Acute Myocardial Infarction, Pulmonary Embolism, and a Suspicious Aortic Mass: A Case of Complex Differential Diagnosis and Management

An ascending aortic mass is an uncommon finding.^[1] The mass etiology needs to be rapidly established due to its impact on the evolution and prognosis of the case. Usually, floating aortic thrombus appears either on a pathological aorta or in hypercoagulable hemodynamic conditions. The ascending segment is described as the least common location of an aortic thrombus.^[2–4] Due to its low incidence, there are no strong and clear recommendations about the optimal treatment. The management should therefore be individualized, discussed, and concluded by a Heart Team.

A 44-year-old female presented to the emergency room of a local hospital with posterior chest pain and dyspnea for 2 weeks. The patient’s history was significant for severe anemia secondary to uterine fibroma (confirmed on biopsy) and ilio-femoral-popliteal deep vein thrombosis, with no pulmonary embolism on a CT scan, performed 4 months prior to this presentation. She was on coumadin therapy for 3 months and stopped all medication 1 month before admission. According to the medical records from the emergency room, she was hemodynamically stable, with normal blood pressure (120/80 mmHg), elevated heart rate (110 bpm), normal oxygen saturation level (98%), normal heart sounds, clear lung fields, and no peripheral edema. Screening transthoracic echocardiography revealed a mobile mass in the aortic root, apparently attached to the posterior aortic valve annulus. The patient was admitted, and empirical antibiotic therapy was initiated for suspected infective endocarditis. Within a few hours after admission, the patient developed angina with elevated troponin levels and ST elevation in leads V2 to V6. She was urgently transferred to our cardiology clinic for further evaluation and treatment with a diagnosis of suspected infective endocarditis on native aortic valve and anterior STEMI.

On admission in our clinic the patient was hemodynamically stable, with refractory angina and persistent ST elevation in leads V2 to V6 (Figure 1). Laboratory tests showed elevated troponin levels (hs c-TnI 16203 ng/L) and D-dimers (>5.0 mcg/ml), severe anemia (6 g/dl), and a significant inflammatory syndrome (CRP 98 mg/dl) with normal white blood cell count. Transthoracic and transesophageal echocardiography confirmed the presence of a 2.1/1.1 cm irregular, mobile mass attached to the aortic root wall at the level of the left sinus of Valsalva with no impact on the aortic valve (Figures 2 and 3). Moderate left ventricular systolic dysfunction (LVEF 40%) with anterior wall hypokinesia was also noted. There was no evidence of significant valvular disease or intracardiac vegetations. Due to the proximity of the ascending aortic mass to the left coronary sinus, invasive evaluation of the coronary circulation was deemed impossible, dangerous, with the risk of potential embolization of fragments from the mass into the left main coronary artery. Moreover, since there was a high likelihood of associated pulmonary embolism, we proceeded with a full-body CT scan, which showed multiple renal and splenic infarcts, as well as bilateral peripheral pulmonary emboli; the scan confirmed the ascending aortic mural mass at the level of the left sinus of Valsalva (Figures 4A and B). Coronary CT angiography showed normal epicardial coronary arteries and a Calcium score of 0.

Figure 1

Figure 2

Figure 3

Figure 4A

Figure 4B

Our working diagnoses were bilateral low risk PE, anterior STEMI (likely embolic), and an ascending aortic mass of unknown etiology. The main differentials for the ascending aortic mass that we considered were floating aortic thrombus, vegetation, and tumor. The patient was started on systemic anticoagulation with unfractionated heparin (targeting both PE and a possible thrombus) and empirical antibiotic treatment as per endocarditis guidelines (given the suspicion of endocarditis and the inflammatory syndrome). Blood cultures were also taken, which turned out to be negative at 24 hours and remained negative after 14 days. A thrombophilia panel was positive for protein C deficiency. At this point, an aortic thrombus seemed very likely and considering the very high embolic risk and the lack of response to conservative therapy, the patient was sent to surgery for excision of the aortic mass. No aortic wall abnormalities were noted during surgery (Figure 5). Following successful excision, the histopathological examination confirmed the mass as being a thrombus (Figure 6). The inflammatory markers normalized postoperatively and antibiotic therapy was stopped after 10 days. The patient was discharged on systemic lifelong anticoagulation with vitamin K antagonist and heart failure therapy.

Figure 5

Figure 6

At discharge, the patient was asymptomatic. Transthoracic echocardiographic evaluation revealed no lesions at the level of the ascending aorta (Figures 7A and B), and persistent anterior wall motion abnormality.

Figure 7A

Figure 7B

This is a case of complex intertwining pathology in a young patient presenting with dyspnea and chest pain. The surprising finding of an aortic mass at the level of the left sinus of Valsalva raised important clinical questions with regard to its differential diagnosis and management.

Differential diagnoses included infective endocarditis (albeit the patient did not meet sufficient criteria for definite diagnosis) and tumor of unknown etiology. The definitive confirmation was obtained on histopathology.

In the absence of aortic aneurysm, the incidence of aortic mural thrombi is low (0.45%).^[5] Several causes have been linked to their development, including atheromatous aortic disease, structural aortic abnormalities, malignancy, immunological disorders, trauma, and steroid use.^[6,7] In our case, the only significant factor predisposing to thrombus formation identified was protein C deficiency.

No definitive guidelines exist on the optimal management of these patients. While conservative treatment with systemic anticoagulants is preferred by many, there is a significant risk of persistence of the aortic mural thrombus (38%) and an important proportion of patients develop recurrent arterial embolization (21%).^[2] Thrombolysis carries a significant risk of distal embolization (especially if the attachment site is lysed first) and is generally not considered an option. The experience with minimally invasive endovascular treatment is scarce and it runs the risk of guidewire manipulation as well as unknown long-term effects.^[8,9] Surgical treatment remains the definitive choice, especially when embolic events have already occurred,^[3] as in the case of our patient. Nonetheless, a literature review comparing anticoagulation to open surgery identified no significant difference in mortality rates, except for situations with hemodynamic instability, which was found to be an independent predictor of mortality.^[2]

Although ascending aorta floating thrombus is a relatively rare finding, the condition has potential catastrophic complications in the absence of rapid and specific management. Surgical resection can be the definite treatment modality, especially in situations in which the mass etiology is uncertain, when the thrombus persists with anticoagulant therapy, or presents a high embolic risk.^[4,9]