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.