Pericardiocentesis for cardiac tamponade is a commonly performed procedure which may lead to complications such as perforation of the (right) ventricle, laceration of a coronary artery, pneumothorax and ultimately death. Transient left ventricular dysfunction has been described by various authors [
1‐
7]. Case reports describe patients with pulmonary oedema [
1,
3,
5], cardiogenic shock [
2,
4] and acute adult respiratory distress syndrome [
6]. Global myocardial dysfunction [
4,
5] as well as regional dysfunction [
1,
2], as in our case, are described. The underlying mechanism is poorly understood. Multiple factors are considered to play a role. During tamponade, external compression of the myocardium leads to reduced stroke volume and cardiac output. Compensatory mechanisms include tachycardia and expansion of the intravascular volume. Catecholamine levels are generally high with vasoconstriction [
8]. Sudden release of pericardial constraint through pericardiocentesis could lead to a disproportionate increase in end-diastolic volume of the right ventricle compared with the left ventricle and a temporary mismatch in ventricular outputs. This could lead to a sudden increase in left ventricular end-diastolic pressure and, in the presence of high afterload through vasoconstriction and a suddenly developed normal or negative intrapericardial pressure, to an acute increase in left ventricular wall stress and left ventricular failure [
2]. Other mechanisms postulated are myocardial stunning because of mismatch of oxygen distribution across the myocardial wall or altered coronary blood flow due to high pericardial pressures [
7]. In our case there was akinesia of the anterior wall and developing Q waves in the anterior leads, but no elevation of the cardiac enzymes, excluding myocardial infarction. Also, the regional akinesia as well as the Q waves and negative T waves appeared to be completely reversible. Other authors have performed myocardial perfusion studies [
1] or coronary angiograms [
2] in cases like this but found no evidence of coronary artery disease. The exact mechanism for this observation is not known. Other reversible cardiomyopathies, such as thyrotoxicosis-induced cardiomyopathy, Tako Tsubo cardiomyopathy or peripartum cardiomyopathy are also known to produce these ECG changes and echocardiographic abnormalities [
9,
10]. Because of the possible impact on the haemodynamics of the acute left ventricular overload which can follow abrupt relief of cardiac tamponade, it might be wise not to remove a large pericardial effusion too quickly. In cardiac tamponade intrapericardial pressure declines rapidly after evacuation of the first 50–200 ml of pericardial fluid. Therefore some authors have suggested that pericardial fluid should be removed only until tamponade physiology disappears and after that gradually [
1‐
3].