Download Prognostic value of T peak-to-end Interval for risk stratification after

Prognostic value of T peak-to-end Interval for risk stratification after acute
myocardial infarction
Tarek A. Rahman,MD – Minia University Hospital – Egypt
Abstract
Aim: Fatal Arrhythmia is the main cause of sudden death in patients with acute myocardial infarction
either during hospital admission or in post-discharge period. Our aim is to identify groups at high risk of
arrhythmic mortality by using a simple bed-side test in Electrocardiogram.
Background: Trans-mural dispersion of repolarization (TDR) in patients with ST elevation myocardial
infarction is the main trigger of arrhythmias. The potential value of measuring the interval between the
peak and end of the T wave (Tpeak-Tend, Tp-Te) as an index of spatial dispersion of repolarization is a
parameter thought to be capable of reflecting dispersion of repolarization and thus may be prognostic tool
for detection of arrhythmic risk. Little is known about its use for identifying risk of arrhythmias in acute
myocardial infarction and this must be approached with great caution and require careful validation.
Methods: A prospective analysis of data from 564 patients admitted to our CCU by acute myocardial
infarction along a period of two years from January 2012 to December 2013 was done. After exclusion of
valvular, congenital lesions, HOCM, IDCM, pericardial diseases, accessory pathway, any Bundle branch
block, metabolic disorders and re-perfusion arrhythmia. Analysis of TpTe interval and its dispersion was
done for all patients and a Holter-24h was performed after one month. Patients were then classified into
two groups based on Lown grading score for arrhythmia: Group-I (441 patients) with no or minimal
arrhythmias (Lown score <3), and Group-II (123) with high grade arrhythmias (Lown score ≥3). Inhospital predischarge echocardiography was done for all patients to evaluate left ventricular functions and
presence of myocardial aneurysm. Signal average ECG was done to detect low amplitude signals (LAS).
Pre-disharge coronary angiography was done for all patients.
Results: Statistical analysis of the results revealed that, Group (II) patients carry a significantly higher
numbers of obese, diabetic, and hypertensive patients. Most of patients in this group were smokers,
having a higher creatinine levels, and exposed previously to cerebral insults in a significantly higher
values than group (I) .Also, group (II) patients need a significantly higher doses of diuretic and ACEIs
than group (I). The percentage of anterior wall infarction is significantly higher in group (II), with higher
inferior wall affection in group (I). TpTe interval and dispersion between both groups revealed that, a
higher TpTe interval was found in group (II) than group (I) and this was linked to occurrence of sudden
death or malignant VT and deterioration in Lv functions than in group (I). Also, patients in group-II
exposed to re-infarction and cardiogenic shock in a statistically significant values (p<0.01) than group (I).
Strong correlation is present between prolonged TpTe and presence of late potentials in SAECG.
Conclusion: TpTe was significantly and independently associated with increased odds of SCD and is
linked to deterioration of Lv functions and myocardial aneurysms. It's highly correlated to presence of
LAS and associate with seveity of cornary lesions. Patients with prolonged TpTe intervals and
dispersions were likely to develop fatal arrhythmias.
Key Indexing Terms: Tp-Te interval – Ventricular arrhythmias - sudden death - Heart failure
Tarek M. AbdelRahman,MD
Department of Cardiology,
Faculty of Medicine, El-Minia
University, El-Minia, Egypt
e-mail: [email protected]
Abbreviations and Acronyms
AP - action potential
ECG - electrocardiogram
STEMI – ST elevation myocardial infarction
TDR - transmural dispersion of repolarization
Tp-Te - Tpeak-Tend interval
VF - ventricular fibrillation
VT - ventricular tachycardia
EAD – early after depolarization
LAS – low amplitude signals
AMI – acute myocardial infarction
Introduction:
Amplification of spatial dispersion of repolarization, particularly transmural dispersion of
repolarization (TDR), within the ventricular myocardium has been suggested to underlie
arrhythmogenesis in different cardiac diseases, such as the Brugada, short QT, long QT syndromes, and
Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT).(1)
Numerous studies (2,3) have highlighted the heterogeneity that exists among the cells that comprise
ventricular myocardium, demonstrating unique electrophysiologic and pharmacologic profiles for
epicardial, endocardial, and M cells in a number of species, including man. Differences in the time-course
of repolarization of these three predominant ventricular myocardial cell types contribute prominently to
the inscription of the electrocardiographic T wave recorded in the precordial leads V5
These differences in action potential (AP) morphology lead to the development of opposing
voltage gradients on either side of the M region, which contribute to inscription of the T wave, especially
those inscribed in the precordial leads (Fig. 1). The interplay between these opposing transmural forces
determines the height and width of the T wave and the extent to which the T wave may be interrupted,
resulting in a bifid or notched appearance.(4)
Figure 1: Voltage gradients on
either side of the M region are
responsible for inscription of the
electrocardiographic T wave
Recent studies have identified TDR and other forms of spatial dispersion of repolarization as the
principal substrate and early afterdepolarization (EAD)-induced extrasystoles as the most common trigger
for the development of lethal arrhythmias.(5)
During bradycardia or because of a repolarization-prolonging insult, the action potential of the M
cells is more vulnerable to prolongation compared with the other 2 cell types,(6) likely because of larger
late-sodium and sodium/calcium exchange currents and a weaker, slowly activating delayed rectifier
current.(7) TpTe corresponds with transmural dispersion of repolarization in the ventricular myocardium, a
period during which the epicardium has repolarized and is fully excitable, but the M cells are still in the
process of repolarization and are vulnerable to the occurrence of early afterdepolarizations.(8,9)
One of the challenges ahead is to identify a means to quantitate spatial dispersion of repolarization
and TDR non-invasively. In this study, we discuss the potential value of the interval between the peak
and end of the T wave (Tpeak-Tend, Tp-Te) as an index of spatial dispersion of repolarization in patients
with ST elevation myocardial infarction and to stratify them according to the risk of ventricular
arrhythmias.
This parameter is thought to be capable of reflecting changes in spatial dispersion of
repolarization, including TDR, and thus may be prognostic tool for detection of arrhythmic risk under a
variety of conditions.(10) Little is known about its use for identifying risk of arrhythmias in acute
myocardial infarction and this must be approached with great caution and require careful validation.
Because of the interval from the peak of the T wave to the end of the T wave [TpTe]) is a measure
of transmural dispersion of repolarization in the left ventricle, its prolongation representing a period of
potential vulnerability for reentrant ventricular arrhythmias.(11) Many studies confirm that, Prolonged
TpTe has been associated with increased risk of mortality in congenital and acquired long-QT syndromes,
in hypertrophic cardiomyopathy with troponin I mutations, and in patients undergoing primary
percutaneous coronary intervention for myocardial infarction.(10-12)
There are findings from the bench that link TpTe to mechanisms of ventricular arrhythmia. Using
a canine myocardial wedge preparation model, Antzelevitch and coworkers (13,14) explored the genesis of
TpTe as well as the potential mechanisms that link TpTe prolongation to increased risk of ventricular
arrhythmogenesis.
If conditions are favorable, these early afterdepolarizations can lead to reentry and its
perpetuation, resulting in polymorphic ventricular tachycardia or ventricular fibrillation. Hence, a
prolonged TpTe likely corresponds to an extended vulnerable period and given the right conditions, could
increase risk of ventricular arrhythmogenesis.(15)
In our study, we try to detect these changes in Tp-Te interval and document its relation to
occurrence of different ventricular arrhythmias among patients admitted to our CCU by St-elevation
myocardial infarction STEMI. Moreover, to detect its safe and risky limits.
Material and methods:
Study Participants:
A prospective analysis of data from 564 patients admitted to our CCU by acute myocardial
infarction along a period of two years from January 2012 to December 2013 was done . Demographic
data as regards Age, Sex and BMI. History and clinical examination are taken after their consent, history
of co-morbidity, hypertension, diabetes, renal disease, current smoker, previous AMI, previous CABG,
Killip class, prior stroke, prior PCI, HF, and shock
Exclusion criteria were: valvular and congenital lesions, HOCM, IDCM, pericardial diseases,
accessory pathway, any Bundle branch block, any metabolic disorders and re-perfusion arrhythmia .
(1) 12-Leads surface ECG:
ECG was done for all participants using ECG-machine Fukuda Denshi Climax machine.(filter
range 0.5 Hz to 150 Hz, AC filter 60 Hz, 25 mm/s, 10 mm/mV), Measurements of TpTe intervals and its
dispersion were conducted manually using digital onscreen software at a pre-discharge day and in a stable
clinical conditions. A 12-leads ECG is used and all patients were in sinus rhythm.
Measurement of TpTe interval and TpTe dispersion:
TpTe interval was measured from Tpeak to Tend n lead V5.(16) If V5 was not suitable, leads V4
and V6 in that order were measured.(10) The end of the T wave was defined as the intersection of the
tangent to the down slope of the T wave and the isoelectric line when not followed by a U wave or if
distinct from the following U wave. If a U wave followed the T wave, the T-wave offset was measured as
the nadir between the T and U waves. (17) If the T-wave amplitude was<1.5 mm in a particular lead, or
morphologically distorted that lead was excluded from analysis. For more confirmation we allow a third
observer to measure TpTe by subtracting Qp from QT, as shown in figure (2)
T-peak-to-T-end dispersion defined as the difference between the maximum and minimum Tpeak-to-T-end interval in all ECG leads. ECG readers were blinded to case status.
Figure (2) : Examples of different patients for measurements of QT and TpTe intervals
(2) Signal-averaging ECG:
SAECG was done for all patients using a commercially available machine ( HP-Page-Writer,
Hewlette-Packard, Inc.USA). ECG was recorded in sinus rhythm and signals from a number of beats
were averaged to achieve a noise level less than 0.3 uV and then the signals were amplified, digitized and
filtered with 40Hz High pass filter-band. The Gomes Criteria was used to identify positive late potentials
if ( QRS> 114, RMS-40 uV <20, and LAS40 >38).
(3) Trans-thoracic Echocardiography:
Echocardiography using a commercially available GE vivid 3 echo machine equipped with 2.5 –
3.5 MHz transducer was done for all patients to examine for LV volumes including (end-diastolic EDV,
end-systolic ESV) through which calculation of LVEF% is made by Simpson's Biplane method. Also,
recording wall motions abnormalities, Tie index, MR severity and presence of aneurysm.
(4) Coronary Angiography:
Diagnostic coronary angiography (CA) was done for all patients before discharge using a flatpanel GE-imaging system. All subjects were in the fasting sedated state. CA was performed from the
arterial femoral approach after local groin infiltration of 10-20 ml xylocaine 2% using modified
seldinger's technique after injection of 5000 IU of Heparin, 6F JL then JR coronary catheters were used to
engage the corresponding arteries. The study was conducted with a General Electric Innova 2000
angiographic unit (GE medical system Milwaukee, WI, USA).
(5) Holter-24h Monitorring :
The patients were seen one month after hospital discharge in the arrhythmia outpatient clinic to
receive a Holter-machine. Holter-24h-monitoring and Analysis was done using cardioline Holter
Scanning System (cardioline, SPA, Italy) which consisted of a recorder, analyzer, electrocardiogram
writer and reporter. The recorder is a battery-operated device , which continuously records ECG signals
on a magnetic tape for subsequent analysis. It permitted continuous recording of two separate ECG leads
for 24 hours. Analysis of the recordings was accomplished with ECG analyzer of Cardio-line system,
which allowed playback of tapes at high speed and full arrhythmia analysis after elimination of artifacts
to detect any ventricular arrhythmias. The tapes were subsequently analyzed by the Marquette 8000 laser
scanner run with its arrhythmia analysis program to identify and label each QRS complex. The data file
was over read and corrected when appropriate by one of the investigators who was unaware of the clinical
course of the patients.
All episodes of nonfatal arrhythmic events, re-infarction, and revascularization procedures were
carefully recorded. Information about deceased patients was obtained from family members, their general
practitioners, and the hospitals they had been admitted to. Particular attention was given to the
circumstances of each death. The primary end point of the study was prospectively defined as a composite
end point of all-cause mortality, documented sustained VT, and resuscitated ventricular fibrillation.
Secondary end points of the study were (1) all-cause mortality and (2) arrhythmic events (defined as
sudden cardiac death, documented sustained VT, and resuscitated ventricular fibrillation). Sudden death
was defined as instantaneous, unexpected death or death within 1 hour of symptom onset not related to
circulatory failure. Sustained VT was defined as a documented tachycardia of ventricular origin at a rate
of≥100 bpm and lasting for >30 seconds or resulting in hemodynamic collapse
Documentation of ventricular arrhythmias is recorded and patients were classified according to
Lown grading score (18) into two groups. Group-I: with Lown score less than 3 with no or minor
arrhythmias and group-II with high grade arrhythmias of Lown score ≥ 3
The Lown-grading system to evaluate the ventricular premature beats as follows:
grade 0= no ventricular premature beats,
grade 1= lower than 30 ventricular premature beats/hr,
grade 2= more than 1 ventricular premature beats/min or 30 ventricular premature beats/hr,
grade 3= multiform ventricular premature beats or ventricular couplets were present,
grade 4= 4A = repetitive VPBs - couplets (2 in a row)
4B = repetitive VBPs - runs of ventricular tachycardia (3 in a row)
grade 5= early-cycle ventricular premature beats (R on T phenomenon)
Statistical Methods:
Data were collected and analyzed by Statistical Package for Social Sciences (SPSS) version 13
Data are given as mean (SD) for both numbers and percentages and compared using Chi-square and the
Student t test. A probability level of p-value ≤ 0.05 was considered as statistically significant in all tests.
Correlation between TpTe and both SAECG and severity of cornary lesions were made using the Pearson
correlation coefficient (r).
Limitations:
As is the case for QTc, the difficulty in locating T-wave end when the T-wave morphology is flat
or multiphasic may affect TpTe measurements. However, we overcome this by measuring the dispersion
of Tp-Te interval. Readers were blinded, so any such errors would be unrelated to case status. Therefore,
any bias introduced by this error would be unlikely to affect the validity of the findings. A subset of
patients may be skipped from research because a high percent of SCD may be unfortunate first
manifestation of their illness and are unlikely to have undergone any cardiac investigations. Finally, a
large number of cases is essential to clarify a cut-off value and a percentile for which risk is inevitable.
Results
Patients demographic data, Co-morbidity and medications are listed in Table (I).
Group (I): N= 441
(78.2%)
Age (yrs)
52 ± 4
Height (cm)
167 ± 4
Weight (kg)
85 ± 2
BMI (kg/m2)
29.2 ± 4
Gender male, n (%)
361 (81%)
Hypertension, n (%)
272 (61%)
Diabetes mellitus, n (%)
283 (64%)
Hyperlipidemia, (n %)
382 (86%)
Serum creatinine (mg%)
1.3±0.2
Current smoker, n (%)
259 (58%)
Previous Stroke, n (%)
6 (1.3%)
Medications used during admission period
ASA, n (%)
366 (83%)
Clopidogrel , n (%)
106 (24%)
ACEI, n (%)
194 (44%)
ARB, n (%)
128 (29%)
B-Blockers, n (%)
392 (89%)
CCB, n (%)
71 (16%)
Statin, n (%)
163 (37%)
Diuretics, n (%)
53 (12%)
OAD/Insulin, n (%)
283 (64%)
Co-morbidity
Demographic
Parameter
Group (II): N= 123
(21.8%)
50 ± 6
157 ± 8
88 ± 6
34.3 ± 5
98 (80%)
98 (79%)
102 (83%)
108 (87%)
1.5±0.3
90 (73%)
4 (3.2%)
NS
0.02
0.06
0.01
NS
0.01
0.01
NS
0.03
0.01
0.01
99 (81%)
27 (22%)
76 (62%)
38 (31%)
107 (87%)
17 (14%)
46 (38%)
78 (64%)
102 (83%)
NS
NS
0.01
NS
NS
NS
NS
0.01
0.01
P
It was shown that, the group (II) carry a significantly higher numbers of obese, diabetic and
hypertensive patients. Most of patients in this group were smokers, having a higher creatinine levels and
exposed previously to cerebral insults in a significantly higher values than group (I). Also, group (II)
patients need a significantly higher doses of diuretic and ACEI than group (I) during the admission period
The site of infarction is categorized in table (2):
Site of MI
Group-B
(N=123)
83 (68%)
P value
Anterior MI
Group-A
(N=441)
211 (47%)
- extensive anterior
- antero-septal
- antero-lateral
Inferior MI
86 (19%)
98 (22%)
27 (6%)
233 (53 %)
44 (35%)
23 (18%)
18 (15%)
40 (32%)
0.01
- localized inferior
- infero-lateral
- infero-posterior
174 (39%)
35 (8%)
24 (6%)
21 (17%)
11 (9%)
8 (6%)
0.01
It was found that, percentage of anterior wall infarction is significantly high in group (II) representing
68% of cases with higher inferior wall affection in group (I) 53% of cases in a statistically significant
value (p 0.01).
Figure (3): Localization of infarction site in group (I) and group (II)
TpTe interval and dispersion between both groups revealed that, a higher TpTe interval was found in
group (II) in a value of 86±16 msec than 62±14 msec in group (I). Also, increased TpTe dispersion in
group (II) than group (I) in a value of (26±6 msec & 18±4 msec respectively) as shown in table(3) and
figure (4). At the end of the study, we made a correlation between reported cases as sudden death or
malignant VT and found all of them having Tp-Te interval more than 100 msec and a dispersion more
than 30 msec.
Table (3) TpTe interval and dispersion between two groups
Parameter
TpTe interval (msec)
TpTe dispersion (msec)
Group (I)
N= 441
Mean
SD
62
14
18
4
Group (II)
N= 123
Mean
SD
86
16
26
6
P
0.001
0.001
TpTe interval in both groups
TpTe Dispersion in both groups
35
120
30
100
25
80
20
Group-I
60
Group-II
Group-I
Group-II
15
40
10
20
5
0
0
Figure (4): Tp-Te interval and Tp-Te dispersion in both groups
Echocardiographic findings revealed a significant deterioration in Lv functions in group (II) versus group
(I) as shown in table (4).
Table (4): Echocardiographic findings in both groups
Echocardiograhic Finding
Lv end diastolic dimension (LVEDD)
Lv end systolic dimension (LVESD)
Ejection Fraction (EF %)
Fractional shortening (FS %)
Tei-Index
MR jet area width (Cm2)
Evidence of myocardial aneurysm
Group-I
(N=441)
47±1.2
31±1.1
61±4
26±2.1
0.52±0.13
1.5±0.4
0
Group-II
(N=123)
56±2.4
45±1.6
44±1.5
16±2.1
0.64±0.68
3.1±0.2
4±0
P value
0.001
0.001
0.001
0.001
0.001
0.001
0.001
Data from admission period and one month Holter-24h monitoring revealed, documented VT in 16
patients in group II versus 9 patients in group I, resuscitated VF in 8 patients in group-II versus only 2
cases in group-I, sudden death in 4 patients in group-II versus only one case in group-I, Re-infarction
occurred in 21 case of group-II versus 8 cases in group-I and cardiogenic shock in 23 patients in group-II
versus 4 cases in group-I. as shown in figure (5).
Arrythmias and sudden death in both groups
25
20
15
group (I)
group (II)
10
5
0
Cardiogenic
Shock
Re-infarction
Sudden Death
VF
VT
Figure (5): Arrhythmias and events between both groups
SAECG Data revealed increased QRS duration and low amplitude signals with lower RMS-40 in group-II
versus group-I in a statistically significant values (p 0.001), as shown in table (5)
Table (5): Comparison of SAECG results between the two groups.
Parameter
QRS duration (msec)
RMS-40 (msec)
LAS (msec)
Group (I)
N= 441
Mean
SD
96
6
100
12
10
2
Group (II)
N= 123
Mean
SD
102
10
44
4
36
6
P
0.001
0.001
0.001
Coronary Angiographic results using QCA "quantitative coronary lesion assessment" revealed a severer
lesions in Left main territory in group-II than group-I in a statistically significant values (p 0.001).
However, group-I showed a higher affection in RCA territory than group-I but, less severe percentage of
stenosis in the affected vessels as shown in table (6).
Table (6): Comparison of coronary angiographic findings between the two groups.
Coronary artery
Left Main artery (LM)
Left anterior descending A (LAD)
Diagonal branch artery (DA)
Left circumflex artery (LCx)
Obtuse marginal artery (OM)
Right coronary artery (RCA)
Group (I)
N= 441
Mean
SD
0
0
40%
10%
50%
10%
60%
10%
50%
10%
60%
10%
Group (II)
N= 123
Mean
SD
40%
10%
80%
15%
90%
10%
45%
5%
40%
5%
40%
10%
P
0.001
0.001
0.001
0.001
0.001
0.001
Correlation between TpTe interval and number of LAS in SAECG was made and revealed a strong
positive linear correlation between both parameters in (r)= 0.98 and (p) 0.001 as shown in figure (6-A)
and a positive correlation between prolonged TpTe and severity of coronary lesions with (r)= 0.96 and (p)
0.001 as shown in figure (6-B).
Correlation between TpTe and % of
CA stenosis (fig 6-B)
Correlation between TpTe and LAS
fig-6-A
120
60
40
20
TpTe Interval
80
80
60
40
0
37
33
29
25
21
17
13
Low Amplitude Signals
9
5
1
20
37
33
29
25
21
17
13
9
5
1
TpTe interval
Figure (6): Correlation between TpTe and LAS (A) and Percent of coronary stenosis (B)
Conclusions:
TpTe was significantly and independently associated with increased odds of SCD among subjects
with STEMI. Also, increased TpTe interval and dispersion is linked to deterioration of Lv functions and
myocardial aneurysm. Arrhythmias were very frequent in a subset of groups that having a prolonged TpTe interval and increased dispersion. TpTe is positively correlated to presence of Late-potentials in
SAECG and to the perecent of coronary stenosis in angiographic findings. Measurement may extend the
value of repolarization beyond the QTc, particularly in situations where QTc is either normal or not valid
because of prolongation of QRSD. Prolonged TpTe has potential for enhancement of SCD and risk
stratification and warrants evaluation in additional, larger populations.
Discussion
Arrhythmic events are likely to occur during the natural course of acute myocardial infarction
which may be a direct cause of mortality or deterioration of cardiac functions in such patients. Many
studies tried to demonstrate an association between an increase in Tpeak-Tend and arrhythmic risk but
they are notwithstanding.(19-21) Direct validation of Tpeak-Tend measured at the body surface as an index
of TDR is still lacking and guidelines for such validation have been suggested.(22)
Because precordial leads view the electrical field across the ventricular wall, Tpeak-Tend would
be expected to be most representative of TDR in these leads. The precordial leads are unipolar leads
placed on the chest that are referenced to Wilson central terminal. The direction of these leads is radially
toward the "center" of the heart, the center of the Einthoven triangle. Unlike the precordial leads, the
bipolar limb leads, including leads I, II, and III, do not look across the ventricular wall. While TpeakTend intervals measured in these limb leads may provide an index of TDR, they are more likely to reflect
global dispersion, including apico-basal and interventricular dispersion of repolarization.(23,24)
% of Stenosis
100
100
Another important consideration is that TDR can be highly variable in different regions of the
ventricular myocardium, particularly under pathophysiologic conditions. Consequently, it is important to
measure Tpeak-Tend independently in each of the precordial leads and it is inadvisable to average TpeakTend among several leads.(25) So, in our study we overcome this averaging by measuring the dispersion
between the longest and shortest TpTe interval.
A large increase in TDR is likely to be arrhythmogenic because the dispersion of repolarization
and refractoriness occurs over a very short distance (the width of the ventricular wall), creating a steep
repolarization gradient.(26, 27) It is the steepness of the repolarization gradient rather than the total
magnitude of dispersion that determines its arrhythmogenic potential. Apico-basal or interventricular
dispersion of repolarization is less informative because it may or may not be associated with a steep
repolarization gradient and thus may or may not be associated with arrhythmic risk.(26, 27)
Our study conclude a direct association between Tp-Te interval prolongation and increased its
dispersion to increased events of fatal arrhythmias in group-II patients more than group-I in a statically
significant values which confirm increased TDR in group-II.
Topilski et al.(11)found that QT, QTc and Tpeak-Tend intervals were strong predictors of Torsade
de pointes, with the best single discriminator being a prolonged Tpeak-Tend. Watanabe et
al.(27)demonstrated that prolonged Tpeak-Tend is associated with inducibility as well as spontaneous
development of ventricular tachycardia (VT) in high risk patients with organic heart disease.(27)
We found that, patients in group-II having a prolonged Tp-Te interval in a value of (78±12 msec
versus 62±14 msec in group-I and this made them more prone to many arrhythmic events. Lubinski et
al(28) observed that patients with CAD and inducible ventricular tachycardia had a higher TpTe (74±14
versus 63±16 ms;P<0.004). In addition he measures TpTe/QT ratio and expressed in his research that a
higher percentage (21±4% versus 17±3%;P=0.02) was found in arrhythmic group than those who
survived myocardial infarction without inducible ventricular tachycardia.(28)
In this study, we tried to detect the value at which Tp-Te interval is risky, and found that,
increased Tp-Te interval more than 102 msec and a dispersion more than 36 msec -which is the mean plus
two SD- carry an ultimate risk of SD and fatal arrhythmias.
In a study made by Harrmark C., et al.,(29) who studied TpTe in acute myocardial infarction. They
observed that, a TpTe values >100 ms during acute myocardial infarction and >113 ms in the setting of
acquired bradyarrhythmias have been described as “high risk” in the literature. In our study, the majority
of subjects with a TpTe value >100 ms were at high risk. Our findings are comparable with a smaller
study of patients with acute myocardial infarction that evaluated overall mortality (not SCD) in which 10
of 11 patients who died had TpTe >100 ms.(29)
This fact is supported from data by Lubinski et al,(28) who reported that the mean TpTe observed
in subjects with CAD and inducible ventricular tachycardia was relatively low (74±14 ms). However,
further studies are needed for establishing cutoffs for patients at risk of SCD in the community.
In our study, we noticed a high percentage of smokers in group-II who are linked to increased
mortality and arrhythmias. This fact is confirmed nowadays by a study made by Hakan Tasolar et.
Al.,(30) in 2013 who studied Tp-Te interval in 45 chronic smoker and confirm a direct relationship
between smoking and prolongation of Tp-Te interval as a predictor for ventricular arrhythmias and
sudden death. (30)
In our study, a left ventricular aneurysm was found only in patients of group-II who are
characterized by longer Tp-Te interval and increased dispersion and that is confirmed by many authors
who reported a link between presence of Lv aneurysm and deterioration of Lv functions and refractory
arrhythmias after myocardial infarction. (31,32)
Left ventricular structural lesions result in complex electrophysiological changes, but those mainly
responsible for arrhythmias are conduction slowing, changes in the refractory period, inhomogeneous
activation and repolarization. We review the literature and report our personal experience of the
prognostic value of TpTe interval and its dispersion added to Holter and SAECG data and found a strong
correlation of prolongation of TpTe to presence of ventricular late potentials. This is supported in a study
in 2007 made by Bounhoure et al., who use a programmed ventricular stimulation and succeeded to select
the best candidates for defibrillator implantation and resynchronization. (33)
Another study made by Chu et al., 2007, to detect the favorable impact of three month statin therapy on
arrhythmias and sudden death revealed strong correlation of TpTe and late potentials as non-invasive
tools to stratify arrhythmic susceptibility which –by the way- conclude that, the favorable antiarrhythmia
effect of atorvastatin (10 mg/day) therapy cannot be directly reflected by analyzing these noninvasive
ECG risk stratification parameters in low-risk patients with hypercholesterolemia. (34)
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