Elevated troponin levels in absence of coronary artery disease

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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 [9],
                    the diagnosis of acute coronary syndrome and myo-                 renal insufficiency [10], cerebrovascular accidents
                    cardial infarction [1]. In the past traditional en-               [11] or prolonged strenuous endurance exercise
                    zyme evaluation left patients with small myocar-                  [12]. In contrast, as far as we know, there has been
                    dial injury and cellular death undiagnosed [2];                   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 [1]. In general, elevated troponin levels are              in final diagnosis and correct treatment [9]. 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 [3]. 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 [4], myocarditis [5], pulmonary em-                  ease are discussed.
                    bolism [6], sepsis [7], congestive heart failure [8],

                    Case presentations
                    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-
No financial
                    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 [9] 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

Figure 1
                                                                                              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-
composite endpoint
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-
recurrent ischaemia
prompting urgent                                                                              scribed had a low TIMI risk score with no other
revascularisation);                                                                           risk factor except elevated troponin in three and
adapted from [13].
                                                                                              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 [13]. 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:

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