Background Perioperative myocardial infarction after minimally invasive mitral valve surgery is uncommon. Recognized mechanisms include iatrogenic circumflex coronary injury and coronary embolism, but embolization of papillary muscle tissue has not been well described. Case summary A 76-year-old woman underwent minimally invasive mitral valve repair for severe mitral regurgitation caused by P3 prolapse. Inferior ST-segment elevation developed after aortic unclamping and persisted despite repeated de-airing. Because the patient remained haemodynamically stable and transoesophageal echocardiography did not show a definite new regional wall-motion abnormality, she was initially observed closely. Persistent ST-segment elevation and mild lateral wall hypokinesis two hours after intensive care unit admission prompted emergency coronary angiography, which demonstrated complete occlusion of the posterolateral branch of the left circumflex coronary artery. Aspiration thrombectomy restored Thrombolysis In Myocardial Infarction grade 3 flow. Histopathological examination of the retrieved material showed that all identifiable tissue fragments consisted of striated cardiac muscle, supporting papillary muscle tissue embolism. The patient recovered without residual regional wall-motion abnormality. Discussion Papillary muscle tissue can be disrupted during subvalvular manipulation and embolize to a coronary artery after restoration of forward flow. Persistent or recurrent ST-segment elevation after mitral valve surgery should prompt early coronary angiography even when air embolism is initially suspected and haemodynamics remain stable.
Abstract Background Takotsubo cardiomyopathy may be complicated by dynamic left ventricular outflow tract obstruction (LVOTO) due to basal hyperkinesis in response to apical akinesis. In turn, this can lead to complications such as mitral regurgitation (MR) and systolic anterior motion (SAM) of the mitral valve, resulting in hypotension and potentially cardiogenic shock. Case Summary A 72-year-old woman presented with chest pain and ST elevation. Coronary angiography was normal, with left ventriculography and subsequent transthoracic echocardiography (TTE) confirming a diagnosis of Takotsubo cardiomyopathy. She developed refractory cardiogenic shock from severe LVOTO with SAM and MR, unresponsive to traditional therapies such as intravenous fluids, beta-blockade, and vasopressors. Serial TTE demonstrated progression of a small pericardial effusion with evolving tamponade physiology. Emergent pericardiocentesis resulted in immediate improvement of the LVOT gradient, elimination of valvular pathologies and rapid haemodynamic recovery. Discussion LVOT obstruction due to hyperdynamic basal contraction and mitral SAM is a known cause of cardiogenic shock, particularly in cardiomyopathies where apical ballooning is a feature. Progressive pericardial effusion and cardiac tamponade may critically exacerbate LVOTO, MR and mitral SAM through preload reduction and render standard LVOT-directed therapy ineffective. As early recognition and treatment of tamponade physiology can be lifesaving, failure to respond to LVOT-directed therapy should warrant urgent repeat echocardiography.
Abstract Background Cardiac myxomas are rare but represent the most common primary cardiac tumour. Most are sporadic, solitary, and associated with a low risk of recurrence. Recurrent, multiple, or atypically located cardiac myxomas should raise suspicion of an underlying hereditary syndrome, particularly Carney complex. Case summary a 24-year-old man presented with pulmonary embolism caused by a right atrial cardiac myxoma and underwent complete surgical resection. Fourteen years later, he presented with systemic peripheral arterial emboli due to a left atrial myxoma and again underwent surgery. At routine echocardiographic follow-up two years later, an asymptomatic recurrent atrial myxoma was detected and he underwent his third cardiac surgery. Genetic evaluation subsequently identified a likely pathogenetic PRKAR1A variant, molecularly confirming the diagnosis of Carney complex. Discussion Recurrence after complete resection of sporadic myxoma is uncommon, and routine long-term echocardiographic surveillance is therefore not universally recommended. However, young age at presentation, recurrent or multiple tumours, atypical cardiac locations, or other features suggestive of Carney complex should prompt genetic evaluation and closer follow-up. Recognition of Carney complex has important implications for lifelong surveillance and multidisciplinary management.
Abstract Background Cement-augmented pedicle screw fixation is an established technique in complex spinal surgery, but intracardiac and pulmonary cement embolization remain feared complications. Management is poorly standardized, particularly when percutaneous retrieval is attempted and fails. Case summary A 58-year-old woman with severe scoliosis underwent long-segment vertebral arthrodesis (T3–S1) at multiple levels. Intraoperative ventricular arrhythmia prompted postoperative imaging, which revealed a linear cement embolus spanning the right ventricular outflow tract and crossing the pulmonary valve. Percutaneous retrieval was attempted due to high-risk anatomical positioning but resulted in cement fragmentation and distal embolization into bilateral pulmonary segmental arteries. Following multidisciplinary reassessment confirming the absence of hemodynamic compromise, the strategy was de-escalated to anticoagulation and close surveillance. The patient recovered uneventfully. Discussion This case uniquely illustrates the management decision pathway when percutaneous retrieval fails. Fragmentation with distal embolization away from the pulmonary valve may represent an acceptable procedural endpoint permitting de-escalation to conservative management. The intraoperative arrhythmia served as a critical sentinel event guiding early diagnosis in the context of cement-augmented pedicle screw fixation, which is underrepresented in bone cement embolization literature compared to vertebroplasty/kyphoplasty.
