Short communication S W I S S M E D W K LY 2 0 0 3 ; 1 3 3 : 4 3 9 – 4 4 1 · w w w . s m w . c h 439
Peer reviewed article
Elevated troponin levels in the
absence of coronary artery disease
after supraventricular tachycardia
Michael J. Zellweger, Beat A. Schaer, Thomas A. Cron, Matthias E. Pfisterer, Stefan Osswald
Cardiology Department, University Hospital, Basel, Switzerland
Generally speaking elevated troponin levels supraventricular tachycardia without evidence of
are consistent with the diagnosis of acute coronary coronary artery disease and very low risk scores for
syndrome and haemodynamically relevant coro- acute coronary syndrome are described and dis-
nary artery stenosis. However, they may also point cussed.
to minor myocardial injury in other circumstances.
Four patients with elevated troponin levels after Key words: troponin; supraventricular tachycardia
Elevated troponin levels play a pivotal role in tachycardia with haemodynamic compromise ,
the diagnosis of acute coronary syndrome and myo- renal insufficiency , cerebrovascular accidents
cardial infarction . In the past traditional en-  or prolonged strenuous endurance exercise
zyme evaluation left patients with small myocar- . In contrast, as far as we know, there has been
dial injury and cellular death undiagnosed ; no report evaluating elevated troponin levels after
these patients were wrongly classified as having av-nodal reentry tachycardia (AVNRT).
unstable angina or, worse, non-cardiac chest pain. Patients with positive troponin levels due to
Troponin elevation now identifies these patients as conditions other than acute coronary syndrome
a subgroup at high risk for subsequent cardiac may receive inappropriate therapy and face delays
events . In general, elevated troponin levels are in final diagnosis and correct treatment . In in-
observed in the setting of acute coronary syndrome terpreting troponin results it is important to take
with ongoing myocardial damage and haemody- into account the context of the patient’s clinical
namically significant stenosis . However, several presentation.
conditions with elevated troponin and normal In the present report four patients with
coronary arteries are not linked to acute coronary supraventricular tachycardia (AVNRT) and ele-
syndromes or coronary artery intervention, such as vated troponin levels without coronary artery dis-
pericarditis , myocarditis , pulmonary em- ease are discussed.
bolism , sepsis , congestive heart failure ,
Case 1 testing, echocardiography and gated myocardial perfusion
A 48-year-old female with a history of supraventric- (SPECT) were performed. These investigations revealed
ular tachycardia since adolescence underwent minor sur- normal left ventricular function without evidence of is-
gery, after which 2 prolonged episodes of supraventricu- chaemia. Relevant coronary artery disease was therefore
lar tachycardia occurred. In addition, the patient devel- ruled out.
oped atypical chest pain, which she had never experienced During electrophysiological testing AVNRT was eas-
before, and it was for this reason that she was referred for ily reproducible (cycle length 355 ms, 170 bpm) and was
cardiac work-up. In addition to atypical chest pain, the tro- successfully treated by slow pathway ablation. Subse-
ponin and creatine kinase levels were slightly elevated quently the patient remained free from chest pain and
support declared. (Table 1). ECG after tachycardia revealed no abnormali- further tachycardia.
ties compared to baseline. Before electrophysiological
Elevated troponin levels in the absence of coronary artery disease after supraventricular tachycardia 440
Table 1 Patient tachycardia duration troponin I creatine kinase TIMI risk score
Tachycardia and (beats per minute) (hours)
laboratory findings. 1 170–240 6 3.5 (normal <2 mg/l) 267 (normal <170 U/l) 0/1
2 175–250 22 10 (normal <2 mg/l) 214 (normal <200 U/l) 0/1
3 210 7 32 (normal <2 mg/l) 329 (normal <200 U/l) 0/1
4 180 11⁄2 1.32 (normal <0.5 ng/ml)* 170 (normal <170 U/l) 2
It is worth noting that troponin and creatine kinase levels are consistent with peak levels.
* In this patient a troponin test with another upper limit was used.
Case 2 dia which he had been unable to terminate on his own. In
A fifty-year-old male with an unremarkable medical contrast to former episodes this one was further associated
history developed light-headedness, dizziness, shortness with chest pain and shortness of breath. On admission the
of breath and nausea in the course of his daily work. After patient still complained of chest pain and the ECG showed
a near-fainting episode he was referred to the emergency supraventricular tachycardia (cycle length 286 ms; 210
room for cardiac evaluation and therapy. On admission the bpm) most probably consistent with AVNRT. The ECG
patient was asymptomatic with respect to anginal chest obtained after conversion to sinus rhythm (adenosine)
pain. ECG showed atrial fibrillation with rapid ventricu- afforded no evidence of ischaemia. In view of remark-
lar response and elevated troponin and creatine kinase lev- ably high troponin and CK levels (table) the patient under-
els (Table 1). After treatment and conversion to sinus went coronary angiography, which revealed normal coro-
rhythm (no changes to previously acquired ECGs) the pa- nary arteries, normal left ventricular ejection fraction
tient underwent further work-up with treadmill stress (71%), volumes and left enddiastolic ventricular pressure
testing and subsequent stress echocardiography. Neither (10 mm Hg). Additional echocardiography confirmed
of these examinations provided any clue to coronary ar- these findings and demonstrated normal thickness of left
tery disease. However, supraventricular tachycardia (cycle ventricular walls. In a first approach the patient was treated
length 250 ms; 250 bpm) occurred during recovery from medically and did well.
the stress echo and at this point in time the patient expe-
rienced the same symptoms as those which had prompted Case 4
hospital admission. In retrospect it may be hypothesised A 57-year-old female patient was referred with dizzi-
that atrial fibrillation at first presentation was secondary ness of sudden onset and chest pain. On their way back to
to the AVNRT. the hospital the paramedics diagnosed supraventricular
The results of electrophysiological testing were con- tachycardia (table) which was successfully treated by in-
sistent with AVNRT and slow-pathway modulation was travenous adenosine. After conversion to sinus rhythm the
successfully performed. After treatment the patient did patient became symptom-free. However, the ECG
well and did not experience chest pain or recurrent sus- showed slight ST depression in infero-lateral leads. In
tained tachycardia. view of this, elevated troponin levels and several cardio-
vascular risk factors, echocardiography was performed
Case 3 with normal results and coronary angiography showed
A 44-year-old male, who in the past had had recur- normal coronary arteries, normal left ventricular ejection
rent episodes of supraventricular tachycardia which he had fraction (67%), volumes and left ventricular end-diastolic
always successfully treated by vagal manoeuvres, was ad- pressure (4 mm Hg). In a first approach the patient was
mitted after experiencing a recurrent episode of tachycar- treated medically and did well.
All these patients had supraventricular tachy- Despite the fact that “clinical” coronary artery
cardia without evidence of coronary artery disease. disease was ruled out in all of these patients, ele-
However, all had elevated troponin levels and vated troponin levels may point to myocardial in-
three even elevated creatine kinase levels on ad- jury during AVNRT.
mission. It can be postulated that the creatine ki- The mechanism of myocardial injury in an ob-
nase elevation was due to myocardial injury in two viously normal heart is unclear. It may be specu-
of the patients. In the first patient with only slightly lated that increased demand during a relatively
elevated troponin levels creatine kinase elevation long period of rapid tachycardia is combined with
was very probably due to the surgical procedure a reduced oxygen supply to the myocardium due
the patient had undergone one day before tachy- to the shortened diastole during tachycardia. It is
cardia. With regard to the ECG changes, only one of interest that no correlation between the extent
patient had slight ST depression just after conver- of marker elevation and duration and rate of tachy-
sion to sinus rhythm. It is worth noting that ST al- cardia was seen in these patients.
terations during AVNRT are not evidence for the This observation is in accordance with a re-
presence of ischaemia. They are frequently ob- cently published report  describing 21 patients
served without other evidence of ischaemia and who had elevated troponin levels despite a normal
with a normal ECG after conversion to sinus or only mildly abnormal coronary angiogram
rhythm. (<50% diameter loss without complex features or
S W I S S M E D W K LY 2 0 0 3 ; 1 3 3 : 4 3 9 – 4 4 1 · w w w . s m w . c h 441
tude, the risk score was calculated by assigning a
TIMI risk scores: The
event rate is consis- value of 1 when a variable was present and then
tent with risk of the classifying patients in the test cohort by the num-
at 14 days (all-cause
ber of risk factors present. Event rates increased
mortality, myocardial significantly as the TIMI risk score increased (Fig-
infarction and severe ure 1). It is worth noting that all four patients de-
prompting urgent scribed had a low TIMI risk score with no other
revascularisation); risk factor except elevated troponin in three and
adapted from .
only one additional risk factor in one. Thus, the
presence of an acute coronary syndrome in these
four patients was unlikely.
Generally speaking, elevated troponin levels
thrombus). Troponin release was attributed to are consistent with the diagnosis of acute coronary
tachycardia (4 supraventricular, 2 ventricular), syndrome and haemodynamically significant coro-
physical exertion, pericarditis and congestive heart nary artery stenosis. However, it must be borne in
failure in 29%, 10%, 10% and 5% respectively. mind that troponin results (as also other easily
46% of patients had no identifiable cause for the available laboratory variables) need to be inter-
troponin elevation. preted in the context of the patient’s clinical pres-
Elevated troponin levels must thus be inter- entation. The TIMI risk score provides a useful
preted in the clinical context. In patients with tool in the clinical evaluation of patients with ele-
unstable angina and non-ST elevation myocardial vated troponin levels. In the absence of clinical
infarction, the TIMI risk score is a simple, prog- coronary artery disease, troponin levels may point
nostically important scheme which characterises a to minor myocardial injury, as shown by this re-
patient’s risk of death and ischaemic events, and port on four cases of supraventricular tachycardia
provides a basis for clinical and therapeutic deci- (AVNRT).
sion-making . The TIMI risk score takes into
account the patient’s age, risk factors for coronary
artery disease, existence of >50% prior coronary Correspondence:
stenosis, ST deviation, number of severe anginal Stefan Osswald, MD
events 24 h prior to hospital admission, use of as- Cardiology Department
pirin and elevated serum cardiac markers (creatine University Hospital
kinase MB fraction and/or cardiac-specific tro- Petersgraben 4
ponin level). Since the estimated parameters for CH-4031 Basel
each of the 7 predictors were of a similar magni- E-Mail: email@example.com
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