肥厚性梗阻型心肌病60例心电图分析

1996年以来 ,我院共收治肥厚性梗阻型心肌病患者 6 0例。现将其心电图表现分析报告如下。资料与方法 :本组男 4 2例 ,女 18例 ;年龄 (40± 12 )岁。入选标准 :1有明显的临床症状。2二维超声心动图示左室流出道 <10 mm,舒张末期室间隔厚度≥ 15 mm,室间隔 /左室后壁≥ 1.3。全部病例均于常规记录 12导联心电图检查前 3天停用血管活性药物。结果 :本组合并心电图异常改变 5 8例 ,其表现为 :1ST-T改变最常见 (30例 ) ,T波深度倒置 >1m V (最深达2 .5 m V) ,其中 、av F、V4 - V6 倒置 15例 , 、 、av F导联倒置 5例 , 、 、av F、V4 - V…     

72例肥厚性梗阻型心肌病心电图分析

目的　探讨肥厚性梗阻型心肌病与心电图异常的关系。方法　对 72例肥厚性梗阻型心肌病患者心电图资料进行分析。结果　本组合并心电图异常改变 6 9例 (95 8% ) ;伴ST段压低 4 4例(6 1 1% ) ,T波异常倒置 36例 (5 0 % ) ;左室大和高电压 30例 (41 7% ) ;心电轴左偏 2 7例 (37 5 % ) ;异常Q波 2 1例 (2 9 2 % ) ;P波时限增宽 18例 (2 5 2 % ) ;右侧胸前导联r波递增序列异常 18例 (2 5 % ) ;合并心房纤颤 4例 (5 5 % ) ;QRS时限 >0 12秒 ,伴束支阻滞或室内阻滞 2例 (2 7% ) ;心电图正常 3例。结论　肥厚性梗阻型心肌病与心电图异常具有相关性     

肥厚性梗阻型心肌病化学消融术早期心电图变化

目的:探讨肥厚性梗阻型心肌病导管化学消融术(PTSMA)治疗早期的心电图变化。方法:3例肥厚性梗阻型心肌病人均经超声心动图,左室造影,左室一左室流出道测压确诊,在心电图(ECG)、血压监测下,先做冠脉造影,后行PTSMA术,用无水酒精消融第一或第二间隔支,术后第1周连续心电监护并每日记录心电图,观察其演变情况,术后2周和4周复查ECG。结果:3例患者均出现剧烈胸痛,术后几分钟有2例出现一过性的Ⅲ度房室传导阻滞(Ⅲ°AVB),2例于术后30分钟发生尖端扭转性室速伴阿-斯综合症发作,经心脏电复律后转复。心电图表现为下壁Q波心梗1例,前间壁非Q波心梗2例,3例均有室性早搏,另见右束支传导阻滞(RBBB)1例。结论:肥厚性梗阻型心肌病化学消融术后早期心电图多表现心肌梗死,常见而严重的表现是Ⅲ°AVB和室速。束支阻滞和室性早搏也很常见,但多为一过性的。     

起搏器治疗肥厚梗阻型心肌病

历史回顾虽然用起搏器治疗肥厚梗阻型心肌病被认为是一种新的治疗方法，但早在本世纪６０年代末期，一些最初的报告已提示了双腔起搏的血流动力学好处。Ｈａｓｓｅｎｓｔｅｉｎ和Ｗｏｌｔｅｒ［１］在１９６７年的一份病例报告中，首先认识到心室起搏能降低左室流出道的压...     

化学消融治疗肥厚性梗阻型心肌病2例

1临床资料病例1:男性,55岁,于半年前开始出现乏力,近20余日出现活动后胸闷,无心慌、黑蒙、晕厥,心脏彩超发现肥厚梗阻性心肌病(室间隔上段)。入院查体:血压106/86mmHg(1mmHg=0.133kPa),颈静脉无怒张,双肺呼吸音清,心前区无隆起,心尖部闻及Ⅳ级收缩期杂音,胸骨左缘3、4肋间可闻及Ⅱ～Ⅲ级收缩期杂音,较粗糙,腹软,肝脾未触及,双下肢无浮肿。实验室检查:血尿便常规、血生化、肝功等无异常,血沉29mm/h;心电图示窦性心律,V3～V6病理性Q波,V3～V5T波改变;胸片未见异常;心脏超声示心脏各房室大小正常,室间隔上段增厚,厚约1.46cm,下段变薄,室间…     

化学消融治疗一例肥厚性梗阻型心肌病的护理

经皮间隔心肌消融术 (ＰＴＳＭＡ)是通过介入方法 ,用无水乙醇消融梗阻肥厚的室间隔心肌相关动脉 ,造成室间隔心肌局限的治疗性心肌梗死 ,使室间隔变薄 ,收缩功能降低 ,左室流出道 (ＬＶＯＴ)扩大 ,降低或消除左室流出道压力阶差(ＬＶＯＴＧ)改善临床症状[1 ] 的非外科治疗方法。 1995年 ,Ｓｉｇ ｗａｒｔ将其应用于肥厚梗阻型心肌病 (ＨＯＣＭ)的治疗并获得成功 ,此后 ,其它学者的研究进一步证实了这一疗法的安全性及有效性[2 ] ,国内也有类似报道 ,我院 2 0 0 0年 11月 14日成功地为一例肥厚性梗阻型心肌病病人施行了室间隔化学消融术 ,并…     

肥厚梗阻型心肌病的起搏治疗

对药物治疗抵抗的肥厚梗阻型心肌病患者,起搏治疗日益受到重视。本文就肥厚梗阻型心肌病的病理基础,起搏治疗的机 制及对预后的影响作一简要综述。     

肥厚梗阻型心肌病的心脏起搏治疗

心脏起搏治疗肥厚梗阻型心肌病是目前最新的一种方法，本文综述有关治疗效果，机理，适应症和进展等有关问题。     

Mitral valve endocarditis in hypertrophic cardiomyopathy: case report and literature review

Mitral endocarditis complicating hypertrophic cardiomyopathy occurs predominantly on the left ventricular aspect of the anterior mitral valve leaflet in the presence of outflow tract obstruction. It is a rare condition and the estimated cumulative 10 year probability of developing endocarditis in patients with obstruction is < 5%. Combined mitral valve replacement and septal myectomy has been reported in this setting. A case of community acquired Staphylococcus aureus mitral valve endocarditis is reported in a previously asymptomatic young man with hypertrophic obstructive cardiomyopathy. The potential treatment options are discussed.     

Mavacamten,a novel revolutionizing therapy in hypertrophic obstructive cardiomyopathy: A literature review

Hypertrophic cardiomyopathy (HCM) is one of the most common inherited cardiac diseases, defined as a left ventricular wall thickness of ≥15 mm, in the absence of other causes of abnormal ventricular loading. A major hallmark of this disease is the presence of left ventricular outflow tract obstruction, which develops in up to three quarters of patients, referred to as obstructive hypertrophic cardiomyopathy. Current treatment is offered to symptomatic patients, based on the presence of documented left ventricular obstruction, aimed at reducing symptoms and disease progression. This is achieved through pharmacological empirical therapy, surgery, alcohol ablation and/or pacing. Mavacamten is a first-in-class allosteric inhibitor of cardiac myosin that promises to provide clinicians with targeted therapy for these patients. The aim of this review is to provide a general overview of the modern approach to the diagnosis and management of HCM, as well as to integrate all the current knowledge on mavacamten, in anticipation of a future change in the treatment algorithm of patients with HCM.     

The case for surgery in obstructive hypertrophic cardiomyopathy

Relief of left ventricular (LV) outflow obstruction in patients with hypertrophic cardiomyopathy (HCM) and disabling symptoms refractory to maximum medical management has historically been a surgical problem. Surgical septal myectomy permanently abolishes systolic anterior motion of the mitral valve and mitral regurgitation, while normalizing LV pressures and wall stress. Also, these salutary goals are achieved without encumbering patients with post-procedural devices (e.g., pacemakers or defibrillators) or creating potentially arrhythmogenic substrates, as may occur with alcohol septal ablation. Procedural morbidity and mortality risk with myectomy is similar to, and in some institutions less than those for alcohol septal ablation. Over four decades, reports from numerous centers worldwide have consistently and unequivocably documented the benefits of surgery on hemodynamic and functional state, restoring normal and acceptable quality of life to patients of all ages by largely reversing the complications of heart failure. Long-term survival after myectomy is similar to that of the general population and superior to non-operated patients with obstruction. The LV outflow tract morphology in HCM is heterogeneous and not uncommonly includes congenital anomalies of the mitral valve apparatus for which the surgeon has the flexibility to adapt the repair, often employing an extended myectomy. In the current atmosphere of increasing and perhaps excessive enthusiasm for newer catheter-based interventions, it is a critical time to promote and re-emphasize that surgery is the time-honored (and presently the most effective) treatment strategy for relieving heart failure-related disability resulting from dynamic LV outflow obstruction in HCM, and is the primary treatment option for this subgroup of severely symptomatic drug-refractory patients.     

Right ventricular involvement in hypertrophic cardiomyopathy: a case report and literature review

Although hypertrophic cardiomyopathy (HCM) is classically considered a disease of the left ventricle, right ventricular (RV) abnormalities have also been reported. However, involvement of the right ventricle in HCM has not been extensively characterized. The literature regarding prevalence, genetics, patterns of involvement, histologic findings, symptoms, diagnosis, and treatment of RV abnormalities in HCM is reviewed. To highlight the salient points, a case is presented of apical HCM with significant RV involvement, with an RV outflow tract gradient and near obliteration of the RV cavity, in the absence of a left intraventricular gradient. Right ventricular involvement in HCM appears to be as heterogeneous as that of the left ventricle. The spectrum extends from mild concentric hypertrophy to more unusual severe, obstructive disease. While in some cases the extent of RV involvement correlates with left ventricular (LV) involvement, predominant RV disease can be seen as well. While the genetics of RV involvement have not been well characterized, histologic findings appear to be similar to those in the left ventricle, suggesting similar pathogenesis. Significant RV involvement may result in RV outflow obstruction and/or reduced RV diastolic filling, with potentially increased incidence of severe dyspnea, supraventricular arrhythmias, and pulmonary thromboembolism. The optimal treatment for patients with significant RV disease is unknown. Medical and surgical therapies have been attempted with variable success; experience with newer techniques such as percutaneous catheter ablation has not been reported. Further characterization of RV involvement in HCM is necessary to elucidate more clearly the clinical features and optimal treatments of this manifestation of HCM.     

Evolution of dilated cardiomyopathy from hypertrophic obstructive cardiomyopathy: a case report

A 20-year-old woman whose echocardiograms showed a rare evolution from hypertrophic to dilated cardiomyopathy during a nine year observation period is described. This patient was initially diagnosed as having hypertrophic obstructive cardiomyopathy (HOCM) at the age of 12 years. Her echocardiogram showed marked thickening of the interventricular septum (IVS) and left ventricular posterior wall (LVPW), asymmetric septal hypertrophy (ASH) and systolic anterior motion of the mitral valve (SAM). Chest radiography revealed a prominent left ventricular border and a cardiothoracic ratio of 0.52. At 18 years of age she experienced onset of palpitation during the 16th week of pregnancy. Her echocardiogram recorded in June 1980 revealed a thickened IVS and LVPW with resolution of the SAM and of the narrow cavity. At 20 years of age she became pregnant again and was admitted to our hospital for the third time at 24 weeks gestation. On admission her blood pressure was 122/60 and her pulse was 56, and moist rales were audible over both lung fields. Peripheral edema was noted. Chest radiography revealed moderate cardiomegaly, a cardiothoracic ratio of 0.66, and congestion of the pulmonary vasculature. An echocardiogram showed thinning of the IVS and LVPW with hypokinesis and dilatation of the cavity compatible with dilated cardiomyopathy (DCM). She delivered a boy on July 15th 1982 at 32 weeks gestation following which she developed marked congestive heart failure. She expired one month later. A chest radiograph made one day before death revealed marked cardiomegaly, a cardiothoracic ratio of 0.76, prominent pulmonary vasculature and a pleural effusion. Autopsy was refused; therefore the terminal DCM-like features were not clarified pathologically. However, the slow progression from HOCM to HCM during eight years and then rapid progression from HCM to DCM during four months was most impressive.     

Multiple lentiginosis and hypertrophic obstructive cardiomyopathy

Two patients with Multiple Lentiginosis (ML) had hypertrophic cardiomyopathy with severe obstruction of the right and left ventricular outflow tracts. ML is a rare syndrome in which there is a typical skin pigmentation disorder together with various other abnormalities like slight mental retardation, sensorineural deafness, genital and skeletal anomalies and sometimes a characteristic facies. Obstruction of the right ventricular outflow tract is frequent in such patients. The association of ML and obstructive hypertrophic cardiomyopathy has been recently reported. A critical examination of the literature in addition to our clinical observations suggests that the biventricular obstructive hypertrophic cardiomyopathy may play a major role in the clinical feature of ML syndrome.     

Sudden death and obstructive hypertrophic cardiomyopathy

Sudden death is the most common cause of death in obstructive hypertrophic cardiomyopathies. Ventricular arrhythmias appear to be involved most frequently. The typical clinical picture is that of a young, asymptomatic male subject with a family history of sudden death and obstructive hypertrophic cardiomyopathy. The electrocardiogram at rest, the left ventricular pressure gradient, and the width of the septum are not good predictive criteria. Holter monitoring with the discovery of a run of ventricular tachycardia is the only method which identifies a subgroup at high risk for sudden death. Treatment with beta blockers does not protect patients with obstructive hypertrophic cardiomyopathy from sudden death and only combined therapy with an antiarrhythmic agent can control ventricular rhythm disturbances and decrease the number of sudden deaths in this condition.