Abstract:

Elevated Cardiac Enzymes Associated With Supraventricular Tachycardia In the Absence of Coronary Artery Disease

Mahreen Majid M.D; Patrycja Galazka, MD; Islam Abudayyeh, MD Department of Medicine, Advocate Lutheran General Hospital

Introduction: In the absence of angiographically visible coronary lesions, elevated troponin I is seen in up to 15 percent of those undergoing angiography for suspected coronary artery disease. It is reported in a variety of conditions that are not linked to acute coronary syndrome. Elevated cardiac enzyme levels are uncommonly seen in patients with supraventricular tachycardia with normal coronary arteries. Methods: In this retrospective case review study we evaluated a series of 5 patients age 33 to 60 years presenting to the emergency room with complaints of prolonged palpitations and shortness of breath. Results: The ECG in each case demonstrated a narrow-complex tachycardia, and initial troponin I levels were elevated ranging from 0.05 to 5 (abnormal >0.04). Further evaluation with cardiac catheterization, nuclear imaging stress tests, and echocardiogram demonstrated normal ejection fraction, normal wall motion, and no evidence of coronary artery disease. Electrophysiology testing confirmed supraventricular re-entry tachycardia. Conclusions: The patients’ elevation in troponin I could not be explained by coronary artery disease. The mechanism of cardiac enzyme elevation in the setting of prolonged tachycardia is unclear. In the absence of coronary artery disease and other conditions that may raise troponin I levels such as renal failure it was felt that the only likely factor causing the elevation would be the tachycardia. The tachycardia was demonstrated on EP study. Based on this retrospective case review, elevated cardiac enzymes should be interpreted in the context of a patient’s clinical presentation

Introduction:

In the absence of angiographically visible coronary lesions, elevated troponin I is seen in up to 15 percent of those undergoing angiography for suspected coronary artery disease. It is reported in a variety of conditions that are not linked to acute coronary syndrome. Elevated cardiac enzyme levels are uncommonly seen in patients with supraventricular tachycardia with normal coronary arteries.

References:

The patients’ elevation in troponin I could not be explained by the imaging stress tests, echocardiograms, or cardiac catheterization which was angiographically free of disease. Cardiac enzyme elevations in the setting of angina-type pain were associated with intermediate to high risk and therefore often the basis for invasive evaluation, or stress testing. The mechanism of cardiac enzyme elevation in the setting of prolonged tachycardia is unclear. It may be associated with increased demand and reduced coronary supply during diastole, or elevated ventricular end-diastolic pressures. In the absence of such disease and other conditions that may raise troponin I levels such as renal failure it was felt that the only likely factor causing the elevation would be the tachycardia. The tachycardia was demonstrated on EP study. Based on this retrospective review we feel that elevated cardiac enzymes should be interpreted in the context of a patient’s clinical presentation. Risk-stratifying the patients based on their TIMI risk-scores before obtaining cardiac enzymes in the setting of prolonged tachycardia may improve the positive predictive value of the diagnostic tests, and reduce unnecessary testing. At this time there is no large study to specifically show the cardiac enzymes are elevated in other forms of tachycardia in the absence of coronary artery disease, but sporadic cases do show that there are elevations with conditions such as atrial fibrillation.

Methods:

We present a series of 5 patients age 33 to 60 years presenting to the emergency room with complaints of prolonged palpitations and shortness of breath. Initial physical exam was unrevealing except for the tachycardia. Troponin I levees greater than 0.04 were considered abnormal. Our patient series included values between 0.05 to 5. These levels are consistent with patients who can present with in variety of settings such as STEMI, NSTEMI, myocarditis, cardiac contusion, and type II MI.

Results:

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The ECG in each case demonstrated a narrow-complex tachycardia, and initial troponin I levels were elevated ranging from 0.05 to 5. Further evaluation with cardiac catheterization, nuclear imaging, stress tests, and echocardiogram demonstrated normal ejection fraction, normal wall motion, and no evidence of coronary artery disease. Electrophysiology testing confirmed re-entry tachycardia such as atrioventricular node, and atrioventricular reentry tachycardia as the cause of elevation of these troponins.

Discussion:

Figure 2. Normal Left Coronary Artery

Figure 1.LV Gram showing normal LV function during diastole and systole

Figure 3. Normal Right Coronary Artery

Figure 4. 12 Lead ECG showing AVNRT with

2 : 1 Block from EP Study

1. Redfearn DP, Ratib K, Marshall HJ, Griffith MJ: Supaventricular tachycardia promotes release of troponin I in patients with normal coronary arteries. International Journal of Cardiology 2005; 521-522.2. Zellweger MJ, Schaer BA, Cron TA, Pfisterer ME, Osswald S: Elevated troponin levels in absence of coronary artery disease after supraventricular tachycardia. Swiss Med Wkly 2003; 133; 439-441.3. Patane S, Marte F, Di Bella, G: Abnormal troponin I levels after supraventricular tachycardia. Internal Journal of Cardiology 2009; 57-59.