Thromboembolic phenomenon from aortic aneurysms in the setting of thrombolytic therapy for acute occlusive vascular syndromes is a rare but severe event. The mortality in such cases is comparable with aortic rupture [1] . Thus, clinicians should be aware that vascular aneurysms, like aortic aneurysms, are potential sites of embolic showers and should be thought and carefully considered in patients with vascular diseases especially before fibrinolytic treatment is accomplished. In such cases, the identification of the source of the embolization and the definition of the characteristics of the emboli are central to the best treatment option that should be applied in order to add survival chances in this life-threatening complication.

A 67-year-old male patient with no previous history of cardiovascular disease was admitted to the emergency room of a secondary hospital with a history of 4 hours of chest pain. Diagnosis of an infero-posterior ST-eleva- tion myocardial infarction (STEMI) was done. Immediate pharmacologic thrombolysis with streptokinase was performed and clinical and electrocardiographic reperfusion criteria were achieved. However, the patient developed two episodes of ventricular fibrillation, which were immediately resolved with electrical cardioversion and controlled with amiodarone infusion. Due to the electrical instability, he was transferred to a tertiary cardiologic center. Upon admission, the patient still met reperfusion criteria, with no chest pain. However, he started complaining of pain on both legs and feet. Physical examination showed pale and cold feet with bilateral peripheral pulses present. The pain on his lower limbs worsened needing continuous morphine infusion and his abdomen started to distend. Due to the signs of lower limbs ischemia, cardiac catheterization was deferred and a doppler ultrasonography of the limbs was performed. Diffuse atherosclerosis and decreased arterial blood flow were found, with no signs of gross obstructive lesions, suggesting an impairment of the microcirculation. Over the next hours the abdominal distention got worse and abdominal pain developed. Furthermore, laboratory exams showed rising levels of BUN and creatinine and very high levels of serum creatine phosphokinase (CPK 15,554 U/L), amylase (258 U/L) and aminotransferases (AST 2111 U/L; ALT 1621 U/L). The patient was transferred to an intensive care unit. He evolved with acute renal failure and severe lactic metabolic acidosis. Hemodialysis therapy was started. Transesophageal echocardiography revealed an ejection fraction of 55% with akinesia of the inferior wall and no signs of aortic dissection or intraventricular thrombus. Abdominal ultrasonography revealed a large abdominal aortic aneurysm (8.5 ´ 7.5 cm in diameter and 16.0 cm of extension) with a high burden of thrombus. Lactic acidosis continued to worse and CPK levels reached 35,230 U/L. After the second day, despite intensive medical care, multiple organ failure developed and the patient died. On necropsy, a large abdominal aortic aneurysm (AAA) was found (Figure 1 and Figure 2) filled with a big, friable, and mobile thrombus. Signs of systemic microembolization and diffuse mesenteric, hepatic, kidney and skeletal muscle ischemia were also observed (Figure 3).

In this case report, we present a catastrophic thromboembolic event from an AAA triggered by thrombolytic therapy in a patient with acute STEMI. Unlike the hemorrhagic complications of thrombolytic therapy, this patient developed a fatal embolic complication with the definitive diagnosis confirmed by histopathology. Of note, in the literature, most of the few cases similar to the present one had only presumptive diagnosis [1] .

Thromboembolism from an AAA is a serious clinical manifestation of this disease. It is the first manifestation of an AAA in 5% of patients [1] . Mortality in these cases is comparable with rupture [1] . Series of reports describe mortality higher than 70% in patients with embolic events after thrombolysis [2] .

Clinically, this patient presented signs of lower limbs ischemia few hours after fibrinolysis, but pulses were palpable. Interestingly, Wingo and colleagues have reported that only 15% of the patients had a pulse deficit in cases similar to the present one [2] .

In this patient, systemic inflammation following acute myocardial infarction [3] - [5] associated with the lysis of the thrombus laid on the surface of the aneurysm by thrombolytic treatment acted synergistically, leading to the disruption of a chronic thrombus and to distal and massive embolization.

Both AAA and atherosclerotic plaques of the aorta are manifestations of systemic atherosclerosis, and are common in the elderly and in patients with coronary artery disease [6] . Main risk factors for thromboembolic

events include the thickness of the plaque, the presence of thrombus and/or ulceration, plaque mobility and cardiovascular procedures [1] . Although thromboembolic phenomena from an AAA are rarely reported, it’s frequently described that fibrinolytic and anticoagulant therapy might provoke atheroembolism (embolism of cholesterol) [7] .

The indication for fibrinolytic treatment in an attempt to open the occluded coronary artery frequently underestimates systemic complications. Furthermore, the emergency condition of an acute coronary syndrome restricts an investigation of risk factors for complications, before the indication of the thrombolytic procedure. So, the benefit of an early thrombolysis for an acute myocardial infarction should balance the risks of possible complications related to treatment. In patients with aortic aneurism or other emboligenic sources, the choice of treatment should be carefully considered.

Due to unavailability of primary percutaneous coronary intervention (PCI) at the first hospital, thrombolysis was indicated and accomplished its initial target. The patient didn't have any contra-indications for thrombolysis. He had a large AAA unknown so far, but even if he had this diagnosis previously, this would not be a formal contra-indication for thrombolytic therapy.

If thromboembolism occurs in great arteries, surgical or percutaneous embolectomy procedures may be effective treatments [8] [9] . However, in the present case, treatment of microembolic showers is less effective and is based on the use of heparin sodium, intensive support and treatment of end-organ dysfunction. The use of high-dose heparin is indicated due to its potential to reduce tissue damage [10] , as it may improve collateral flow and decrease permeability changes [11] - [13] . Moreover, heparin may suppress tissue plasminogen activator and matrix metalloproteinase production [14] . These two substances can contribute to plaque instability.

In summary, aortic aneurysms and emboligenic sources must be considered in patients with clinical indications for thrombolytic therapy.

Besides bleeding complications, the indication of thrombolytic therapy should take into account factors related to embolic complications, like aortic aneurysms. These aneurysms should always be concerned in patients with vascular disease, especially during fibrinolytic treatment.

We would like to thank all the members of MASS research group for putting together all the forces to publish this paper.

This work was supported by Zerbini Foundation.