Introduction:
The pericardium normally houses between 10 - 50 milliliters of plasma ultrafiltrate. If and once fluid accumulates above such physiologic amount, pericardial effusion sets in by definition. The ramifications that could follow are ultimately governed by the rate of accumulation of the fluid, whether incremental over a prolonged period of time, or swift over a short one. Eventually, this may lead to cardiac tamponade as defined by an intra-pericardial pressure exceeding pressures of the intra-cardiac chambers, causing life-threatening derangements in hemodynamics [1]. Transthoracic Echocardiogram (TTE) remains the gold standard modality in diagnosing cardiac tamponade with the sign of early diastolic right ventricular (RV) collapse exhibiting 100% specificity [2]. However, essential focus should be placed on correlating the patient’s clinical status and assessing for the presence of hypotension, jugular venous distention (JVD) and distant heart sounds in order to make appropriate clinical decisions. There are multiple, distinguishable etiologies that may introduce the development of pericardial effusion and a possible cardiac tamponade sequelae, but one that is often overlooked, underestimated, and substituted with an idiopathic label is the adverse effect of medications [3]. Throughout literature, only a handful of medications have been implicated as triggers of such pericardial disease. In clinical trials as well as prospective and retrospective studies, the platelet reducing agent anagrelide has been shown to cause cardiovascular adverse events such as heart failure (HF), myocardial infarction, cardiomyopathy, arrhythmia, pericarditis, and although rare, pericardial effusion. Anagrelide is used for the treatment of essential thrombocythemia (ET), polycythemia vera and myeloproliferative disorders [4-6]. There has been one case reported of pericardial effusion after the introduction of anagrelide in an essential thrombocythemia patient [7]. We present a case of an 84-year-old female with anagrelide-induced pericardial effusion progressing to cardiac tamponade.