扩张型心肌病患者血清尿酸浓度的动态变化

目的探讨扩张型心肌病(DCM)心力衰竭(心衰)患者血清尿酸浓度的变化规律及其临床意义。方法比较DCM(46例)不同心功能状态下尿酸浓度;比较22例DCM心衰控制前后的尿酸浓度;比较DCM中左室内径≥65mm(26例)和＜65mm(16例)患者的尿酸浓度;比较DCM入院时未用利尿剂及正在服用利尿剂患者的尿酸浓度;比较DCM中血尿素氮＞7.5(18例)和≤7.5mmol/L(28例)患者的尿酸浓度。结果DCM心功能Ⅱ、Ⅲ、Ⅳ级的尿酸分别为(303±34)、(403±95)和(595±190)mmol/L;心衰控制前后尿酸浓度为〔(609±218)和(414±147)mmol/L(P＜0.01)〕;左室内径≥65mm者尿酸明显高于＜65mm者;入院时服与未服利尿剂者尿酸无明显差异(P＞0.05);血尿素氮＞7.5与≤7.5mmol/L者尿酸浓度无明显差别(P＞0.05)。结论DCM心衰患者尿酸浓度增高,独立于服用利尿剂及肾功能不全,且随着心衰加重而明显增高,是反映心衰患者病情严重程度的一个指标。     

血清尿酸水平与扩张型心肌病心衰患者的关系

目的：探讨扩张型心肌病心衰患者血清尿酸浓度的变化规律及其临床意义。方法：比较扩张型心肌病（DCM,96例）不同心功能和其他状态下的尿酸浓度。结果：DCM心功能Ⅱ、Ⅲ、Ⅳ级患者的尿酸分别为（303±34）mmol／L,（403±95）mmol／L和（595±190）mmol／L,各级间比较差异具有显著性（P〈0．01）;与心衰控制前比较,心衰控制后尿酸浓度明显降低[（609±218）mmol／L比（414±147）mmol／L,P〈0．01];左室内径≥65mm者尿酸浓度明显高于〈65mm者[（572±183）mmol／L比（425±112）mmol／L,P〈0．01];人院时服与未服利尿剂者尿酸浓度无明显差异（P〉0．05）;BUN〉7．5mmol／L与≤7．5mmol／L者尿酸浓度无明显差异（P〉0．05）。结论：扩张型心肌病心衰患者尿酸浓度升高,升高程度与心衰严重程度有关,而独立于服用利尿剂及肾功能不全;血清尿酸浓度是反映心衰患者病情严重程度的一个指标。     

扩张型心肌病患者血清可溶性细胞间黏附分子与血管功能和心功能的关系

目的:观察扩张型心肌病(DCM)患者外周血中可溶性细胞间黏附分子-1(sICAM-1)的水平及与血管功能和心功能的关系.方法:DCM患者65例,正常对照组49例.用酶联免疫吸附法测定2组血清中sICAM-1的水平;用无创动脉功能测定仪测定大动脉弹性指数(C1)和小动脉弹性指数(C2).用NYHA分级评价心功能.结果:①DCM组外周血sICAM-1的水平显著高于正常对照组,而DCM组C2显著低于正常对照组,2组间C1差异无统计学意义;②血清sICAM-1与C2呈负相关.sICAM-1是影响C2的重要因素;③随着心功能下降,血清中sICAM-1的水平逐渐升高,两者呈等级相关.结论:DCM患者心功能和血管内皮功能下降与sICAM-1升高有关.     

扩张型心肌病患者运动前后血清肌钙蛋白I水平变化

目的 观察扩张型心肌病患者在症状限制性运动试验和运动训练期后心肌钙蛋白I变化.方法 20例扩张型心肌病中度心力衰竭患者[(NYHA分级Ⅱ一Ⅲ级,射血分数(31.7±9.3)%]与15例轻度心力衰竭患者及10例无心力衰竭受试者进行对比观察,他们均经历了症状限制性运动试验和单期运动训练(达最大心率的80%以上,持续时间30 min),分别测定其基础cTnI值、症状限制性试验后和运动训练后1～5h时的.TnI值.结果 症状限制性运动试验后,中度心力衰竭患者cTnI值由(38±19)pg/ml增加到(75±29)pgtnd,其中5例中度心力衰竭患者和4例轻度心力衰竭患者的cTnI值升高到100 pg/ml以上.无心力衰竭的受试者无论是静息时或是运动后其cTnI值均较低(P＜0.05).结论 扩张型心肌病中度心力衰竭患者在症状限制性运动试验后其.cTnI值增加,其水平达到轻微的心肌损伤水平,这一现象对患者预后的影响值得进一步研究.     

维吾尔族男性冠心病心力衰竭与血清尿酸的相关性

目的：探讨维吾尔族男性冠心病患者心力衰竭与血清尿酸浓度的相关性。方法：218例维吾尔组男性冠心病患者,按左室射血分数（LVEF）分三组,LVEF≥50％组（对照组,72例）、40％〈LVEF〈50％组（71例）、LvEF≤40％组（75例）,比较三组血清尿酸浓度的变化;所有患者心功能再参照NYHA分级分为Ⅰ级组（37例）、Ⅱ级组（80例）、Ⅲ级组（67例）、Ⅳ级组（34例）,比较四组血清尿酸浓度的变化;按冠脉粥样斑块的稳定型再分为急性冠脉综合征（ACS,101例）组和稳定型心绞痛（SAP,117例）组,比较血清尿酸浓度的变化及血尿酸和LVEF的相关性。结果：LVEF≥50％组、40％〈LVEF〈50％组、LVEF≤40％组三组血清尿酸浓度依次增高．各组间差异均有显著性（P〈0．05）,血尿酸与LVEF呈负相关（r=-0．408,P〈0．01）。按NYHA分级分组,心功能Ⅳ级组血尿酸高于其余三组．心功能Ⅲ级组血尿酸高于心功能Ⅰ、Ⅱ级组,差异均有显著性（P均〈0．05）,心功能Ⅱ级组与心功Ⅰ级组血尿酸差异无显著性（P=0．62）;ACS组血清尿酸浓度明显高于SAP组（P〈0．01）。Pearson相关分析显示SUA与LVEF呈负相关（r=-0．408,P〈0．01）。结论：血清尿酸增高与心力衰竭严重程度密切相关,是心功能恶化的预测因子,也是心血管急性事件的预测因子。     

卡维地洛治疗扩张型心肌病心力衰竭患者的疗效

目的：观察卡维地洛治疗扩张型心肌病心力衰竭患者的临床疗效。方法：选择扩张型心肌病心力衰竭患者82例,采用随机分组的方法分为卡维地洛组（42例）和常规治疗组（40例）,卡维地洛组在常规治疗基础上加用卡维地洛3．125～25mg2次／d。比较两组左室舒张期末内径（LVEDd）、左室收缩期末内径（LVEsd）、左房内径（LAD）、左室射血分数（LVEF）、6min步行距离（6MWD）等指标变化情况。结果：治疗6个月后,两组患者心功能均有改善,卡维地洛组总有效率显著高于常规治疗组（90．5％比72．5％,P〈0．05）;两组治疗后患者的LVEDd、LVESd、LVEF及6MWD均有显著改善（P〈0．05）,且与常规治疗组比较,卡维地洛组治疗后患者的LVEDd[（59．1±9．6）mm比（54．2±10．2）mm]、LVESd[（46．1±8．7）mm比（41．4±12．2）mm]显著缩小,LVEF[（42．1±10．5）％比（48．4±9．6）％]及6MWD[（264．52±51．23）m比（309．26±45．24）m]显著增加（P均〈0．05）。结论：在常规治疗基础上加用卡维地洛可明显改善扩张型心肌病心力衰竭患者的疗效。     

参附注射液治疗扩张型心肌病心力衰竭的效果

1对象和方法1.1对象20008年1月～2009年12月我院住院患者100例,诊断标准参照扩张型心肌病(DCM)的诊断标准[1],心功能分组标准参照美国纽约心脏病学会(NYHA)制定的标准[2],纳入标准:符合诊断标准并年龄为18～45岁;心功能Ⅱ～Ⅳ级的充血性心力衰竭(CHF);超声心动图证实左室射血分数(LVEF)<50%;符合1971年美国Framingham心衰诊     

普伐他汀对扩张型心肌病患者心功能及细胞因子的影响

目的 观察普伐他汀对扩张型心肌病(DCM)心力衰竭患者心功能及血清肿瘤坏死因子(TNF-α)、白细胞介素-6(IL-6)水平的影响.方法 选择DCM心力衰竭患者68例,随机分为治疗组(35例)及对照组(33例).对照组给予常规纠正心力衰竭药物治疗,治疗组在常规治疗基础上加用普伐他汀,10 mg,每晚一次.治疗前及后6个月后行心脏彩超检查,测定左心室舒张末内径(LVEDd)、左心室射血分数(LVEF),测定血清TNF-α、IL-6浓度.结果 两组患者治疗6个月时LVEDd均较治疗前显著缩小(P＜0.05),LVEF较治疗前显著提高(P＜0.05).治疗6个月时治疗组与对照组比较LVEF较对照组显著提高(P＜0.05),LVEDd有进一步缩小趋势,但差异无统计学意义.治疗6个月时,治疗组血清TNF-α(146.26±1.27和174.58±1.42,P＜0.05)、IL-6(25.56±1.79和35.23±1.87,P＜0.05)水平较治疗前显著下降,对照组较治疗前无明显变化.结论 普伐他汀可明显改善DCM心力衰竭患者心功能,降低血清TNF-α、IL-6水平,有利于DCM的治疗.     

卡维地洛治疗扩张型心肌病心力衰竭疗效观察

目的　评价第三代 β受体阻滞剂卡维地洛治疗扩张型心肌病 (DCM)心力衰竭的临床疗效。方法　 6 2例 DCM心力衰竭患者在接受常规治疗 (洋地黄、利尿剂、血管紧张素转换酶抑制剂 )病情稳定后 ,随机分为卡维地洛组和美多心安组。均从小剂量 (卡维地洛组 ,2 .5 m g bid;美多心安组 ,6 .2 5 m g bid)缓慢递增。检测治疗前后 DCM患者左心室功能和结构的变化以及血液中内皮素 - 1(ET- 1)、心钠素 (ANP)和血管紧张素 (Ang )的改变。结果　治疗 6个月后 ,两组心脏功能分级均明显改善 ,左心室射血分数 (L VEF)、短轴缩短率 (FS)、左心室射血前期与射血时间比(PEP/ L VET)、舒张早期峰值血流速度 (PFVE)、舒张早期峰值血流速度与舒张晚期峰值血流速度比 (PFVE/ PF-VA)均明显增加 ,卡维地洛组较美多心安组 L VEF增加更为明显。两组左心房内径 (L AD)、左心室收缩末期内径(L VSD)、左心室舒张末期内径 (L VDD)明显减小 ,卡维地洛组 L VSD减小较美多心安组更明显。治疗后血浆中ET- 1、ANP和 Ang 均明显降低。结论　卡维地洛和美多心安都能够改善 DCM心力衰竭患者左心室收缩和舒张功能 ,逆转左心室重构 ,卡维地洛较美多心安疗效更佳。     

培哚普利对老年心力衰竭患者血中可溶性细胞间黏附分子-1和细胞凋亡抑制因子的影响

目的　观察培哚普利对老年慢性心力衰竭 (CHF)患者循环血中可溶性细胞间黏附分子 1(sICAM 1)和细胞凋亡抑制因子 (Fas Apo 1)水平的影响。方法　用酶联免疫方法检测 5 3例老年CHF患者治疗前后及 2 5例健康老年人血中sICAM 1和Fas Apo 1水平。结果　老年CHF患者sICAM 1和Fas Apo 1水平分别为 (6 0 2 .6 1± 14 8.5 8) μg Lvs(0 .2 7± 0 .0 8) μg L ,显著高于 2 5例健康老年人 (178.5 4± 31.0 1) μg Lvs (0 .12± 0 .0 4 ) μg L ,且随着心功能损害程度加重而升高 ,各组间比较差异有显著性意义。培哚普利组与治疗对照组治疗前后血中sICAM 1和Fas Apo 1浓度水平差异有显著性意义 ,培哚普利组较治疗对照组治疗后血中sICAM 1和Fas Apo 1下降明显。结论　外周血中sICAM 1和Fas Apo 1水平可反映老年CHF的程度 ;培哚普利可明显降低老年CHF患者血中sICAM 1和Fas Apo 1的水平 ,从而保护和改善心功能。     

Increased plasma adhesion molecule levels in patients with heart failure who have ischemic heart disease and dilated cardiomyopathy

BACKGROUND: Inflammatory mechanisms, including leukocyte activation, appear to play a pathogenetic role in the development of heart failure. Vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) are important mediators of leukocyte adhesion to vascular endothelium. The plasma levels of the soluble form of these molecules may be elevated in chronic inflammation. METHODS AND RESULTS: We measured plasma VCAM-1 and ICAM-1 levels (in nanograms per milliliter) with the commercially available enzyme-linked immunosorbent assay method in 12 patients (9 male, 3 female, aged 64 +/- 8 years) with dilated cardiomyopathy and heart failure, in 23 patients (23 male, aged 65 +/- 9 years) with ischemic cardiomyopathy and heart failure, and in 11 healthy control subjects (8 male, 3 female, aged 49 +/- 14 years). Plasma ICAM-1 levels were higher both in patients with dilated cardiomyopathy (363 +/- 77 ng/mL, P <.05) (mean +/- SEM) and in those with ischemic heart disease (320 +/- 32 ng/mL, P <.05) than in control subjects (225 +/- 29 ng/mL). VCAM-1 levels were also higher in both groups with heart failure (664 +/- 73 ng/mL) than in control subjects (551 +/- 60 ng/mL). VCAM-1 levels were higher in patients with class IV compared with those with class II and III heart failure. CONCLUSIONS: Plasma adhesion molecule levels are increased in patients with heart failure and are unrelated to the presence or absence of angiographically demonstrable atherosclerotic coronary artery disease. The plasma level of VCAM-1 correlates with the severity of heart failure.     

卡维地洛对不伴有心力衰竭的扩张型心肌病患者冠状动脉血流储备的影响

目的:利用无创经胸负荷超声心动图评价不伴有心力衰竭的扩张型心肌病(DCM)患者冠状动脉血流储备(CFR)以及卡维地洛治疗对其影响。方法:入选不伴有心力衰竭的DCM患者40例,正常对照组30例。DCM患者在常规药物治疗基础上,加用卡维地洛至目标剂量或最大耐受剂量,治疗前后行常规超声及负荷超声检测,并评价CFR。结果:①治疗前,DCM组较正常对照组左房内径、左室舒张末期内径明显增加,左室射血分数(LVEF)、二尖瓣舒张早期和晚期峰值血流速度比值减低(P0.05);治疗1个月后各项指标与治疗前差异无统计学意义,而6个月后左房内径、左室舒张末期内径和LVEF有所改善,但与正常对照组仍有差异。②治疗前DCM组较正常对照组舒张期最大峰值血流速度(hCFV)和CFR降低(P0.05)[hCFV:(63.72±5.81)∶(81.65±8.47)cm/s,P0.05;CFR:2.57±0.31∶3.20±0.29,P0.05];治疗1个月、6个月后hCFV和CFR均较治疗前升高(P0.05),1个月后DCM组与正常对照组比较hCFV和CFR仍减低[hCFV:(70.75±6.08)∶(81.65±8.47)cm/s,P0.05;CFR:2.81±0.30∶3.20±0.29,P0.05],6个月后与正常对照组之间各指标差异无统计学意义[hCFV:(78.93±6.88)∶(81.65±8.47)cm/s,P0.05;CFR:3.13±0.36∶3.20±0.29,P0.05]。结论:不伴有心力衰竭的DCM者hCFV和CFR减低,经卡维地洛治疗1个月和6个月后均可有效改善;负荷超声检测CFR可以早期评价卡维地洛治疗效果。     

冠心病合并心力衰竭患者血清脂联素水平变化

目的探讨冠心病合并心力衰竭患者血清脂联素水平的变化及其临床意义。方法选择冠心病患者60例、冠心病合并心力衰竭患者60例[其中心功能（NYHA）Ⅱ级18例、心功能Ⅲ级27例、心功能Ⅳ级15例]、健康对照组25例,测定血清脂联素并对其变化进行两两比较。结果冠心病合并心力衰竭患者血清脂联素为（14．22±5．34）mg／L;冠心病无心力衰竭组血清脂联素为（4．79±1．61）mg／L;健康对照组为（6．98±1．62）mg／L,两两比较差异有统计学意义（P〈0．01）。冠心病合并心力衰竭患者随着心功能分级的升高,血清脂联素水平也显著升高[NYHAII级为（9．25±2．71）mg／L,NYHAⅢ级为（13．72±3．38）mg／L,NYHAIV级为（18．0±6．72）mg／L,P〈0．01]。结论合并心力衰竭的冠心病患者血清脂联素水平是升高的,且随着心功能分级的升高,血清脂联素水平也明显升高。血浆脂联素可能参与冠心病及心力衰竭的发病机制,血清脂联素水平变化对心力衰竭的进展和程度有一定的指导意义。     

Acute hemodynamic and neurohumoral effects of moxonidine in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Elevated plasma norepinephrine (PNE) has been shown to be an important predictor of morbidity and mortality in patients with congestive heart failure (CHF). Moxonidine selectively stimulates imidazoline receptors located in the medulla, which centrally inhibit sympathetic outflow. PNE is suppressed and peripheral vasodilation reduces systemic blood pressure. This study evaluated the acute neurohumoral and hemodynamic effects of a single dose of oral moxonidine in 32 patients (22 men, mean ± SD age 66 ± 10 years) with CHF. All patients were in New York Heart Association functional class III and stabilized on chronic therapy with diuretics, digitalis, and angiotensin-converting enzyme inhibitors. The mean PNE concentration was 509 ± 304 pg/ml at baseline. Patients underwent invasive hemodynamic monitoring after double-blind randomization to either placebo (n = 12), moxonidine 0.4 mg (n = 9), or moxonidine 0.6 mg (n = 11). Moxonidine produced a dose-dependent, vasodilator response compared with placebo. Analysis of the time-averaged change from baseline over 6 hours demonstrated that moxonidine 0.6 mg caused significant reductions in mean systemic arterial pressure (p <0.0001), mean pulmonary arterial pressure (p <0.005), systemic vascular resistance (p <0.05), pulmonary vascular resistance (p <0.01), and heart rate (p <0.05). Stroke volume was unchanged. PNE was reduced substantially (−180 pg/ml at 4 hours, p <0.005) and the reduction was highly correlated with the baseline level (r = −0.968). Moxonidine was well tolerated in this single-dose study and resulted in a modest, dose-dependent, vasodilator response, with substantial reductions in systemic and pulmonary arterial blood pressure. Trials designed to evaluate the clinical efficacy of chronic moxonidine therapy in CHF added to conventional therapy would be appropriate.     

Acute hemodynamic and neurohumoral effects of moxonidine in congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy

Elevated plasma norepinephrine (PNE) has been shown to be an important predictor of morbidity and mortality in patients with congestive heart failure (CHF). Moxonidine selectively stimulates imidazoline receptors located in the medulla, which centrally inhibit sympathetic outflow. PNE is suppressed and peripheral vasodilation reduces systemic blood pressure. This study evaluated the acute neurohumoral and hemodynamic effects of a single dose of oral moxonidine in 32 patients (22 men, mean ± SD age 66 ± 10 years) with CHF. All patients were in New York Heart Association functional class III and stabilized on chronic therapy with diuretics, digitalis, and angiotensin-converting enzyme inhibitors. The mean PNE concentration was 509 ± 304 pg/ml at baseline. Patients underwent invasive hemodynamic monitoring after double-blind randomization to either placebo (n = 12), moxonidine 0.4 mg (n = 9), or moxonidine 0.6 mg (n = 11). Moxonidine produced a dose-dependent, vasodilator response compared with placebo. Analysis of the time-averaged change from baseline over 6 hours demonstrated that moxonidine 0.6 mg caused significant reductions in mean systemic arterial pressure (p <0.0001), mean pulmonary arterial pressure (p <0.005), systemic vascular resistance (p <0.05), pulmonary vascular resistance (p <0.01), and heart rate (p <0.05). Stroke volume was unchanged. PNE was reduced substantially (−180 pg/ml at 4 hours, p <0.005) and the reduction was highly correlated with the baseline level (r = −0.968). Moxonidine was well tolerated in this single-dose study and resulted in a modest, dose-dependent, vasodilator response, with substantial reductions in systemic and pulmonary arterial blood pressure. Trials designed to evaluate the clinical efficacy of chronic moxonidine therapy in CHF added to conventional therapy would be appropriate.     

The effects of simvastatin on the incidence of heart failure in patients with coronary heart disease

Background: Although treatment of myocardial overload effectively reduces death from progression of heart failure, it is not known whether the retardation of progressive coronary artery disease obtained with lipid lowering treatment will prevent the onset and consequences of heart failure in patients without previous symptoms of heart failure.Methods and Results: In the Scandinavian Simvastatin Survival Study, 4444 patients with coronary heart disease without evidence of heart failure were randomized to placebo (n = 2223) or simvastatin 20–40 mg (n = 2221) and followed for more than 5 years. Among the patients who received placebo, 228 (10.3%) were diagnosed with heart failure during follow-up evaluation compared with 184 (8.3%) of patients who received simvastatin (P < .015). Mortality was 31.9% in the placebo group and 25.5% in the simvastatin group among patients who developed heart failure. These compare with 9.2 and 6.6%, respectively, among non-heart failure patients. There were 45 hospitalizations because of acute heart failure in the placebo group and 23 in the simvastatin group (NS). Patients who developed heart failure were more likely to have suffered a recurrent myocardial infarction and have a history of diabetes, peripheral artery disease, and hypertension than patients who did not develop congestive heart failure.Conclusion: Long-term prevention with simvastatin reduces the occurrence of heart failure in a cohort of patients with coronary heart disease without previous evidence of congestive heart failure.     

扩张型心肌病心室重构伴充血性心力衰竭的危险因素分析

目的:探讨扩张型心肌病(DCM)后心室重构(VRM)伴充血性心力衰竭(CHF)的危险因素。方法:选择DCM患者NYHA分级Ⅱ～Ⅳ级,且左心室射血分数(LVEF)<40%的96例为观察组;心功能Ⅰ级,LVEF≥40%的35例患者为对照组,比较2组临床资料,在单因素分析基础上,采用Logistic多因素逐步分析方法确立DCM后VRM伴CHF的独立危险因素。结果:单因素分析结果显示,观察组中男性患病率、心房颤动(房颤)及脉压≥70mmHg(1mmHg=0.133kPa)者较对照组高,差异有统计学意义(P<0.01)。Logistic逐步回归分析脉压≥70mmHg、房颤为DCM后VRM伴CHF的独立危险因素。结论:脉压≥70mmHg、房颤是DCM后VRM伴CHF的独立危险因素。     

冠心病和充血性心力衰竭患者的心率变异性

本文采用标准差法及心率变指数法分析了冠心病、充血性心力衰竭及正常人各５０例的心率变异性，结果发现冠心病及充血性心力衰竭者的心率变异值显著低于正常人。心衰组中，心衰程度越重者，心率弈异赵低。且心率变异与心胸比值及ＰＥＰ／ＬＶＥＴ呈负相关，与心脏指数呈正相关。急性心肌梗死者的心率变趔氏于陈旧性心肌梗死和心绞痛者。２４例心肌梗死者查心室晚电位，晚电位阳性者的心率变异值显著低于晚电位阴性者，提示两者结合可     

扩张型心肌病伴心衰患者肝细胞生长因子浓度与心功能的关系

目的探讨扩张型心肌病伴心衰患者血清肝细胞生长因子（HGF）浓度与心功能的关系。方法检测试验组扩张型心肌病伴心功能不全患者（NYHA心功能Ⅰ级15例、Ⅱ级16例、Ⅲ级15例、Ⅳ级17例）和26名健康对照者血清HGF浓度、NT—proBNP浓度、LVEDD值和LVEF值,比较各组各项指标的差异;同时探讨血清HGF浓度和上述指标的相关性。结果HGF浓度、NT—proBNP浓度、LVEDD值和LVEF值对照组分别为（323±29）pg／ml、（251±102）pg／ml、（42±7）mm和（57±11）％;NYHA心功能Ⅰ级组分别为（492±47）pg／ml、（973±112）pg／ml、（50±6）mm和（50±7）％;NYHA心功能Ⅱ级组分别为（607±68）pg／ml、（1229±214）pg／ml、（54±9）mm和（48±9）％;NYHA心功能Ⅲ级组分别为（662±94）pg／ml、（4208±1562）pg／ml、（59±16）mm和（42±7）％;NYHA心功能Ⅳ级组分别为（1028±135）pg／ml、（6963±2129）pg／ml、（66±19）mm和（38±6）％,各组间比较差异均有统计学意义（P〈0．05）.血清HGF浓度和NT—proBNP浓度呈正相关,相关系数为0．79;血清HGF浓度和LVEDD值呈正相关,相关系数为0．73;血清HGF浓度和LVEF值呈负相关,相关系数为-0．69。结论扩张型心肌病伴心功能不全患者血清HGF浓度和心功能不全的严重程度有关,可以作为心功能不全严重程度的预测因子。     

Anaemia and coronary artery disease severity in patients with heart failure

BACKGROUND: Anaemia is common in heart failure (HF) and associated with higher mortality. Exacerbation of myocardial ischemia in patients with heart failure, coronary disease, and anaemia patients has been suggested as a potential mechanism underlying this association. AIMS: The aim of this study was to evaluate the hypothesis that greater CAD severity would exacerbate the adverse effects of anaemia in HF. METHODS: We examined data on patients with symptomatic heart failure (NYHA class > or = II) undergoing coronary angiography between 1995 and 2003 (n = 4951). Patients with primary valvular or congenital heart disease were excluded. Cox proportional hazards modeling was used to evaluate the relationship between coronary disease severity (as defined by no. of diseased vessels) and hemoglobin concentration. RESULTS AND CONCLUSIONS: In patients with symptomatic HF undergoing coronary angiography, we found an interaction between hemoglobin and CAD severity (p = 0.003 for interaction). Contrary to our hypothesis, the mortality hazard associated with anaemia was greatest in patients without CAD and progressively lower with increasing CAD severity. These data suggest that anaemia may exert its effect on HF outcomes through mechanisms beyond simply the exacerbation of myocardial ischemia.