The localization of fibrinolytic areas in normal and atheromatous human coronary arteries was studied by the histochemical fibrin slide technique. Fibrinolytic activity was caused by a plasminogen activator. The activator, occasionally observed at sites in the normal endothelial lining, was abundantly present in relation to vessels in the normal adventitia. The pathological adventitia contained an increased number of active sites and endothelium covering an atherosclerotic plaque was richer in fibrinolytic sites than the normal endothelium. Within the vascularized plaque, fibrinolytically active capillaries could be traced from their origin in the vasa vasorum or, occasionally, in the endothelium. The results confirm and extend previous observations obtained in assays after extraction. They present patterns similar to those observed in normal tissue repair.ADDITIONAL KEY WORDS vessels capillaries tissue repair plasminogen activator• Assays of thromboplastic and fibrinolytic activities of extracts of the layers of the normal arterial wall of animals and man have been reported (1-4). In man the aortic intima is rich in thromboplastin with little or no fibrinolytic activity suggesting that fibrin formation may occur readily while fibrin resolution is delayed. The intima of the atherosclerotic aorta contains less thromboplastin than the normal intima (5-7), while the media and adventitia have higher fibrinolytic activity (assayed as plasminogen activator) than the normal layers (7). However, separation of the layers of the wall is more difficult in the pathological samples, and the limited amounts available make determinations less accurate. With the histochemical fibrin slide technique, plasminogen activator has been localized to the vascular endothelium, especially