Introduction Acquiring Data Filtering Data Post MI Patients Indications/Uses False Positives/Negatives Conclusion |
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I. INTRODUCTION - What is a VLP?
All VLPs are microvolt signals that are part of the terminal portion of the QRS complex. These signals persist into the ST-T segment. They represent areas of delayed ventricular activation which are manifestations of slowed conduction velocity. Slowed conduction results with ischemia or deposition of collagens after an acute myocardial infarction. This causes the preserved myofibrils to separate from their neighbors causing the activation wave to seek other or slower routes. VLPs may be detected more readily when they occur in the areas of the heart that normally activate late in ventricular activation such as the posterobasal, posterolateral and inferiolateral segments of the myocardium. This explains why VLPs are often detected in patients with right coronary artery/inferior wall MI versus those with left anterior descending artery/anterior MI. But sometimes there is just no difference between these groups. Occasionally VLPs will not be detected unless the heart is stressed (extrastimuli or higher pacing rates).
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II. Acquiring the Data:
There are two types of averaging processes used: temporal and spatial. Spatial averaging has a potential advantage in that it eliminates the variation between serial SAECGs induced by changes in heart rate, voltages, and ventricular activation time. However, most studies use temporal averaging because of a greater noise reduction is possible due to the ability to collect a larger number of complexes. Spatial averaging has not been studied prognostically in the post MI patient group.
Hence, the most common method is the TEMPORAL averaging method. This method acquires multiple highly amplified QRS complexes over time. For effective averaging there are four areas to keep in mind, they are:
QRS duration < = 114ms the waveforms must have a common reference or fiducial point so that averaging of similar sampling points in each complex can be accomplished noise must be random with an unrelated to the cardiac fiducial point (Gaussian distribution) artifacts cannot occur at the same time with each waveform. The lead placement for temporal signal-averaging is shown below:
Horizontal leads (x- and x+): 4th intercostal level at the midaxillary lines
Vertical Leads (y- and y+): suprasternal notch and the anterior-superior iliac crest
Anterior/Posterior Leads (z- and z+): V2 position and directly posterior
This placement optimizes the capture of the signal regardless of its vector orientation and avoids the cardiac impulse which would introduce a repetitive electrode artifact that would not be eliminated by the signal averaging process.
These are called "orthogonal X, Y and Z" leads. Ventricular Late Potentials (VLP) were found to be well detected by these leads.
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III. Filtering the Data and Calculating the Vector Magnitude:
After temporal averaging, the complexes are filtered to eliminate low frequency components of the QRS complex (plateau or repolarization phase). Interference form low frequency artifact declines abruptly with 10-20 Hz filtration, gradually with 20-50 Hz, and is stable at 50-100 Hz filtration. Filtering enhances detection of high-frequency low-amplitude signals corresponding to disorganized wavefronts of activation. The only filtering method that is recommended by the AHA/ACC/ESC Policy Statement on SAECG Standards, as well as the ACC Expert Consensus Document on SAECG, is the Bidirectional Butterworth Filter. Corner frequencies of 25 - 100 Hz are still used, but 40 - 100 Hz is the most common due to its reproducibility.
After filtering each lead, the resulting vector magnitude (VM) is calculated from the standard equation (x2 + y2 + z2)1/2.
Note the normal results of the three commonly measured parameters (filter setting at 40 - 100 Hz):
QRS duration < = 114ms Duration of the terminal potential under 40 µ V RMS* voltage of the last 40 ms of the VMC> 20 µ V *RMS is "root mean square"
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IV. Post MI Patients and SAECG
Approximately 20-52% of post MI patients will have abnormal SAECGs. The abnormalities are seen less often in non-Q wave myocardial infarction and very commonly seen in Q wave myocardial infarctions. They are also less often seen in myocardial infarctions that have a lower CPK level. Patient's who suffer an acute Inferior wall MI and those who form BBB after MI are at a 12 fold increase for abnormal SAECGs. In patients post MI without sustained ventricular tachycardia, SAECGs were abnormal in 7-15%, in those with sustained ventricular tachycardia, abnormalities of the SAECG were observed in 73-100%.
Patient Population
Patients who suffer MI
Patients who suffer MI without sustained VT
Patients who suffer MI with sustained VT
Patients with normal / non cardiac history without sustained VT
Patients with normal / non cardiac history with sustained VT Abnormal SAECGs
20-52%
7-15%
73-100%
0-6%
20%
Ventricular late potentials (VLPs) can show up as early as 3 hours post-MI or as late as 8 weeks post MI. The first 24-48 hours following an acute myocardial infarction are the most unstable. This causes VLP incidences to increase throughout this early period. VLPs have been found to be most prevalent in the 6-30 day interval post MI. Approximately 93% of SAECGs are able to be recorded in the 6-14 day post MI period. Obtaining the SAECG during this time period avoids the instability of the immediate post infarction period. At least one week should separate the event from the SAECG acquisition. In the absence of MI the appearance of a new VLP is rare. Transient VLPs associated with MI are uncommon with 58-70% of positive SAECGs obtained 7-40 days post MI remaining positive even 2 to 6 months later. A variety of reasons have been proposed as explanations for the SAECG becoming normal again. These include: development of collateral circulation decreasing ischemia and recovery of the "stunned" myocardium. However, none of these have been proven.
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V. The Indications and Uses of SAECGs
The most commonly demonstrated use for SAECGs is the ability of it to predict the likelihood of sustained ventricular tachycardia, ventricular fibrillation, and sudden cardiac death in patients post MI. Probably the most important is its ability to predict who will not have these events! Ventricular fibrillation is predicted much less well than VT. Sudden death prediction is compromised by its multiple variety in mechanisms.
The most useful statistics are the predictive values with the NEGATIVE studies. The ability of the SAECG to predict sustained VT is somewhat imperfect, but proven better than studies that just quantify ventricular ectopic activity counts and depressed left ventricular function. In a variety of studies there has been no correlation between Holter detected VEA density and SAECG criteria suggesting differing VEA mechanisms. Oddly, in one study, there was documented and increase in VEA with exercise but the SAECG showed an improvement in patients with left ventricular dysfunction.
Patients undergoing radiofrequency ablation for VT may not show significant normalization of the SAECG, but their VT may not be reinduceable due to reentrant pathway being disrupted thus preventing completion of the reentrant circuit. If the post ablation SAECG normalizes, there is a 90-100% chance that a subsequent arrhythmia will not occur.
Patient's with unexplained syncope can profit from SAECG. Sustained VT has been reported as the cause of syncope in 25 to 40% of patients. Its strength again is its negative predictive value being able to exclude sustained VT or VF from the etiology of the syncope. A normal study does not eliminate sustained VT as a cause of syncope if the arrhythmia is from an automatic focus and therefore does not preclude the indication for EP testing in patients with unexplained syncope.
Other uses for SAECG testing include monitoring the patient who has recently had cardiac transplant as well as those who have received thrombolysis therapy. Follow-up of patient post MI, post thrombolytic therapy and possible post angioplasty with the SAECG shows some promise with a normal SAECG predicting a patent vessel.
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VI. False Positive and False Negative SAECGs
Patients with atrial flutter and atrial fibrillation have shown false positive SAECGs. Attempts have been made to apply the SAECG techniques to the P wave to assess patients susceptibility to atrial fibrillation or atrial flutter. However these are of questionable success.
Differing lead placement and filtration techniques can result in differing test results. VLPs can disappear if the same data is reprocessed at a higher filter frequency. False negatives can also occur when the ventricular arrhythmia is due to triggered automaticity. False positives may sometimes due to detection of delayed ventricular activation that is inadequate to complete a reentrant circuit or not an adequate trigger to set off the arrhythmia.
VII. Interventional Effects
Pharmacologic Effects
All drugs that slow conduction and prolong QRS may also prolong VLPs. Even with EP guided effective antiarrhythmic therapy, VLPs may not be abolished.
The presence of a normal SAECG in a patient presenting with sustained VT or VF while taking antiarrhythmic drugs suggests that the original rhythm disturbance was drug related proarrhythmic.
A malignant arrhythmic disturbance in a patient taking an antiarrhythmic drug and who has an abnormal SAECG may intimate:
an ineffective drug
an inadequate level of an effective drug
a spontaneous new unrelated arrhythmia
Differentiating the small group of patients who will benefit from antiarrhythmics versus those in whom they are harmful is important. The SAECG, through its strong correlation with the results of EP studies, may be a useful non-invasive screen to select patients for treatment or, more important, to select those needing no treatment.
DC Countershock
SAECGs obtained after DC countershock are similar to those obtained at baseline.
Non-pharmacologic
Bypass surgery has no demonstrable effect on the commonly measured SAECG parameters.
Successful catheter ablation results in no change in the SAECG.
Exercise
The cause of sudden cardiac death in athletes during exercise is most often due to coronary artery disease in those individuals greater than 35 years of age; and hypertophic cardiomyopathy in patients less than 35 years of age.
Detection of those prone to exercise induction of lethal arrhythmias is very important. In small studies of patients, physical exertion even to extremes of marathon running has been shown to improve the measure parameters of a patient's SAECG. The SAECG therefore seems to be of little use in screening prior to exercise to predict arrhythmia or sudden cardiac death.
Aging
Aging was noted to induce no change in the patient's SAECG.
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Conclusion:
SAECG is very reliable in detecting VLPs caused by slowed conduction resulting in endocardial or epicardial fragmented potentials. The knowledge of their presence in patients without MI has not as yet been overwhelmingly helpful. In post MI patients, especially when coupled with an abnormal LV ejection fraction and high grade ventricular ectopy, the abnormal SAECG suggests the need for at least considering EP testing for inducibility of a sustained ventricular arrhythmia. A negative SAECG post MI coupled with a normal EF obviates the need for further testing for the patient's potential of having sustained ventricular arrhythmia. SAECGs performed post cardiac transplant and post PTCA are still being evaluated as a mechanism to detect early rejection or acute closure of vessel. Even though the presence of VLPs may indicate the presence of a reentry pathway, the ability to sustain an arrhythmia is not reliable. The SAECG offers no information about the triggers necessary to initiate the tachycardia.
References:
AHA/ACC/ESC Policy Statement: "Standards for the Analysis of Ventricular Late Potentials Using High Resolution or Signal-Averaged Electrocardiography: A Statement by a Task Force Committee of the European Society of Cardiology, the American Heart Association and the American College of Cardiology. JACC Vol. 17, No. 5, April 1991:999-1006.
Download the ACC Expert Consensus Document on Signal Averaged Electrocardiography published in the Journal of the American College of Cardiology,: Vol 27, No 1, Jan 96:238-49. You will need to also download the free Adobe Acrobat PDF Reader. Please allow for sufficient download time.
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