Abstract

Thebeisan veins are microfistulous connections between a coronary arterial branch directly to a ventricular or atrial chamber. Extensive thebesian veins that empty into the left ventricle can cause typical chest pain symptoms, troponin elevation, and ischemic EKG changes from coronary steal leading to acute coronary syndrome in extreme cases. Literature review exposed a consistent pattern of EKG findings among patients with extensive thebesian veins involving all three major coronary arteries. We present a case study as an example of this rare anatomic finding of extensive thebesian veins draining into the left ventricle causing acute coronary syndrome in a symptomatic patient with elevated troponin and ischemic changes on EKG. This same EKG pattern that is present in our patient was discovered to be consistent among available case studies reviewed that had included an EKG tracing in their report. A newly proposed association between the ischemic changes on EKG due to extensive thebeisan veins and those of a severe proximal left anterior descending coronary artery stenotic lesion was discovered. The newly discovered consistency in the EKG pattern with acute coronary syndrome caused by extensive thebesian veins is the same pattern as that seen in Wellens Syndrome.

Highlights

  • A coronary artery fistula is an abnormal luminal connection between a coronary artery and either a vein, another artery, or even a ventricular chamber.[1]

  • When a significant number of microfistulae exist, leftto-left shunting occurs, meaning blood that should be continuing downstream in the arterial system has taken an alternative pathway creating a new circuit of blood flow that doubles back on itself

  • The patient was admitted with a diagnosis of Acute Coronary Syndrome (ACS) non-ST segment elevated myocardial infarction in which the EKG did not display ST segment elevations, but labs were consistent with myocardial injury

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Summary

INTRODUCTION

A coronary artery fistula is an abnormal luminal connection (i.e., communication via a tubular structure) between a coronary artery and either a vein, another artery, or even a ventricular chamber.[1]. The patient was admitted with a diagnosis of ACS non-ST segment elevated myocardial infarction in which the EKG did not display ST segment elevations (as seen in most cases of acute myocardial infarction), but labs were consistent with myocardial injury (elevated troponin level) Her physicians were concerned that the culprit artery causing ischemic disease was the Left Anterior Descending (LAD) based on her EKG findings meeting criteria for Wellens Syndrome. She reported currently undergoing an extremely stressful economic situation, which raised concern for possible Takotsubo Cardiomyopathy (i.e., stress induced cardiomyopathy) in which there is no coronary artery disease, but severe left ventricular myocardial dysfunction that is present with EKG changes mimicking ACS. This would entail optimizing her CAD medication regimen according to current guidelines, minimizing her CAD risk factors, and monitoring to ensuring she has no symptom recurrence

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