of hypertension-induced LVH, induce abnormalities in the signaling transduction system of cardiac myocytes (beta-receptor, G-protein, cyclases, calcium channel, phosphokinase, etc.), and influence protein expression of cardiac myocytes. The increased expression of structural proteins will gradually enhance cardiac contractility, but uncontrolled expression of cardiac fibrils will result in cardiac hypotrophy and enlargement of the ventricular chamber. Risk factors Prevalence of LVH and ventricle remodeling in hypertensive patients is influenced by age, body fat, and genetic factors. The prevalence of LVH is correlated with patient age, i.e., older age means a higher risk of LVH.[34] The left ventricular mass index (LVMI) is distinctly higher in obese patients; and like high systolic and diastolic pressure, obesity (high body mass index) during childhood and adult is distinctly related with eccentric and concentric hypotrophy.[35] Moreover, the left ventricle mass (LVM) displays the obvious difference in patients with a similarly increased segment of blood pressure, suggesting that genetic factors are involved in the development of LVH. Gene polymorphisms associated with both the sympathetic nervous system and RAAS system is correlated with the prevalence of LVH and the impairment of cardiac functions. Gene polymorphism in the sympathetic nervous system and RAAS is related with LVH, yet it has not been identified as the cause or consequence of LVH.[27,36] High-salt diet is also involved in LVH; there have been animal experiments which showed that high-salt diets could induce LVH.[37,38] The damage of hypertension-related left ventricular hypertrophy Reducing coronary flow reserve Because the myocardium is totally dependent on aerobic metabolism, an increase in myocardial oxygen consumption requires an increased coronary blood flow, and this is achieved by dilatation. The ability of the heart to autoregulate coronary perfusion in response to metabolic demands is called coronary flow reserve. Some studies find that in hypertension patients with LVH, the CRF is significantly reduced and the risk of ischemic heart diseases is increased. This can easily induce ischemic disease and increase the risk of death.[39-41] Impairing left ventricle functions In hypertensive patients with LVH, left ventricle hypotrophy will further impair left ventricle functions and finally induce development of heart failure regardless of the contractile status with the left ventricle. Compared with patients suffering from left ventricle systolic dysfunction, LVH patients are more inclined to suffer from left ventricular diastolic dysfunction. Studies show that both the increase in LVM and relative wall thickness (RWT) significantly increase the risk of left ventricle diastolic dysfunction in hypertensive patients.[39,42,43] However, about 13% of concentric LVH patients with normal left ventricle systolic function progress to left ventricle systolic dysfunction within 3 years post-follow-up.[44] Increasing risk of arrhythmia A meta-analysis including 12 studies reveals that risk of arrhythmia in patients with hypertensive-induced LVH is 3 times higher than hypertensive patients without LVH.[45] LVH diagnosed by ECG suggests an obvious increase in SCD risk,[46,47] and reversing LVH can prominently reduce the prevalence of SCD.[48] LVH is also a major risk factor for arterial fibrillation (AF).[49,50] For every 1, standard deviation increase in left ventricular mass, the risk of AF was increased by 1.20 times.[51,52] Increasing major cardiovascular events and risk of death The reduction of endpoints in NIDDM with the angiotensin II antagonist losartan study showed that chronic kidney disease combined with LVH is an predictor of increased CK level in plasma/end-stage renal disease (Hazard Ratio (HR) = 1.42; P = 0.03) and cardiovascular event (HR = 1.68; P = 0.001).[53] The Framingham study shows that persons who acquire ECG-LVH have an eightfold increased risk of CVD death and a six-fold increased risk of CHD death.[54] The following studies coherently verify that ECG-LVH is associated with the incidence of cardiovascular diseases, death from cardiovascular disease, and death from all causes.[55-60] Furthermore, there is a continuous relation between LVH severity and CVD risks.[61] Significance of reversing left ventricular hypertrophy Preclinical and clinical researches have verified that blood pressure control can effectively reverse LVH.[62,63] Regression of LVH can decrease the risk of cardiovascular events, regardless of endpoint reduction of blood pressure.[64,65] Therefore, more attention should be paid to patients with hypertension-induced LVH, and early prevention and/or regression of LVH should be one of the therapeutic targets for clinical hypertension treatment. Reducing risk of cardiovascular events Some studies revealed that prevention/regression of ECG-LVH could significantly reduce morbidity and mortality from cardiovascular events. A meta-analysis including five studies and comprising 2449 patients found that compared with patients of LVH persistence/LVH development, the total risk of cardiovascular events was reduced by 46% in patients of LVH regression/persistent normal.[66] Mathew et al.[8] found that prevention and regression of ECG-LVH are associated with reduced clinical endpoints including the risk of death, myocardial infarction, stroke, and congestive heart failure.[7] A total of 941 prospectively identified patients aged 55-80 years with essential hypertension and electrocardiographic LV hypertrophy had LV mass measured by echocardiography at enrolment in the The Losartan Intervention For Endpoint reduction (LIFE) trial and thereafter are followed up annually for a mean (standard deviation of 4.8 (1.0) years for CV events. The LIFE study used a composite endpoint of CV death, myocardial infarction, or stroke. The multivariable Cox regression model showed a strong association between lower LV mass index and reduced rate of the composite cardiovascular end point. Risk of cardiovascular event declined 22% (P = 0.009) for 1 reduction of LVMI standard deviation (25.3 g/m2). Reduction of LVMI was proved to be a more suitable predictor for reduced risk of cardiovascular events than the decrease of blood pressure. Lower LVMI is associated with lower rates of all clinical endpoints, including CV death (HR = 0.62; P = 0.0001), stroke (HR = 0.76; P = 0.02), myocardial infarction (HR = 0.85; P = 0.33) and all-cause mortality (HR = 0.72; P = 0.002).[64,65] Other benefits In addition to reducing the risk of cardiovascular events, Okin et al.[67] found new benefits of antihypertensive therapy. Electrocardiographic hypertrophy was evaluated over time in 7998 hypertensive patients without diabetes at baseline in the Losartan Intervention for endpoint reduction in hypertension (LIFE) study. During a mean follow-up of 4.6 ± 1.2 years, resolution or continued absence of LVH during antihypertensive therapy is associated with a lower likelihood of new-onset diabetes. Diagnosis and Differential Diagnosis of Hypertension-Associated Left Ventricular Hypertrophy The diagnostic criteria for hypertensive-associated LVH include three aspects as follows: (1) the definitive diagnosis of hypertension; (2) the definitive diagnosis of LVH; and (3) elimination of other causes of LVH. The clinical diagnosis methods for left ventricular hypertrophy The diagnostic approaches include ECG, ECHO, and cardiac magnetic resonance (CMR). These methods have different sensitivity, specificity, costs and feasibility, as shown in Figure 1. When it comes to clinical use, the individualized diagnostic method should be considered.Figure 1:: Diagnostic pathway for hypertension-associated left ventricular hypertrophyElectrocardiography ECG is simple and practical. It is recommended by a majority of guidelines as the most optical method for LVH diagnosis. The sensitivity of ECG to LVH is relatively lower than other approaches, and its diagnostic sensitivity for mild and modest/severe LVH is 7%-35% and 30%-60%, respectively.[68] The specificity of ECG is much higher than its sensitivity, especially for severely hypertensive patients, the specificity is as high as 80%-90%. Obesity markedly attenuates the validity and performance of ECG criteria for LVH detection.[69] There are ethnic differences in ECG criteria for LVH and the African heritage strongest independent predictor of decreased ECG specificity.[70,71] There are a variety of ECG-LVH criteria in the guidelines and in the scientific and medical literature. Each method has advantages and disadvantages. The most prevalent criteria are listed: Sokolow-Lyon voltage >3.5 mV (2013 ESH/ESC guidelines for hypertension, 2014 Japanese guidelines for hypertension) or Sokolow-Lyon voltage >3.5 mV (2010 Chinese guidelines for prevention and treatment of hypertension) Cornell product >224 mV·ms (2013 ESH/ESC guidelines for hypertension) R aVL >1.1 mV (2013 ESH/ESC guidelines for hypertension) Left ventricular voltage (such as RV5 >2.5 mV) can be used as a simple criterion for primary diagnosis.[72] It was reported that ECG-LVH was associated with an increased risk of overall mortality, cardiovascular events, and stroke mortality.[73] Another study revealed that in addition to ECG-LVH, various electrocardiographic abnormalities, such as asymmetric inverted T-wave and ST-segment depression, were independent risk factors for cardio-cerebral vascular diseases.[74] Echocardiography ECHO is more sensitive than ECG in the diagnosis of LVH, and the LVMI normalized by body surface area (BSA) or height is utilized for detection of LVH; the former method is more widely used than the latter one. The generally accepted method for LVMI calculation is the “cube” method. The criteria for the diagnosis of LVH recommended by “The 2013 ESH/ESC Guidelines for Hypertension Treatment,” ‘2015 Taiwan Hypertension Guidelines’ and ‘The 2014 Japanese Guidelines for Hypertension are listed as follows: LVMI ≥115 g·m-2 (male), LVMI ≥95 g·m-2 (female). Computational formula: LVM (g) = 0.8 × 1.04 × ([LVDd + IVST + LVPWT] 3-LVDd3) + 0.6 LVDd: Left ventricle diastolic diameter; IVST: Interventricular septum thickness; LVPWT: Left ventricular posterior wall thickness. LVMI (g·m-2) = LVM (g)/BSA (m2) Body surface area: Male (m2) = (m2) = 0.0057 × height (cm) + 0.0121 × body weight (kg) + 0.0882 Female (m2) = 0.0073 × height (cm) + 0.0127 × body weight (kg)-0.2106. According to RWT (RWT, RWT = (2 × LVPWT)/LVDd) and the geometrical configuration of left ventricular hypotrophy/remodeling in LVH, the guidelines also clarifies LVH into three subtypes, as shown in chart 2 [Table 2].[75]Table 2: Classification of geometrical configuration of left ventricular hypertrophy/remodelingThe recommended abnormal criteria in 2015 EACVI/ASE adult hypertension echocardiographic examination are IVST and/or PWT >11 mm (male) and IVST and/or PWT >10 mm (female).[76] This is a more sensitive approach for diagnosis of concentric hypotrophy/remodeling, and LVH with concentric hypotrophy is the most reliable criteria for prediction of cardiovascular diseases,[75] therefore, except for LVMI, using IVST and PWT as prognostic criteria for LVH is reasonable. In clinical practice, IVST or PWT usually be used to diagnose LVH when LVMI is not available.[18,77] IVST or PWT ≥11 mm is used as earlier diagnostic criteria of LVH. However, the sensitivity, specificity, and universality of this method need further study. ECHO examination should be conducted individually: in patients with a moderate risk of cardiovascular events, ECHO may checkout LVH which cannot be determined by ECG. In ECG-LVH patients, ECHO can quantitatively evaluate hypertrophic condition with much higher accuracy and to define its geometric construction and dangerous level. In hypertensive patients with symptoms of heart failure, ECHO can help to diagnose the underlying disease. Cardiac magnetic resonance Among all kinds of noninvasive diagnostic approaches for LVH, CMR is the most reproducible. There is research that the LV volume and function determined by CMR can be at the of and the of repeatability of ECHO is as as and There are for CMR such as by body and higher Therefore, ECHO is a diagnosis method than a detection method for LVH. Diagnostic pathway for hypertension-associated left ventricular hypertrophy A diagnostic pathway is shown in Figure 1. methods have different [Table For hypertensive patients, the methods adopted should be to diagnosis of LVH, and the cause of disease are important for a in the The diagnostic method should be to disease and hypertension-associated LVH from LVH by other disease is also of electrocardiogram, echocardiogram, and cardiac magnetic resonance in diagnosis of left ventricular Diagnostic pathway for left ventricular hypertrophy with different for Hypertension-Associated Left Ventricular Hypertrophy blood pressure is the therapeutic of LVH LVH patients should treatment as early as to lower blood pressure, effectively reverse LVH, and reduce the of cerebrovascular and cardiovascular Blood pressure treatment targets for left ventricular hypertrophy patients LVH is an independent and dangerous factor for cardiovascular events. to lower blood pressure can effectively reverse LVH and reduce the risk of of guidelines for management of hypertension that all LVH patients should to reduce blood The Chinese guidelines for hypertension recommended the blood pressure target is The 2015 Taiwan guidelines for hypertension and the 2014 Japanese guidelines for hypertension not have a target for blood pressure. In the is to reduce the blood pressure of hypertensive patients to and of for left ventricular hypertrophy The used for of blood pressure include angiotensin calcium and and as or in some with of antihypertensive can the clinical symptoms of LVH through a decrease in blood pressure, but these antihypertensive by different mechanisms and show different on LVH. A meta-analysis shows that there is a difference (P = five antihypertensive in ability to reverse LVH. 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LIFE study is the and the only cardiovascular endpoint research into hypertension-associated LVH The study is conducted hypertensive patients with electrocardiographic LVH, who or antihypertensive treatment. follow-up or primary endpoints, of patients had used of losartan was used blood pressure could not that with antihypertensive therapeutic losartan treatment is associated with 13% (P = lower of the composite CV endpoints CV mortality and lower risk of stroke (P = lower risk of new-onset arrhythmia and lower risk of new-onset diabetes Meanwhile, losartan is more in reversing At the reversing was found in of concentric remodeling and of concentric hypotrophy patients, and it is well that both concentric remodeling and hypotrophy are independent risk factors of the composite CV In about of the of losartan are to reversing of LVH. LIFE research shows that compared with reversing of LVH, progression and of LVH are related with a higher risk of cardiovascular on this is recommended as the for treatment of patients with hypertension-associated LVH in different guidelines for management of with the and of by cardiac and LVH. and show LVH reversing in clinical high and may have advantages in reversing LVH, but the clinical research is not can of as well as reverse and LVH. A study conducted patients with hypertensive-associated LVH shows that was as as in LVH regression and blood pressure control of P = However, the of of should be and there is a of endpoint research that it can reverse LVH and reduce cardiovascular events. Because blood pressure target and LVH regression are these guidelines the following to combined with of or should be adopted to lower the blood pressure. in a are also recommended to and therapeutic of Hypertension-Associated Left Ventricular Hypertrophy of blood pressure control of blood pressure control Diagnosis and of hypertension-associated left ventricular hypertrophy of hypertension-associated LVH by ECG is recommended in all patients with hypertension of hypertensive patients by ECHO in medical and LVMI is recommended as a The criteria LVMI g·m-2 (male), LVMI ≥95 g·m-2 the simple of septum or posterior wall of left ventricle mm mm For medical ECHO examination is not patients with ECG should be to that are for ECHO For LVH that cannot be in the CMR should be adopted for diagnosis. of ECG is the method for of hypertension-associated LVH ECHO is the main method for diagnosis of hypertension-associated LVH CMR is the diagnostic method for LVH with ECHO should take LVMI as a examination of hypertension-associated left ventricular hypertrophy weight are important and lifestyle for hypertensive-associated LVH For patients with hypertension-associated LVH, is the patient to target blood pressure, a of for with of is and is medical without may other or but there are clinical For hypertension-associated LVH patients with systolic or diastolic dysfunction, higher heart rate (HR or arterial of heart is recommended For patients who cannot target blood pressure, the combined of is recommended For hypertension-associated LVH of and is include and LVH and Blood pressure follow-up clinical and should be in patients with an diagnosis of hypertension-associated LVH, and the of pressure should be In the earlier the follow-up of hypertension-associated LVH can be at of the blood pressure not the target treatment with at 3 kinds of antihypertensive it is recommended to the patient to a hypertensive or for further treatment. 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Diabetes mellitus has become a devastating global epidemic. Patients with diabetes suffer a high prevalence of diabetic cardiomyopathy (DCM). DCM is a type of cardiac problem independent of any preexisting macro- and micro-vascular diseases. The pathophysiological basis underlying diabetes-induced cardiac damage is rather complex and multifactorial. Although a number of risk factors including oxidative stress, apoptosis, and aberrant intracellular Ca2+ metabolism have been postulated to play a role in the onset and development of cardiac anomalies within diabetes, the precise mechanisms responsible for DCM remain elusive. This mini-review discusses the latest findings of mechanisms involved in the progression of cardiomyopathy in diabetes. We emphasize the role of the lysosomal cysteine protease, cathepsin K, and its downstream calcineurin/nuclear factor of activated T-cells signaling in the prevention and treatment of DCM.

Objective: This study was carried out to determine the correlation between arachidonic acid metabolites and vascular endothelial dysfunction in older Chinese patients diagnosed with type 2 diabetes mellitus. Methods: High-resolution ultrasound was employed to measure ow-mediated dilation (FMD) and sub - lingual nitroglycerin-induced dilation (NID) of the brachial artery. Serum 14,15-dihydroxyeicosatrienoic acid (14,15-DHET), the end-product of 14,15- epoxyeicosatrienoic acid (14,15-EET) and 6-keto-prosta - glandin F1α (6-keto-PGF1α), the end-product of prostacyclin (PGI2), were measured in 60 healthy elder - ly volunteers, 78 senile diabetic patients without nephropathy (SD) and 58 senile diabetic patients with nephropathy (SDN). Results: Compared to healthy elderly volunteers, serum 14,15-DHET and 6-keto-PGF1α levels were re - duced by 50% in SD. No further decline was observed in SDN. 6-keto-PGF1α was associated with FMD, but not with NID in the brachial artery of healthy elderly volunteers. Brachial FMD and NID were im - paired in all diabetic patients. The correlation between FMD and 6-keto-PGF1α or 14,15-DHET was lost in diabetic subjects. On the other hand, NID was positively correlated with 6-keto-PGF1α or 14,15-DHET in SD. Only NID and 6-keto-PGF1α correlation persisted in SDN. In addition, brachial artery dysfunction was negatively correlated with urinary albumin excretion and serum triglyceride in SDN patients. Conclusions: Impaired brachial artery vasodilation was associated with reduced PGI2 and EET produc - tion in older Chinese subjects with type 2 diabetes.