缬沙坦治疗心力衰竭临床观察

目的：探讨血管紧张素（hng）Ⅱ受体拮抗剂缬沙坦在治疗心功能不全中的临床疗效。方法：选择NYHA心功能分级Ⅲ-Ⅳ级、左室射血分数（LVEF）≤50％的患者60例，随机分为缬沙坦和卡托普利组，于服药前及服药后6个月后观察临床症状，超声心动图。结果：两组用药后左室射血分数（LVEF），心输出量（CO），心脏指数（CI）及左室舒张末内径（LVEDD）等指标均有改善（P〈0．05）。结论：缬沙坦和卡托普利均能改善左心室收缩舒张功能。     

Prenatal exposure to maternal undernutrition induces adult cardiac dysfunction

An adverse environmental experience of the growing fetus may lead to permanent changes in the structure and function of organs that may predispose the individual to chronic diseases in later life; however, nothing is known about the occurrence and mechanisms of heart failure. We employed a rat model in which pregnant dams were fed diets containing either 180 g (normal) or 90 g (low) casein/kg for 2 weeks before mating and throughout pregnancy. The ejection fraction (EF) of the pups exposed to the low-protein (LP) diet was severely depressed in the first 2 weeks of life and was associated with an increase in cardiomyocyte apoptosis. This early depressed cardiac function was followed by progressive recovery and normalization of the EF of the offspring in the LP group. The left ventricular (LV) internal diameters were increased between 24 h and 84 d (12 weeks) of age in the LP-exposed group. Although between 3 d and 2 weeks of age the LV wall of the heart in the LP group was thinner, a progressive increase in LV wall thickness was seen. At 40 weeks of age, although the EF was normal, a two-fold elevation in LV end-diastolic pressure, reduced cardiac output, decreased maximum rates of contraction and relaxation, and reduced mean arterial pressure were observed. Our findings demonstrate that exposure of the developing fetus to a maternal LP diet programs cardiac dysfunction in the offspring in later life.     

Absence of cardiac valve dysfunction in obese patients treated with sibutramine.

OBJECTIVE: Serotonin-releasing agents prescribed as weight-loss medications have been implicated as a cause of acquired aortic and mitral valve abnormalities. Sibutramine hydrochloride (MERIDIA) is a serotonin and norepinephrine reuptake inhibitor with proven efficacy of weight reduction. The purpose of this study was to determine the incidence of cardiac valve disease in sibutraminetreated patients. RESEARCH METHODS AND PROCEDURES: Obese patients with type 2 diabetes mellitus enrolled in an ongoing double-blind, placebo-controlled, parallel-arm, 12-month study of sibutramine (followed by a 12-month open label extension) underwent transthoracic echocardiographic imaging and color Doppler interrogation for assessment of cardiac valve anatomy and function. RESULTS: A total of 210 patients were evaluated. Of these, 133 were receiving sibutramine (72 in the double-blind period), and 77 were receiving placebo. The mean+/-Standard Deviation age was 54+/-9 years, and the mean duration of treatment was 229+/-117 days (approximately 7.6 months). The prevalence of left-sided cardiac valve dysfunction was low and similar for the two treatment groups (sibutramine 3/133, or 2.3%; placebo 2/77, or 2.6%). All five cases were cases of aortic insufficiency; four were mild, one was severe (in a placebo patient). All three sibutramine cases were patients over age 50; two had a history of systemic hypertension. CONCLUSION: The prevalence of left-sided cardiac valve dysfunction was not higher than background in obese patients treated with sibutramine for an average of 7.6 months.     

High-sugar intake does not exacerbate metabolic abnormalities or cardiac dysfunction in genetic cardiomyopathy

ObjectiveA high-sugar intake increases heart disease risk in humans. In animals, sugar intake accelerates heart failure development by increased reactive oxygen species (ROS). Glucose-6-phosphate dehydrogenase (G6PD) can fuel ROS production by providing reduced nicotinamide adenine dinucleotide phosphate (NADPH) for superoxide generation by NADPH oxidase. Conversely, G6PD also facilitates ROS scavenging using the glutathione pathway. We hypothesized that a high-sugar intake would increase flux through G6PD to increase myocardial NADPH and ROS and accelerate cardiac dysfunction and death.MethodsSix-week-old TO-2 hamsters, a non-hypertensive model of genetic cardiomyopathy caused by a δ-sarcoglycan mutation, were fed a long-term diet of high starch or high sugar (57% of energy from sucrose plus fructose).ResultsAfter 24 wk, the δ-sarcoglycan–deficient animals displayed expected decreases in survival and cardiac function associated with cardiomyopathy (ejection fraction: control 68.7 ± 4.5%, TO-2 starch 46.1 ± 3.7%, P < 0.05 for TO-2 starch versus control; TO-2 sugar 58.0 ± 4.2%, NS, versus TO-2 starch or control; median survival: TO-2 starch 278 d, TO-2 sugar 318 d, P = 0.133). Although the high-sugar intake was expected to exacerbate cardiomyopathy, surprisingly, there was no further decrease in ejection fraction or survival with high sugar compared with starch in cardiomyopathic animals. Cardiomyopathic animals had systemic and cardiac metabolic abnormalities (increased serum lipids and glucose and decreased myocardial oxidative enzymes) that were unaffected by diet. The high-sugar intake increased myocardial superoxide, but NADPH and lipid peroxidation were unaffected.ConclusionA sugar-enriched diet did not exacerbate ventricular function, metabolic abnormalities, or survival in heart failure despite an increase in superoxide production.     

Combined renal and cardiac transplantation for severe left ventricular dysfunction in end-stage renal failure.

Successful treatment of severe cardiac failure in a patient with end-stage renal failure by combined renal and cardiac transplantation is described. The possible causes of myocardial disease in the dialysis population are discussed.     

Rats in acute withdrawal from ethanol exhibit left ventricular systolic dysfunction and cardiac sympathovagal balance shift

There is strong evidence that sympathovagal balance plays an important role in the progression of cardiac dysfunction in non-alcoholics. The purpose of this investigation was to determine whether a pattern of continuous ethanol intake and withdrawal modulates the cardiac sympathovagal balance and left ventricular (LV) systolic function in rats. Male Wistar rats were treated with a continuous ethanol liquid diet for 49 days, and then subjected to 1-day withdrawal and 21-day abstinence. Cardiac sympathovagal balance and LV systolic function were evaluated based on heart rate variability (HRV), Western blotting, and echocardiography. Longitudinal data obtained from the same rats showed that the 49-day continuous ethanol treatment induced LV systolic dysfunction, expressed by decreased fractional shortening and ejection fraction. At the 1-day withdrawal, LV systolic dysfunction was deteriorated, and the low-frequency power/high-frequency power (LF/HF) ratio in HRV was elevated because of the depressed HF and the increased LF. Western blot analysis showed an increased expression of myocardial tyrosine hydroxylase and a decreased expression of myocardial acetylcholine. All anomalies were recovered to baseline values with 21-day abstinence. We concluded that acute withdrawal from a 49-day continuous ethanol regimen is sufficient to promote the shift of cardiac sympathovagal balance toward sympathetic predominance and reduced vagal tone, contributing to the further deterioration of LV systolic function in rats. Those providing medical care for alcoholics should be aware of this enhanced susceptibility to LV systolic dysfunction with abrupt termination of a continuous ethanol regimen.     

Congenital heart abnormalities and cardiac dysfunction: how prenatal diagnosis changed the chances for survival]

Because of the rapid development of sonography, there are many new informations on embryonal and fetal circulation and pathophysiology of decompensation. Echocardiography is a useful tool to follow intrauterine therapy. Authors have examined the effect of prenatal diagnosis on the prevalence of heart abnormalities, terms of cardiac surgery, perinatal mortality and mortality due to heart abnormalities or decompensation. During five years they have found 187 severe heart abnormalities. Because of parental request 90 pregnancies have been terminated. Following prenatal diagnosis in 16 cases planned surgery of the newborn, in 14 cases planned cesarean sections have been done. From 64 transplacentar treatments 44 patients have survived. Authors have found, that prenatal diagnosis had good effect on short term survival rate but had no effect on long term survival rate. Fetal echocardiography has selective and therapeutic effect. The selective effect depends on second trimester screening. The therapeutic effect was significant in cases of arrhythmias and decompensation.     

胸腔生物电阻抗法无创血流动力学监测对新生儿脓毒症患儿心功能障碍的预测价值

目的 探讨胸腔生物电阻抗法无创血流动力学监测(NHM-BIA)预测新生儿脓毒症(NS)患儿心功能障碍(CD)的价值。方法 选择2017年1月至2020年11月,西安交通大学附属儿童医院新生儿重症监护病房(NICU)收治的152例NS患儿为研究对象。采用回顾性研究方法,根据NS患儿是否并发CD,将其分为研究组(n=53,并发CD)与对照组(n=99,未并发CD)。对2组患儿性别、出生胎龄、出生体重、危重新生儿比例,血清N-末端脑利钠肽前体(NT-proBNP)、高敏肌钙蛋白(hs-cTn),肌酸激酶同工酶MB(CK-MB),心房、室内径及射血分数,以及心率、每搏输出量指数(SI)、心排血量(CO)、心指数、每搏输出量变异度(SVV)、校正流动时间(FTC)、外周血管阻力(SVR)、外周血管阻力指数(SVRI)、心肌收缩指数(ICON)、收缩时间比(STR)等NHM-BIA指标采用成组t检验、Mann-Whitney U检验与χ²检验进行统计学比较。对NS患儿并发CD的影响因素进行多因素非条件logistic回归分析。绘制NHM-BIA不同指标预测NS患儿并发CD的受...     

原发性高血压患者合并低水平白蛋白尿与左室不良构型及舒张功能的关系

目的 探讨原发性高血压患者合并低水平白蛋白尿(晨尿白蛋白10～30mg/L)与左室构型及舒张功能的关系.方法 301例未经系统治疗的原发性高血压患者按晨尿白蛋白水平分为三组:正常组107例(晨尿白蛋白＜10 mg/L),低水平白蛋白尿组127例(晨尿白蛋白10～30 mg/L),微量白蛋白尿组67例(晨尿白蛋白＞30 mg/L).分别测量各组患者的血压、身高、体重,检测血肌酐(SCr)、血尿素氮(BUN)、尿酸(UA)、空腹血糖(FBG)、口服葡萄糖耐量试验2 h血糖(2hPG)、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C),并进行心脏超声检查,测量左室舒张末期内径(LVEDD)、左室后壁厚度(LVPWT)、室间隔厚度(IVST).多普勒超声心动图测定二尖瓣舒张早期血流速度峰值(E)、舒张晚期血流速度峰值(A),计算E/A,并测定E峰减速时间(DT)和左室等容舒张时间(IVRT),评估左室舒张功能.根据公式计算左室质量指数(LVMI)、相对室壁厚度(RWT),比较各组LVMI、RWT、左室构型及左室舒张功能.结果 尿白蛋白水平与LVMI呈显著正相关(r=0.43,P＜0.01).低水平白蛋白尿组与正常组比较,IVST、LVPWT、RWT、LVMI均显著升高(P＜0.01),左室正常构型比例降低(P＜0.01),向心性重构、向心性肥厚发生率升高(P＜0.05),A升高(P＜0.05),E/A显著降低(P＜0.01).301例患者左室舒张功能不全发生率为28.6%(86/301),正常组、低水平白蛋白尿组、微量白蛋白尿组左室舒张功能不全发生率分别为12.1%(13/107)、33.9%(43/127)及44.8%(30/67),微量白蛋白尿组、低水平白蛋白尿组左室舒张功能不全发生率均显著高于正常组(P＜0.01).结论 合并低水平白蛋白尿的原发性高血压患者左室不良构型及左室舒张功能不全发生率升高.

Abstract：

Objective To investigate the relationship between low-grade albuminuria and unfavourable cardiac geometric adaptations and left ventricular diastolic dysfunction in non-treated essential hypertensive(EH ) patients. Methods Three hundred and one patients of EH were divided into three groups acording to morning urine albumin concentration ( MU AC ): normoalbuminuria (NAU) group ( 107 cases,MUAC ＜ 10 mg/L) ;low-gradealbuminuria (LGAU) group ( 127 cases, MUAC 10-30 mg/L); microalbuminuria (MAU) group (67 cases, MUAC ＞ 30 mg/L). The blood pressure,body height and weight was measured for all the patients. The serum creatinine (SCr),blood urea nitrogen (BUN), uric acid (UA),fasting plasma glucose (FBG), plasma glucose 2 hours after oral glucose load (2hPG), total cholesterol (TC), triglyceride (TG) and low density lipoprotein cholesterol (LDL-C) were detected by automatic biochemical analyzer.Echocardiogram exarmination was performed to detect left ventricular end-diastolic diameter (LVEDD), left ventricular end-diastolic posterior wall thickness (LVPWT) and interventricular septum thickness at end-diastole (IVST). Color Doppler ultrasound was used to measure indicators of left ventricular diastolic function, including peak E velocity of mitral diastolic flow (E) and peak A velocity of mitral diastolic flow ( A ), calculated E/A, measured the deceleration time of peak E ( DT ), and isovolumic relaxation time (IV RT ).Left ventricular mass index (LVMI) and relative wall thickness(RWT) were calculated by formula, and LVMI,RWT,left ventricular configuration diastolic dysfunction was compared. Results The level of MUAC had positive relationship with LVMI (r = 0.43 ,P ＜ 0.01 ). Compared with that in NAU group, IVST, LVPWT,RWT, LVMI increased (P ＜ 0.01 ), the ratio of left ventricular normal configuration decreased (P ＜ 0.01 ), the incidence of concentric reconstitution, concentric hypertrophy increased (P ＜ 0.05 ), A increased (P ＜ 0.05 ),and E/A decreased (P ＜ 0.01 ) in LGAU group. The total incidence of left ventricular diastolic dysfunction was 28.6%(86/301 ),12.1%(13/107),33.9%(43/127) and 44.8%(30/67)in NAU group,LGAU group and MAU group. The incidencerates of left ventricular diastolic dysfunction in LGAU group and MAU group were higher than that in NAU group (P ＜ 0.01 ). Conclusion LGAU is positively related to incidence of unfavourable cardiac geometric adaptations and left ventricular diastolic dysfunction in EH patients.     

Early detection of cardiac dysfunction: use of the myocardial performance index in patients with anorexia nervosa.

OVERVIEW: Patients with anorexia nervosa have functional cardiac abnormalities secondary to their nutritionally depleted state. These abnormalities include decreased left ventricular (LV) mass and varying degrees of LV systolic dysfunction. Assessment of LV diastolic function and quantitative assessment of right ventricular function are not routinely performed. The myocardial performance index (MPI) is a relatively new, simple, quantitative measure of global myocardial function. The purpose of this study was to evaluate left and right ventricular function in 13 patients with anorexia nervosa with the MPI and compare it to more commonly used echocardiographic measures of ventricular function.     

Heart rate variability analysis: a useful assessment tool for diabetes associated cardiac dysfunction in rural and remote areas

OBJECTIVE: Cardiovascular complications are the main cause of death in people with diabetes. Early, asymptomatic changes are due to autonomic nervous system dysfunction, which if identified can lead to improved health. This study used detrended fluctuation analysis to identify changes in heart rate variability (HRV) associated with short-time electrocardiograph (ECG) recordings. The aim of the study was to determine whether heart rate variability analysis on short ECG recordings has the potential to be a useful adjunct to clinical practice. DESIGN: Comparative design with three independent simple random samples. SETTING: University-based research project. PARTICIPANTS: Forty-eight people with no diabetes or cardiovascular complications had a 20 min ECG recorded, which was subsequently analysed using mathematical procedures. All participants also had a lying-to-standing autonomic nervous system test. Data was analysed using a Student t-test. RESULTS: Heart rate variability expressed as a numeric value (alpha(1)), is reduced in disease states. We found a significant difference in alpha(1)(P = 0.03) between the ECG recordings of the diabetes and control groups. In addition lower alpha(1)values were obtained from people identified with autonomic dysfunction within the diabetes group. CONCLUSION: The importance of our findings is that abnormal HRV identifies people with cardiovascular disease, irrespective of diabetes status, that may have autonomic neuropathy. HRV analysis is easily implemented by primary health care providers and has the potential to lead to improved health care by reducing inequity in rural areas and specifically addressing cardiovascular complications associated with diabetes.     

Autonomic dysfunction

The autonomic nervous system is closely involved in the majority of bodily functions. Different disease processes and a variety of drugs can result in autonomic dysfunction, some with minor but others with major consequences. This review considers factors which relate to the recognition, investigation and principles of management of such disorders.     

Sexual dysfunction

Drug treatment of sexual dysfunction has often been unwise and lacked a sound physiological basis. However, medication has a small but important role in treatment, the most usual being the reversal of hypogonadism. Recent advances in the drug treatment of erectile dysfunction are also very promising.     

Endothelial dysfunction

The endothelium is a major regulator of vascular tone, releasing vasoconstrictive (endothelin, cyclooxigenase-dependent factors, including prostanoids and oxygen free radicals) and vasodilating (endothelium--derived nitric oxid, endothelium--derived hyperpolarizing factor) mediators. These biologically active substances control not only the vascular tone but the vascular structure and permeability, coagulation and fibrinolysis, as well inflammatory response of the vascular wall. In endothelial dysfunction the balance in the endothelial production of vasodilating and vasoconstricting substances is altered resulting an apparent decrease in endothelium-dependent relaxations. Endothelial dysfunction is an important event in the pathogenesis of the early phase of atherosclerosis and hypertension. The testing and monitoring of endothelial dysfunction include tests of endothelium-dependent vasomotion, as well as circulating markers of endothelial damage. Further methods are needed to build up a panel of tests which measure the extent of endothelial dysfunction (= subclinical atherosclerosis), predict the subsequent risk and response to therapy.     

Acetaldehyde-induced cardiac contractile dysfunction may be alleviated by vitamin B1 but not by vitamins B6 or B12

AIMS: Chronic alcohol exposure leads to a deficiency of group B vitamins and increased risk of alcoholic cardiomyopathy characterized by impaired ventricular contractility. This study was designed to examine the effect of group B vitamin supplementation on short-term exposure of the main alcohol metabolite acetaldehyde (ACA)-induced cardiac contractile dysfunction in rat ventricular myocytes. METHODS: Mechanical contractile properties were evaluated by an IonOptix SoftEdge system. Protein damage and apoptosis were determined by protein carbonyl and caspase-3 assays, respectively. RESULTS: Short-term (4-6 h) culture of myocytes with ACA (10 microM) depressed peak shortening amplitude, maximal velocity of shortening/relengthening, shortened duration of shortening but not the duration of relengthening. ACA exposure also enhanced protein carbonyl formation and apoptosis in ventricular myocytes. The toxin-induced mechanical defects, protein damage and apoptosis were ablated by vitamin B1 (10 microM), an essential vitamin required for DNA synthesis and repair. Vitamin B6 (10 microM) attenuated ACA-induced impairment of shortening duration. Vitamin B12 (1 mM) attenuated ACA-induced reduction in maximal velocity of shortening/relengthening. Unlike vitamin B1, none of the other ACA-elicited alterations in myocyte mechanical function were affected by vitamin B6 or vitamin B12. Vitamin B6 and vitamin B12 partially, but significantly, attenuated the ACA-induced carbonyl formation without affecting ACA-induced apoptosis. CONCLUSIONS: These data provide evidence that vitamin B1 supplementation may be protective for ACA-induced cytotoxicity through protection against protein damage and apoptotic cell death in ventricular myocytes.