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A Series of Unfortunate Events: Prinzmetal Angina Culminating in Transmural Infarction in the Setting of Acute Gastrointestinal Hemorrhage

DOI: 10.1155/2013/641348

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Prinzmetal angina or vasospastic angina is a clinical phenomenon that is often transient and self-resolving. Clinically it is associated with ST elevations on the electrocardiogram, and initially it may be difficult to differentiate from an acute myocardial infarction. The vasospasm induced in this setting occurs in normal or mildly to moderately diseased vessels and can be triggered by a number of etiologies including smoking, changes in autonomic activity, or drug ingestion. While the ischemia induced is usually transient, myocardial infarction and life-threatening arrhythmias can occur in 25% of cases. We present the case of a 65-year-old female where repetitive intermittent coronary vasospasm culminated in transmural infarction in the setting of gastrointestinal bleeding. This case highlights the mortality associated with prinzmetal angina and the importance of recognizing the underlying etiology. 1. Introduction Coronary vasospastic angina also known as Prinzmetal angina is a discrete clinical entity characterized as episodic angina pectoris in association with ST-segment elevations on electrocardiogram in the absence of high-grade coronary artery stenosis. These episodes usually occur at rest and often between the midnight and early morning hours [1]. The etiology of Prinzmetal angina is believed to be focal spasm of the smooth muscle layer of the arterial wall. These spasms occur in normal or mildly diseased vessels in the absence of any preceding increase in myocardial demand [1–4]. Transient ischemia is responsible for the anginal symptoms, while myocardial infarction can develop in a percentage of patients. Myocardial infarction and life-threatening arrhythmias are believed to occur in 25% of untreated patients with Prinzmetal angina [5]. The major risk factor contributing to vasospastic angina is thought to be an active smoking history [6]. Other possible triggers include changes in autonomic activity, the use of ephedrine-based products, cocaine ingestion guide wire or balloon dilatation, and magnesium deficiency [7–10]. It is usually diagnosed before 50 years of age with a higher prevalence in females and in the Japanese population [11]. Diagnosis may be challenging and includes ambulatory monitoring for ST segment elevations as well as exercise stress testing. In some scenarios intracoronary provocative tests can be performed in the catheterization lab to secure the diagnosis. Acetylcholine and ergonovine are the most widely used drugs for these tests. Treatment modalities have focused on calcium channel blockers for prevention and


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