CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 4, July/August 2022 AFRICA 223 obvious evidence of contrast extravasation. It is likely that the guide wire was inadvertently pushed into the distal end of an atrial branch, especially as damage to this branch was identified during the second angiography. We suggest, therefore, that the cause of LatD in this case was perforation of the epicardial collateral branch of the right coronary artery. Blood from this perforation entered the endocardial false lumen but did not rupture the pericardium. The first symptom experienced by the patient was chest pain, followed by gradually worsening hypoxia. The chest pain was caused by an intimal tear and hypoxia was secondary to obstruction of mitral valve inflow or the pulmonary vein orifice, which led to congestive heart failure and low-output syndrome. The left atrium is especially susceptible to these issues, because it can be easily compressed by an intramural haematoma.2 Our case emphasises the importance of utilising patients’ clinical manifestations and underlying conditions in the performance of differential diagnoses. Upon recurrence of chest pain after PCI, the first consideration is acute stent thrombosis. Accordingly, the spectrum of myocardial enzymes should be analysed, an ECG should be performed, and coronary angiography should be strongly considered. At the same time, bedside echocardiography should be performed to exclude pericardial effusion or pericardial tamponade, and CTA should be performed to exclude acute aortic dissection. In the case of our patient, while the first bedside echocardiography following PCI showed no abnormality, a substantial haematoma in the left atrium became apparent after the onset of symptoms. We therefore concluded that while bedside echocardiography is an important monitoring tool following PCI, it is equally important to monitor patients’ symptoms, including chest pain and hypoxia. Of course, for some complex cases or cases with unclear histories, multimodal examinations, including echocardiography, CTA and magnetic resonance imaging (MRI), may be required for diagnosis.1,2 Due to the rarity of LatD, clear guidelines for diagnosis and treatment have yet to be established.2,9 Clinicians therefore must remain vigilant in the identification of LatD and the differentiation of its distinct clinical manifestations (stable and unstable LatD) prior to making decisions concerning treatment. Determining the stability of the LatD separation influences the choice of treatment. Two general treatment options, surgical repair and close observation, are currently available. Prompt intra-operative diagnosis and surgical repair are recommended in any case of haemodynamic instability that is accompanied by rapid expansion of the haematoma. Such instability may result in occlusion of the left atrial cavity, pulmonary vein or mitral valve.10 In previously reported cases, prompt surgical repair has been undertaken in most patients (73.4%; 63 of 87 cases).2 Surgeons have a variety of available surgical approaches. Maeda et al.11 first reported surgical repair of LatD through left thoracotomy in 1985. Since then, several different surgical approaches have been described.12 Most operative repair approaches focus on evacuation of the haematoma, obliteration of the false lumen, and repair of the entry injury.13 In our case, the surgical procedure involved closing of the endocardial false lumen via intermittent suture to protect the entrance of the bilateral pulmonary vein. In order to prevent the reformation of a haematoma, a drainage window was reserved for decompression due to potential uncertainty regarding the site of haemorrhage. This surgical procedure was deemed successful, as the patient recovered fully without incident. We and others have therefore observed significant benefit from a surgical approach, and we suggest that clinicians take a more aggressive approach to LatD, especially for those patients with obvious haematoma enlargement or rapid progression of symptoms. In addition, despite clear divisions of work between cardiovascular medicine and cardiac surgery departments, co-operation among teams and the delivery of detailed information are particularly important in PCI cases in order to facilitate diagnoses and decision making regarding treatment plans.14 In particular, LatD should be considered by medical and surgical teams when contrast agent infiltration of myocardial tissue is found during PCI. Conclusion As cases of coronary artery total occlusion increase, the application of retrograde PCI is becoming more common. Therefore, we should expect more frequent incidents of rare but dangerous complications, especially LatD. Rapid diagnosis of LatD is essential, and multimodal examinations, including echocardiography, CTA and MRI, can help. Careful examination of test results and clinical symptoms of PCI patients can help to guide clinical decisions. For patients with minimal symptoms, close observation is likely to be the best option. For patients with haemodynamic disorders, however, active surgical intervention is recommended. This study was funded by China International Medical Foundation (CIMF) (No CIMF-Z-2016-23-1823). References 1. Gallego P, Oliver JM, Gonzalez A, Dominguez FJ, Sanchez-Recalde A, Mesa JM. Left atrial dissection: pathogenesis, clinical course, and transesophageal echocardiographic recognition. J Am Soc Echocardiogr 2001; 14: 813–820. 2. Fukuhara S, Dimitrova KR, Geller CM, Hoffman DM, Tranbaugh RF. Left atrial dissection: an almost unknown entity. Interact Cardiovasc Thorac Surg 2015; 20: 96–100. 3. Cereda AF, De Luca F, Lanzone AM, Cottini M, Pastori L, Sangiorgi G. Case report and systematic review of iatrogenic left atrial dissection in different cardiovascular specialties: A common treatment for an uncommon complication? Catheter Cardiovasc Interv 2020; 95: E30–E36. 4. Vadgaonkar V, Yousif N, Sabde S, Slais S, Darwish A, Tarief H, et al. Spontaneous left atrial multiseptated intramural dissecting hematoma. Echocardiography 2020; 37: 1682–1686. 5. Bhattacharyya S, Khattar R, Lindsay AC, Senior R, Di Mario C. Ventricular septal mass formation after retrograde chronic total occlusion percutaneous coronary intervention. Circulation 2013; 128: 2167– 2168. 6. Barbeau GR, Senechal M, Voisine P. Delayed abrupt tamponade by isolated left atrial compression following coronary artery perforation during coronary angioplasty. Catheter Cardiovasc Interv 2005; 66: 562–565. 7. Tsukui H, Iwasa S, Yamazaki K. Left atrial dissection related to retrograde cardioplegia cannula insertion. Heart Vessels 2016; 31: 819–821.
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