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: firstname.lastname@example.org
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 ± 0.220.06
Type of device < 0.001
Single-chamber14 (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 hr35.97 [22.89, 70.20]21.63 [11.44, 35.77] < 0.001
0-8 hr diff erence22.02 [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 hr 3.70 [2.70,4.90] 3.06 [2.25,4.03]0.001
24 hr 3.22 [2.51,4.21]3.01 [2.38,3.54]0.02
0-8 hr diff erence 0.94 [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
1. Tereshchenko LG, Faddis MN, Fetics BJ,
Zelik KE, Efimov IR, Berger RD. Transient local
injury current in right ventricular electrogram
after implantable cardioverter-defibrillator
shock predicts heart failure progression.
J Am Coll Cardiol 2009; 54: 822-8.
G. Davoodi et al. Download full-text
2. Cevik C, Perez-Verdia A, Nugent K.
Implantable cardioverter defibrillators and
their role in heart failure progression.
Europace 2009; 11: 710-5.
3. Alaiti MA, Maroo A, Edel TB. Troponin levels
after cardiac electrophysiology procedures:
review of the literature. Pacing Clin
Electrophysiol 2009; 32: 800-10.
4. Schluter T, Baum H, Plewan A, Neumeier D.
Effects of implantable cardioverter
defibrillator implantation and shock
application on biochemical markers of
myocardial damage. Clin Chem 2001; 47:
5. Hurst TM, Hinrichs M, Breidenbach C, Katz N,
Waldecker B. Detection of myocardial injury
during transvenous implantation of
J Am Coll Cardiol 1999; 34: 402-8.
6. Sonel AF, Shalaby A, McConnell JP,
Czarnecki T, Hogen S, Zahid M, Amidi M.
Detectable troponin levels predict poor
prognosis in patients with left ventricular
dysfunction undergoing internal defibrillator
implantation. Pacing Clin Electrophysiol 2007;
7. Larsen GK, Evans J, Lambert WE, Chen Y, Raitt
MH. Shocks burden and increased mortality
in implantable cardioverter-defibrillator
patients. Heart Rhythm 2011; 8: 1881-6.
8. Blendea D, Blendea M, Banker J,
McPherson CA. Troponin T elevation after
implanted defibrillator discharge predicts
survival. Heart 2009; 95: 1153-8.
9. Lee TH, Rouan GW, Weisberg MC, Brand DA,
Cook EF, Acampora D, Goldman L. Sensitivity
of routine clinical criteria for diagnosing
myocardial infarction within 24 hours of
hospitalization. Ann Intern Med 1987; 106:
10. Lindahl B, Toss H, Siegbahn A, Venge P,
Wallentin L. Markers of myocardial damage
and inflammation in relation to long-term
mortality in unstable coronary artery disease.
FRISC Study Group. Fragmin during Instability
in Coronary Artery Disease. N Engl J Med 2000;
11. Tsutamoto T, Kawahara C, Nishiyama K,
Yamaji M, Fujii M, Yamamoto T, Horie M.
Prognostic role of highly sensitive cardiac
troponin I in patients with systolic heart
failure. Am Heart J 2010; 159: 63-7.
12. Bradfield J, Tung R, Boyle NG, Shivkumar K.
Managing patients with ICD shocks and
programming tachycardia therapies during
acute heart failure syndromes. Heart Fail Rev
2011; 16: 449-56.
13. Adams JE, 3rd, Bodor GS, Davila-Roman VG,
Delmez JA, Apple FS, Ladenson JH, Jaffe AS.
Cardiac troponin I. A marker with high
specificity for cardiac injury. Circulation 1993;
14. Chia S, Senatore F, Raffel OC, Lee H,
Wackers FJ, Jang IK. Utility of cardiac
biomarkers in predicting infarct size, left
ventricular function, and clinical outcome
after primary percutaneous coronary
intervention for ST-segment elevation
myocardial infarction. JACC Cardiovasc
Interv 2008; 1: 415-23.
15. EASE Guidelines for Authors and Translators of
Scientific Articles to be Published in English:
European Association of Science Editors
(EASE). J Tehran Heart Cent 2011; 6: 206-10.
16. Epstein AE, DiMarco JP, Ellenbogen KA,
Estes NA 3rd, Freedman RA, Gettes LS,
Gillinov AM, Gregoratos G, Hammill SC,
Hayes DL, Hlatky MA, Newby LK, Page RL,
Schoenfeld MH, Silka MJ, Stevenson LW,
Sweeney MO, Smith SC Jr, Jacobs AK,
Adams CD, Anderson JL, Buller CE,
Creager MA, Ettinger SM, Faxon DP,
Halperin JL, Hiratzka LF, Hunt SA, Krumholz
HM, Kushner FG, Lytle BW, Nishimura RA,
Ornato JP, Page RL, Riegel B, Tarkington LG,
Yancy CW; American College of Cardiology/
American Heart Association Task Force on
Practice Guidelines (Writing Committee to
Revise the ACC/AHA/NASPE 2002 Guideline
Update for Implantation of Cardiac
Pacemakers and Antiarrhythmia Devices);
American Association for Thoracic Surgery;
Society of Thoracic Surgeons. ACC/AHA/HRS
2008 Guidelines for Device-Based Therapy
of Cardiac Rhythm Abnormalities: a report of
the American College of Cardiology/
American Heart Association Task Force on
Practice Guidelines (Writing Committee to
Revise the ACC/AHA/NASPE 2002 Guideline
Update for Implantation of Cardiac
Pacemakers and Antiarrhythmia Devices)
developed in collaboration with the American
Association for Thoracic Surgery and Society
of Thoracic Surgeons. J Am Coll Cardiol 2008;
17. Christ M, Popp S, Pohlmann H, Poravas M,
Umarov D, Bach R, Bertsch T. Implementation
of high sensitivity cardiac troponin T
measurement in the emergency department.
Am J Med 2010; 123: 1134-42.
18. Altin T, Akyurek O, Vurgun K, Beton O, Sayin T,
Kilickap M, Karaoguz R, Guldal M, Erol C.
Effect of transvenous cardiac
resynchronization therapy device
implantation on cardiac troponin I release.
Pacing Clin Electrophysiol 2007; 30: 1356-62.
19. Katus HA, Remppis A, Scheffold T, Diederich
KW, Kuebler W. Intracellular compartmenta-
tion of cardiac troponin T and its release
kinetics in patients with reperfused and
nonreperfused myocardial infarction.
Am J Cardiol 1991; 67: 1360-7.
20. Hamm CW. Risk stratifying acute coronary
syndromes: gradient of risk and benefit.
Am Heart J 1999; 138(1 Pt 2): S6-11.
21. Boos CJ, Gough S, Wheather M, Medbak S,
More R. Effects of transvenous pacing on
cardiac troponin release. Pacing Clin
Electrophysiol 2004; 27: 1264-68.
22. Ng SM, Krishnaswamy P, Morrisey R,
Clopton P, Fitzgerald R, Maisel AS. Mitigation
of the clinical significance of spurious
elevations of cardiac troponin I in settings of
coronary ischemia using serial testing of
multiple cardiac markers. Am J Cardiol 2001;
87: 994-9; A994.
23. Morady F. Radio-frequency ablation as
treatment for cardiac arrhythmias.
New Engl J Med 1999; 340: 534-44.
24. Missov E, Mair J. A novel biochemical
approach to congestive heart failure: cardiac
troponin T. Am Heart J 1999; 138 (1 Pt 1): 95-9.
25. Jeremias A, Gibson CM. Narrative review:
alternative causes for elevated cardiac
troponin levels when acute coronary
syndromes are excluded. Ann Intern Med 2005;
26. Hsieh BP, Rogers AM, Na B, Wu AH, Schiller NB,
Whooley MA. Prevalence and prognostic
significance of incidental cardiac troponin T
elevation in ambulatory patients with stable
coronary artery disease: data from the Heart
and Soul study. Am Heart J 2009; 158: 673-9.
27. Latini R, Masson S, Anand IS, Missov E, Carlson
M, Vago T, Angelici L, Barlera S, Parrinello G,
Maggioni AP, Tognoni G, Cohn JN. Prognostic
value of very low plasma concentrations of
troponin T in patients with stable chronic
heart failure. Circulation 2007; 116: 1242-9.
28. Masson S, Anand I, Favero C, Barlera S, Vago T,
Bertocchi F, Maggioni AP, Tavazzi L, Tognoni G,
Cohn JN, Latini R. Serial measurement of
cardiac troponin T using a highly sensitive
assay in patients with chronic heart failure:
data from 2 large randomized clinical trials.
Circulation 2012; 125: 280-8.
29. Tung R, Zimetbaum P, Josephson ME. A
critical appraisal of implantable
cardioverter-defibrillator therapy for the
prevention of sudden cardiac death.
J Am Coll Cardiol 2008; 52: 1111-21.