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).