心尖肥厚型心肌病的心电图特征

目的探讨心尖肥厚型心肌病的心电图特点。方法对29例心尖肥厚型心肌病的常规12导联心电图进行分析。结果患者V3～V5导联R波电压增高、ST段压低，均表现为V4〉V5〉V3，T波对称性倒置，呈V4〉V5〉V6。V3～V6导联同导联R波高度与T波倒置深度、ST段压低深度呈负相关（P均〈0．05），T波倒置深度与ST段压低深度呈正相关（P〈均0．01）。结论常规心电图显示胸导联R波电压增高伴ST-T特征性改变，要高度考虑心尖肌肥厚性心肌病。     

心尖肥厚型心肌病患者心电图的诊断意义

目的探讨心尖肥厚型心肌病患者的心电图特征性改变及临床诊断意义。方法分析38例心尖肥厚型心肌病患者的心电图及超声心动图资料。结果心尖肥厚型心肌病合并有心电图异常和超声心动图异常改变者38例(100%),其中伴胸前导联巨大倒置T波≥0.2mV～0.3mV,以V3～V4最明显29例(76%);左胸V4～V6导联R波电压增高,且RV4>RV5>RV6者26例(68.4%);ST段压低,以V3～V4最明显者29例(76%);超声心动图示心尖部肥厚达15mm或以上伴心尖部心腔狭小者38例。结论心电图对心尖肥厚型心肌病具有早期诊断价值和预测意义。     

50例心尖肥厚型心肌病患者心电图特点分析

对2002～2006年确诊的50例心尖肥厚型心肌病(AHCM)患者的心电图进行回顾性分析,结果发现50例患者均有左胸导联T波倒置及ST段压低,呈典型的Tv4＞Tv5＞Tv3者30例,左胸导联R波电压增高44例,Rv4＞Rv5＞Rv6者35例.认为胸前导联T波倒置伴R波振幅增高为AHCM的特征性心电图表现,临床应注意与冠心病、心肌梗死等鉴别.     

心尖肥厚型心肌病病人MRI表现及心电图特点分析

目的研究心尖肥厚型心肌病MRI表现和心电图的特点,探讨MRI在心肌肥厚型心肌病中的诊断价值。方法对临床确诊的26例心尖肥厚型心肌病病人MRI表现、心电图资料进行回顾分析。结果 26例病人心脏MRI均提示心尖部心肌肥厚,TAHCM14例,P-AHCM12例,8例T-AHCM舒张期左室表现为典型的"黑桃心"征象。26例病人行心肌首过灌注及延迟强化MRI扫描,11例延迟增强显示心尖部肥厚心肌内不规则增强高信号。26例病人心电图均存在ST-T改变:其中26例左胸导联产生的对称倒置的T波,11例表现为巨大T波倒置(42.3%);16例表现胸前导联R波振幅增高(61.5%);17例出现ST段下移(65.4%);T波倒置深度与心尖部室壁厚度无相关性,但T-AHCM、P-AHCM两组11例延迟强化阳性病例,均表现为巨大T波倒置,两组肥厚心肌的延迟增强阳性率无统计学意义。结论在心尖肥厚型心肌病中,MRI可以准确诊断,延迟强化能够解释心电图中巨大倒置T波原因。     

心尖部肥厚型心肌病的影像学诊断特点

目的 探讨心尖部肥厚型心肌病影像学检查特点,总结更为合理的诊断和治疗方法.方法 回顾性分析我院2004年1月至2010年1月期间60例诊断为心尖部肥厚型心肌病患者的临床表现,心电图、超声心动图、冠状动脉造影、左室造影、256层螺旋CT及心脏磁共振检查的特点,以及治疗后随访1年的心血管事件.结果 60例患者中56例表现为V1～V6导联 ST段压低,T波倒置,尤以V4 T波深倒;1例为完全性右束支传导阻滞;2例表现为AVR抬高,V3～V6导联ST段压低,T波倒置;1例Ⅲ、V1 T波倒置,V2～V6 T波双向.超声心动图异常改变48例（80%）,其中38例表现为不同程度的心尖部肥厚,厚度均≥15 mm,最厚可达22～24 mm.冠脉造影41例,仅有1例为前降支中段狭窄约70%,2例为前降支近中段肌桥形成,其余38例冠脉血管均正常.左室造影32例表现为左室腔舒张末期呈＂黑桃＂形改变,9例表现为＂猫舌＂状.10例患者行256层心脏及冠脉CTA检查,2例发现前降支近中段肌桥,8例冠脉正常;10例患者表现为心尖部增厚,厚度为15～21 mm.9例患者行心脏磁共振（CMR）检查,7例发现心尖部肥厚,厚度14～28 mm.结论 心尖部肥厚型心肌病容易误诊为冠心病.结合心电图和超声心动图可进一步明确,左心室造影、多层螺旋CT及心脏MRI为该病的诊断提供了确诊的依据.     

右室心尖部起搏时体表心电图V1导联呈右束支阻滞图形分析

目的分析右室心尖部起搏患者V1导联呈现右束支阻滞图形的特点、出现的可能机制以及鉴别诊断方法。方法选取北京大学人民医院2005—2007年于右室心尖部植入起搏电极的患者,分析患者完全右室起搏时V1导联呈右束支阻滞图形患者的超声心动图、胸部X线等资料,并与同期V1导联呈左束支阻滞图形变化的右室起搏患者以及植入左室心外膜电极的患者的临床资料以及体表心电图特点进行对比。结果共有9例患者术后完全心室起搏时V1导联呈右束支阻滞图形,术后超声心动图以及胸部X线检查证实起搏电极均位于右心室,QRS波平均电轴为-61.7±15.6,与随机选取50例术后体表心电图呈左束支阻滞的右室电极植入患者心电图相比,QRS波电轴差异无统计学意义(P>0.05),与7例行左室心外膜起搏者QRS波电轴差异有统计学意义(P<0.05)。呈右束支阻滞者其肢体导联I、aVL导联QRS波均直立,与呈左束支阻滞患者相同,而左室心外膜起搏者其I、aVL导联QRS波为负向。结论当患者V1导联呈右束支阻滞形态时可通过I、aVL导联QRS波形态和QRS波电轴可以判断是否为右室起搏。     

第18课 罕见的束支传导阻滞

这份心电图(图1)是一例无症状、无器质性心脏病的52岁女性患者,该患者至门诊部是因常规心电图显示若干异常:①QRS电轴90°,②QRS时间0.14s,③肢体导联QRS形态提示束支传导阻滞,但仅根据这些尚难确定究竟是哪一种(右或左)束支传导阻滞。初看时,Ⅰ和aVL导联粗钝的S波提示右束支传导阻滞,而下壁导联的QRS形态(单相R波和继发性ST-T改变)较支持左束支传导阻滞伴电轴相对右偏。④胸导联(图形)使该问题更复杂化,因为V1导联(图形)提示右束支传导阻滞,而V5和V6导联呈单相R波完全与左束支传导阻滞相一致;此外,V5导联呈典型左束支传导阻滞时…     

心电图对肥厚型心肌病的诊断价值

目的通过回顾分析心尖肥厚型心肌病(AHCM)患者的12导联心电图特点,探讨其对AHCM的诊断指导价值。方法对2014年12月~2016年12月于河南省安阳地区医院心内科就诊的60例AHCM患者作为观察组,与同时期我院正常体检人群50名为对照组。行12导联心电图,进行回顾性分析,比较两组人群的心电图变化情况及有无特征性变化等。结果观察组患者心电图表现为胸导联T波倒置伴ST段下移及左室高电压表现;胸导联QRS波群时间延长,且QRS波群振幅在不同导联上变化明显,均超过正常值;在ST段分别表现为V3~V6和Ⅱ、Ⅲ、a VF下移;且有42例出现V3~V6 T波倒置。患者左胸导联R波电压增高,ST段压低,0.05m V,T波对称性倒置,左胸导联同导联R波高度与T波倒置深度,ST段压低深度呈负相关(P0.05),T波倒置深度与ST段压低深度呈正相关(P均0.01)。结论心电图诊断对心尖肥厚型心肌病有辅助指导价值,对AHCM患者早期行心电图检查可提高其疾病确诊率。     

不同原因右胸导联T波倒置的比较

探讨不同原因右胸导联T波倒置的心电学特征,以利于对不同特征右胸导联T波倒置的原因识别。对74例由不同原因所致右胸导联T波倒置患者常规12导联心电图T波倒置的分布规律、倒置的深度以及是否同时伴有ST段改变、其它导联的T波倒置及其演变过程进行分析。结果:①右室起搏后电张调整性T波呈V1~V2V5~V6,并伴Ⅱ、Ⅲ、aVF导联T波倒置,不伴ST段改变。②急性肺栓塞后TV1~V3倒置往往在发病1~2h后按一定的顺序相继出现,依次为TV1→TV2→TV3→TV4;倒置深度V1>V2>V3>V4,随病情好转,其T波恢复的顺序则相反。③Brugada综合征或Brugada心电图征呈TV1>TV2>TV3伴STV1~V3下斜型或马鞍型抬高及右束支阻滞或类右束支阻滞,R′>R。④妊娠晚期亦表现为TV1~V3倒置,倒置深度V1>V2>V3,与急性肺栓塞后的T波改变类似。结论:不同原因右胸导联T波倒置的心电学特征亦异,认识这些特征,有利于对其病因的识别。     

心尖肥厚型心肌病18例临床分析

目的:对心尖肥厚型心肌病辅助检查进行分析,探讨其临床诊断价值。方法:以心电图、超声心动图、磁共振、冠状动脉造影及左室造影等检查方法检测18例心尖肥厚型心肌病。结果:18例心电图显示胸前导联T波倒置呈TV4>TV5>TV3,R波振幅增高以RV4>RV3> RV5;超声心动图左室心尖室壁舒张期厚度(17.22±14.20mm)与心室间隔基底段厚度(1.07±0.23mm)之比为1.60±0.16;4例冠状动脉造影检查后排除冠心病;6例因超声心动图不典型而行磁共振心脏成像检查后确诊。结论:标准12导联心电图显示胸前导联T波倒置伴R波增高应高度怀疑心尖肥厚型心肌病,可进一步行超声心动图或磁共振检查确诊。     

Clinical implication of left precordial T wave inversions in the presence of complete right bundle branch block

This study was designed to elucidate whether left precordial negative T waves are electrocardiographic indicators for the diagnosis of hypertrophic cardiomyopathy (HCM) even in the presence of complete right bundle branch block (CRBBB). In 7 consecutive patients with CRBBB accompanied by negative T waves in at least one of the left precordial leads (V4, V5, V6, maximal negativity; 1.06 +/- 0.40 mVol) (left precordial negative T wave group) and in 15 randomly selected CRBBB patients without left precordial T wave inversions (control group), echocardiography was performed to rule out underlying diseases causing left ventricular overload and to identify candidates for magnetic resonance (MR) imaging. None had anginal pain indicating ischemic heart disease. When 2-dimensional echocardiography indicated left ventricular hypertrophy with wall thickness > or = 15 mm, the magnitude and distribution of hypertrophy were scrutinized on contiguous left ventricular MR short-axis images. The diagnostic criterion of HCM was the demonstration of hypertrophy with a wall thickness of 20 mm or more on the left ventricular MR short-axis images. All patients in the left precordial negative T wave group had negative T waves in both I (negativity; 0.27 +/- 0.17 mVol) and aVL (negativity; 0.23 +/- 0.14 mVol), whereas none in the control group did. The diagnostic criterion for HCM was fulfilled in six patients in the left precordial negative T wave group. However there were no patients who fulfilled the criterion in the control group. Negative T waves were recorded in the I (negativity; 0.30 +/- 0.17 mVol), aVL (negativity; 0.25 +/- 0.14 mVol), V4 (negativity; 1.03 +/- 0.46 mVol), V5 (negativity; 0.83 +/- 0.37 mVol) and V6 leads (negativity; 0.31 +/- 0.31 mVol) in all patients with HCM, while they were recorded in only 6% of the patients without HCM. In conclusion, the existence of left precordial negative T waves in the presence of CRBBB strongly indicates HCM.     

Electrocardiographic differentiation between acute pulmonary embolism and acute coronary syndromes on the basis of negative T waves

Negative T waves in precordial leads are often seen in patients with acute coronary syndrome (ACS), but also occur in those with acute pulmonary embolism (APE). However, little attention has been given to differences in negative T waves between patients with these 2 diseases. The present study examines the value of electrocardiograms for discriminating between 40 patients with APE and 87 patients with ACS who had negative T waves in the precordial leads (V(1) to V(4)) on the admission electrocardiogram. In 77 patients (89%) with ACS, the culprit lesion was confirmed angiographically to be located in the left anterior descending coronary artery. Pulmonary P waves, S(1)S(2)S(3) pattern, S(1)Q(3)T(3) pattern, low voltage, and clockwise rotation were specific for APE, but sensitivities of these findings were very low. In patients with APE, negative T waves were commonly present in leads II, III, aVF, V(1), and V(2), but were less frequent in leads I, aVL, and V(3) to V(6) (p <0.05). Negative T waves in leads III and V(1) were observed in only 1% of patients with ACS compared with 88% of patients with APE (p <0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of APE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V(1) allows APE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads.     

Atypische hypertrophe Kardiomyopathie mit verkalktem, linksventrikul?rem Spitzenthrombus

A case of atypical hypertrophic cardiomyopathy (HCM) with a calcified apical thrombus is presented. A 42 year old asymptomatic patient was admitted for evaluation of an abnormal electrocardiogram (ECG) which was recorded when the patient suffered from a bronchitis. The ECG showed giant negative T-waves in leads II, III, aVF, V3 to V6 associated with high QRS voltages in the precordial leads. The chest X-ray and fluoroscopy demonstrated a calcification in projection to the apical region of the heart. Echocardiography and the left ventricular (LV) cineangiography showed hypertrophy of the apical LV myocardium and an obliteration of the apical LV cavity. Magnetic resonance imaging identified a calcified thrombus in the apical cavity of the LV in the setting of an atypical HCM.     

Valsartan decreases type I collagen synthesis in patients with hypertrophic cardiomyopathy.

BACKGROUND: Fibrosis, as well as myocyte hypertrophy, is the major determinant of prognosis in hypertrophic cardiomyopathy (HCM). Valsartan, an angiotensin II type 1 receptor blocker, may improve myocardial fibrosis in patients with HCM. METHODS AND RESULTS: Twenty-three patients with HCM were randomly divided into 2 groups: 11 patients had valsartan added to conventional treatment (V group) and 12 patients received the conventional therapy (C group). Plasma concentrations of brain natriuretic peptide (BNP), troponin T (TnT), aldosterone (ALDO), procollagen type I (PIP) and procollagen type III aminoterminal peptide (PIIINP) were measured before and 12 months after this study. Left ventricular wall thickness (LVWT) and ejection fraction (LVEF) were measured by echocardiography. PIP was decreased in the V group (123.2+/-63.1 ng/ml to 102.8+/-37.6, p<0.05), but unchanged in C group (110+/-40.5 ng/ml to 119.9+/-47.4, p=0.22). ALDO concentration was unchanged in the V group (88.5+/-26.2 pg/ml to 91.2+/-26.8, p=0.27), and increased in C group (92.6+/-36.6 ng/ml to 116.0+/-33.3, p<0.05). BNP, PIIINP, and TnT were unchanged by the treatment. There was no significant difference between the 2 groups in either LVWT or LVEF. CONCLUSION: Valsartan suppresses the synthesis of type I collagen in patients with HCM and this was associated with suppression of the increase in ALDO.     

Apical hypertrophic cardiomyopathy: diagnosis with contrast-enhanced echocardiography--a case report

Apical hypertrophic cardiomyopathy is a rare form of hypertrophic cardiomyopathy (HCM) recognized by a unique spadelike configuration on the left ventriculogram. Two-dimensional echocardiography is another useful tool in the diagnosis of this condition. The diagnosis may be difficult and may mimic akinesia or apical thrombus in some patients with poor acoustic windows. A 50-year-old woman with typical angina and left ventricular hypertrophy with T wave inversion in leads V3-V6, II, III and aVF is presented. Apical HCM was diagnosed with contrast-enhanced echocardiography and confirmed by finding a spadelike configuration on the left ventriculogram. Apical HCM should be considered in patients in whom symptoms and ECG findings mimic ischemic heart disease. Contrast-enhanced echocardiography is a reliable and simple method in the diagnosis of apical HCM.     

Variability of negative T wave in hypertrophic cardiomyopathy: possible role of beta-adrenergic function

To investigate the variability and the mechanism of negative T waves in hypertrophic cardiomyopathy (HCM), especially giant negative T waves in apical hypertrophy, from view point of adrenergic function, ECG was studied by treadmill exercise test and under administrations of beta-adrenergic agonist (isoproterenol) and antagonist (propranolol) in 33 patients with HCM and negative T waves. Apical hypertrophy was seen in 16 cases, and giant negative T waves were seen in 24 cases. By treadmill exercise test, negative T waves became less deep in all cases of HCM (-1.2 +/- 0.5 mV-----0.6 +/- 0.5 mV, p less than 0.001). The higher exercise level the patients attained, the less deep the negative T waves became. Isoproterenol caused the same reversal of negative T waves as the exercise test, but heart rate and rate pressure product attained by isoproterenol were significantly smaller than those by exercise. R wave amplitude did not change with isoproterenol. Propranolol made negative T waves deeper at rest and inhibited the reversal of negative T waves caused by exercise. In conclusion, negative T wave in HCM, especially giant negative T wave in apical hypertrophy, is variable. Beta-adrenergic function may be at least one of its mechanisms.     

Concordance of distinguishing electrocardiographic features during sinus rhythm with the location of accessory pathways in the Wolff-Parkinson-White syndrome

Knowledge of the location of accessory pathways in patients with Wolff-Parkinson-White (WPW) syndrome is pertinent to patient management. Despite the recognition that features of delta waves present during maximal preexcitation reflect ventricular activation at different sites around the anulus fibrosus, the value of electrocardiographic patterns observed during sinus rhythm, when ventricular preexcitation is often not maximal for identifying accessory pathway locations, has not been determined. In this study, 12-lead electrocardiograms recorded during sinus rhythm from 66 patients with WPW syndrome were analyzed for delta-wave polarity, QRS axis in the frontal plane, the pattern of precordial R-wave transition, and concordance between electrocardiographic patterns and the site of the accessory pathway determined using catheter and intraoperative computer mapping. Electrocardiograms from patients with left lateral sites showed negative delta waves in leads I or aVL, a normal QRS axis and early precordial R-wave transition (20 of 24 patients); left posterior sites manifested negative delta waves in II, III and aVF and a prominent R wave in V1 (14 of 16 patients); posteroseptal sites had negative delta waves in II, III and aVF, a superior QRS axis and an R less than S in V1 (all 16 patients); right free wall locations manifested negative delta waves in aVR, a normal QRS axis, and R-wave transition in V3-V5 (6 of 6 patients); and anterior septal sites had negative delta waves in V1 and V2, a normal QRS axis, and R-wave transition in V3-V5 (4 of 4 patients). Characteristic electrocardiographic patterns were not observed in 5 patients because of insufficient preexcitation. Each had a left lateral or left posterior pathway. Overall, the proposed electrocardiographic criteria derived during sinus rhythm identified correctly the accessory pathway location in 60 of 66 patients (91%). Thus, the electrocardiogram provides the physician with a reliable noninvasive means of regionalizing the location of accessory pathways in patients with WPW syndrome.     

Electrocardiogram in dilated cardiomyopathy

The authors describe the main electrocardiographic features in 90 cases of dilated cardiomyopathy. The patients were divided into tree groups: in group I were the patients with electrocardiographic signs of left ventricular hypertrophy, in group II the patients with complete left bundle branch block and in group III the cases with right bundle branch block, was held in the group I 64 patients (71%), in the group II 22 (24.6%) and in the group III four case (4.4%). Seventy two cases (80%) showed arrhythmias. Atrial fibrillation was observed in 20 patients (28%), supraventricular tachycardia in two (3%), atrioventricular block, of the 1st and 2nd degree, in eight (11%), ventricular arrhythmias in 63 (87.5%) and supraventricular arrhythmias in 42 (58%). In the 64 patients, with left ventricular hypertrophy, 60 (93.75%) showed very important S waves in, at least two right precordial leads. Fourty four patients (73.3%) had rS pattern in right precordial leads, from V1 to V4, with the R waves in V5 and V6 with normal, low and height amplitude. A first degree left bundle branch block was recorded in 16 cases (25%), a pathologic Q waves in 22 (37.5%), low voltage in limb leads in 24 (37.5%), left atrial enlargement in 36 (56%), right atrial enlargement in two (3%) and atrial fibrillation in 10 (16%). In the 22 patients from the group II six (27%) had left atrial enlargement, two (9%) had right atrial enlargement and six (27%) atrial fibrillation. In the four patients from group III two (50%) had an incomplete right bundle branch block, two (50%) the complete form and all had atrial fibrillation.     

Ventricular Tachyarrhythmia Associated with Hypertrophic Cardiomyopathy: Incidence,Prognosis, and Relation to Type of Hypertrophy

VT Associated with HCM . Objective: To assess the incidence, characteristics, and prognosis of ventricular tachyarrhythmia in hypertrophic cardiomyopathy (HCM). Patients: The study consisted of 66 consecutive patients with HCM who were admitted to Niigata University Hospital between 1992 and 2005. Their clinical characteristics and ECG morphology were investigated according to the type of HCM. Results: The type of HCM was asymmetric hypertrophy (ASH) in 34 patients (51%), obstructive HCM (HOCM) in 9 (14%), apical HCM (ApHCM) in 14 (21%), and midventricular obstruction (MVO) in 9 (14%). The cause of admission was ventricular tachyarrhythmia in 25 patients (38%), unexplained syncope in 11 (17%), and heart failure in 30 (45%). Sustained monomorphic ventricular tachycardia (SMVT) occurred in 19 patients and ventricular fibrillation in 6. In the 19 patients with SMVT, 12 had MVO and 3 of these had previous apHCM. Six of the 19 patients with SMVT had ASH, and 3 had abnormal apical wall motion. In 14 patients, the SMVT appeared to originate from the apical aneurysm based on the morphology of the tachycardia. Ventricular tachyarrhythmia recurred in 14 of the 25 patients (56%), and 4 of the 18 patients with an ICD had electrical storm. ASH with abnormal wall motion of the LV apex or MVO was recognized in the 4 patients with electrical storm; they commonly had abnormal Q waves and ST elevation in leads V4–V6. Conclusion: Ventricular tachyarrhythmia was responsible for 38% of hospitalizations in HCM, and SMVT occurred in patients with MVO and/or with abnormal wall motion of the LV apex. Electrical storm was more common in patients with ST elevation in precordial leads V4–V6. (J Cardiovasc Electrophysiol, Vol. 21, pp. 991‐999, September 2010)     

Chronologic electrocardiographic changes in patients with hypertrophic cardiomyopathy associated with cardiac troponin 1 mutation

Background Deletion of lysine 183 (K183del) in the cardiac troponin I (cTnI) gene is one of the mutations that causes hypertrophic cardiomyopathy (HCM). However, the phenotypic expression of this mutation has not been well established. Methods and Results We analyzed 10 probands with HCM associated with a K183del in the cTnI gene, as well as their family members. Forty-seven of these 80 subjects were found to be carriers and 33 were noncarriers. In the carrier subjects, electrocardiogram (ECG) abnormalities were initially noted during the early teenage years preceding echocardiographic abnormalities. Abnormal Q waves were found first and most frequently compared with other ECG abnormalities. Abnormal Q waves were frequently observed in leads II, III, aVF, V5, and V6 in teenage patients, whereas they were observed in many leads in patients >20 years old. The youngest of the 11 patients who had sudden cardiac death among studied pedigrees was a 14-year-old boy. Conclusions These results suggest that the first phenotypic manifestation in patients with HCM associated with a K183del mutation in the cTnI gene is abnormal Q waves in leads II, III, aVF, V5, and V6 during the early teenage years. To prevent sudden death in family members of patients with this mutation, it may be necessary to genetically diagnose it before age 10 years and to pay careful attention to any development of abnormal Q waves. (Am Heart J 2002;143:289-93.)