急性心肌缺血患者与健康人室性期前收缩发生部位的对比研究

目的:对比研究急性心肌缺血患者与健康人室性期前收缩发生部位的差异.方法:选择12导联同步心电图检测的177例室性期前收缩患者,其中急性心肌缺血患者87例、健康体检者90例,计算不同起源部位室性期前收缩发生率,并对比分析.结果:急性心肌缺血患者左心室前壁(20.7%)及心尖部期前收缩发生率(13.8%)、V左心室期前收缩总发生率(51.7%)显著高于健康体检者(分别为3.3%,2.2%,23.3%);健康体检者右心室流出道期前收缩发生率(61.1%)、右心室期前收缩总发生率(76.7%)显著高于急性心肌缺血患者(分别为31.0%,48.3%).结论:急性心肌缺血患者以左心室期前收缩常见.     

老年2型糖尿病患者不同部位室性期前收缩窦性心率震荡及连续心率减速力及临床意义

目的研究老年2型糖尿病(T2DM)不同部位室性期前收缩窦性心率震荡及连续心率减速力(DRs)的特点及其临床意义。方法选取同步12导联动态心电图监测的582例老年T2DM室性期前收缩患者,根据宽大畸形QRS波形态对室性期前收缩起源部位进行定位,对比不同部位室性期前收缩的窦性心率震荡(震荡起始TO;震荡斜率TS)及DRs指标。结果右心室流出道、右心室心尖部、左心室心尖部早搏TO、TS、DRs异常率分别为9.6%、13.4%、6.8%,8.5%、12.0%、4.3%,7.9%、13.2%、5.3%,差异无统计学意义(P>0.05)。左心室流出道期前收缩的TO、TS、DRs异常率分别为23.7%、29.9%、15.5%,均明显高于以上三个部位(P<0.05)。结论老年T2DM合并左心室流出道期前收缩患者,窦性心率震荡减弱,DRs降低,易引起恶性心律失常,具有心源性死亡高危性,临床上应给予高度重视。     

不同心电学特征的单发室性期前收缩对心脏瞬时泵血功能的影响

目的:研究无基础心脏病患者室性期前收缩的心电学特征对左心室瞬时泵血功能的影响,深入理解室性期前收缩导致心肌病的机制。方法:收集中南大学湘雅二医院、湖南省人民医院收治的体检人群中无明确心脏器质疾病的室性期前收缩患者71例,分析每例患者室性期前收缩的心电图特征(联律间期、起源位置及QRS时限),并在室性期前收缩发生瞬间利用心脏彩超监测左心功能,包括左心室射血分数(LVEF)、每搏输出量(SV)及左心室舒张末期容积(LVEDV)。并利用SPSS 13.0统计软件分析心电图特征与左心室泵血功能的关系。结果:与窦性心律相比,室性期前收缩发生时LVEF减少31.5%(37.5%∶69%,P<0.05),LVEDV减少46%(52 ml∶97 ml,P<0.05),SV减少63.6%(24 ml∶67 ml,P<0.05)。与左心室流出道及非流出道比较,右心室流出道起源的室性期前收缩时LVEF减少更加明显(P<0.05)。与左心室流出道及非流出道比较,右心室流出道及右心室非流出道起源室性期前收缩对SV减少的影响更大(P<0.05)。不同起源的室性期前收缩对LVEDV的影...     

射频导管消融治疗中窦性心律胸导联移行对室性心律失常起源点鉴别的价值

前面12 期我们已经连续介绍了室性期前收缩/ 室性心动过速射频导管消融(下称消融)治疗的适应证、定位基本原则、右心室流出道及其邻近结构和三尖瓣环、二尖瓣环、左心室间隔部、心外膜及心大静脉(GCV)最远端、希氏束旁、特发性左心室壁瘤合并室性心动过速、左冠状动脉窦起源室性期前收缩经右心室流出道优先传导和起源于右心室间隔部室性期前收缩/ 室性心动过速的心电图特征及消融治疗.     

右心室间隔部室性期前收缩/室性心动过速的心电图特征及射频导管消融治疗

前面11期我们已经连续介绍了室性期前收缩 / 室性心动过速射频导管消融（下称消融）治疗的适应证、定位基本原则、右心室流出道及其邻近结构和三尖瓣环、二尖瓣环、左心室间隔部、心外膜及心大静脉（GCV）最远端、希氏束旁、特发性左心室室壁瘤合并室性心动过速及左冠状动脉窦起源的室性期前收缩经右心室流出道优先传导的心电图特征及消融治疗.本文介绍右心室间隔部不同起源室性期前收缩/室性心动过速的心电图特征及消融治疗体会.     

左心室心尖起源的频发室性期前收缩伴左侧旁道一例射频消融

文献报道经导管射频消融(RFCA)治疗的室性期前收缩(PVCs)多起源于心室流出道尤其多源于右心室流出道(RVOT)，对于左心室心尖部来源的频发室性期前收缩行RFCA治疗罕有报道；而同时伴发隐匿旁道者，更未见之于文献。     

不同起源部位室性期前收缩与动态心电图判定心肌缺血部位的关系

室性期前收缩是临床上较为常见的一类心律失常,主要见于老年人群中〔1〕。研究表明,正常人亦可能出现室性期前收缩,而且其发生的概率随着年龄的增长呈现上升的趋势〔2〕。有文献报道老年不同部位室性期前收缩与心肌缺血之间存在一定的关联〔3〕。本研究探讨不同起源部位室性期前收缩与动态心电图判定老年人心肌缺血的联系。     

右心室不同部位起搏对左心室收缩功能的影响

目的:比较右心室心尖(RVA)及流出道间隔部(RVOT-S)起搏对左心室收缩功能的影响,探讨合理的右心室起搏部位。方法:自2007年8月~2009年12月,36例左室收缩功能正常的完全性房室传导阻滞患者,随机纳入RVA和RVOT-S起搏组,起搏器植入12月后分别测定左室射血分数(LVEF),左室收缩末容量(LVESV),主动脉瓣口速度时间积分(VTI),主动脉与肺动脉瓣开放时间差(QAO-QP),房颤负荷(AFb),自动模式转换(AMS),血浆脑钠尿肽原(NT-proBNP)变化,QRS波宽度,比较两组的差别。结果:起搏12月后RVOT-S组LVEF及VTI明显高于RVA组(均P<0.05);LVESV,QAO-QP,NT-BNP,AFb,AMS及QRS波宽度明显低于RVA组(均P<0.05)。结论:与RVOT-S组相比,RVA长期起搏可导致明显左右心室间以及左室内收缩不同步及左室重构,减低左心室收缩功能,对心室依赖起搏患者应首选RVOT-S为心室电极植入部位。     

室性期前收缩的体表心电图定位及射频导管消融治疗

室性期前收缩是临床上最常见的心律失常，虽然心室的各个部位均可发生室性期前收缩，但其存在好发区域。目前研究发现右心室流出道及其延伸部位（主肺动脉干）是最常见的好发部位，约占室性期前收缩的70％左右，其次是左心室流出道左冠状窦内、左冠状窦下及左心室间隔部和房室环（二尖瓣环和j尖瓣环）等是较常见的好发区域，     

急性心肌梗死行经皮冠状动脉介入治疗病人合并频发室性期前收缩对短期预后的影响

目的观察合并频发室性期前收缩对经皮冠状动脉介入(PCI)治疗的急性心肌梗死病人短期预后的影响。方法回顾性分析2015年1月—2018年1月我院接受PCI治疗的合并室性期前收缩急性心肌梗死病人228例,其中合并频发室性期前收缩26例(11.4%),偶发室性期前收缩202例。观察并比较频发室性期前收缩和偶发室性期前收缩病人临床资料和介入治疗数据,采用Logistic回归进行多因素分析,明确住院期间发生主要心血管不良事件(MACE)的独立危险因素。结果频发室性期前收缩组病人年龄大于偶发室性期前收缩组(P0.05),频发室性期前收缩组心力衰竭、心源性休克发生率均高于偶发室性期前收缩组(P0.05)。频发室性期前收缩组冠状动脉3支病变发生率高于偶发室性期前收缩组,PCI术后梗死相关血管恢复心肌溶栓试验血流3级构成比低于偶发室性期前收缩组(P0.05);频发室性期前收缩组MACE发生率高于偶发室性期前收缩组(P0.05)。Logistic回归分析结果显示:心源性休克、血流心肌梗死溶栓治疗3级是急性心肌梗死住院期间MACE的独立危险因素。结论急性心肌梗死后并发频发室性期前收缩提示病人冠状动脉病变广泛且严重,急诊PCI术中发生血流改善更差,术后发生无复流风险增加,心源性休克、血流心肌梗死溶栓治疗3级是影响短期预后的独立危险因素。合并频发室性期前收缩病人左心功能明显减低,提示长期预后不良。     

Study on the relationship between myocardial ischemia assessed by 24-hour ambulatory electrocardiogram and ventricular premature beat originating from different positions in older adults

BackgroundMyocardial ischemia is a common reason of ventricular premature beat, and it plays an important role in arrhythmia in older adults. We could often see the report about the diagnosis and radiofrequency catheter ablation of ventricular arrhythmia from the right ventricular outflow tract, Haissaguerre et al. (2002) [1], Miyamoto et al. (2010) [2], Nakagawa et al. (2008) [3], Zhu et al. (1995) [4]. However, no study to date has examined the relation of myocardial ischemia and ventricular premature beat originating from different positions. In this article, we studied the incidences of myocardial ischemia of ventricular premature beats originating from different positions in older adults.MethodsWe located the original positions of ventricular premature beats according to the shape of the wide and malformed QRS waves in 12 leads synchronizing ECG. We used synchronism 12-lead ambulatory 24 hour electrocardiograms to examine 531 aged patients with ventricular premature beats, calculated the incidences of myocardial ischemia of the ventricular premature beats originating from different positions.ResultsThe incidence of myocardial ischemia of ventricular premature beats from the right ventricular outflow and the left ventricular outflow were 52.31% and 51.42% respectively. The incidence of myocardial ischemia of ventricular premature beat from the right ventricle anterior wall and the left ventricle anterior wall were 53.57% and 73.47% respectively. The incidence of myocardial ischemia of ventricular premature beat from the right ventricular apex and the left ventricular apex were 55.10% and 74.42% respectively. The total incidence of myocardial ischemia of right ventricular premature beats and left ventricular beats were 52.92% and 61.65% respectively.ConclusionsThe total incidence of myocardial ischemia of left ventricular premature beats was higher than that of right ventricular premature beats. The highest incidence of myocardial ischemia of ventricular premature beats was that from the left ventricular apex and anterior wall. The incidence of myocardial ischemia of ventricular premature beats was more than 50% in older adults.     

超高龄高血压病左室肥厚与神经体液因素及室性早搏的相关性研究

目的探讨超高龄（>80岁）高血压病左室肥厚与部分神经体液因素之间的关系及与室性早搏、心肌缺血的相关性。方法60例病人分2组超高龄高血压病伴左室肥厚30例为A组；单纯超高龄高血压病30例为B组。对比观察心率变异、肾素（Ren）、血管紧张素（AT-Ⅱ）、醛固酮（Ald）、胰岛素峰值（Ins）、24小时动态心电图和血压等指标。结果(1)A组病人交感神经张力明显增高，迷走神经活性下降不明显；交感神经张力增高与室性早搏的发生有关；室性早搏与心肌缺血具有相关性；(2)A组病人与Ald及Ins水平有关，与Ren和AT-Ⅱ无明显相关；(3)A组病人与室性早搏和心肌缺血具明显相关。结论超高龄高血压病左室肥厚患者交感神经张力增高，Ald及Ins水平升高，与室性早搏、心肌缺血具有正相关。     

超高龄高血压病左室肥厚与神经体液因素的相关性

目的 探讨超高龄（〉８０岁）高血压病左室肥厚与部分神经体液因素之间的关系及与室性早搏、心肌缺血的相关性。方法 ６０例病人分２组：超高龄高血压病伴左室肥厚３０例为Ａ组;单纯超高龄高血压病３０例为Ｂ组。对比观察心率变异、肾素、血管紧张素（ＡＴ－Ⅱ）、醛固酮、胰岛素峰值、２４ｈ动态心电图和血压等指标。结果 ①Ａ组病人交感神经张力明显增高,迷走神经活性下降不明显;交感神经张力增高与室性早搏的发生有关;室性     

Characterization of left ventricular mechanical function during arrhythmias by two-dimensional echocardiography. II. Location of the site of onset of premature ventricular systoles

Two-dimensional echocardiography was applied experimentally in a closed chest dog model with intact pericardium to determine the location, magnitude and extent of contractile response during pacing from discrete ventricular sites. Midventricular short-axis tomographic images obtained during regular sinus rhythm and subsequent premature ventricular beats provided comparative measurements of global and segmental systolic changes of cross-sectional luminal areas and myocardial wall thickness. Computer-assisted standardized analysis of segmental systolic fractional area change and wall thickening was used to map left ventricular contraction during normal rhythm and premature beats of 70% coupling interval, induced alternately from anterior and lateral aspects of the mid-left ventricular short-axis cross-sectional plane. A characteristic pattern consisting of early systolic contraction and wall thickening was followed by paradoxical motion and wall thinning in late systole in segments corresponding to the region of direct electrical stimulation. Statistical analysis of segment by segment function indicated a maximal amount of premature beat contractile derangement at the site of the stimuli. Pacing from a right ventricular wall site in the midventricular plane caused a similar premature beat response at the anterior aspect of the interventricular septum. It is concluded that two-dimensional echographic analysis of segmental ventricular function can identify the location of electrical stimuli, and thus might noninvasively characterize regional patterns of contraction associated with ectopic foci during arrhythmias.     

Two-dimensional echocardiographic and left ventriculographic evaluations of left ventricular diverticula

Twenty cases of left ventricular diverticula were gleaned from 4,300 consecutive angiocardiographic records (13 males and seven females whose age ranged from 17 to 78 years with a mean of 52 +/- 16 years). Their findings were compared with those of 16 patients with left ventricular aneurysms due to myocardial infarction. In only one patient was a diverticulum first detected by two-dimensional echocardiography before left ventriculography was performed. None of the patient had an associated midline thoracoabdominal defect. Five patients had premature ventricular beats, two of whom had ventricular tachycardia. Three patients complicated mitral valve prolapse and three atrial septal defect. Of the 20 patients, four each had two diverticula, as opposed to 16 others who each had a single diverticulum. The diameter of the diverticula ranged from eight to 70 mm. The sites of 14 diverticula were along the inferior wall; five in the anterior wall; four in the apex. Morphologically 15 diverticula were bulky outpouchings, six were tongue-like, and three hammocking. All diverticula exceeding 15 mm in diameter and originated near the mitral ring could always be detected in the short-axis view of two-dimensional echocardiography. However, those originating in the apex or of a tongue-like configuration could rarely by detected. Comparative two-dimensional echocardiographic analyses of 16 diverticula, 16 left ventricular aneurysms, and 16 normal left ventricular walls disclosed that the left ventricular aneurysmal wall had a higher echo intensity, but the diverticula had the same wall echo intensity as the normal left ventricular wall. Left ventricular end-diastolic wall thickness in an aneurysm (7.6 +/- 1.5 mm) was lower (p less than 0.01) than the normal left ventricular wall (11.1 +/- 1.3 mm), but it did not differ from the normal left ventricular wall in any case of diverticulum (10.2 +/- 1.5 mm). The percent wall thickening ratio in aneurysms (-3.6 +/- 10.7%) was lower (p less than 0.01) than the normal left ventricular wall (39.8 +/- 10.9%), but it did not differ from the normal left ventricular wall in diverticula (45.8 +/- 16.6%). Regional fractional shortening in the diverticula (41.3 +/- 9.2%) did not differ from that in the normal left ventricular wall (34.5 +/- 5.2%). In conclusion, a small diverticulum without a midline thoracoabdominal defect is not rare, and two-dimensional echocardiography is the diagnostic method of choice in many cases based on the echo features described above.     

Right ventricular myocardial infarction with anterior wall left ventricular infarction: an autopsy study

Right ventricular myocardial infarction has been reported to occur exclusively in association with inferior left ventricular infarction. To determine the frequency of right ventricular myocardial infarction in association with anterior left ventricular myocardial infarction, all hearts with anterior myocardial infarction studied over a 3-year period were examined for evidence of right ventricular necrosis or scar. Of 97 hearts with anterior myocardial infarction, 13 (13%) had anterior right ventricular myocardial infarction. The right ventricular infarcts involved from 10% to 50% (mean 28%) of the circumference of the right ventricular free wall from base to apex. The associated left ventricular infarcts were all anteroseptal and large and involved from 36% to 67% (mean 50%) of the total area of the left ventricular free wall and septum. Nine of the 13 patients underwent equilibrium radionuclide angiography and six had demonstrable right ventricular regional and global dysfunction. Thus, right ventricular myocardial infarction does occur with anterior wall left ventricular infarction, and right ventricular dysfunction may be demonstrable by radionuclide angiography. Further investigation is needed to define the hemodynamic characteristics, clinical importance, and therapeutic implications of anterior right ventricular myocardial infarction.     

Sites of origin of ventricular premature beats in patients with and without cardiovascular disease evaluated by body surface mapping

The site of origin of ventricular premature beats (VPBs) was estimated by QRS maps and its distribution in two patient groups was studied. VPB origin was determined by comparing the body surface map of VPBs with that during electrical stimuli applied at various sites of the ventricle. Subjects were 100 patients without obvious underlying cardiovascular disease (Group N) and 289 patients with various heart diseases (Group D). Nine sites of origin of VPB were identified. In group N, VPBs of right ventricular origin were noted in 69%, those of left ventricular origin in 6%. There was a relatively high incidence of VPBs with foci estimated to be the divisions of the left bundle branch, and the age of patients with these VPBs was young. In Group D, VPBs of left ventricular origin showed a higher incidence (34.6%) and those of right ventricular origin a lower incidence (41.2%) than those in group N. The data suggest that VPBs originating from the apex and base of the ventricle strongly indicate the presence of basic heart disease and that VPBs originating in or near the divisions of the left bundle branch in younger subjects do not necessarily indicate cardiac disease.     

Impaired right ventricular filling in old myocardial infarction

To evaluate ventricular filling and interactions between right and left ventricles in patients with old myocardial infarction, right and left ventricular time-volume curves were analyzed from a cineangiographic study of 10 normal subjects (Group 1), 10 patients with old anterior myocardial infarction (Group 2) and 10 patients with old inferior myocardial infarction (Group 3). Volumes of both ventricles were calculated from each frame over an entire cardiac cycle using Simpson's method. From time-volume curves, peak ejection rates, peak filling rates and atrial kick rates were obtained for both ventricles and these parameters were normalized by end-diastolic volume. All patients were in sinus rhythm with heart rates less than 80 beats/min. There were no significant differences among the 3 groups in end-diastolic pressure of both ventricles and mean pulmonary artery pressure. Left ventricular ejection fractions were significantly lower in Groups 2 and 3 than in Group 1 (p less than 0.001, p less than 0.005, respectively), although there were no significant differences in end-diastolic volume indexes of either ventricle among the 3 groups. Peak left ventricular ejection rate and peak filling rates of the left and right ventricles were lower in Group 2 than in Group 1 (p less than 0.01, p less than 0.05, p less than 0.01, respectively) and peak filling rate of the right ventricle in Group 2 correlated with the peak filling rate of the left ventricle and left ventricular ejection fraction (r = 0.64, r = 0.64, respectively). Peak filling rate of the right ventricle in Group 2 correlated inversely with left ventricular peak negative dp/dt (r = -0.72), but no correlation was found between peak filling rate of the right ventricle and left ventricular end-diastolic volume index or mean pulmonary artery pressure. Peak ejection rate of the left ventricle and peak filling rates of both ventricles in Group 3 were lower than in Group 1 (p less than 0.02, p less than 0.02, p less than 0.01, respectively) and no correlation was found between peak filling rates of both ventricles. Wall motion of the right ventricular septal portion was slightly reduced in 5 patients in Group 2. In all patients in Group 3, right ventricular wall motion centering around the right ventricular diaphragmatic portion was reduced. These results suggest that in old inferior myocardial infarction, right ventricular wall motion abnormality results in impaired right ventricular filling, whereas in old anterior myocardial infarction, right ventricular filling is reduced indirectly due to impaired left ventricular filling.     

Protective role of collaterals in patients with coronary artery occlusion

We reviewed the clinical, hemodynamic and angiographic data of 105 patients with right coronary artery occlusion and of 82 patients with left anterior descending coronary artery occlusion, subdivided into 3 groups by the presence and quality of collaterals to the occluded coronary (absent, poor or good collaterals). We found that patients with right coronary artery occlusion and good collaterals had a lower frequency of diaphragmatic myocardial infarction (60%) than patients with absent collaterals (100%) (P < 0.01). In addition, in patients with old diaphragmatic myocardial infarction, both poor and good collaterals were associated with a lower frequency of severe asynergy of the diaphragmatic left ventricular segments at left ventriculography (54% and 14%, respectively), compared to patients with no collaterals to the right coronary artery (92%, P < 0.02 vs. poor collaterals, P < 0.001 vs. good collaterals). In contrast, in patients with left anterior descending coronary artery occlusion, the presence of either poor or good collaterals to the left anterior descending coronary artery was not associated with a lower frequency of old anterior myocardial infarction, or, in patients with old anterior myocardial infarction, with a less severe asynergy of the anterior left ventricular segments.Our results suggest that collaterals are effective in protecting the diaphragmatic left ventricular wall in patients with right coronary artery occlusion, but not the anterior left ventricular wall in patients with left anterior descending coronary artery occlusion.