S pontaneous coronary artery dissection (SCAD) is an unusual cause of acute myocardial ischemia (1). It is more common in younger patients and in women, and has a propensity to affect patients without traditional cardiovascular risk factors (2). The tendency to affect women in high estrogenic states suggests that the hormonal and thrombogenic status of the patient may play etiological roles in SCAD. Similar factors have been implicated in increased cardiovascular event rates observed in young patients undergoing chemotherapy for testicular cancer (3). Despite this, no cases of SCAD occurring during cisplatin-based chemotherapy for testicular cancer have been reported.The presentation, outcome and management of acute spontaneous coronary artery dissection have been described extensively (4)(5)(6)(7)(8). In all of these reports, there was either no angiographic follow-up of patients who survived the acute event or follow-up angiography demonstrated complete healing of the dissection. The long-term outcome of the dissection that persists is less well described (9,10).We report a case of chronic coronary artery dissection that had its onset during a course of bleomycin-etoposide-cisplatin therapy for testicular cancer. The implications of testicular cancer and chemotherapy, and the significance of chronic coronary artery dissection persistent on angiography will be discussed.
CASE PRESENTATIONA 36-year-old man presented with a history of lightheadedness, shortness of breath and left-sided chest tightness after several minutes of playing hockey. Emergency medical services arrived at the scene and found the patient in monomorphic ventricular tachycardia at approximately 300 beats/min (Figure 1). The patient underwent electrical cardioversion, with almost immediate resolution of his symptoms. On admission to a local hospital, his troponin I peaked at 0.6 μg/L (10 times the upper limit of normal), and his electrocardiogram (ECG) showed significant Q waves in leads II, III and AVF, as well as ST depression in the inferolateral leads. The Q waves in the inferior leads were unchanged from previous ECGs recorded since July 1994. At the time of the current presentation, the patient was taking ramipril and Lipitor (Pfizer, Canada). He did not smoke and rarely used alcohol. He was started on acetylsalicylic acid, clopidogrel, enoxaparin and metoprolol by the referring centre, and was transferred to a tertiary care centre for further investigation.His medical history was relevant. At the age of 24 years he developed testicular cancer, which was treated with four cycles of chemotherapy following orchiectomy. During his last course of bleomycin-etoposide-cisplatin chemotherapy, the patient developed left chest, neck and shoulder discomfort, and presented to the hospital 12 h later. Serial ECGs revealed the development of a Q wave inferior infarction and poor R wave progression across precordial leads on serial tracings. He did not receive thrombolysis, and cardiac catheterization was not performed. He was sent home on acetylsalic...