ST elevation occurring during stress testing

Abstract

A case is presented of significant reversible ST elevation occurring during treadmill testing, and the coronary anatomy and subsequent course are described, indicating that ischemia is a potential cause of this electrocardiographic finding. M any conditions can cause electrocardiographic (ECG) ST elevation. Significant ST elevation is defined by at least 1 mm elevation in the limb leads or 2 mm elevation in the precordial leads above the isoelectric point (1). With regard to myocardial infarction, diagnostic ST elevation in the absence of left ventricular hypertrophy or left bundle-branch block is defined by the European Society of Cardiology/ACCF/AHA/World Heart Federation Task Force for the Universal Definition of Myocardial Infarction as new ST elevation at the J point in at least two contiguous leads of !2 mm in men or 1.5 mm in women in leads V2ÁV3 and/or of !1 mm in other contiguous chest leads or the limb leads (2). In addition to ST elevation myocardial infarction, other causes include early repolarization, left ventricular hyper-trophy, hypertrophic cardiomyopathy, ventricular aneur-ysm, left bundle-branch block, pericarditis, myocarditis, aortic dissection, Prinzmetal's angina, Takotsubo cardio-myopathy, and Brugada syndrome (1, 3). Furthermore, non-cardiac conditions, such as pulmonary thromboem-bolism, pneumothorax, and atelectasis, can also present with similar ECG changes (1, 3). Thus, ST segment elevations are not specific for myocardial infarction and should be distinguished among the many potential causes. We present a case of exercise-induced ST segment elevation associated with atypical symptoms and caused by ischemia. Case A 75-year-old Caucasian male with a past medical history of hypertension, hyperlipidemia, and abnormal hemoglo-bin A1c (6.5) was found to have an abnormal ECG by his primary care physician on routine evaluation. His wife had noted that he appeared to have slowed down a bit, but he denied chest pain or exertional dyspnea. Baseline ECG revealed poor R wave progression suggesting prior anteroseptal infarction (Fig. 1). The patient had no history of symptoms suggesting myocar-dial infarction. A stress echocardiogram was performed. During exercise, ST elevation developed in lead V3 and increased progressively over the next 3 min. The test was terminated at 7 min because of dyspnea and the ECG changes, at which time the heart rate had increased to 150 (Fig. 2). No chest pain or arrhythmias were noted. Both dyspnea and ST elevation resolved 4 min after cessation of exercise. No ST changes were noted in other leads. Physio-logic pulse and blood pressure responses were noted: blood pressure rose from 130/70 to 160/75, and heart rate dropped from maximal rate of 150 down to 100 within 2 min after exercise. Resting echocardiography revealed a mildly dilated left ventricle, normal wall thickness, and an ejection fraction of 50%, with mild antero-apical hypokinesis at rest, and dyskinesia immediately post-exercise. No other wall motion abnormalities were noted. Coronary angio-graphy was advised. The study revealed a 60Á70% eccentric stenosis of the left main coronary artery, a 70% long proximal stenosis of the left anterior descending (LAD), followed by a 99% mid-LAD stenosis, with the distal vessel being filled by right-sided collaterals. Additionally, a small LAD diagonal was totally occluded, and the circumflex had a 70% heavily calcified obtuse marginal branch stenosis. The right coronary artery (RCA) revealed minimal JOURNAL OF COMMUNITY HOSPITAL INTERNAL MEDICINE PERSPECTIVES ae