Effect of thrombolytic therapy in acute myocardial infarct on incidence of ventricular late potentials

The aim of thrombolytic therapy for acute myocardial infarction is reperfusion of the infarction-related vessel. Ventricular late potentials detected by signal averaging have been demonstrated to be related to slow and inhomogeneous conduction within damaged cardiac tissue. In 75 patients with first myocardial infarction the effect of thrombolysis on ventricular late potentials was studied. Reperfusion of the infarction-related vessel could be demonstrated by coronary angiography in 53 (71%) patients. In 22 patients (29%) there was no reperfusion. In the 53 patients with successful thrombolysis the incidence of late potentials was significantly lower (9%) than in the 22 patients without reperfusion (50%). The lower incidence of late potentials may demonstrate improved ventricular electrical stability.     

Reduction in the frequency of ventricular late potentials after acute myocardial infarction by early thrombolytic therapy

Ventricular late potentials are strong predictors of arrhythmic events after acute myocardial infarction (AMI). To assess the effect of intravenous thrombolysis on the incidence of ventricular late potentials, 223 consecutive patients surviving a first AMI were included in the present study: 59 patients (53 men, 6 women, mean age +/- standard deviation 55 +/- 10 years) received intravenous recombinant tissue-type plasminogen activator (100 mg over 3 hours, group A) and 164 patients (123 men, 41 women, mean age 61 +/- 11 years) received conventional medical treatment (group B). A time-domain signal-averaged electrocardiogram and a high-resolution beat-to-beat recording (gain 10(6), filters 100 to 300 Hz) were performed at 10 +/- 3 days after AMI. There was no difference between group A and B patients in terms of AMI location (anterior in 28 of 59 vs 80 of 164, difference not significant [NS]), mean left ventricular ejection fraction (55 +/- 10 vs 55 +/- 13%, NS), or presence of heart failure (New York Heart Association class III or IV in 12 of 59 vs 40 of 164, NS). The incidence of ventricular late potentials was 10% (6 of 59) in group A and 24% (39 of 164) in group B (p less than 0.05). Among the 146 patients who underwent coronary arteriography, the incidence of ventricular late potentials was 13% (10 of 80) in patients with a patent infarct-related artery and 26% (17 of 66) in patients with an occluded infarct-related artery (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of a beta-blocker on ventricular late potentials in patients with acute anterior myocardial infarction receiving successful thrombolytic therapy

Late potentials (LP) detected on the signal-averaged electrocardiogram (SAECG) predict arrhythmic events after acute myocardial infarction (AMI). It is also well established that successful thrombolytic therapy reduces the incidence of LP. Our aim was to evaluate the effects of a beta-blocker on LP in patients receiving thrombolytic therapy. We studied 40 patients presenting with anteroseptal AMI (< 6 hours). All patients received thrombolytic therapy and were evaluated with coronary angiography at predischarge. Eighteen patients received metoprolol (5 mg IV on admission followed by 50 mg BID). SAECG recordings were obtained serially using an ART system (40-250 Hz filter, noise < 0.5 mV) prior to thrombolytic therapy, after 48 hours and after 10 days. LP was defined as posi-tive if the SAECG met at least 2 of the Gomes criteria. Changes observed in SAECG recordings after thrombolytic therapy were correlated with angiographic and clinical data with regard to the usage of BB. The frequencies of LP before and after thrombolytic therapy were compared with the McNemar test. There were no significant differences between the clinical characteristics, risk factors, and angiographic findings (including infarct related artery patency and LV functions) of the groups. Baseline SAECG findings were also similar between the groups. The incidence of LP significantly decreased after TT in the BB group, however, this change was not observed in patients who did not receive BB (P = 0.012, McNemar test). Beta-blockers reduce the incidence of LPs following thrombolytic therapy in patients with anterior AMI. This might be explained by the possible beneficial effect of BB on the arrhythmogenic substrate.     

心肌再灌注对犬心室晚电位的影响

对犬进行冠状动脉二期结扎,建立心肌梗死模型,应用心表组合电极标测心室晚电位,观察再灌注对其影响。结果发现:心室晚电位阳性再灌犬,晚电位100％转阴。未灌犬无一例转阴。心室晚电位阳性再灌犬恶性心律失常发生率与晚电位阴性再灌犬相比,无显著差异。提示1.再灌注是使心室晚电位转阴的可靠方法;2.心室晚电位与再灌注心律失常无关;3.对急性心肌梗塞后心室晚电位阳性者,应积极进行心肌再灌注治疗。     

The origin of late potentials in patients with ventricular tachycardia after myocardial infarction

In order to study the origin of late potentials, their distribution was analyzed in 16 patients who had undergone surgery for arrhythmia due to ventricular tachycardia following myocardial infarction. The potentials were measured in sinus rhythm using 63 unipolar leads placed on the chest before the operation, then on the epicardium and endocardium during the operation. Epicardial and/or endocardial activity extending beyond the QRS complex measured from unfiltered chest signals and characterized by slowed propagation at the edge or inside of necrotic regions, stable from one beat to the next, and showing simple (39 per cent), double (34 per cent) or fragmented (27 per cent) deflections on the electrocardiograms were observed in 5/6 patients without bundle-branch block and in 5/10 patients with block. Similar activity but which did not extend after the QRS was detected in the 6 other patients. For signals filtered at 55 Hz, a close correlation between the distribution of chest, epicardial and endocardial potentials was observed, thus allowing approximate location of the origin of late potentials from the chest. Anterior or apical sites corresponded to close extrema in the precordial region, whereas the other sites were associated with more distant extrema. An analysis of potential distribution thus gives a better understanding of the electrogenesis of late potentials as well as their detection on the chest.     

急性心肌梗死冠状动脉自发再通对心室晚电位的影响

137例急性心肌梗死病人发病后1周内做冠脉造影。冠脉完全闭塞65例(组1),不全闭塞72例(组2),冠脉自发再通率为53%。组2晚电位检出率显著低于组1,左室射血分数显著高于组1。逐步多元回归分析示肌酸激酶峰值及冠脉持续闭塞为影响晚电位检出率的两个自变量(皆 P<0.05)。     

Importance of myocardial infarct artery patency on the prevalence of ventricular arrhythmia and late potentials after thrombolysis in acute myocardial infarction.

Sustained infarct artery patency is an important determinant of survival in patients with acute myocardial infarction. We studied 61 patients with acute myocardial infarction who received intravenous recombinant tissue-type plasminogen activator, aspirin or heparin within 6 hours of symptom onset, to determine if infarct artery patency after intravenous thrombolytic therapy influences myocardial electrical stability as measured by the prevalence of spontaneous ventricular ectopy or late potential activity. Infarct artery patency was determined by angiographic evaluation 2.5 +/- 3 days after infarction. Forty-eight patients (79%) had a patent infarct-related artery and 13 (21%) patients had an occluded vessel. The mean number of ventricular premature complexes (VPCs)/hour (p less than 0.01) and the prevalence of late potentials (54 vs 19%; p less than 0.03) were significantly higher in patients with an occluded versus patent-infarct related vessel. Although VPC frequency and late potentials were not influenced by the time to thrombolytic treatment, patients with a patent infarct-related artery had a lower prevalence of late potentials regardless of whether treatment was initiated less than or equal to 2 hours (25% patent vs 50% occluded; p = not significant) or 2 to 6 hours (16% patent vs 55% occluded; p greater than 0.03) after symptom onset. Thus, successful thrombolysis decreases the frequency of ventricular ectopic activity and late potentials in the early postinfarction phase. The reduction in both markers of electrical instability may help explain why the prognosis after successful thrombolysis is improved after acute myocardial infarction.     

Prognostic significance of late ventricular potentials after acute myocardial infarction

The prognostic significance of late ventricular potentials recordedfrom the body surface using high-gain amplification and signalaveraging was assessed prospectively in 160 patients (mean age56±8.3 years) after recent acute myocardial infarction(median day of study 25.5). Late potentials were recorded in 81 out of 160 patients (50.6%);a duration of less than 20 ms was observed in 33 patients (20.6%),whereas late potentials of 20 ms duration or more were presentin 48 patients (30%). The mean duration of late potentials was27 ± 16.5 ms. There was no significant correlation withthe frequency and type of spontaneous ventricular arrhythmiasduring 10–24 h Holter monitoring. The follow-up period was 7.5±3.2 months (mean ±s.D.;maximum 15.8 months). In 136 patients (85%) the course afterdischarge was uneventful. Sudden cardiac death occurred in sevenpatients (4.4%) after 3.7± 3.4 months (range 0.7–8.3months). Sustained ventricular tachycardia was documented infour cases 2.9± 1.3 months after myocardial infarction,all having late potentials. The overall incidence of ventriculartachycardia in patients with late potentials of 20 ms durationand more was four out of 48 patients (8.3%) increasing to 16.6%(three out of 18 patients) if only patients with late potentialsgreater than 40 ms were considered. Sudden cardiac death occurredin three of 79 patients (3.8%) without late potentials. In patientswith late potentials less than 40 ms duration, the incidenceof sudden death was 3.2% (two out of 63 patients), but it increasedto 11.1% (two out of 18 patients) with late potentials of 40ms duration or more. Ventricular tachycardia or sudden deathoccurred in 21.7% of patients with late potentials and anteriorwall infarction compared to 5.4% in patients with late potentialsand inferior wall infarction (P<0.05). Only one of 79 patients(1.3%) without late potentials died non-suddenly from a cardiaccause (reinfarction) compared to three of 81 patients (3.7%)with late potentials irrespective of duration. Thus, this prospective multicentre pilot study suggests thataveraging might be a promising non- invasive technique for theidentification of patients prone to ventricular tachycardiaor possibly even sudden death after recent acute myocardialinfarction.     

The effect of statin therapy on ventricular late potentials in acute myocardial infarction

AIMS: To determine whether early statin therapy in acute myocardial infarction has any effect on ventricular late potentials which are considered as a noninvasive tool for evaluation of arrhythmogenic substrate. METHODS AND RESULTS: Study population consisted of prospectively enrolled 72 patients presenting with acute myocardial infarction (<6 h). Thirty-four of the patients were randomized to pravastatin (40 mg/day) on admission irrespective of lipid levels. All patients received thrombolytic therapy. Signal-averaged ECG recordings were obtained serially prior to thrombolytic therapy, 48 h after and 10 days later. Late potentials were defined as positive if signal-averaged ECG met at least two of Gomes criteria: filtered total QRS duration >114 ms, root mean square voltage of the last 40 ms of the QRS <20 mV, or the duration of the terminal low (<40 mV) amplitude signals >38 ms. Changes observed in signal-averaged ECG recordings after thrombolysis were evaluated statistically with regard to statin usage. There were no significant differences between the clinical characteristics of the two randomized groups. There was a significant decrease in the rates of late potentials between the first and third signal-averaged ECG recordings after thrombolytic therapy in pravastatin group. Pravastatin group also had lower incidence of ventricular arrhythmias compared with control group (26 vs. 63%, P=0.021). The in-hospital cardiovascular event rates were also lower in statin group. CONCLUSION: Early use of pravastatin reduces the incidence of late potentials following thrombolytic therapy in acute myocardial infarction. Statin therapy also seems to be reducing the incidence of in-hospital ventricular arrhythmias. These beneficial effects of statins might be explained through prevention of new myocardial ischemic episodes due to early plaque stabilization or regulation of endothelial and platelet functions.     

Effect of pre-infarction angina on ventricular late potentials in patients with acute myocardial infarction and successful thrombolysis

OBJECTIVE: Pre-infarction angina is considered as a good clinical model of ischaemic preconditioning which facilitates myocardial protection. Late potentials (LP) have prognostic significance following acute myocardial infarction (AMI). It is also well established that thrombolytic therapy reduces the incidence of LP. Our aim was to evaluate the relationship between pre-infarction angina and LP in patients receiving successful thrombolytic therapy. METHODS AND RESULTS: We prospectively studied 55 patients presenting with AMI (<6 hours). All patients received thrombolytic therapy and were evaluated with coronary angiography at predischarge. Signal-averaged recordings (SAECG) were obtained serially prior to thrombolysis, 48 hours after and 10 days later. Pre-infarction angina was present in 14 (25%) patients. There were no significant differences between the clinical characteristics and angiographic findings of the groups. Baseline SAECG parameters of the groups were also similar. After thrombolysis, the 48th hour values of LAS (the duration of the terminal low amplitude signals), and both the 10th day values of LAS and RMS (root mean square voltage of the last 40 ms of the QRS) were significantly better in the pre-infarction angina group. The mean filtered QRS duration and RMS 40 values changed significantly at the 10th day recordings of patients with pre-infarction angina [QRS duration, 110+/-34 ms before to 91+/-11 ms after (p = 0.039); RMS 40, 40+/-17 microV before to 50+/-14 microV after (p = 0.02)]. The incidence of LP significantly decreased after thrombolytic therapy in the pre-infarction angina group, however, this change was not observed in patients without angina. CONCLUSION: Presence of pre-infarction angina reduces the incidence of LP following thrombolysis in AMI. This might be explained by the possible beneficial effect of ischaemic preconditioning on the arrhythmogenic substrate.     

Determinants of improved left ventricular function after thrombolytic therapy in acute myocardial infarction

Many studies have been performed to evaluate the efficacy of thrombolytic therapy in achieving reperfusion, salvaging myocardium and enhancing survival. This review discusses the concordance between the results of these clinical studies and the observations made in experimental animals of the effect of reperfusion on the recovery of left ventricular function. The evaluation of functional recovery is affected by the timing of the measurement and the sensitivity of the method for detecting regional abnormalities. In addition, the underlying coronary anatomy also determines outcome, so that infarct location, collateral circulation and the degree of coronary obstruction merit consideration. Two factors are of paramount importance in determining the amount of myocardium salvaged, the recovery of left ventricular function and the reduction in mortality. These factors are: the time delay until reperfusion is achieved and the adequacy of the coronary reflow. The close agreement between studies measuring the effect of reperfusion on left ventricular function and studies with mortality as the end point provides indirect evidence that enhancement of survival in patients treated with thrombolytic agents is mediated by recovery of ventricular function.     

Effect of antiarrhythmic therapy on delayed potentials detected by the signal-averaged electrocardiogram in patients with ventricular tachycardia after acute myocardial infarction

The ability of class I and class II antiarrhythmic drugs to either abolish delayed potentials or modify their timing was investigated in 39 patients with spontaneous ventricular tachycardia (VT) after myocardial infarction. Before the study all patients had delayed potentials on the signal-averaged electrocardiogram and inducible VT with programmed stimulation. These investigations were repeated during 67 trials of oral antiarrhythmic therapy (mexiletine 25, quinidine 24, metoprolol 13, disopyramide 2, procainamide 1, drug combinations 2). Delayed potentials were abolished in only 5 trails (7%), which was within the baseline variability of 8.5% for detection of delayed potentials. In the 7 trials in which VT inducibility was suppressed, delayed potentials persisted in 6 and mean ventricular activation time was virtually unchanged (151 ms before drug therapy, 152 ms after). Quinidine, mexiletine and metoprolol caused no consistent change in ventricular activation time. There was also no change in mean ventricular activation time (164 ms before and 163 ms after drug treatment) in patients in whom spontaneous VT did not recur with drug therapy during follow-up. Thus, the tested antiarrhythmic drugs had no consistent effects on presence or timing of delayed potentials on the signal-averaged electrocardiogram, even when VT inducibility was suppressed or recurrence of spontaneous VT was prevented.     

Relationship between myocardial viability and ventricular late potentials in patients with history of myocardial infarction

AIM. To study relationship between presence and volume of viable myocardium and registration of late ventricular potentials in patients with history of myocardial infarction. MATERIAL AND METHODS. High resolution ECG, dobutamine stress echocardiography and Holter ECG monitoring were carried out 34 patients (mean age 54.1-/+3.1 years) with history of documented myocardial infarction. RESULTS. According to data of dobutamine stress echo patients were divided into 2 groups: with irreversible myocardial dysfunction (n=16, group 1) and with hibernating myocardium (n=18, group 2). Ventricular late potentials were registered in 3 (18.7%) and 11 (61,1%) patients in groups 1 and 2, respectively. Group 2 patients more often had high-grade ventricular arrhythmias. There was no association between presence of ventricular late potentials and Lown grade of ventricular arrhythmias on Holter ECG. Duration of filtered QRS (QRSt) complex correlated directly with index of regional wall motion abnormality, end-diastolic volume, and negatively - with total ejection fraction. CONCLUSION. Among myocardial infarction survivors patients in whom dobutamine stress echo detects viable myocardium significantly more often have ventricular late potentials and high grade ventricular arrhythmias compared with patients with myocardial scars without viable myocardium.     

Effects of early captopril therapy after myocardial infarction on the incidence of late potentials

Background: Late potentials (LP) on signal‐averaged electrocardiography (SAECG), recorded 6 to 30 days after an acute myocardial infarction (AMI), identify patients at risk for late arrhythmic events. Angiotensin‐converting enzyme (ACE) inhibitors have been shown to reduce ventricular remodeling and cardiovascular mortality after AMI. Hypothesis: The aim of this study was to investigate the effect of early (< 24 h) administration of captopril on the presence of LP on Days 6–30 after AMI. Methods: The study included 117 patients with a first AMI; 63 patients (53 men and 10 women, aged 59±12 years), 35 with an anterior and 28 with an inferior AMI (44 thrombolyzed), received early captopril therapy. The control group consisted of 54 age‐matched patients (39 men and 15 women, aged 60 ± 12 years), 19 with an anterior and 35 with an inferior AMI (31 thrombolyzed, p = NS), who did not receive early therapy with an ACE inhibitor. The mean left ventricular ejection fraction was similar in both groups (48 vs. 46%). Time domain analysis of SAECG was performed using a band‐pass filter of 40–250 Hz. Late potentials were considered present if any two of three criteria were met: (1) Filtered QRS duration (QRSD) > 114 ms, (2) root‐mean‐square voltage of the last 40 ms of the QRS complex (RMS) > 20 m?V, and (3) duration of low amplitude (< 40 m?V) signal of the terminal portion of the QRS (LAS) > 38 ms. Results: In the two groups of patients there were no differences in mean values of SAECG parameters. No patient was receiving any antiarrhythmic drugs. In the captopril group LPs were present in 9 of 63 patients (14%) and in the control group in 17 of 54 patients (31 %) (p =0.046). There was no difference in the number of patients with a patent infarct‐related artery in the two groups (76 vs. 59%). Conclusion: Captopril treatment early after an AMI reduces the incidence of LPs recorded on Days 6–30 and may thus favorably affect the arrhythmogenic substrate.     

Long-term effect of thrombolytic therapy on left ventricular ejection fraction after acute myocardial infarction

To assess the long-term effect of thrombolytic therapy on left ventricular (LV) systolic function, 222 patients with acute myocardial infarction treated with intravenous tissue plasminogen activator within 4 hours of symptom onset underwent assessment of LV ejection fraction (EF) by radionuclide equilibrium angiography at hospital discharge and 1 year later. Mean EF at hospital discharge (46 ± 12) was similar to that at 1 year (45 ± 13). Stepwise multivariate linear regression analysis identified EF at discharge and patency of the infarct-related artery before discharge as independent predictors of EF change at 1 year (p = 0.0002 and 0.003, respectively). Random assignments to invasive versus conservative treatment strategies or to early versus delayed β-blocker therapy did not affect EF change during follow-up. No significant deterioration of EF was observed in patients with larger infarcts. However, EF decreased from 45 ± 10 at hospital discharge to 39 ± 12 (p = 0.005) at 1-year follow-up in a subgroup of patients with history of prior infarction.

Thus, patients with acute myocardial infarction, treated with intravenous tissue plasminogen activator early after onset of symptoms, appear to have stable LV function between hospital discharge and 1 year follow-up. The change in EF between hospital discharge and 1 year can be predicted from the EF value at discharge, patency of the infarct-related artery before discharge and history of previous myocardial infarction.     

链激酶溶栓治疗急性心肌梗死对左心室功能的改善作用

为评价链激酶溶栓治疗急性心肌梗死（ＡＭＩ）对左心室功能的影响，应用二维超声心动图对２６例接受链激酶溶栓治疗的ＡＭＩ患者和２７例未溶栓的ＡＭＩ患者，分别在急性期及６个月后随访时测量并计算左心室容积（ＥＤＶ和ＥＳＶ），射血分数（ＥＦ）以及室壁运动指数（ＧＷＭＩ和ＲＷＭＩ）。以上各项指标在急性期时比较各组无显著性差异；在随访期再通组ＥＦ值明显高于未通组和未溶栓组，再通组左室容量减小。急性期各组心功能无差异，随访时再通组心功能较未通组显著改善。提示:链激酶溶栓能明显减轻ＡＭＩ患者的左心室扩张，改善左心室功能和长期预后     

Management of patients after thrombolytic therapy for acute myocardial infarction

The coronary artery thrombus that causes acute myocardial infarction can be lysed, and reperfusion can be achieved, in the first few hours after infarction. However, the infarct vessel will reocclude in 15-30% of patients, and this event is frequently associated with pain, reinfarction, arrhythmias, or death. The risk of reocclusion is greatest in patients with high-grade residual stenosis after thrombolysis. Percutaneous coronary angioplasty may be performed safely after thrombolytic therapy. Angioplasty effectively decreases the degree of residual stenosis, and may thereby reduce the risk of reocclusion and consequent ischemic events. However, a substantial proportion of patients with acute infarction are not suitable candidates for angioplasty. Coronary artery bypass surgery has also been safely performed within several days after thrombolytic therapy. Further studies are needed to determine which patients will benefit most from this aggressive approach to acute myocardial infarction.