Precordial T-wave inversion of “cardiac memory” pattern after high-dose methylprednisolone pulse therapy

Abstract

‘‘Cardiac memory’’ (CM) refers to T-wave abnormalities that manifest on resumption of a normal ventricular activation pattern after a period of abnormal ventricular activation, such as ventricular pacing, transient left bundlebranch block, ventricular arrhythmias, or Wolf–Parkinson– White syndrome [1]. Pacing-induced T-wave inversion (TWI), the most common clinical example of CM, is usually localized to precordial and inferior leads [1, 2]. Postpacing CM often produces striking precordial TWI that may persist for long periods of time after the pacing is discontinued, thus obscuring their causal relationship. As a result, TWI due to CM represents an important confounder in the diagnosis of myocardial infarction [2, 3]. Diagnostic features to differentiate by vector direction analysis pacinginduced CM from TWI that results from ischemia and infarction have been described only recently: the combination of (a) positive TaVL, (b) positive or isoelectric TI, and (c) maximal precordial TWI [ TWIIII was 92% sensitive and 100% specific for CM, discriminating it from ischemic precordial TWI [4]. The use of corticosteroids with caution is recommended in patients with congestive heart failure because long-term use has been associated with fluid retention and hypertension. Potentially severe side effects of high-dose pulse corticosteroid therapy are noted. Problems included arrhythmias, myocardial infarctions, and sudden death [5]. In one early report, most of the patients had underlying renal disease and/or were undergoing renal transplantation; all of the patients having the cardiovascular reactions associated with the corticosteroid received individual doses of at least 250 mg of methylprednisolone or its equivalent. However, cause–effect relationship between high-dose corticosteroid therapy and severe cardiovascular reactions has not been scientifically proven by a controlled trial [6]. Severe complications of pulse methylprednisolone, mainly cardiovascular, are strongly related to underlying comorbidities. In one recent study of 146 consecutive patients treated by three pulses of 250, 500 or 1,000 mg/day methylprednisolone for various eye diseases, 88.4% had one ore more side effect(s), mainly transient and of mild intensity; myocardial ischemia was observed in 2.1% with known coronary insufficiency or high cardiovascular risk; blood pressure levels of at least 180/110 mmHg were recorded in 3.4%; bradycardia occurred in 14 patients (9.7%), with symptomatic in one patient [7]. We report a case of a young adult who developed atypical angina at rest associated with precordial ECG changes with TWI after a 4 days pulse methylprednisolone therapy. On May 20, 2007, the 26-year-old man was admitted because of the feeling of a lump of gradual onset in the throat and with pain radiating to the jaw. There was no chest discomfort. Symptoms were constantly present, aggravated by swallowing but otherwise independent of daily activities and neither worsened by respiration nor exacerbated when lying down. There were no associated complaints like belching, vomiting, diaphoresis, dyspnea, syncope or palpitation. Five days before, on May 15, a 4 days course of high dose methylprednisolone therapy of 1,000 mg per day intravenously had been initiated for the treatment of idiopathic orbital inflammatory syndrome (IOIS) also known as J. Rottensteiner A. Kaneppele I. Stockner G. Panizza C. J. Wiedermann (&) Division of Internal Medicine 2, Department of Internal Medicine, Central Hospital of Bolzano, Lorenz Bohler Street 5, 39100 Bolzano (BZ), Italy e-mail: christian.wiedermann@asbz.it