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Ann Thorac Surg 2002;73:1324-1326
© 2002 The Society of Thoracic Surgeons
a Department of Cardiac Surgery, Royal Victoria Hospital, Belfast, Northern Ireland
b Regional Medical Cardiology Centre, Royal Victoria Hospital, Belfast, Northern Ireland
Accepted for publication August 2, 2001.
* Address reprint requests to Dr Badmanaban, Department of Cardiac Surgery, Royal Victoria Hospital, Grosvenor Rd, Belfast BT12 6BA, Northern Ireland
e-mail: balaji{at}talk21.com
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| Introduction |
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A 59-year-old male power station worker with no previous history of ischemic heart disease presented to our teaching hospitals emergency department in extremis. He had developed sudden onset of chest pain radiating to his legs approximately 1 hour previously. He was hypotensive, tachycardic, and diaphoretic. His neck veins were not noted to be distended.
Electrocardiography demonstrated sinus tachycardia without evidence of myocardial ischemia. Ultrasound examination of the abdomen was undertaken to exclude a ruptured abdominal aortic aneurysm and was normal. There was a lactic acidosis with blood pH at 7.16 and a base deficit of 16.5 mmol/L. Computed tomography of the thorax excluded thoracic aortic dissection but demonstrated a significant pericardial effusion. No invading extrapericardial lesion was seen. A transthoracic echocardiogram (Fig 1) confirmed the presence of a pericardial effusion containing echodense material with evidence of right ventricular diastolic collapse. Transesophageal echocardiography confirmed previous findings. The patient was transferred to the cardiac catheterization laboratory. A pericardial effusion with marked pulsus paradoxus was noted. Fluoroscopic pericardiocentesis was unsuccessful due to the solid nature of the effusion. Coronary angiography demonstrated dissection of the left anterior descending and circumflex arteries (Fig 2). The left main coronary artery was involved by implication. Angiographically, the coronary arteries appeared relatively free from atherosclerotic occlusive disease.
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On the 6th postoperative day, the patient had an episode of syncope associated with melena. Upper gastrointestinal endoscopy revealed an ulcer in the posterior wall of the second part of the duodenum, which was injected with adrenaline, and helicobacter eradication started. Aspirin was withheld and clopidogrel was later introduced. Follow-up echocardiography at 2 weeks showed good left ventricular function with no residual pericardial effusion. There was no recurrence of melena.
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Spontaneous coronary dissection is also associated with angiitis, sarcoidosis, Marfans syndrome, and previous renal transplantation [5]. Cystic medial necrosis has been documented in some patients [2]. The left anterior descending, right coronary, circumflex, and left main coronary arteries are involved with decreasing frequency, respectively [6].
In contrast to aortic dissection, hypertension is not a risk factor, and the primary site of coronary wall dissection is usually the outer third of the tunica media or between the tunica media and the external elastic lamina [5]. Hemorrhage into the coronary wall is postulated to initiate dissection with luminal compromise by the expanding hematoma. Intimal tears representing a starting point for dissection are rarely identified [6]. Various changes in the coronary vessel wall and vasa vasorum as found in pregnancy probably contribute to pathogenesis [6].
A significant number of patients die suddenly [3]. Patients who survive to reach hospital usually present with ischemic syndromes ranging from stable angina to acute myocardial infarction [2]. The diagnosis is difficult to make, and many cases are identified at autopsy; a high degree of clinical suspicion in the typical patient, grouped together with early angiography, is required. Optimal patient management is not yet defined. Anticoagulants, anti-platelets, or thrombolytic therapy may worsen the dissection [2]. Patients who are managed conservatively often have a suboptimal outcome with survivors progressing to subsequent myocardial infarction, sudden death, or disabling angina [4].
Percutaneous coronary artery stenting is the treatment of choice for suitable dissections following angioplasty and has been successfully undertaken for spontaneous dissections, including those with multivessel involvement. Surgery was the preferred option in our case because of the need for evacuation of hemopericardium, lesion morphology with left main involvement, and arterial rupture.
The aim of surgery is to restore blood flow to the compromised myocardium and prevent propagation of the dissection [4]. The preferred conduit in an elective process is the internal mammary artery because of its long-term patency [4], but in our case, because of the time constraints, saphenous vein grafts were used.
Our case is unusual in that a patient of atypical profile presented not with myocardial ischemia but with cardiac tamponade. It is also important to note that further bleeding was arrested following grafting and repair of the dissection. This association has only been described in 1 other patient in the literature [1]. It is probable that the hematoma dissected through the wall of the artery resulting in free rupture and hemopericardium, rather than accumulating intramurally and compressing the vessel lumen. This case represents a rare survivor following surgery for a coronary artery dissection presenting as cardiac tamponade.
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