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.     

Ventricular fibrillation in the initial phase of acute myocardial infarct

In order to determinate the incidence, predictivity and prognosis of ventricular fibrillation in the early phase of acute myocardial infarction a series of 301 patients with acute myocardial infarction consecutively assisted by the Mobile Coronary Care Unit of Florence was analyzed. 151 patients (50.2%) received intensive care within 2 hours from the onset of the symptoms, 75 patients (24.9%) received intensive care between the second and sixth hour. 38 patients (12.6%) had at least one episode of ventricular fibrillation. 30% of the episodes of ventricular fibrillation happened within 1 hours from the onset of the symptoms, 47.4% within 2 hours, 74% within 6 hours. Serious arrhythmias complicated the early phase of acute myocardial infarction, but only sinus bradycardia seems to have a significant predicativity of ventricular fibrillation (P less than 0.05). We found that hospital survival resuscitated patients is strictly related to the time between early symptoms and the episode of ventricular fibrillation: 91% of the patients with ventricular fibrillation within 1 hour were discharged alive from hospital, 71% of those with ventricular fibrillation within 6 hours, 20% of those with ventricular fibrillation beyond 6 hours (P less than 0.01). The high rate and the favourable prognosis of ventricular fibrillation in the early phase of acute myocardial infarction must lead to a widespread implementation of rapid response emergency care systems away from hospital.     

Ventricular late potentials and left ventricular function after early enalapril treatment in acute myocardial infarction

In conclusion, late potentials measured at discharge are associated with a lack of improvement in left ventricular function after AMI, and enalapril treatment seems to reduce the presence of late potentials.     

Late ventricular potentials in acute and rehabilitative periods of myocardial infarct

The study was undertaken to examine 121 individuals: 48 apparently healthy subjects, 43 patients with angina pectoris and 42 patients with acute myocardial infarction (MI). Late ventricular potentials (LVP) were recorded in 6.2% of healthy subjects, 25.6% of patients with angina and 40.5% of those with MI in the first 24 hours, 28.5% on day 3, and 45.2% on day 14 of the onset of infarction. They were not recorded in 35.7% of MI patients. On days 3-4 of MI, the presence of LVP depended on the severity of diastolic left ventricular dysfunction; on day 14, LVP occur more frequently with circular than with anterior MI; in days 3 and 14, LVP were recorded much more frequently with Q wave; the total R-wave amplitude in leads V2-V4 is of definite importance for LVP in anterior MI, whereas that in 35 leads is of definite significance in posterior MI.     

Ventricular late potentials in myotonic dystrophy

OBJECTIVE: To determine the prevalence of ventricular late potentials, as determined by signal-averaged electrocardiography, in patients with myotonic dystrophy. DESIGN: Cross sectional, with blinded analysis of all electrocardiographic data. SETTING: Outpatient departments of a Veterans Affairs medical center and a tertiary care private hospital. PARTICIPANTS: Twenty-four patients with myotonic dystrophy. Patients were excluded from the study if they had either a history suggestive of significant ventricular arrhythmias or electrocardiographic evidence of a bundle-branch block. Two comparison groups were also formed; one group included 44 healthy employees at the tertiary hospital and the other, 30 cardiac patients with inducible ventricular tachycardia. MAIN RESULTS: A time-domain analysis of the signal-averaged electrocardiograms showed that 75% of patients with myotonic dystrophy met one criterion for the presence of late potentials, 67% met two criteria, and 29% met all three criteria. Spectrotemporal mapping in these patients showed markedly abnormal spectral peaks with a mean factor of normality that was significantly lower than that of the normal volunteers; the frequency of electrocardiographic abnormalities approached that seen in patients with known ventricular tachycardia. The presence of late potentials correlated directly with the length of the PR interval and inversely with left ventricular fractional shortening. CONCLUSIONS: In our study, the prevalence of late potentials on signal-averaged electrocardiography in patients with myotonic dystrophy approached that seen in cardiac patients with inducible ventricular tachycardia. It is possible that ventricular arrhythmias play a role in the occurrence of sudden death in some patients with myotonic dystrophy.     

Ventricular late potentials in normal subjects

Low-amplitude late potentials detected in the terminal part of ventricular activation have been evaluated as a possible means of identifying patients prone to sustained ventricular tachyarrhythmias. These signals are usually absent in those without such arrhythmias and in normal subjects. 67 healthy subjects, with no suggestion of cardiac disease from examination or electrocardiograms, were studied in an effort to report the incidence of late potentials in normal subjects. Three subjects met the criteria for abnormal late potentials (4%); the vectormagnitude complexes of these subjects were indistinguishable from those seen in patients with spontaneous sustained ventricular tachycardia after myocardial infarction. Measured indices from our subjects were compared with those of normal subjects studied by other investigators utilizing similar analytic techniques and similar software and equipment. Explanations are considered for the occurrence of false-positives. It is concluded that the incidence of late potentials in normal subjects is very low and thought to represent some type of false-positive expression related either to the recording or analytic technique. However, in certain instances, the occurrence of late potentials in a seemingly normal person may be a predictor of underlying structural pathology.     

Ventricular late potentials in athletes]

Ventricular late potentials detected by signal averaging have a high predictive value for the origin of malignant ventricular tachyarrhythmias in patients with coronary artery disease. We examined 35 male sportsmen aged from 22 to 33 years. Clinical examination, ECG at rest, echocardiography and signal averaging were performed. In nine of the 35 sportsmen (26%) ventricular late potentials were detected. In a control group of 20 nonsportsmen none had late potentials. The nine sportsmen with late potentials all had electrocardiographical and echocardiographical signs of left-ventricular hypertrophy. Of the 26 sportsmen without ventricular late potentials five had left-ventricular hypertrophy. Ventricular late potentials are not rare in sportsmen. They seem always to appear together with left-ventricular hypertrophy.     

Behavior of late ventricular potentials in acute experimental myocardial ischemia

Locally retarded depolarizations of the ischaemic myocardium are regarded as frequent trigger mechanisms of dangerous ventricular arrhythmias. Up to now, however, there are scarcely systematic investigations concerning their concrete developmental conditions in man, since late potentials can be made evident only by means of expensive invasive methods or signal mediation techniques. Therefore, an animal model should be built, which is suitable for the control of new therapy conceptions with antiarrhythmic drugs. The investigations were performed on 22 pigs in whom under insufflation anaesthesia altogether 10 pressure, flow and contractility parameters as well as 6 epicardial ECG signals were continuously recorded. The episodes of ischaemia were caused by LAD occlusions of different duration and intensity. Typical late potentials could be registered in 5 animals who all had survived complete interruptions of the coronary blood flow of longer than 10 min. The mean duration of the late potentials was 20 +/- 9.2 ms, their amplitudes reached from 150 to 600 microV. Also with regard to time and cycle constancy, the delay of the late Q-potential and the morphology they corresponded to the homogeneous phenomenon, known from man. They always could be derived only from electrodes outside the immediate zone of ischaemia. Neither partial occlusions nor complete interruption of the coronary blood flow in intervals shorter than 10 minutes led to the development of a late potential. The animal model used altogether appears very suitable to investigate the medicamentous influencibility of arrhythmogenic areas of the myocardium under direct control of the dynamic behaviour of ventricular late potentials.     

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.     

Ventricular fibrillation threshold in acute myocardial infarction and its relation to myocardial infarct size.

The effect of myocardial infarct size on ventricular fibrillation threshold (VFT) was evaluated by determining changes in VFT during acute myocardial infarction and relating those changes to infarct size. Infarct size was estimated from gross measurement and from serial changes in serum CPK activity in 25 dogs. VFT reduction correlated well with gross infarct size (r=0.92). This suggests that the severity of electrical instability during AMI is related to the size of the developing infarct, and that appropriate therapeutic interventions to reduce infarct size during this time may also render the heart more electrically stable.     

Late potentials and computerized averaging electrocardiogram in acute myocardial infarct: evaluation of myocardial reperfusion

Myocardial reperfusion after thrombolytic therapy in acute myocardial infarction can be directly demonstrated with coronary angiography or it can be assessed thanks to indirect markers of reperfusion, such as modifications in the "averaged" QRS complex. We assessed the presence of late potentials in 37 patients within 5 hours of acute myocardial infarction onset and evaluated their disappearance or modification after reperfusion. Signal-averaged electrocardiogram, obtained computerizing QRS complexes filtered through Simson's bidirectional filter (25-250 Hz), was serially recorded in each patient: at admission, as well as 12 hours, 3 and 10 days following urokinase and/or heparin therapy. Other indirect markers of reperfusion (incidence of ventricular arrhythmias, serum CK-MB level, ST elevation) were contemporaneously evaluated. All patients underwent coronary angiography between 6 and 83 days after acute myocardial infarction. Late potentials (Total QRS greater than 115 ms; Under 40 microV greater than 39 ms; RMS Last 40 ms less than 25 microV) were present only in 25% of patients, and they always disappeared after successful thrombolysis. On the contrary if ischemia-related vessel occlusion persisted, late potentials persisted as well or else were first recorded on the 3rd or 10th day following acute myocardial infarction. Quantitative analysis of the "averaged" QRS complex showed a statistically significant reduction in QRS duration (-9.1 +/- 12.7 ms) 3 days after acute myocardial infarction in reperfused patients (group A, n = 24), while no significant reduction in the total QRS (-1 +/- 6.7 ms) was observed in non-reperfused cases (group B, n = 13), (p less than 0.05 group A vs group B). So, 10 ms reduction in total QRS duration was a good marker of reperfusion, with specificity = 92% and sensitivity = 54%; marker sensitivity was even higher (= 79%) when coupled with serum CK-MB peak within 12 hours of therapy (diagnostic accuracy = 84%). In conclusion, even if late potentials have a low prevalence in acute myocardial infarction (25%) their disappearance correlates with myocardial reperfusion. Furthermore, a reduction in total QRS duration greater than or equal to 10 ms can itself be a good marker of successful thrombolysis.     

Ventricular late potentials in familial amyloidotic polyneuropathy

We investigated the occurrence of ventricular late potentials (LPs) in patients with familial amyloidotic polyneuropathy (FAP) and the possible association with ventricular arrhythmia on Holter electrocardiography and echocardiographic data. Fifty-five patients and 94 healthy controls were studied. LP were found in 46% of the FAP patients older than 60 years and in 15% of the controls (P = .02), whereas no difference was found in individuals younger than 60 years. The occurrence of LP was associated with nonsustained ventricular arrhythmia in the older FAP patients (P = .04). Older patients with LP had increased ventricular septum thickness (P = .02) and left posterior wall thickness (P = .01), as compared with those without LP. In conclusion, ventricular LPs are common in the FAP patients older than 60 years and associated with nonsustained ventricular arrhythmia and increased thickness of the left ventricular wall. Long-term follow-up studies are required to find the prognostic significance of these new findings.     

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.