Electrophysiological Basis of Ventricular Late Potentials

EL-SHERIF, N., ET AL.: Electrophysiological Basis of Ventricular Late Potentials. The presence of late potentials on the body surface recording was correlated with ventricular activation maps of reentrant circuits in the postinfarction canine model of reentrant excitation. Late potentials were found to correlate with delayed myocardial activation. However, during a reentrant rhythm complete diastolic activity on the body surface could not be detected if the mass of electrically active cells was too small and/or if very slow conduction in part of the reentrant circuit generated low amplitude extracellular potentials. Myocardial zones responsible for late potentials during a basic rhythm (e.g., sinus rhythm) may not necessarily be part of the critical zone of slow conduction during reentrant activation. Dynamic changes in late potentials are not amenable to temporal signal averaging techniques but could be detected by a high resolution beat-to-beat recording. A thorough understanding of the electrophysiological limitations of late potentials in the signal-averaged ECG could result in better utilization of the technique in clinical practice as well as in the development of new approaches for the detection of the arrhythmogenic substrate.     

Prognostic Implications of Loss of Late Potentials Following Acute Myocardial Infarction

The prognosis of patients following myocardial infarction is adversely affected by the finding of late potentials at the time of hospital discharge. Loss of late potentials has been previously reported during seriai testing during the first year after infarction, but it is not known whether such patients remain at risk of arrhythmic events. This study prospectively followed 243 patients after myocardial infarction. Late potentials were observed in 92 patients (group 1) at the time of hospital discharge. Of these patients, 23 no longer had late potentials at G-week follow-up and 8 had had an arrhythmic event (sudden death or ventricular tachycardia). In patients with loss of late potentials, overall QRS duration had decreased from 109 ± 11 msec at discharge to 104 ± 11 msec (P < 0.01), terminal QRS voltage rose from 15 ± 4 μV to 31 ± 9 μV (P = 0.001), and late potential duration fell from 42 ± 6 msec to 28 ± 6 msec (P = 0.001) at the 6-week study. Predictors of loss of late potentials were: initial duration of the QRS duration (P < 0.001) and terminal voltage (P < 0.005); non-Q wave infarction (P < 0.001); and being a male (P < 0.05). After the 6-week assessment, 11 additional arrhythmic events occurred during median follow-up of31 months. The risk of arrhythmic events was similar in patients with loss of late potentials and those who retained late potentials in group I (9% vs 11%, P - NS) but significantly greater than palients with no late potentials at discharge (group II, 2%). Of those patients with events beyond 6 weeks, a normal signal-averaged ECG (either lost late potentials or group II) was observed in 6/11 (55%) patients on at least one occasion prior to the occurrence of the event. Hence, a significant number of arrhythmic events occurring ≥ 6 weeks after myocardial infarction occur in palients with a normal signal-averaged ECG even when late potentials are initially present. “Loss’ of late potentials does not necessarily confer an improved prognosis in terms of risk of arrhythmic events.     

急性右室心肌梗死对下壁心肌梗死的临床特征和预后干预的分析

目的 :分析急性右室心肌梗死对急性下壁心肌梗死的临床特征和预后干预的意义。方法 :将急性单纯性下壁心梗患者列入第一组 ,将急性下壁心梗合并右室心梗的患者列为第二组。分析两组的临床特征和院内病死率。结果 :2 17例患者 ,其中 ,第一组 96例 ,第二组 5 2例。发生低血压第一组 9例 (占 9.36 % ) ,第二组 31例 (占 5 9.6 2 % )。发生快速心律失常 (包括阵发性室上性心动过速 ,阵发性心房颤动 ,频发室性早搏 ,非持续性室性心动过速第一组 12例 (占 12 .5 0 % ) ,第二组 17例 (占32 .6 9% )。发生缓慢心律失常 (包括窦性心动过缓 ,房室传导阻滞 )第一组 14例 (占 14 .5 8% ) ,第二组 2 5例 (占 4 8.0 8% )。诊断心功能不全第一组 11例 (占 11.4 6 % ) ,第二组 14例。血清肌酸酶平均峰值第一组 1349.2± 2 11.7U/L ,第二组 2 814 .6±35 2 .7U/L。以上数据两组有显著差异 (P <0 .0 5 )。院内病死率第一组 8.14 % ,第二组 34%。静脉溶栓、急诊PTCA和未行再灌注治疗的院内病死率在第一组分别为 3.4 5 % ,4 .2 6 % ,和 30 % ,在第二组分别为 10 % ,11.76 %和 80 %。结论 :合并右室心梗时 ,急性下壁心梗患者临床表现更为复杂 ,严重 ,院内病死率增高。积极行溶栓或急诊PTCA治疗 ,可显著降低院内病死率。     

Late Potentials in a Porcine Model of Anterior Wall Myocardial Infarction and Their Relation to Inducible Ventricular Tachycardia

In this study, normal values for signal averaged electrocardiographic parameters were assessed in healthy pigs (n = 100) and the development of late potentials after myocardial infarction (n - 41) in relation to inducible ventricular tachycardia was investigated. Normal values are: filtered QHS duration (QRS) ± 78 msec; root mean square voltage of the averaged QRS complex (V_tot) ± 51 μV, and duration of terminal activity below 30 μV (D₃₀) ± 37 msec. The distribution of the root mean square voitage in the last 30 msec (V₃₀) was biphasic. Two weeks after myocardial infarction, QRS was prolonged from 55 ± 10 to 66 ± 19 msec (P < 0.002), D₃₀ was prolonged from 19 ± 6 msec to 28 ± 13 (P < 0.002). V₃₀ was decreased from 107 ± 135 μV to 45 ± 77 (P < 0.02). The total voltage (V_tot) was decreased from 195 ± 78 to 123 ± 61 μV (P < 0.002). In four pigs (19%) late potentials developed. Sustained ventricular tachycardia was inducible in 11 pigs (52%), ventricular fibrillation in two pigs (10%) and eight pigs (38%) were noninducible. Three of 11 inducible pigs and one of the noninducible pigs had a late potential. The incidence of late potentials and their relation to inducibie sustained ventricular tachycardia is comparable to the situation in man. Therefore, this pig model is an attractive alternative to the commonly used dog models.     

Determinants of the Natural Course of Ventricular Late Potentials After Thrombolytic Therapy for Acute Myocardial Infarction

The intraindividual changes of ventricular late potentials and their possible determinants were examined prospectively in 88 consecutive patients (male: 75; mean age: 58 ± 9 years) after thrombolytic therapy for acute myocardial infarction. Late potential analysis was performed 4 weeks and 12 months after acute myocardial infarction. At the same time, a left heart catheterization was performed to assess the extent of coronary heart disease and left ventricular ejection fraction. The incidence of late potential 4 weeks after acute myocardial infarction was 15% (13/88 patients). Eighteen percent (16/88) of the patients revealed changing results of late potential analysis: 9 patients lost late potential (late potential pos./neg.) 1 year after acute myocardial infarction and 7 patients presented new formation of late potential (late potential neg./pos.). Preserved late potentials were found in four patients (late potential pos./pos.). Late potential analysis remained negative in 68 patients (late potential neg./neg.). There was no influence of age, gender, site of infarction, clinical course, and medical treatment on the natural course of late potential. Changing results of late potential analysis seemed to be correlated with the evolution of left ventricular ejection fraction and the dynamics of coronary heart disease. In the group late potential pos./pos., comparable values for left ventricular ejection fraction were measured at both examinations, whereas late potential neg./neg. had a significant increase in ejection fraction. In the group late potential pos./neg., a significant improvement in left ventricular function was also measured. In contrast, the late potential neg./pos. group tended to have lower left ventricular ejection fractions 1 year after infarction. In the late potential neg./pos. and late potential pos./pos. groups, the extent of coronary artery disease returned to conditions comparable to baseline despite an initial reduction after coronary revascularization performed 4 weeks after infarction. Late potential neg./neg. and late potential pos./neg. revealed a stable benefit gained from coronary revascularization with a persistent reduction in the number of diseased vessels. Dynamic changes in the results of the signal-averaged ECG 1 year after thrombolytic therapy for acute myocardial infarction were observed in 18% of the patients. These changes seem to be correlated with the evolution of left ventricular function and the dynamics of coronary artery disease.     

Right Ventricular Disarticulation Procedures: The Role of Late Potentials in the Genesis of Postoperative Ventricular Arrhythmias

Arrhythwogenic right ventricular disease may be associated with life-threatening and drug refractory ventricular arrhythmias. Right ventricular disarticulation procedures are effective antiarrhythmic surgical approaches in selected patients. This study examined the role of late potentials in the postoperative development of new ventricular arrhythmias, and showed that right ventricular isolation is effective, probably because it destroys the tissue giving rise to late potentials. Total disarliculation is associated with fewer postoperative arrhythmias than partial isolation procedures. Total disarticulation may be the surgical approach of choice in such patients.     

急性心肌梗塞合并左室附壁血栓的超声研究

本文以５３２例急性心肌梗塞患者为对象，以心脏超声为手段，检出左室附壁血栓３７例，占各部位梗塞的７％，前壁梗塞的１３％，明显低于欧美的报告。该血栓易发生于前壁、大面积梗塞及室壁运动障碍的患者，于心梗发病后２±２天出现于左室心尖部，其形态多为附壁形，少为伸探形。继发周围动脉栓塞２例（５．４％）。５例（１４％）演变为机化型血栓，其余于入院后第１９±８天溶解消失     

超声心动图评估右室心肌梗死与心肌灌注造影的对比研究

目的研究右室心肌梗死（RVI）的超声心动图表现特征及与心肌灌注造影（MCE）的对比研究。 方法9条麻醉开胸犬,均结扎右冠状动脉近端,致急性右室心肌梗死。超声心动图记录梗死前后右室短轴和四腔切面,于左室腔内团状注射5%白蛋白微气泡悬浮液,通过负性显影的方法,确定右室梗死的范围和侧支血流状态,红四氮唑磷酸缓冲液（ETT）染色心肌标本。 结果阻断右冠状动脉后,右室横径增大,右室游离壁室壁变薄,右室游离壁及室间隔矛盾运动,右室射血分数下降,P〈0.05。MCE显示右室游离壁灌注缺损,负性显影区弧长（5.57±0.32）cm,占右室壁总弧长70%。梗死区边缘延迟显影。ETT心肌染色显示右室游离壁呈非透壁性、密集点状灶性坏死,其间有存活心肌。 结论右室腔扩大、梗死区室壁变薄及运动异常、室间隔矛盾运动、右室心功能减低是右室心肌梗死的超声心动图表现特征。MCE能准确地评估心肌梗死的范围和侧支的血供情况,与病理研究结果相一致。     

QT离散度及心室晚电位对心肌梗塞急性期室性心律失常的预测价值

目的：研究QT离菜度（QTd)及心室晚电位（VLP）对心肌梗塞急性期室性心律失常的预测价值。方法：计算48例急性心肌梗塞患QTd,其中34例行VLP检测。结果：12例严重室性心律失常组QTd,校正的QT离散度（QTcd)明显延长,VLP阳性率明显高于无室性心律失常组（P＜0．01）,结论：QTd和VLP检测对心肌梗塞急性期发生室性心律失常有较高预测价值。     

彩色多普勒超声观察陈旧性心肌梗死部位与左室功能改变

目的　应用彩色多普勒超声观察陈旧性心肌梗死患者的定位与左室功能。方法　观察对象为 4 2例心肌梗死患者和 4 0例正常人。根据心肌梗死部位 ,分为前壁梗死组 (OMI- AN) 2 0例 ,下壁心肌梗死 (OMI-IN) 2 2例。用多普勒超声心动图研究了左室收缩和舒张功能 ,Tei指数的定义为 :左室等容收缩期加等容舒张期之和除以射血时间。结果　OMI- IN组梗死部位瘢痕组织范围大于 OMI- IN,分别是 OMI- IN(4.1± 2 .1) cm,OMI-IN (2 .3± 2 .5 ) cm,(P <0 .0 1) ,OMI- IN,OMI- IN和对照组左室舒张末内径分别为 (5 7.6± 6 .2 ) mm,(5 2 .5± 5 .1) mm,和 (47.2± 3.7) mm (P <0 .0 1) ;左室射血分数 (EF)分别是 4 8.6± 7,5 8.0± 7和 6 5 .8± 9(P<0 .0 5 ) ;E/ A比值分别为 0 .99± 0 .14 ,0 .72± 0 .2 5和 1.3± 0 .2 3(p <0 .0 5 ) ;Tei指数分别是 0 .72± 0 .14 ,0 .4 9± 0 .18和 0 .38± 0 .12 ,(p <0 .0 0 1) ;舒张早期充盈时间 (DT) OMI- IN组短于 OMI- IN组。结论　心肌梗死部位与左室收缩及舒张功能有关 ,OMI- IN组梗死范围较大 ,左室功能亦低于 OMI- IN患者。     

Spatial Differences of the Duration of Ventricular Late Fields in the Signal-Averaged Magnetocardiogram in Patients with Ventricular Late Potentials

Magnetocardiography (MCG) allows one to noninvasively localize cardiac electrical activity in three dimensions. It was the purpose of this study to obtain information about the spatial variations of signal-averoged ventricular Jate magnetic fields recorded by a biomagnetic multichannel system. Biomagnetic signals of 170–600 heart cycles obtained hy the 37-channel system KRENIKON^R (Siemens Medical Engineering Group) were simultaneously averaged in all channels. The absolute values of the filtered signals (digital, bidirectional, four-pole butterworth, bandpass filter [3-dB range, 40–250 Hz]) were calculated in each channel. The noise level was determined within the TP segment. The onset of the terminal low amplitude signals (TLAS) was defined when the signals became lower than 1/23 of R_maxof the QRS complex for the channel with the largest filtered QRS complex after filtering. The TLAS ended when the signal was lower than twice the standard deviation (2 sigma) above the mean noise level. Ventricular late fields were defined as present when the TLAS had a duration of more than 39 msec. In this study, five patients with ventricular late potentials (four with sustained ventricular tachycardia) and three healthy individuals were examined. Ventricular late fields were detected in the patient group in 2–15 MCG channels with a mean length of 49.6 msec (43–60 msec). The spatial distribution of the ventricular late fields was consistently found to exhibit maximum duration in a certain area. In the normal subjects no ventricular late fields were detected. Thus, MCG is able to detect ventricular late fields and their spatial variations. In addition to the information obtained hy signal averaging from the surface ECG, averaging of biomagnetic signals with a multichannel device can reveal spatial inhomogeneity of delayed myocardial excitation.     

High Resolution ECG and Left Ventricular Volume After Acute Myocardial Infarction

The presence of ventricular late potentials (LPs) early after acute myocardial infarction (AMI) was recently reported to correlate with left ventricular dilatation subsequent to AMI. We assessed prospectively the relationship between LP (time domain) in the late phase of AMI and left ventricular end-diastolic volume (EDV) measured by equilibrium radionuclide angiocardiography 4 weeks and 12 months after AMI. In 80 consecutive patients 4 weeks and 12 months after thrombolytic therapy for AMI, LP and EDV were deter mined (EDV1, EDV2). There was no significant correlation between QRS duration (r = 0.18), RMS40 (r = 0.08), or LAS40 (r = 0.1) and EDV1 or EDV2 in patients with or without LP at baseline. In both groups (patients with [n = 15] and without LP [n = 65]), EDVl and EDV2 were comparable (128 ± 32 mL vs 126 ± 35 mL; 114 ± 40 mL vs 117 ± 36 mL; P = NS). In addition, there was no significant difference between EDVl and EDV2 in patients who developed new LP (n = 6) or lost LP (n = 9) 12 months after AMI. In contrast to LP in the very early phase after AMI, there seems to be no significant correlation between the high resolution ECG in the late phase after thrombolytic therapy for AMI and left ventricular EDV.     

The Effects of Direct Current Countershock on Ventricular Late Potentials

Signal averaging is a noninvasive method of recording ventricular late potentials. These late potentials are present in many patients with sustained ventricular tachycardia. Analysis of ventricular late potential characteristics may develop as a useful marker of antiarrhythmic drug efficacy. Often antiarrhythmic drugs are tested acutely in the electrophysiology laboratory after direct current countershock (DC shock). The purpose of this study was to investigate the effects of DC shock delivered for cardioversion of sustained ventricular tachycardia or fibrillation on ventricular late potentials. Signal averaged electrocardiograms (SAEKGs) were recorded before and after 13 DC shocks. There was no significant change in QRS duration, duration of the high frequency filtered QRS, or duration of the high frequency signal under 40 microvolts. There was a small increase in the root mean square amplitudes of the terminal 40 milliseconds (41 microV to 49 microV). This degree of change is felt to be clinically insignificant. Except for one trial, no late potential appeared or disappeared after electrical cardioversion. We have shown that ventricular late potentials are only slightly altered by programmed ventricular stimulation, induced sustained ventricular tachycardia or ventricular fibrillation, and DC countershock. To analyze changes in ventricular late potentials after antiarrhythmic drug administration in the electrophysiology laboratory, in those patients requiring DC countershock, comparisons should be made to postshock SAEKGs rather than those obtained prestudy.     

Effect of Right Ventricular Apical Pacing in Survivors of Myocardial Infarction

Background: Much information is available regarding the possible negative effects of long-term right ventricular (RV) apical pacing, which may cause worsening of heart failure. However, very limited data are available regarding the effects of RV pacing in patients with a previous myocardial infarction (MI).
Methods and Results: We screened 115 consecutive post-MI patients and matched a group of 29 pacemaker (PM) recipients with a group of 49 unpaced patients, for age, left ventricular (LV) ejection fraction, and site of MI. During a median follow-up of 54 months, echocardiograms showed a decrease in LV ejection fraction in the paced group, from 51 ± 10 to 39 ± 11 (P < 0.01), and a minimal change in the unpaced group, from 57 ± 8 to 56 ± 7 (P = 0.98). Similar change was observed in systolic and diastolic diameters and volumes.
Conclusions: The study showed that, in post-MI patients, RV apical pacing was associated with a worsening of LV function, suggesting that, among MI survivors, the need for a PM is a marker of worse outcome .     

Left Ventricular Free-Wall Rupture Occurring During Programmed Ventricular Stimulation in a Patient With Recent Myocardial Infarction

In this report we describe a patient who died during programmed ventricular stimulation due to a rupture of the left ventricular free wall at the site of a recent myocardial infarction. The patient was a 75-year-old male who presented with an extensive anterior wall myocardial infarction complicated by sustained ventricular tachycardia occurring 8 days after admission. Cardiac catheterization revealed total occlusion of left anterior descending coronary artery and an anteroapical aneurysm. The patient died due to electromechanical dissociation during electrophysiological testing 11 days after myocardial infarction. Postmortem examination showed a rupture of the left ventricular free wall at the site of the myocardial infarction and distant from the site of catheter placement. It is suggested that caution be taken in choosing patients for electrophysiological studies who have had recent large myocardial infarctions with ventricular aneurysm.     

Prediction of Arrhythmic Events After Acute Myocardial Infarction Using Two Methods for Late Potentials Recording

One hundred consecutive patients recovering from an acute myocardiai infarction underwent, prior to home discharge, signal-averaged electrocardiography (ECG), left ventriculography. and 24-hour Holter ECG recording. The signal-averaged ECG was recorded and analyzed using two procedures: the orthogonal bipolar XYZ lead configuration with a bidirectional filter: and a precordial unipolar lead configuration with a uonrecursive digital filter. An abnormal signal-averaged ECG was seen in 40% of patients with the XYZ system and in 30% of patients in the precordial method, abnormal ejection fraction (< 40%) in 24% of patients and high grade ectopy activity in 22%. During the 24-month follow-up period, 12 patients (12%) had an arrhythmic event defined as either sudden death (11 patients) or sustained ventricular tachycardia (1 patient). Neither the signal-averaged ECG with the XYZ configuration, the abnormal ejection fraction, nor the high grade ectopy were able to statistically predict a higher arrhythmic event rate. The signal-averaged ECG with the precordial configuration was able to statistically predict a higher arrhythmic event rate, P < 0.03; odds ratio = 3.96. The combination of the orthogonal XYZ configuration signal-averaged ECG with the ejection fraction (P < 0.01, odds ralio = 7.33), or with ejection fraction and Holter monitoring (P < 0.06. odds ratio = 6.17) was able to predict a higher arrhythmic event rate. The combination of the precordial configuration signal-averaged ECG with the ejection fraction (P < 0.002, odds ratio = 14.4), or with ejection fraction and Holter monitoring (P < 0.06. odds ratio =10) was able to better predict a higher arrhythmic event rate. The combination of a normal or abnormal signal-averaged ECG and ejection fraction gave a sensitivity, specificity, positive, or negative value prediction of arrhythmic events of 60%, 90.6%, 37.5%, and 96%, respectively. It must be emphasized that the number of arrhythmic events during the 2-year follow-up was small and further study is required to determine the true predictive value of each method for arrhythmic events.     

Loss of Late Potentials After Radiofrequency Catheter Ablation of Recurrent Ventricular Tachycardia in a Patient with Right Bundle Branch Block

The case of a patient with a history of myocardial infarction and recurrent ventricular tachycardia undergoing attempted radiofrequency catheter ahlation with loss of late potentials is described. Prior to energy delivery fractionated, late activation could be found using the signal-averaged ECC despite the presence of a right bundle branch block. After successful catheter ablation, the clinical ventricular tachycardia was no longer inducible and the signal-averaged ECG, recorded the next day, showed marked changes indicating loss of late potentials. Our report emphasizes the possibility of late potential recordings despite the presence of bundle branch block.     

Late Ventricular Potentials and Spontaneous and Induced Ventricular Arrhythmias in Dilated or Hypertrophic Cardiomyopathies. A Prospective Study About 83 Patients

In a series of 83 patients with dilated (DCM) (n = 56) or hypertrophic cardiomyopathies (HCM) (n = 27), were performed 24-hour-Holter monitorings, exercise stress testings, noninvasive recordings of late ventricular potentials (LVP), and programmed ventricular stimulations (PVS) (sinus rhythm and three cycles of stimulation, two extrastimuli, two right ventricle sites) (n = 53). in order to appreciate the frequency of ventricular premature depolarisations (VPDs), to correlate these results with myocardial vulnerability to TV induction, and to compare electrophysiologic and hemodynamic results. Holter monitoring showed that 80% of group A patients had VPDs (75% Lown's grade 3 or over) and 63% in group B (37%≥ grade 3). LVP were found in 15/56 DCM, and 2/27 HCM; in comparison with a control group of 32 normal subjects, the prevalence of LVP was only significant for DCM group. LVP were more frequent in cases of VPD's ≥ Lown's grade 3 at Holter monitoring in DCM group, (33% versus 7% if VPDs ≤ Lown's grade 3) and HCM group (20% versus 0) but the correlation was not significant. Exercise stress testing, conducted only in group E, revealed about 20% of VPDs. PVS provoked ventricular arrhythmia (>5 QRS) in 13 out of 33 cases in group A and in 2 out of 20 cases in group B. There was no significant correlation between the results of these methods of study and those of hemodynamic or echocardiographic explorations except for cardiac index in group A flower when LVP were present, and VPDs ≥ grade 3 during Holter) and end diastolic diameter (larger when PVS provoked fewer ventricular arrhythmias). In group B, PVS induced monomorphic VT in 2/3 patients with syncopes. Thus: (1) ventricular arrhythmias are frequent in cardiomyopathies but LVP had a significant prevalence only in dilated forms; (2) in DCM monomorphic induced VT reproduce spontaneous crisis, whereas in HCM it is possible to provoke VT in patients with syncopes but without this clinical arrhythmia; (3) in DCM as in HCM, ventricular arrhythmia can be independent from hemodynamic disorders.     

Study of Late Potentials and Ventricular Arrhythmias in Hypertensive Patients with Normal Electrocardiograms

Introduction: Although an increase in the occurrence of ventricular arrhythmias has been observed in hypertensive patients, some basic questions remain unresolved regarding the prevalence and the pathophysiology of these arrhythmias. The basic aims of this study were as follows: (1) to examine the incidence and severity of ventricular arrhythmias in a substantial number of hypertensive patients without electrocardiographic indications of hypertrophy; and (2) to examine the correlation between late potentials, hypertrophy, and ventricular arrhythmias in these patients. Materials and Methods: We studied 78 consecutive patients (31 men, 47 women), aged 60.5 ± 7.8 years, with a history of hypertension but a normal electrocardiogram. All patients had an echocardiographic study, 24-hour ambulatory monitoring, exercise test, and signal-averaged electrocardiogram. The latter was analyzed using a 40-to 250-Hz filter and with a noise level ± 0.3 μV. Results: Of the 78 patients studied, 21 (26.9%) had severe ventricular arrhythmias, while 57 (73.1 %) had either no ventricular ectopics or sporadic isolated ventricular extrasystoles. Left ventricular hypertrophy, defined by echocardiography, was found in 58 patients (74.3%), of which 16 (27.58%) had severe ventricular arrhythmias. Five (25%) of the 20 patients without hypertrophy also had severe ventricular arrhythmias (P = NS). Ventricular late potentials were recorded in 19 (24.5%) of the 78 patients. Of these, 11 (57.89%) had severe arrhythmias, while of the 59 patients without late potentials 10 (16.94%) had severe ventricular ectopic activity. Conclusions: In hypertensive patients without electrocardiographic signs of hypertrophy, the higher prevalence of ventricular arrhythmias does not appear to be related to left ventricular hypertrophy but is correlated with the existence of ventricular late potentials.     

直接经皮冠状动脉介入治疗对急性心肌梗塞后左室重构的影响

目的:研究直接经皮冠状动脉介入治疗(直接PCI)及常规药物治疗对急性心肌梗塞(AMI)后左室重构的影响。方法:应用超声心动图对65例AMI患者进行随访。结果:12~24个月随访显示:直接PCI组患者的心功能分级、再次住院数及死亡数较常规治疗组显著降低(P<0.05)。左室收缩末容积(LVESV)较常规治疗组减小(P<0.01),但左室射血分数(LVEF)增高(P<0.01),球形指数(SI)显著增加(P<0.01),室壁运动指数(WMI)显著降低(P<0.05),左室质量指数(LVMI)也显著降低(P<0.01)。AMI后1个月及12~24个月随访显示:常规治疗组AMI患者12~24个月时LVESV、LVEF及SI较1个月时显著改变(P<0.01),但WMI及LVMI无显著差异(P>0.05)。直接PCI组AMI患者除WMI在12~24个月时较1个月时显著降低(P<0.01)外,余指标均无显著差异(P>0.05)。结论:直接PCI治疗能够明显改善AMI后患者的左室重构,使AMI后心衰、再次住院及死亡发生率降低。