Fatty acid metabolism assessed by 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume-overloaded hearts

BACKGROUND: The peroxisome proliferator-activated receptor (PPAR) alpha is a member of the nuclear receptor superfamily and regulates gene expression of fatty acid utilization enzymes. In cardiac hypertrophy and heart failure by pressure-overload, myocardial energy utilization reverts to the fetal pattern, and metabolic substrate switches from fatty acid to glucose. However, myocardial metabolism in volume-overloaded hearts has not been rigorously studied. The aim of the present study was to examine fatty acid metabolism and protein expressions of PPARalpha and fatty acid oxidation enzymes in volume-overloaded rabbit hearts. METHODS: Volume-overload was induced by carotid-jugular shunt formation. Sham-operated rabbits were used as control. Chronic volume-overload increased left ventricular weight and ventricular cavity size, and relative wall thickness was decreased, indicating eccentric cardiac hypertrophy. (125)I-iodophenyl 9-methylpentadecanoic acid (9MPA) was intravenously administered, and animals were sacrificed at 5 min after injection. The 9MPA was rapidly metabolized to iodophenyl-3-methylnonanoic acid (3MNA) by beta-oxidation. Lipid extraction from the myocardium was performed by the Folch method, and radioactivity distribution of metabolites was assayed by thin-layer chromatography. The protein was extracted from the left ventricular myocardium, and levels of PPARalpha and fatty acid oxidation enzymes were examined by Western blotting. RESULTS: Myocardial distribution of 9MPA tended to be more heterogeneous in shunt than in sham rabbits (P = 0.06). In volume-overloaded hearts by shunt, the conversion from 9MPA to 3MNA by beta-oxidation was faster than the sham-control hearts (P < 0.05). However, protein levels of PPARalpha and fatty acid utilization enzymes were unchanged in shunt rabbits compared with sham rabbits. CONCLUSIONS: These data suggest that myocardial fatty acid metabolism is enhanced in eccentric cardiac hypertrophy by volume-overload without changes in protein expressions of PPARalpha and fatty acid utilization enzymes. Our data may provide a novel insight into the subcellular mechanisms for the pathological process of cardiac remodelling in response to mechanical stimuli.     

Myocardial gene expression of leukaemia inhibitory factor, interleukin-6 and glycoprotein 130 in end-stage human heart failure

BACKGROUND: Studies in different animal models and plasma analyses in humans suggest that members of the interleukin-6 (IL-6) cytokine family may be involved in the pathogenesis of congestive heart failure (CHF). Accordingly, we have examined IL-6-related cytokines in chronic CHF in humans by analysing gene and protein expression in myocardium derived from patients with end-stage heart failure and donor hearts. METHODS: Gene expression of cytokines/receptors of the IL-6 family was documented in myocardial samples using cDNA array hybridization and RNase protection assays. Immunohistochemistry was used to detect leukaemia inhibitory factor (LIF), IL-6 and glycoprotein 130 (gp130) in myocardial tissues. RESULTS: Myocardial gene activity was documented for the majority of IL-6 family cytokines and their receptors. Immunohistochemical analysis localized IL-6, LIF and their common receptor subunit gp130 to myocytes and vascular smooth muscle cells. LIF mRNA levels were enhanced in the left ventricles of CHF patients relative to the left ventricles of donor hearts (patients 4.6 +/- 4.7 vs. donors 0.3 +/- 0.3, P < 0.005). Myocardial IL-6 and gp130 mRNA levels were not statistically different between patients and donors, but in contrast to LIF mRNA expression in heart explants, gp130 mRNA levels were significantly higher in left atrium compared with left ventricle in both patients and donors. CONCLUSIONS: Both mRNA and proteins of gp130 and its ligands IL-6 and LIF are expressed in both nonfailing and failing human myocardium. The elevated LIF mRNA levels in left ventricles from patients with end-stage heart failure suggest a role for LIF in the pathogenesis of CHF.     

β肾上腺素能受体在左室机械辅助减负荷模型中的表达

目的 研究β肾上腺素能受体在左室机械辅助减负荷模型中的表达及其意义,探讨左室减负荷后心肌分子水平的变化.方法 选用Lewis大鼠,结扎冠状动脉左前降支(LAD)诱导心力衰竭(心衰);4周后,心脏移植组将心衰后的心脏及右肺移植到受体大鼠的腹部(通过供体的升主动脉与受体的降主动脉吻合);移植2周后,评价全心重量、左室重量、心肌细胞直径及心肌纤维化程度,采用实时定量聚合酶链反应(PCR)检测β肾上腺素能受体mRNA的表达.以7只正常Lewis大鼠为对照.结果 心衰后增大的心脏、左室重量、左室心肌细胞直径在移植后趋于正常.心衰组左室β1、β2肾上腺素能受体mRNA表达较正常组明显降低(0.09±0.03比0.18±0.04,0.07±0.06比0.12±0.02,均P<0.05);移植组β2肾上腺素能受体mRNA 表达(0.11±0.05)接近正常组(P>0.05),而β1肾上腺素能受体mRNA表达(0.08±0.06)仍低于正常组(P<0.05).结论 左室减负荷后,心肌逆向重构的过程伴随着心肌细胞分子水平改变,如β肾上腺素能受体表达的改变,可能与左室机械辅助后心脏功能的恢复有关.

Abstract：

Objective To study the expression and significance of β adrenergic receptors mRNA in a model of left ventricular mechanical unloading,and explore the change in cardiomyocyte in molecular level after left ventricular unloading.Methods Heart failure was reproduced in Lewis rats by ligating left anterior descending(LAD)artery.After 4 weeks,the failing hearts and right lungs were heterotopically transplanted into the abdomen of the recipients by anatomizing their ascending aorta to the recipients'descending aorta in the heart transplantation group.Two weeks after transplantation,heart weight,left ventricular weight,myocyte diameter and myocardial fibrosis were determined,and β adrenergics receptors mRNA expression was essayed by real-time polymerase chain reaction(PCR).Seven normal Lewis rats served as control.Results The weight of the enlarged heart,left ventricular weight and myocyte diameter of the failing hearts were decreased to normal after transplantation.The levels of β1-and β 2-adrenergic receptors mRNA expression were significantly lowered in heart failure group compared with that of normal group(0.09±0.03vs.0.18±0.04,0.07±0.06 vs.0.12±0.02,both P<0.05).The level of β2-adrenergic receptor mRNA expression in heart transplantation group(0.11±0.05)rose to normal(P>0.05),but β1-adrenergic receptor mRNA expression(0.08±0.06)was lower in heart transplantation group than that in normal group (P<0.05).Conclusion Myocardium reverse remodeling after left ventricular unloading is accompanied by the change in cardiomyocyte in molecular level,such as the change in β adrenergic receptors,which may involve in the improvement of heart function after being supported by left ventricular assist device.     

肌浆网钙转运ATP酶和受磷蛋白在大鼠心肌梗死后的表达变化

目的建立大鼠急性心肌梗死模型,观察心肌梗死后心室重塑过程中肌浆网钙转运ATP酶(Ca-2+ATPase,SERCA)和受磷蛋白(PLB)的表达变化。方法雄性SD大鼠,应用前降支动脉结扎法建立大鼠心肌梗死模型,术后4周观察血流动力学参数,SERCA mRNA和PLB mRNA的表达。结果大鼠心肌梗死后4周,心肌梗死组左心室舒张末压(LVEDP)显著大于假手术组,左心室内压最大上升和下降速率(±dp/dtmax)显著低于假手术组。心肌梗死组心肌组织中SERCA mRNA表达下调,PLB mRNA表达上调。结论大鼠心肌梗死4周后心室收缩和舒张功能已降低,进入了心力衰竭阶段,SERCA mRNA和PLB mRNA的表达变化与心力衰竭的发生发展相关,可能是心肌梗死后心肌收缩和舒张功能失调的重要机制。     

Cardiac adenoviral S100A1 gene delivery rescues failing myocardium

Cardiac-restricted overexpression of the Ca2+-binding protein S100A1 has been shown to lead to increased myocardial contractile performance in vitro and in vivo. Since decreased cardiac expression of S100A1 is a characteristic of heart failure, we tested the hypothesis that S100A1 gene transfer could restore contractile function of failing myocardium. Adenoviral S100A1 gene delivery normalized S100A1 protein expression in a postinfarction rat heart failure model and reversed contractile dysfunction of failing myocardium in vivo and in vitro. S100A1 gene transfer to failing cardiomyocytes restored diminished intracellular Ca2+ transients and sarcoplasmic reticulum (SR) Ca2+ load mechanistically due to increased SR Ca2+ uptake and reduced SR Ca2+ leak. Moreover, S100A1 gene transfer decreased elevated intracellular Na+ concentrations to levels detected in nonfailing cardiomyocytes, reversed reactivated fetal gene expression, and restored energy supply in failing cardiomyocytes. Intracoronary adenovirus-mediated S100A1 gene delivery in vivo to the postinfarcted failing rat heart normalized myocardial contractile function and Ca2+ handling, which provided support in a physiological context for results found in myocytes. Thus, the present study demonstrates that restoration of S100A1 protein levels in failing myocardium by gene transfer may be a novel therapeutic strategy for the treatment of heart failure.     

Changes in gene expression in the intact human heart. Downregulation of alpha-myosin heavy chain in hypertrophied, failing ventricular myocardium.

Using quantitative RT-PCR in RNA from right ventricular (RV) endomyocardial biopsies from intact nonfailing hearts, and subjects with moderate RV failure from primary pulmonary hypertension (PPH) or idiopathic dilated cardiomyopathy (IDC), we measured expression of genes involved in regulation of contractility or hypertrophy. Gene expression was also assessed in LV (left ventricular) and RV free wall and RV endomyocardium of hearts from end-stage IDC subjects undergoing heart transplantation or from nonfailing donors. In intact failing hearts, downregulation of beta1-receptor mRNA and protein, upregulation of atrial natriuretic peptide mRNA expression, and increased myocyte diameter indicated similar degrees of failure and hypertrophy in the IDC and PPH phenotypes. The only molecular phenotypic difference between PPH and IDC RVs was upregulation of beta2-receptor gene expression in PPH but not IDC. The major new findings were that (a) both nonfailing intact and explanted human ventricular myocardium expressed substantial amounts of alpha-myosin heavy chain mRNA (alpha-MHC, 23-34% of total), and (b) in heart failure alpha-MHC was downregulated (by 67-84%) and beta-MHC gene expression was upregulated. We conclude that at the mRNA level nonfailing human heart expresses substantial alpha-MHC. In myocardial failure this alteration in gene expression of MHC isoforms, if translated into protein expression, would decrease myosin ATPase enzyme velocity and slow speed of contraction.     

卡维地洛对充血性心力衰竭大鼠心肌间质基质金属蛋白酶-2表达的干预作用

目的:探讨大鼠充血性心力衰竭心肌间质基质金属蛋白酶-2的表达和心力衰竭的关系及卡维地洛干预对此的影响。方法:110只SD大鼠结扎冠状动脉左主干制备成充血性心力衰竭模型,随机分成心力衰竭对照组和卡维地洛治疗组。两组又随机分为2,4,8周亚组。另设假手术组。应用超声心动图评价大鼠心功能变化。用免疫组化方法检测MMP-2蛋白表达情况。结果:与假手术组相比,心力衰竭对照组基质金属蛋白酶-2的蛋白表达在各亚组明显升高(均P<0.05),而卡维地洛治疗组基质金属蛋白酶-2蛋白表达在4周和8周亚组明显降低(均P<0.05)。超声心动图结果显示大鼠左心室结构和功能呈现动态变化,心功能进行性降低。结论:大鼠心肌梗死后心肌间质内基质金属蛋白酶-2的表达增高,是心室重塑和心力衰竭发生发展的机制之一。卡维地洛可通过抑制基质金属蛋白酶-2的表达而改善心室重塑及心力衰竭。     

Expression of dihydropyridine receptor (Ca2+ channel) and calsequestrin genes in the myocardium of patients with end-stage heart failure.

Cytoplasmic free calcium ions (Ca2+) play a central role in excitation-contraction coupling of cardiac muscle. Abnormal Ca2+ handling has been implicated in systolic and diastolic dysfunction in patients with end-stage heart failure. The current study tests the hypothesis that expression of genes encoding proteins regulating myocardial Ca2+ homeostasis is altered in human heart failure. We analyzed RNA isolated from the left ventricular (LV) myocardium of 30 cardiac transplant recipients with end-stage heart failure (HF) and five organ donors (normal control), using cDNA probes specific for the cardiac dihydropyridine (DHP) receptor (the alpha 1 subunit of the DHP-sensitive Ca2+ channel) and cardiac calsequestrin of sarcoplasmic reticulum (SR). In addition, abundance of DHP binding sites was assessed by ligand binding techniques (n = 6 each for the patients and normal controls). There was no difference in the level of cardiac calsequestrin mRNA between the HF patients and normal controls. In contrast, the level of mRNA encoding the DHP receptor was decreased by 47% (P less than 0.001) in the LV myocardium from the patients with HF compared to the normal controls. The number of DHP binding sites was decreased by 35-48%. As reported previously, expression of the SR Ca(2+)-ATPase mRNA was also diminished by 50% (P less than 0.001) in the HF group. These data suggest that expression of the genes encoding the cardiac DHP receptor and SR Ca(2+)-ATPase is reduced in the LV myocardium from patients with HF. Altered expression of these genes may be related to abnormal Ca2+ handling in the failing myocardium, contributing to LV systolic and diastolic dysfunction in patients with end-stage heart failure.     

p38MAPK信号通路的变化在心力衰竭病人心肌重塑中的意义

目的：了解不同程度充血性心力衰竭（DHF）病人心肌细胞信号传导通路p38MAPK的变化与心肌重塑和心功能的关系。方法：通过手术取材，采用Western blotting技术测定31例瓣膜病所致CHF病人不同心功能组与5例正常人心肌细胞p38MAPK蛋白基础表达和激活情况。结果：瓣膜病所致心力衰竭病人心肌组织呈心肌重塑的病理改变。心衰组p38MAPK基础表达受抑，激活的磷酸化p38MAPK在轻度心衰者降低，重度心衰病人增高，结论：心衰病人心肌细胞存在MAPK信号传导通路的变化。中，重度心衰病人通过激活p38MAPK诱导心肌细胞凋亡，坏死效应，在心功能恶化中发挥重要病理作用。     

肝细胞生长因子对急性失代偿性心力衰竭模型小鼠的保护

背景:肝细胞生长因子是一种心肌营养因子,具有很强的抑制心肌细胞凋亡与心室重构,促血管内皮细胞有丝分裂作用.目的:观察肝细胞生长因子对急性失代偿性心力衰竭模型小鼠的保护作用.方法:将50只昆明小鼠随机分为5组:正常对照组、慢性心力衰竭组、急性失代偿性心力衰竭组、慢性心力衰竭治疗组、急性失代偿性心力衰竭治疗组.采用尾静脉注射阿霉素建立慢性心力衰竭小鼠模型,第7周尾静脉注射细菌脂多糖制作急性失代偿性心力衰竭模型,随后慢性心力衰竭治疗组、急性失代偿性心力衰竭治疗组同时给予尾静脉注射肝细胞生长因子干预.结果与结论:与慢性心力衰竭组比较,慢性心力衰竭治疗组心室壁厚度、左室射血分数值明显增加,白细胞介素6减少,脑钠肽下降,Bax蛋白表达减少,Bcl-2蛋白表达增加,心肌细胞凋亡明显减少(P < 0.01或0.05).与急性失代偿性心力衰竭组比较,急性失代偿性心力衰竭治疗组心室壁厚度、左室射血分数值明显增加,脑钠肽表达下调,白细胞介素6明显下降,Bcl-2蛋白表达增加,Bax蛋白表达减少(P < 0.01或0.05).说明肝细胞生长因子通过抗炎性因子作用,抗心肌细胞凋亡作用明显改善急性失代偿性心力衰竭小鼠的心脏功能.     

法舒地尔对急性心肌梗死大鼠血流动力学及相关蛋白表达的影响

[目的]探讨法舒地尔对急性心肌梗死（AMI）大鼠血流动力学及相关蛋白表达的影响.[方法]取雄性Wistar大鼠,结扎左前降支建立AMI 动物模型,术后24 h存活的大鼠随机分为AMI组、低分子肝素组和法舒地尔组.再随机选取10只大鼠作为假手术组,只在左前降支下穿线不结扎.低分子肝素组4 μL/kg腹腔注射;法舒地尔组给予法舒地尔5 mg/ kg 腹腔注射,2次/日;AMI组和假手术组给予等量生理盐水.4周后分别测血流动力学指标：左心室收缩压（LVSP）、左心室舒张末压（LVEDP）、左心室内压最大上升和下降速率（ ＋ dp/ dtmax、- dp/ dtmax）;western blot检测Caspase-3、Bax及Bcl-2表达的变化.[结果]AMI组大鼠血流动力学指标与假手术组相比,差异有显著性（P〈0.05）.与AMI组相比,低分子肝素组和法舒地尔组大鼠血流动力学指标改善,相关蛋白Bcl-2 表达增加,Caspase-3、Bax表达减少,差异均有显著性（P〈0.05）.[结论]Rho激酶参与了AMI后心肌细胞凋亡及心力衰竭的进展,法舒地尔通过抑制Rho激酶的表达减少细胞凋亡,保护缺血心肌,延缓心力衰竭进程.     

β3受体激动剂对心力衰竭大鼠β3-肾上腺素能受体基因表达及其对细胞凋亡的影响

目的　研究β3受体激动剂 (BRL 37344 )对异丙肾上腺素诱导的心力衰竭 (心衰 )大鼠β3肾上腺素能受体 (β3AR)基因表达水平的影响 ,探讨β3AR在心衰中的作用。方法　将 Wistar大鼠随机分为 : 组(正常对照组 10只 )、 组 (正常用药组 10只 )、 组 (心衰组 30只 )和 组 (心衰用药组 35只 )。 组和 组尾静脉注射 BRL 37344为 0 .4 nm ol· kg- 1 · min- 1 ,每周 2次 ,连续 6周 ; 组和 组尾静脉注射等量生理盐水。 6周后检查以下指标 :血流动力学变化 ;免疫组织化学和 Western Blot法测定 β3AR蛋白表达 ;逆转录聚合酶链反应 (RT PCR)方法测定 β3AR m RNA表达 ;原位缺口末端标记法 (TUNEL)检测心肌细胞凋亡。结果　1与 组比较 , 组、 组、 组左室收缩末压 (PES)、左室压力最大上升速率 (dp/ dtm ax)和左室压力最大下降速率 (dp/ dtmin)逐渐减小 ,左室舒张末压 (PED)和左室等容舒张时间常数 (Tc)逐渐增加。 组与 组比较仅 PED出现统计学差异 (P<0 .0 5 ) ,其余各组间两两比较均有差异 (P<0 .0 1或 P<0 .0 5 ) ;2β3AR蛋白及其 m RNA表达 、 组较 、 组明显增高 , 、 组间比较无显著性差异 ; 组较 组升高更明显。 3 、 组较 、 组心肌细胞凋亡数明显增加 (P均 <0 .0 1) , 、 组间比较无显著性差异     

Effects of cilostazol on thrombospondin-1 (TSP-1) expression changes in the myocardium of diabetic rats

Myocardial protective effects of the phosphodiesterase 3 inhibitor, cilostazol, in streptozotocin-induced diabetic rats were investigated. Four weeks after induction of diabetes, we measured thrombospondin-1 (TSP-1) expression in the left ventricular myocardium. Microstructural and ultrastructural changes were also analysed. Four weeks after the induction of diabetes there were significant differences in body weight and blood glucose between the control, diabetic and cilostazol-treated diabetic animals. TSP-1 expression was significantly increased in the myocardium of diabetic rats compared with the control group. Although significantly higher than the control group, TSP-1 expression was significantly lower in the cilostazol group compared with the diabetes group. There were obvious ultrastructural changes in the myocardium of diabetic rats, which were rarely seen in cilostazol-treated diabetic rats. In conclusion, this study provides experimental evidence that cilostazol treatment of diabetic rats effectively prevents pathological myocardial alterations, possibly via the down-regulation of TSP-1 expression.     

常量卡维地洛对急性心肌梗死近期左心室功能的影响

目的　用超声心动图评价常量卡维地洛对急性心肌梗死后近期左心室功能的影响。方法　 74例急性心肌梗死患者 ,在用药前、用药 6个月后进行超声心动图检查。用修改的Simpson法经心尖四腔和二腔切面测定左心室收缩末容量、舒张末期容量和左室射血分数。结果　卡维地洛组心率比安慰剂组减慢 ,而安慰剂组左心室舒张末期容量和收缩末期容量增加 ,卡维地洛组容量减少。卡维地洛组左心室舒张末期容量指数比安慰剂组显著减少 (t =2 .470 ,P <0 .0 5 ) ;左心室收缩末期容量指数明显减少 (t =2 .6 86 ,P <0 .0 1) ,左心室射血分数增加 (t =2 .5 45 ,P<0 .0 5 )。结论　常量卡维地洛治疗急性心肌梗死 6个月 ,减少左心室容量 ,增加LVEF。     

组织工程化心肌片层移植心肌梗死大鼠的心功能及电生理变化

背景：组织工程化心肌组织在组成结构上类似于心脏组织的三维电偶联网络和肌肉横纹,组织样收缩功能,为病损心肌提供了修复的可能性。目的：观察心肌细胞,胶原复合体移植后心肌梗死大鼠心室肌的心功能及电生理变化。方法：将成年SD大鼠分为假手术组、模型组、移植组,后2组制作心肌梗死动物模型,胸,不结扎冠状动脉。移植组移植心肌细胞与胶原材料复合组织,其他2组不进行移植。而且具有心肌假手术组仅开结果与结论：①左室心功能：与假手术组相比,模型组左室舒张末期内径、左室收缩末期内径均显著增大（P〈0．01）,左室射血分数和左室短轴缩短率显著降低（P〈0．01）;移植组左室舒张末期内径、左室收缩末期内径、左室射血分数和左室短轴缩短率均未见明显增大或降低（P〉0．01）。②左室有效不应期变化：与假手术组相比,模型组梗死周边区有效不应期显著缩短（P〈0．01）;移植组梗死周边区有效不应期较模型组延长,差异有显著性意义（P〈0．01）。③Cx43免疫荧光结果：假手术组、模型组和移植组大鼠缝隙连接蛋白43阳性表达依次呈现阳性,弱阳性,弱阳性。但移植组缝隙连接蛋白43阳性表达高于模型组。结果可见移植的心肌细胞／胶原复合体在组织和结构上形成电偶联网络和收缩偶联,能改善心肌梗死大鼠心室肌的收缩功能及电生理特性。     

Effects of carbon dioxide and pH on myocardial function in dogs with acute left ventricular failure

The present study was undertaken to examine the effects of changes in PaCO2 and pHa on myocardial blood flow and central hemodynamics during acute ischemic left ventricular failure. Six closed-chest dogs anesthetized with pentobarbital were hyperventilated, and CO2 was added to the inspiratory gas to induce: a) normocapnia, b) hypocapnia, c) hypercapnia, and d) hypercapnia with sodium carbonate given to correct pH. Embolization of the left coronary artery with 50-microns microspheres resulted in deterioration of left ventricular function, as indicated by increased left ventricular end-diastolic pressure and mean pulmonary arterial pressure, while cardiac output decreased. During hypocapnia with left ventricular failure, the central hemodynamics remained unchanged, while a minor but nonsignificant decrease in myocardial blood flow was observed. Hypercapnia aggravated the heart failure, as indicated by increased left ventricular end-diastolic pressure, mean right atrial pressure, and mean pulmonary arterial pressure; however, the pump function of the heart was unchanged, as demonstrated by the unaltered cardiac output, heart rate, and mean aortic blood pressure. The changes in the central hemodynamics were reversed when pH was normalized during hypercapnia. Thus, in the present study pH, and not PaCO2, was responsible for the hemodynamic deterioration observed during hypercapnia in the failing heart.     

Myocardial stunning and hibernation in clinical practice

Myocardial stunning and hibernation are both clinically important causes of myocardial dysfunction and are caused by episodes of myocardial ischaemia. Stunning tends to occur acutely and may produce transient but clinically important reductions in left ventricular function in the setting of myocardial infarction, post coronary artery bypass grafting and even following episodes of effort induced angina. Hibernation refers to a chronic down-regulation of myocardial function in response to chronic myocardial ischaemia. Hibernating myocardium may be present in up to 50% of patients with significantly impaired left ventricular function and evidence of heart failure. Importantly, both these entities can be either prevented or ameliorated by preventing or lessening ischaemic burden. There is also evidence that there may be an overlap between these two entities and that hibernating myocardium may result from repeated episodes of myocardial ischaemia causing chronic stunning.     

Myocardial calcification as a rare cause of congestive heart failure: a case report

Myocardial calcification is a manifestation of either metastatic or dystrophic calcium deposition in the myocardium. Dystrophic calcification of the myocardium is most commonly seen in long-term survivors of substantial myocardial infarctions. Current literature has reported only 3 cases of myocardial calcification with normal coronary arteries. We present a case of an 80-year-old woman with multiple admissions over a 5-year period for congestive heart failure. She was found to have a normal left ventricular ejection fraction and normal coronary arteries on left heart catheterization. A high resolution computed tomography (CT) study of the chest revealed extensive left ventricular myocardial calcifications, which were not present 4 years earlier on CT. The patient's history and clinical presentation revealed no etiologic factors for her calcified myocardium.     

双核素心肌显像对老年冠心病CTO病变PCI术的指导意义

目的评价99 Tcm-甲氧基异丁基异腈（99 Tcm-sestamibi,99 Tcm-MIBI）/18F脱氧葡萄糖（18F-fluorodeoxy glu-cose,18F-FDG）双核素心肌灌注/代谢显像技术（DISA）检测冠状动脉完全闭塞导致心力衰竭型冠状动脉粥样硬化性心脏病老年患者存活心肌对经皮冠状动脉支架术（Percutaneous coronary intervention,PCI）后心功能的改善情况。方法 41例经冠状动脉造影证实至少1支以上冠脉闭塞导致心力衰竭型冠心病的老年患者,PCI术前1周行99 Tcm-MI-BI/18F-FDG双核素心肌灌注/代谢显像检查,根据DISA结果,分为有心肌存活组和无心肌存活组。分别比较PCI术前后2组患者血浆BNP值及左室射血分数（LVEF）等心功能指标。结果有心肌存活组经PCI术后LVEF由41.12±5.97升至47.12±4.86,LVFS由16.79±5.64升至25.86±7.43,血NT-proBNP值由4287.25±401.56ng/L降至427.43±91.47ng/L;术前与术后比较,有显著统计学意义;无心肌存活组经PCI术后LVEF由40.03±3.48升至41.31±3.56,LVFS由16.35±5.86升至18.75±3.51,血NT-proBNP值由4495.32±347.72ng/L降至3827.53±97.28ng/L,术前与术后比较,无统计学意义。结论双核素心肌显像能有效检测冠状动脉完全闭塞致心力衰竭型冠心病老年患者存活心肌,而有存活心肌者PCI术后心功能得到明显改善。故双核素心肌显像对老年冠心病CTO病变行PCI术有指导意义。