心肌纤维化的机制及干预治疗

心肌纤维化可发生于包括缺血性心肌病、扩张性心肌病和高血压性心脏病等在内的众多心血管疾病。可使心脏僵硬度增加、心肌舒张以及收缩功能下降,引起心肌电生理紊乱和心律失常。由于心肌纤维化存在上述病理损害,因而其重要性备受临床医师关注,预防和逆转心肌纤维化已成为众多心     

缺血性心脏病患者QT间期离散度的临床探讨

近年来以QT期离散度（QTd）应用于QT间期延长综合征、缺血性心脏病、心功能不全、心肌肥厚以及评价心律失常药物的疗效等方面受到国内外学者的关注。我们对52例缺血性心脏病并心衰患者的op进行测定，并与18例健康人进行比较，分析缺血性心脏病患者的QTd与室性心律失常、摔死和心功能的关系。1临床资料1.1病倒选择全部病例均系住院治疗的缺血性心脏病并心衰患者，且排除电解质紊乱、急性心肌梗塞及使用影响心肌复极的抗心律失常药和先天性QT间期延长综合征等，其中男性31例，女性对例，年龄场一月岁，平均54．6岁；健康对照组男性12例，…     

骨髓干细胞移植治疗缺血性心脏病的护理

缺血性心脏病因心肌供氧和需氧之间不平衡而导致心肌细胞减少、坏死、凋亡,心肌纤维化和心肌瘢痕形成,是影响心脏功能的主要因素,也是导致顽固性心力衰竭乃至死亡的病理基础。目前常规治疗包括药物治疗、介入治疗和手术治疗。上述治疗均不能逆转已坏死的心肌,而心脏移植因其存在供体难求和免疫排斥反应而难以在临床推广。国内外许多动物实验已经证实,骨髓干细胞可以在梗死区促进心肌细胞生成和血管形成,并可使持久性的心功能改善[1]。自体骨髓干细胞移植不存在免疫排斥和伦理问题,可以明显缩小心肌梗死面积,改善心功能[2]。我院心内科在2003…     

缺血性心脏病患者左室舒张功能的临床观察

目的 :探讨缺血性心脏病患者左室舒张功能的变化及其临床意义。方法 :采用彩色多普勒超声诊断仪测定Ve、Va和Ve/Va比值作为左室舒张功能参数 ,测定EF、FS作为左室收缩功能参数。结果 :缺血性心脏病组Ve、Va和Ve/Va比值与对照组相比 ,有显著差异 ;按心功能分级不同 ,上述指标也有差异。结论 :缺血性心脏病患者存在左室舒张功能障碍 ,且早于左室收缩功能障碍 ,左室舒张功能障碍可能是其早期心功能不全的主要原因 ,在治疗上应引起重视     

硬膜外阻滞对缺血性心脏病患者心肌的影响

随着人口老年化,全身性退变及重要器官贮备功能明显降低,缺血性心脏病患者增多。缺血性心脏病是由于冠脉循环改变引起冠脉血流和心肌需求之间不平衡而导致的心肌损害。了解硬膜外阻滞对缺血性心脏病患者的影响,对保证病人安全至关重要。     

冠心病用β受体阻滞剂的注意事项

1　缺血性心脏病合并慢性心功能不全时应禁用β受体阻滞剂鉴于β受体阻滞剂的负性肌力作用,在慢性充血性心衰时应用β受体阻滞剂被认为可加重其心功能不全。事实上对于这种病人在应用血管紧张素转换酶抑制剂、利尿剂及小剂量强心剂基础上,谨慎地小剂量应用β受体阻滞剂是有益处的。其原因为缺血性心脏病合并慢性心功能不全时,由于长期心脏负荷加重及心肌供血不足可使自主神经系统功能发生变化,首先通过压力感受器等反射作用使交感神经兴奋性增强,其次激活了肾素—血管紧张素—醛固酮系统,也使交感神经兴奋性增强,从而使心率增快,心肌收缩力…     

米力农注射液治疗慢性肺源性心脏病心功能不全80例临床分析

慢性肺源性心脏病多发生于老年人,是由肺组织、血管及胸廓的慢性病变引起肺血管阻力增加、肺动脉压力增高,最终导致右心室扩大、心肌肥厚,甚至伴有右心功能不全的心脏病[1]。由于病程中存在慢性缺氧及反复肺感染,引起心功能不可逆性改变,同时,因长期缺氧使心肌变性,在使用过程中易引起洋地黄中毒,加之洋地黄的正性肌力作用使心肌耗氧增加,加重了心肌缺氧,因此,使用洋地黄类     

心脏疾病与心肌细胞凋亡研究进展

近年 ,在种种心脏病的病因和进展中 ,相继报道了细胞凋亡参与心脏疾病的可能性。其中 ,在缺血性心脏病之心肌缺血及再灌注、心功能不全、心律失常中的报道较多。心脏疾病中的细胞凋亡 ,特别是在缺血再灌注过程中的细胞凋亡 ,可加重心肌损伤。因此 ,认识心血管疾病过程中的细胞凋亡有重大意义。1　缺血性心脏病和细胞凋亡1.1　急性心肌梗死时心肌的细胞凋亡　Ｋａｊｓｔｕｒａ等[1] 在不伴有再灌注损伤的兔心肌梗死模型中发现 ,在大量的梗死细胞中可见ＤＮＡ的片断化 ,提示细胞凋亡在梗死灶中占有相当的比重 ,推测细胞凋亡是缺血性心肌损伤的…     

骨髓干细胞移植治疗缺血性心脏病的研究进展

缺血性心脏病指冠状动脉狭窄造成的心肌供氧和需氧之间不平衡而导致的心肌缺血症状，治疗方法主要包括药物治疗、介入治疗及手术治疗，它们能够改善心肌缺血症状。但是对于急慢性心肌梗死患者，上述治疗方法无法逆转已坏死的心肌，因而不能有效改善心脏功能，表现为患者反复发生心力衰竭。其病理生理机制是心肌细胞减少，坏死，凋亡，心肌纤维化和心肌瘢痕形成。如何促进缺血坏死区心肌细胞再生，防止心室重构，已成为缺血性心脏病治疗的关键。近年来，随着分子生物学和细胞生物工程技术的发展以及骨髓干细胞（marrowstemcell，MSC）研究的深入，人们试图通过移植技术将MSC移入受损的心肌组织中并使其增殖再生，以替代坏死心肌，改善心脏功能。本文对骨髓干细胞移植治疗缺血性心脏病的进展作一综述。     

心血管疾病系列问答(11) 缺血性心脏病(冠心病)(上)

问:什么叫做缺血性心脏病? 答:根据1979年国际心脏病学会及协会及世界卫生组织(WHO)临床命名标准化联合专题组的提议,所谓缺血性心脏病是指由于冠状循环改变引起冠状血流和心肌需求之间不平衡而导致的心肌损害。缺血性心脏病包括急性暂时性的和慢性的情况,可由于功能     

The effects of trimetazidine on left ventricular function and physical exercise tolerance in patients with ischemic cardiomyopathy

Trimetazidine is a new metabolic antiischemic agent, which increases the tolerance of cardiomyocytes to ischemia. The aim of the study was to evaluate the effect of additional trimatazidine therapy in patients with ischemic cardiomyopathy (ICMP) in comparison with standard therapy of cardiac insufficiency. According to the results of the study, trimetazidine improves the clinical status, functional class of cardiac insufficiency, left ventricular ejection fraction, in ICMP patients. Trimetazidine increases physical exercise tolerance according to the results of six-minute walking test. Thus, the optimization of myocardial energetic metabolism may be a promising perspective in the treatment of coronary heart disease with systolic dysfunction.     

Signal transduction in heart failure

Heart failure is the final culmination of protracted disease status precipitated by underlying ischemic disease, valvular insufficiency and viral myocarditis. The factors that lead to the development of heart failure are still not fully understood. In mammalian cells, four parallel kinase cascades have been described that finally lead to the activation of members of the mitogen-activated protein kinase(MAPK) family, such as ERKs (p42 and p44), JNK and p38 protein kinase. Apoptosis signal-regulating kinase 1 (ASK1), an upstream activator of JNK and p38, was shown to promote heart dysfunction and dilation as well as cardiac fibrosis. Meanwhile, not only myocyte apoptosis but also myocardial interstitial changes such as extracellular matrix deposition, activation of fibroblasts, and narrowing of vessel lumens play important roles for the progression of heart failure.     

Pathology of sudden cardiac death

Sudden unexpected cardiac death generally occurs in persons with previously unrecognized heart disease. It has become evident that it occurs often enough in patients without any identifiable structural abnormality. Although mechanical cardiac function may seem normal, such patients might have certain discrete anatomic abnormalities, such as myocarditis, focal myocardial fibrosis, hypertrophy of Purkinje-like myocytes, and myocardial disarray. The pathophysiology in patients with acute myocardial infarction (atherothrombosis of the coronary arteries) was discussed.     

Captopril in the treatment of mild cardiac insufficiency in combination with arterial hypertension

The results of clinicoinstrumental investigations in 33 patients with coronary heart disease and coronary heart disease combined with essential hypertension complicated by stage I-II cardiac insufficiency showed that therapy with captopril at a daily dose of 25-75 mg resulted in the correction of cardiac insufficiency in 84% of the patients, with a hypotensive effect in 80%. Captopril improved myocardial contractility, decreased pressure in the pulmonary artery and total peripheral vascular resistance and produced no major side-effects.     

Use of biologically active food additive cardiohels in the treatment of patients with ischemic heart disease

Biologically active food additive (Inrich production) cardiohels was added to the diet of ischemic heart disease patients with hypertension and chronic heart failure stage IIB receiving basic medication with hypotensive, coronarolytic drugs and cardiac glycosides. As shown by control 24-h blood pressure and ECG monitoring, echocardiography, cardiohels has a mild hypotensive effect, improves coronary circulation and microcirculation, myocardial contractility. Mechanism of these positive effects are discussed. Cardiohels is recommended for patients with ischemic heart disease as it allows to reduce the dose of hypotensive and coronarolytic drugs by 35% and cardiac glycosides by 25%, thus lowering the risk of relevand side effects.     

The diagnosis of coronary failure in patients with aortic and mitral valve defects]

The incidence of angina pectoris was investigated and the treadmill test was carried out to assess the presence of myocardial ischemia and heart pump function in 238 patients suffering from mitral and aortal heart disease. Comparison with the coronarography readings has demonstrated that the diagnostic value of the painful syndrome in the health status and anamnesis does not exceed 24%. The appearance of an angina pectoris attack in combination with ischemic alterations on the ECG raised the diagnostic value up to 50%. The authors have distinguished a symptom-complex including the development of angina pectoris, appearance of the ischemic signs on the ECG with the integrity of heart pump function, increasing the diagnostic value of the test up to 83-100%. The integrity or insufficiency of heart pump function were shown to allow differentiation between atherosclerotic and relative coronary insufficiency. The conclusion is drawn about the necessity of carrying out the treadmill test according to the program in patients suffering from heart disease with suspected coronary insufficiency.     

心脏磁共振细胞外容积在高血压性心脏病中的应用

血压长期增高会引起心脏后负荷增加,导致高血压性心脏病。高血压性心脏病的主要改变是左心室肥厚及弥漫性心肌纤维化。通过心脏磁共振T1 mapping测量的细胞外容积作为无创性评估心肌纤维化的手段,在高血压性心脏病的诊断中发挥了重要的作用。作者就高血压性心脏病心肌纤维化的病理生理、高血压性心脏病细胞外容积的特点,治疗后细胞外容积的变化及细胞外容积与心脏磁共振其他技术的在高血压性心脏病中的联合应用进行综述。     

Usefulness of Cardiac Magnetic Resonance in Early Assessment of Cardiomyopathies: Myocardial Fibrosis Is a Common Denominator

Myocardial fibrosis is a common denominator in a wide spectrum of cardiomyopathies; it plays a major role in the pathophysiology of structural remodelling and as a predictor of adverse outcome. Quantification of myocardial fibrosis by invasive biopsy is limited in clinical practice due to the commonly scattered tissue distribution and procedural risks. Late gadolinium enhancement by cardiac magnetic resonance has revolutionized the assessment of ischemic cardiomyopathy by visualization of regional scarring after myocardial infarction. The binary (white-black) principle of contrast development and a requirement for well separated layers of healthy and diseased myocardium is straightforward for clinical decision making in ischemic heart disease, but renders this technique less powerful in conditions where the myocardium is affected diffusely. Recently emerged T1 mapping techniques allow for an individualized quantification of global and regional myocardial signal and are promising tools to separate between healthy and diseased. In this article we review the emerging evidence for T1 mapping techniques and outline the necessary future directions for a successful translational pathway.     

Assessment of myocardial fibrosis by endoventricular electromechanical mapping in experimental nonischemic cardiomyopathy

Cardiac fibrosis plays an important prognostic role in nonischemic cardiomyopathy (NICM), making it a potential therapeutic target. Although electromechanical mapping has been used to identify myocardial scar and facilitate intramyocardial intervention in the setting of ischemic heart disease, its application has not been described in NICM. We assessed the detection of myocardial fibrosis by endoventricular electromechanical mapping in an experimental model of NICM. The NOGA^® XP system was used to perform left ventricular mapping in twelve sheep that had undergone intracoronary doxorubicin dosing to induce NICM and in six healthy control animals. Results for endocardial voltage and mechanical shortening were evaluated against myocardial fibrosis burden, as determined by delayed-enhancement cardiac magnetic resonance and quantitative histomorphometry. Doxorubicin treatment resulted in dilated cardiomyopathy with moderate-severe impairment of left ventricular ejection fraction. Late gadolinium uptake was present in 9/12 doxorubicin animals, while histological fibrosis was approximately doubled compared to controls and was distributed multisegmentally throughout the left ventricle. Cardiomyopathy was associated with widespread reductions in unipolar and bipolar voltage amplitude and endocardial shortening. Each parameter showed an inverse relationship with the burden of fibrosis. Moreover, unipolar voltage and linear local shortening ratio displayed moderate accuracy for identifying myocardial segments with delayed contrast enhancement or increased fibrosis content, with optimal discriminatory thresholds of 7.5 mV and 11.5%, respectively. In this model of NICM, electromechanical mapping shows potential for delineating segmental differences in fibrosis. Pending clinical evaluation, it may therefore have applicability for directing targeted intramyocardial interventions in nonischemic heart disease.     

老年冠心病367例临床分析

目的探讨老年冠心病的临床特点.方法对2001年1月～2004年12月收治的367例老年冠心病住院患者的临床资料进行回顾性分析.结果 367例患者的临床表现为,无明显症状42例、单纯心绞痛92例、单纯心肌梗死56例、单纯心律失常66例、心绞痛或心肌梗死合并心律失常74例、心绞痛或心肌梗死合并心功能不全37例.79例有心肌梗死的病例中,47例表现为Q波心肌梗死;32例表现为非Q波心肌梗死;140例有心律失常的病例中,部分病例有多种心律失常表现,其中房颤51例、室性期前收缩37例、房性期前收缩34例、室内传导阻滞27例、房室传导阻滞12例、病窦综合征8例.结论老年冠心病具有无症状型冠心病多、心绞痛症状不典型者多、心律失常检出率高、易合并心功能不全、多种类型的冠心病合并出现者多、非Q波型心肌梗死发生率高等临床特点.