Discussion
TTS, also known as the ’broken-heart’ syndrome is a unique form of
transient acute left ventricular dysfunction that predominantly affects
post-menopausal women. It mimics acute coronary event in that it
presents with chest pain, ECG changes and elevated cardiac biomarkers.
Most patients report an emotional or physical trigger shortly before the
presentation, however, about 30% of cases lack any obvious trigger (4,
5). The pathophysiology is not fully understood, but several theories
have been proposed to explain the underlying mechanisms. High levels of
plasma catecholamines and neuropeptides have been reported in patients
with TTS (5). Other possible mechanisms include coronary endothelial
dysfunction, various cytokines activation, impaired fatty acid
metabolism in cardiac tissue, and multi-vessel spasm (6). Post-operative
TTS has been previously reported after cardiac surgery such as mitral
valve replacement and atrial myxoma resection and may be explained by
the high catecholamine levels after surgery (7, 8). In addition, delayed
onset TTS has been documented several weeks following mitral valve
surgery, epileptic seizures, or even after routine exercise stress test
(9, 10). Although delayed onset TTS is usually described 24-48 h after
physical or emotional trigger, a wide time range has been reported. In
one series of 25 epileptic patients, post seizure TTS was detected 5-288
hours post-ictally (11). In our case, the most probable trigger for TTS
is the previous surgery with its accompanied stress and pain during the
post-operative days. No other etiology could explain her dramatic
presentation, given the normal angiogram that was performed three weeks
earlier and the lack of fever or any inflammatory markers in her blood
tests. In addition, her echocardiography demonstrated preserved systolic
function of the right ventricle without dilation, findings that actually
exclude massive pulmonary embolism.
Treatment of TTS depends on the patients’ clinical condition.
Hemodynamically stable low risk patients with preserved (or mildly
reduced) systolic left ventricular ejection fraction and without
significant secondary mitral regurgitation may benefit from beta
blockers (12).Cardiogenic shock in TTS may be caused by several
mechanisms including ventricular arrhythmia, left ventricular
dysfunction, right ventricular involvement, and left ventricular outflow
tract obstruction with secondary mitral regurgitation, mechanical
circulatory support may be needed in such cases (13).