Detection of myocardial injury due to defibrillation threshold checking after insertion of implantable cardioverter/defibrillators.
ABSTRACT Possible myocardial damage caused by defibrillation threshold (DFT) control and its extent after insertion of implantable cardioverter/defibrillators (ICD) is still a matter for debate. This study aimed to identify the effect of DFT checking during ICD implantation, compared with permanent pacemaker (PPM) implantation, on the magnitude of myocardial damage as assessed by cardiac troponin-T (cTNT) and CK-MB.
A total of 133 candidates for ICD implantation were enrolled in the ICD group (mean age 60.66 +/- 12.25 years; males 111 [83.5%]) as well as 130 candidates in the PPM group (mean age 69.56 +/- 12.86 years; males 64 [49.2%]). DFT was controlled in all of the ICD patients. Serum levels of cTNT and CK-MB were measured at baseline plus 8 and 24 hours following the procedure. The results were adjusted for age, gender, and other confounding factors. The amount of cTNT rise after 8 and 24 hours in the ICD group was significantly higher than in the PPM group (p < 0.001 for both). These differences remained significant after adjustment for confounding factors. The level of CK-MB rise after 8 and 24 hours was also significantly higher in the ICD group, although it lost its significance after adjustment for age, gender and other confounding variables. There was no significant relationship between the amount of energy delivered and enzyme elevation.
Elevation of cTNT and CK-MB after the ICD implantation was significantly higher than that after the PPM implantation and may be attributed to the DFT testing shock and resulting myocardial injury.
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ABSTRACT: Cardiac-specific Troponins (cTn) I and T have become markers of choice for myocardial injury. We reviewed the literature in order to understand the expected postprocedure cTn rise after electrophysiology procedures. A total of 34 studies and 1,608 patients were included. After external monophasic cardioversion, seven of 442 patients (1.6%) had minimal increase in cTnI (0.1-0.9 ng/mL), and only one of 368 (0.3%) had increase in cTnT (0.11 ng/mL). After internal cardioversion, 17 of 105 (16%) had increase in cTnI (0.7-2.4 ng/mL) but only three (2.9%) were above the cutoff for myocardial infarction (MI) (1.5 ng/mL). During implantable cardioverter-defibrillator (ICD) installation with a mean of 2-7 ICD shocks, 12 of 74 (16%) patients had cTnI >or=1.5 ng/mL (range 1.7-5.5 ng/mL) and 20 of 64 (32%) had cTnT >or=0.1 ng/mL (range 0.26-6.46 ng/mL) considered in the range of clinical MI. Radio frequency ablation (RFA) (n = 496) resulted in significant cTn elevation in 25-100% of patients with ventricular > atrial and linear > focal lesions. Average postprocedure peak cTnI ranged from 0.13 to 6 ng/mL (median: 2.36 ng/mL, max: 15 ng/mL) and cTnT 0.2 to 2.41 ng/mL (median: 0.44 ng/mL, max: 9 ng/mL). Early cTn peak at 2-8 hours was noted after RFA. External cardioversion should not cause a significant increase in cTn; RFA and ICD implantation with shocks often result in an increase in cTn. Interpretation of these markers can be difficult if acute coronary syndrome is suspected in the postprocedure period.Pacing and Clinical Electrophysiology 06/2009; 32(6):800-10. · 1.75 Impact Factor
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ABSTRACT: Implantable cardioverter defibrillator (ICD) implantation is a common approach in patients at high risk of sudden cardiac death. To check for normal function, it is necessary to test the ICD. For this purpose, repetitive induction and termination of ventricular fibrillation by direct current shocks is required. This may lead to minor myocardial damage. Cardiac troponin T (cTnT) and I (cTnI) are specific markers for the detection of myocardial injury. Because these proteins usually are undetectable in healthy individuals, they are excellent markers for detecting minimal myocardial damage. The objective of this study was to evaluate the effect of defibrillation of induced ventricular fibrillation on markers of myocardial damage. This study included 14 patients who underwent ICD implantation and intraoperative testing. We measured cTnT, cTnI, creatine kinase MB (CK-MB) mass, CK activity, and myoglobin before and at definite times after intraoperative shock application. Depending on the effectiveness of shocks and the energy applied, the cardiac-specific markers cTnT and cTnI, as well as CK-MB mass, showed a significant increase compared with the baseline value before testing and peaked for the most part 4 h after shock application. In contrast, the increases in CK activity and myoglobin were predominantly detectable in patients who received additional external shocks. ICD implantation and testing leads to a short release of cardiac markers into the circulation. This release seems to be of cytoplasmic origin and depends on the number and effectiveness of the shocks applied.Clinical Chemistry 04/2001; 47(3):459-63. · 7.77 Impact Factor
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ABSTRACT: The present study was designed to assess the extent of myocardial injury in patients undergoing transvenous implantation of an automatic implantable cardioverter-defibrillator (ICD) using cardiac troponin I (cTNI), which is a highly specific marker of structural cardiac injury. During ICD implantation, repetitive induction and termination of ventricular fibrillation (VF) via endocardial direct current shocks is required to demonstrate the correct function of the device. Transthoracic electrical shocks can cause myocardial cell injury. Measurements of total creatine kinase (CK), CK-MB, myoglobin, cardiac troponin T (cTNT) and cTNI were obtained before and after ICD implantation in 49 consecutive patients. Blood samples were drawn before and 2, 4, 8, and 24 h after implantation. Elevations of CK, CK-MB, myoglobin, cTNT and cTNI above cut-off level were found in 25%, 6%, 76%, 37% and 14% of patients, respectively, with peak cTNI concentrations ranging from 1.7 to 5.5 ng/ml. Cumulative defibrillation energy (DFE), mean DFE, cumulative VF time, number of shocks as well as prior myocardial infarction (MI) were found to be significantly related to a rise of cTNI. Mean DFE > or = 18 J and a recent MI were identified as strong risk factors for cTNI rise. During transvenous ICD implantation myocardial injury as assessed by cTNI rise occurs in about 14% of the patients. Peak cTNI concentrations are only minimally elevated reflecting subtle myocardial cell damage. Patients with a recent MI and a mean DFE > or = 18 J seem to be prone to cTNI rise.Journal of the American College of Cardiology 09/1999; 34(2):402-8. · 15.34 Impact Factor
Address for correspondence:
Gholamreza Davoodi, Associate professor, Department of
Electrophysiology, Tehran Heart Center, North Kargar Street, Tehran,
14111713138, Iran. Tel: +98 21 88029600;
Fax: +98-021-88029731; e-mail: email@example.com
Received 23 November 2012; accepted for publication 31 January 2013.
The implantable cardioverter /defibrillator (ICD)
plays a great role in improving the survival of patients
who are at risk for sudden cardiac death1-2. Myocardial
injury, as detected by the elevation of cardiac specific
enzymes, has been reported following ICD insertion due
to both device-induced shocks and defibrillation thresh-
Detection of myocardial injury due to defi brillation threshold
checking after insertion of implantable cardioverter/defi brillators
Gholamreza DAVOODI, MD; Vahid MOHAMMADI, MD; Akbar SHAFIEE, MD, MSc; Ali KAZEMISAEID, MD;
Saeed SADEGHIAN, MD; Ali VASHEGHANI-FARAHANI, MD; Ahmad YAMINISHARIF, MD
Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.
lators (ICD) is still a matter for debate. This study aimed to identify the eff ect of DFT checking during ICD implantation, compared with permanent pacemaker
(PPM) implantation, on the magnitude of myocardial damage as assessed by cardiac troponin-T (cTNT) and CK-MB.
Methods and results
A total of 133 candidates for ICD implantation were enrolled in the ICD group (mean age 60.66 ± 12.25 years; males
111 [83.5%]) as well as 130 candidates in the PPM group (mean age 69.56 ± 12.86 years; males 64 [49.2%]). DFT was controlled in all of the ICD patients.
Serum levels of cTNT and CK-MB were measured at baseline plus 8 and 24 hours following the procedure. The results were adjusted for age, gender, and
other confounding factors. The amount of cTNT rise after 8 and 24 hours in the ICD group was signifi cantly higher than in the PPM group (p < 0.001 for
both). These diff erences remained signifi cant after adjustment for confounding factors. The level of CK-MB rise after 8 and 24 hours was also signifi cantly
higher in the ICD group, although it lost its signifi cance after adjustment for age, gender and other confounding variables. There was no signifi cant rela-
tionship between the amount of energy delivered and enzyme elevation.
Elevation of cTNT and CK-MB after the ICD implantation was signifi cantly higher than that after the PPM implantation and may be
attributed to the DFT testing shock and resulting myocardial injury.
Possible myocardial damage caused by defi brillation threshold (DFT) control and its extent after insertion of implantable cardioverter/defi bril-
Implantable cardioverter/defi brillator – myocardial injury – defi brillation threshold checking – cardiac troponin T – creatine kinase MB.
old (DFT) checking3-5. Current data suggest that the
elevation of cardiac-specific enzymes following ICD
implantation, as an indicator of myocardial damage, can
influence the outcome in the treated patients6-8. None-
theless, the exact relationship between DFT checking
and the amount of cardiac specific enzyme release and
probable myocardial injury has not been clearly eluci-
Cardiac-specific troponins have been widely accepted
as specific markers of myocardial injury3. Cardiac tro-
ponin T (cTNT) is known as an important diagnostic
and prognostic tool in cardiovascular medicine9-10. High
cTNT levels are detected in acute coronary syndrome
and congestive heart failure as well as many other
cardiovascular disorders11-12. Moreover, manipulations
during electrophysiological interventions can create
myocardial injury of various degrees, which is well
detected by cardiac troponins3. Elevation of creatine
kinase-MB after DFT checking has been reported6,
Acta Cardiol 2013; 68(2): 167-172 doi: 10.2143/AC.68.2.2967274
G. Davoodi et al.
but if it was not induced, other modalities (i.e. 50 HZ or
burst pacing) were used. DFT controlling was performed
by using 10-15 joules of energy initially. If the arrhythmia
failed to respond in the first step, the second step was
using 20-25-joule shocks (10 joules more than in the first
step). In case of failure of the second shock, maximum
output of the device (35-40 J, based on the device) was
given. External shock was reserved as the last resort in
case of failure of all internal shocks. The patients in the
ICD group were finally also compared for the relationship
of the cTNT and CK-MB elevation and the number of
shocks and the amount of energy delivered.
Venous blood samples were drawn at baseline for
measuring serum creatinine. A blood specimen for the
measurement of highly sensitive cTNT and CK-MB was
drawn from the antecubital vein before the procedure
and at 8 and 24 hours thereafter. Measurements of highly
sensitive cTNT and CK-MB were performed by using
an Elecsis 2010 analyzer (Roche Diagnostics, Indian-
apolis, Indiana, USA). Laboratory staff members who
did the measurements were unaware of the patients’
clinical condition. Cut-off points of the Tehran Heart
Center laboratory for cTNT and CK-MB were 24 ng/L
and 6 ng/ml, respectively.
Numerical variables are presented as mean ± SD
(standard deviation), while categorized variables are
summarized by absolute frequencies and percentages.
Continuous variables were compared using the Student
t-test or nonparametric Mann-Whitney U test whenever
the data did not appear to have normal distributions,
and categorical variables were compared using the chi-
square or Fisher’s exact test, as required. Spearman cor-
relation was employed to evaluate the relationship
between the continuous variables. P-values less than 0.05
were considered statistically significant. All the statisti-
cal analyses were performed using PASW Statistics 18.0
(SPSS Inc, Chicago, IL, USA).
The general characteristics of the study population
and the baseline key variables are depicted in table 1.
There were no significant differences between the two
groups in regard to hypertension, hyperlipidaemia and
serum creatinine. However, the groups were significantly
different regarding age, gender, ejection fraction, history
of coronary artery disease and smoking.
although its specificity is much lower than that of cardiac
troponins13. There is, however, a significant correlation
between the elevation of troponins and CK-MB as indi-
cators of myocardial injury14.
The amount of any probable enzyme rise and thereby
myocardial injury that is attributable to DFT checking
compared with the amount of enzyme rise caused by the
implantation procedure per se has yet to be studied.
Therefore, this study aimed to identify the effect of DFT
checking during the ICD implantation, compared with
the PPM implantation on the magnitude of myocardial
damage as assessed by cTNT and CK-MB.
Study design and population
In this prospective study, subjects were recruited
from individuals admitted to the Tehran Heart Center
between September 2009 and March 2011. In total,
133 consecutive candidates for elective ICD implanta-
tion (mean age 60.66 ± 12.25 years; males 111 [83.5%])
were enrolled. The second group consisted of 130 sub-
jects who underwent elective PPM insertion within the
same period (mean age 69.56 ± 12.86 years; males
64 [49.2%]). Patients with a history of myocardial infarc-
tion, unstable angina, cerebrovascular events, surgery,
cardioversion, coronary intervention or angiography
within the previous 30 days, and electrophysiological
testing within 7 days preceding the operation were
excluded beforehand. Demographic characteristics and
medical history variables were recorded for each patient
during an interview and completed from the medical files
if necessary. Written informed consent was obtained from
all the subjects and the study was approved by the Research
Board of the Tehran Heart Center, Tehran University of
Medical Sciences. This manuscript was prepared based
on the EASE Guidelines for Authors and Translators of
Scientific Articles to be Published in English15.
Implantation procedure and DFT checking
The implantation procedure, both for PPM and ICD,
was performed in the cath lab of the Tehran Heart Center
under local anaesthesia with lidocaine and also intrave-
nous meperidine hydrochloride. Indications for the ICD
implantation were primary and secondary prevention
based on the current guidelines16. The number of active
and passive leads was recorded in each group for final
comparison, as screwing active leads into the myocar-
dium may contribute to the increase in cardiac-specific
For DFT checking and after sedation with propofol,
arrhythmia was induced in most cases by T-wave shock,
Myocardial injury following DFT
total of 119 RA leads in both groups, 119 (100%) patients
in the ICD group and 114 (95.7%) patients in the PPM
group had active leads. Also, from a total of 133 RV leads
in the ICD group and 130 leads in the PPM group, 133
and 124 patients had active leads, respectively. There
was no significant difference between the groups in
terms of the number of active and passive leads (p-value
= 0.16 and p-value = 0.17, respectively).
The mean energy delivered during DFT shock was
20.12 ± 11.92. The first DFT shock was successful in
112 (84.21%) patients and only 3 (2.25%) patients
responded to the third attempt. None of the patients
needed external shocks.
In 24 (18.04%) patients in the ICD group and
8 (6.15%) patients in the PPM group, cTNT level at
baseline was above 24 ng/L. CK-MB was above 6 ng/ml
Primary and secondary prevention were the main
indications for the ICD insertion in 60 (45.11%) and
73 (54.9%) individuals, respectively. In the ICD group,
14 (10.5%) patients received single-chamber ICDs,
65 (48.9%) received dual-chamber ICDs and 54 (40.6%)
received cardiac resynchronization therapy defibrillators
The major indications for the PPM implantation were
third-degree heart block in 76 (58.5%), sick sinus syn-
drome in 20 (15.4%), second-degree heart block in
13 (10%), and atrial fibrillation with low ventricular
response in 12 (9.2%) patients. Nine (6.9%) patients
received PPMs for miscellaneous reasons. Single-cham-
ber PPMs were implanted in 12 (9.2%) patients, while
111 (85.4%) patients received dual-chamber pacemakers
and 7 (5.4%) received triple-chamber PPMs. From a
Table 1 Clinical characteristics of patients undergoing ICD and PPM implantation
ICD (n = 133)PPM (n = 130)
Age, (mean ± SD) 60.66 ± 12.2569.56 ± 12.86< 0.001
Male, n (%) 111 (83.5) 64 (49.2) < 0.001
Smoking, n (%) 26 (19.5)8 (6.2) 0.002
Hyperlipidaemia, n (%) 38 (28.6)28 (21.5) 0.2
Diabetes mellitus, n (%) 37 (27.8)23 (17.7) 0.05
Hypertension, n (%)56 (42.1) 67 (51.5)0.13
Coronary artery disease, n (%) 93 (70.5) 24 (18.4) < 0.001
Ejection fraction, %, (mean ± SD) 26.80 ± 9.38 52.52 ± 11.03 < 0.001
Serum creatinine, mg/dl, (mean ± SD) 1.06 ± 0.241.01 ± 0.22 0.06
Type of device < 0.001
Single-chamber 14 (10.5)12 (8.4)
Double-chamber65 (48.8)111 (85.3)
* p-value < 0.05 was considered significant.
54 (40.6)7 (5.3)
Table 2 Serum level of cTNT and CK-MB at baseline, 8 and 24 hours in ICD and PPM groups
cTNT, ng/L, (median [IQR])
19.11 [11.09, 24.48]14.42 [6.59, 20.61] < 0.001
8 hr44.30 [29.69, 84.90]24.61 [13.54, 43.30] < 0.001
24 hr 35.97 [22.89, 70.20]21.63 [11.44, 35.77]< 0.001
0-8 hr diff erence 22.02 [10.88, 48.21]11.02 [2.38, 24.55] < 0.001
0-24 hr diff erence
CK-MB mg/dl (median [IQR])
15.27 [6.39, 38.31] 7.54 [0.99, 17.88]0.001
2.71 [2.01,3.62]2.49 [1.86,3.24] 0.09
8 hr3.70 [2.70,4.90]3.06 [2.25,4.03] 0.001
24 hr3.22 [2.51,4.21]3.01 [2.38,3.54]0.02
0-8 hr diff erence0.94 [0.17, 1.65] 0.52 [0, 1.13]0.003
0-24 hr diff erence
* p-value<0.05 was considered significant.
CK-MB: creatine kinase-MB, cTNT: cardiac troponin T, ICD: implantable cardioverter/defibrillator, IQR: interquartile range, PPM: permanent pacemaker.
0.50 [0, 1.05]0.47 [0, 1.03] 0.43
G. Davoodi et al.
devices and correlated this rise to the mechanical injury
during endocardial lead manipulation and interference
with cardiac venous drainage, resulting in less toxic
metabolite clearance from the heart18. Nevertheless, the
amount of the contribution of DFT shock in the rise in
cardiac markers is not well established.
During the implantation of ICDs, DFT checking is
performed to ensure the proper function of the system
and find the DFT level. Be that as it may, there is a prob-
ability that this shock can damage myocytes. Rise in
cardiac-specific enzymes during the ICD implantation
may be a sign of myocardial cell damage3, but it is not
clear how much of this damage is attributable to DFT
shocks and how much is related to manipulation and
direct mechanical trauma. The present study showed a
significantly higher rise in cTNT in comparison with
cases who received PPM with a more or less similar
procedure except for DFT checking, which can be related
to the DFT shock. Although there was a significant rise
in the cardiac specific enzymes following the ICD
implantation, the correlation between the amount of
energy delivered during DFT shock and the level of rise
was not significant in the present study.
in only 3 (2.25%) patients and all of them belonged to
the ICD group. Medians and interquartile ranges for
cTNT and CK-MB are shown in table 2.
Both cTNT and CK-MB had a significant rise after
8 and 24 hours in the ICD group (table 2). Similarly, the
serum level of both cTNT and CK-MB had a significant
rise in the PPM group, although it was within the normal
range in most cases. However, the mean level of the
cTNT rise after 8 hours in the ICD group was signifi-
cantly higher than that of the PPM group (median [IQR],
35.54 [10.88, 48.21] vs 19.15 [2.38, 24.55], respectively)
(figure 1). A similar finding was also observed for the
24-hour measurements. After adjustment for age and
gender with or without other confounding variables,
including smoking, history of diabetes or coronary
artery disease, and ejection fraction, the difference of
the cTNT rise between the groups remained significant.
Still, after adjustment for the abovementioned factors,
the CK-MB rise was no more significant.
Since some patients had an elevated level of cTNT at
baseline, we selected a subgroup of patients consisting
of 93 patients in the ICD group and 117 patients in the
PPM group with serum levels of cTNT within the nor-
mal range (< 24 ng/ml) to repeat the analysis and check
whether the enzyme rise in this group was also signifi-
cant. The results showed that the median rise of serum
cTNT after 8 and 24 hours in this subgroup was also
significantly different between the ICD and PPM groups
(p = 0.001 and p < 0.001, respectively). The median rise
of CK-MB was only significantly different after 8 hours
between the groups (p = 0.02) but not after 24 hours
(p = 0.47).
There was no significant relationship between the
energy delivered and rise in cTNT and CK-MB (for
cTNT the Spearman correlation was 0.08; p = 0.30; and
for CK-MB the Spearman correlation was 0.03; p = 0.67).
On the other hand, the number of DFT shocks did not
have any influence on the rise of either cTNT or CK-MB
(p = 0.18 and p = 0.41, respectively).
In the present study, we observed a significant rise in
the serum level of cardiac specific biomarkers, i.e. cTNT
and CK-MB, in patients who were treated with ICD
compared to PPM, which can be attributed to the DFT
shock following the ICD implantation. This rise may
exhibit some degrees of myocardial injury, although it
is not correlated with the amount of energy delivered
during DFT checking.
Cardiac troponins are sensitive markers for myocar-
dial injury17. Some studies have shown a rise in cardiac-
specific markers in the wake of implanting cardiac
Fig. 1 Comparing the median rise of cTNT (A) and CK-MB (B)
between the ICD and PPM patients.
Myocardial injury following DFT
shocks and shows the increased risk from non-arrhyth-
mic death in those who receive the ICD discharges29.
This risk has been observed in patients receiving appro-
priate shocks as well as in those receiving inappropriate
shocks. The increased risk in the inappropriate shock
group can be attributed to the harmful effect of the
shocks on the myocardium and requires further elucida-
tion. It has been posited that by utilizing the new lead
technology, and limiting the number of DFT tests, safe
implantation with minimal myocardial injury can be
Our study has some limitations, first and foremost
amongst which is the fact that the sex ratio and mean age
of the patients as well as some few baseline characteristics
in the PPM group were different from those of the ICD
group. We tried to minimize their influence on the results
by adjusting for these variables in the statistical analysis.
The strength of this study lies in its prospective design
and the fact that it does not only comprise a large num-
ber of patients, but it also compares the results with those
patients undergoing a quite similar procedure.
In conclusion, elevation of cardiac specific biomark-
ers after the ICD implantation was significantly higher
compared to that of the PPM implantation, which can
be attributable to DFT shock. Although the exact mech-
anism of enzyme rise is still unknown, it may exhibit
some degrees of myocardial damage. Plausible solutions,
such as identifying the optimal level of energy delivered
during DFT checking, and perhaps skipping DFT check-
ing in specific patient groups in order to prevent further
complications, require more investigations.
The present study was supported by the Tehran Heart
Center and the Tehran University of Medical Sciences.
The authors would like to thank Mr. Roohzendeh and
Mr. Yaghoubzadeh, the laboratory supervisors of the
Tehran Heart Center, for their valuable assistance and
Dr. Arash Jalali for his help with the statistical analysis.
CONFLICT OF INTEREST: none declared.
The exact mechanism of cardiac enzyme release
following DFT or ICD shock is still a matter for debate.
In acute myocardial infarction, cardiac-specific enzymes
rise within 3-4 hours and remain high for several days
due to the gradual degradation of myofibrils and release
of the troponin complex19. Although damage to a small
number of cardiomyocytes is enough to elevate the
serum level of troponins20-21, some studies have posited
that troponins may be released from myocardial cells
without disruption of the cell membranes and cell necro-
sis and are from a cytoplasmic origin4, 22. On the other
hand, the mechanism of enzyme release in ablation and
hyperthermic exposure is thought to be a consequence
of injury to the sarcolemmal membrane23. Given that
the rise in cardiac specific enzymes was transient in the
present study and did not reach the levels usually seen
in acute myocardial infarction, we believe that this ele-
vation may be partly attributable to small and limited
cell injury rather than an extensive myocardial damage.
The rise of CK-MB within normal limits may be a good
proof for this assumption.
A baseline cTNT measurement above the upper
normal range was observed in 32 patients, 24 (75%) of
whom were in the ICD group. This elevation may be a
consequence of several different factors. It has been a
well-established fact that cTNT increases in patients
with congestive heart failure and has a positive correla-
tion with the severity of the disease24. Moreover, an
association between cTNT elevation and high-risk phe-
notypes of cardiac disease such as left ventricular hyper-
trophy, atrial fibrillation, sepsis, hypovolaemia, chronic
kidney disease, and diabetes has also been noted25. Since
we excluded patients who had undergone cardiac manip-
ulation within a 7-day period leading up to the device
implantation or had cardiac events within a 30-day
period before the procedure, the elevated level of cTNT
or CK-MB at baseline in the ICD group can be highly
attributed to other concomitant conditions, particularly
heart failure. The significantly lower ejection fraction
in the ICD group can be a good rationale to explain this
effect. However, we should not forget that cardiac tro-
ponins are highly predictive of future outcomes in car-
diovascular patients26-27. Also, low survival was docu-
mented in patients with elevated levels of cTNT28.
ICDs, albeit life-saving, may speed up the heart fail-
ure progress. The ICD shocks partly contribute to the
exacerbation of heart failure, and probably DFT shocks
are, therefore, no exception2, 7. On the other hand,
limited evidence suggests causal harm from the ICD
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