Rare association of acute pulmonary embolism and type B aortic dissection: anticoagulant therapeutic dilemma

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Ovidiu Mitu1,2, Radu Miftode1,2, Adrian Pintilie2, Antoniu Octavian Petris1,2


1 „Grigore T. Popa” University of Medicine and Pharmacy, Iasi, Romania
2 „St. Spiridon” Clinical Emergency Hospital, Iasi, Romania


Abstract: We report the case of an 88-year-old male who was admitted for presenting acute onset pain in the right lower limb associated with dyspnea. After clinical exam and Doppler echography, the deep vein thrombosis was confirmed. The thoracic angio computed tomography revealed segmentary pulmonary embolism, but also showed aneurysmal dilated ascending aorta and presence of chronic extensive type B aortic dissection with multiple atheroma plaques. Despite the unfortunate association, the anticoagulant treatment was carefully monitored, with no complications or bleeding events. Taking into consideration the thromboembolic event and high atherosclerotic burden, the patient was discharged with no-vel oral anticoagulant and statin, abstaining from antiaggregant therapy. The association of pulmonary embolism with aortic dissection represents a rare condition that raises certain anticoagulant and therapeutic dilemma.

Keywords: pulmonary embolism, aortic dissection, venous thromboembolism, deep vein thrombosis, anticoagulation.

INTRODUCTION
Treatment of pulmonary embolism consists in full dose anticoagulation or even thrombolysis that are associ-ated with high bleeding risk. The presence of aortic dissection in a patient usually represents a contraindi-cation or at least a major precaution for anticoagulant treatment. Nonetheless, the concomitant association of both pathologies is rare but raises specific therape-utic dilemmas.

CASE REPORT
We present the case of an 88-year old male, hyperten-sive, former smoker, who was admitted to the cardio-logy clinic for acute onset pain in the right lower limb associated with recent dyspnea.
His past medical history consisted of previous di-agnosis of chronic obstructive pulmonary disease (COPD) GOLD 1 stage, chronic kidney disease stage 3 and arterial hypertension stage 2 for which the pa-tient received bisoprolol and amlodipine in moderate doses. Clinical examination revealed: obesity grade 1 (body mass index 31 kg/m2), regular cardiac sounds, blood pressure (BP) 140/80 mmHg, 92 bpm, sponta-neous oxygen saturation 88%, mildedema and warmer right lower limb.
Biochemical results showed: normal full blood count, mild dyslipidemia (LDL cholesterol 140 mg/dl), moderate renal function impairment (creatinine clea-rance 54 ml/min/1.73m2), hepatic function and coagu-lation in normal ranges. NTproBNP was slightly elevated (924 pg/ml) while D-dimer value was very high (>5 μg/ml).
The patient presented on admission electrocardio-gram sinus tachycardia 100 bpm, with frequent supra-ventricular premature beats. Transthoracic echocar-diography revealed: non-dilated cardiac cavities, left ventricular ejection fraction 50%, flattened movement of interventricular septum, TAPSE 18 mm, dilated in-ferior vena cava with diminished collapse, ascendant aorta dilated (46 mm) with atheromatosis.
An emergency venous Doppler echography was performed and confirmed the presence of occlusive echogenic material in the right common, superficial and profound femoral vein and partial occlusive in the popliteal vein, all non-compressible and with absen-ce of Doppler signal – highly typical aspect for recent thrombus.
Taking into consideration the clinical presentation, the presence of acute deep vein thrombosis, increased specific biochemical markers and echocardiographic aspects, a pulmonary angio computed tomography (CT) was indicated. The angio CT confirmed partial thrombosis of the right medial, lateral and posterior segmentary pulmonary arteries, the main pulmonary arteries being permeable. Moreover, the CT also revealed aneurysmal dilated ascending aorta (54/45 mm), mild parietal thrombosis of the aortic arch and impor-tant thrombosis of the descendent aorta – suggestive for a chronic type B aortic dissection, along with mul-tiple aortic plaques (Figures 1, 2).
After image confi rmation of acute pulmonary em-bolism and deep vein thrombosis, the anticoagulati-on treatment had to be the treatment of choice but the association of descendent aortic dissection was a major precaution for anticoagulation. However, by computing the simplifi ed Pulmonary Embolism Seve-rity Index (PESI) score, the patient was at high risk (age, COPD and SaO2). Thus, the decision was in favor for starting anticoagulation therapy with unfractioned heparin under strict monitorization of aPTT. Statin therapy was as well introduced taking into conside-ration the high atherosclerotic burden but abstained from introducing the antiplatelet therapy. During ho-spitalization, the patient also developed paroxysmal fast-rhythm atrial fi brillation that responded to amiodarone loading. The clinical evolution was favorable, the lower limb inflammation diminished, the BP was maintained around 120/80 mmHg and heart rate was slightly higher, 70-80 bpm, despite treatment with dil-tiazem associated with amiodarone. The medication at discharge consisted in: low regime of novel oral anti-coagulant (apixaban 2.5 mg bid), diltiazem, amiodarone in prophylactic dose, high statin dose (rosuvastatin 20 mg daily), angiotensin converting enzyme inhibitor and oral venous trophic. One dilemma was for introducing aspirin for the high atherosclerotic burden but taking into consideration the age, the acute thromboembolic pathology and the need for chronic anticoagulant, we decided to postpone the administration of aspirin in prophylactic dose.

Figure 1. Thoracic angio CT: Right segmentary pulmonary embolism (white arrow), respectively dilated ascending aorta and descending aortic dissection (white lines).

Figure 2. Thoracic angio CT: beginning of aortic dissection from the distal part of the aortic arch (white line) along with multiple calcified atheroma plaques.

DISCUSSION
Type A aortic dissection still represents a devastating aortic pathology, with high mortality rates even in surgical treated patients. On the other hand, patients with type B aortic dissection managed medical have the lowest mortality rates. Previous atherosclerosis, along with other risk factors, is a key factor for deve-loping this disease since infl ammation and extracellular matrix degradation lead to remodeling of the aortic wall structure1.
The association of acute pulmonary embolism and type B aortic dissection is rare and the preferred ma-nagement should be based on the predominant symp-tomatology. However, due to anticoagulant treatment for venous thromboembolism, the aortic pathology may evolve leading to bleeding local complications that have been treated with thoracic endovascular aortic repair (TEVAR)2,3. In other situations, non-dissecting ascending aortic aneurysm or, infrequently, type A aortic dissection can mimic pulmonary embolism by subsequent compression and possibly occlusion, lea-ding to diagnostic and treatment confusion4,5.
There are still uncertainties regarding the associa-tion of aortic pathology and venous thromboembolic manifestations. A recent retrospective study demons-trated that aortic aneurysm surgery was associated with an increased risk of venous thromboembo-lism within 6-months post-operation. However, the mechanisms underlying this association remain un-clear6. Another study reported no evidence for sus-taining the use of anticoagulant therapy for deep vein thrombosis prophylaxis in patients undergoing abdo-minal aortic surgery7.
In our case, the patient presented for highly sugges-tive venous thromboembolism manifestations that was confirmed through pulmonary angio CT, but the aortic dissection was a fortuit discovery. Fortu-nately, the evolution was favorable, with no bleeding complications developed under anticoagulant therapy and the treatment for both pathologies remained conservative. Though the theoretical study doses for apixaban in pulmonary embolism patients in the first months is 5 mg bid8, we preferred the 2.5 mg bid dose for chronic surveillance taking into account the age and the renal disease. Another anticoagulant option could have been the vitamin K antagonists but due to the high INR variability and the impossibility of the patient for a close INR check-up we also preferred apixaban. Moreover, another limitation for a higher anticoagulant dosage was represented by the presen-ce of the aortic disease. Nonetheless, the patient will remain under strict surveillance since the anticoagu-lant is mandatory but could affect the aortic pathology leading to several complications that may require in the future TEVAR or surgery. A close follow-up of the patient was scheduled for evaluation of the anticoa-gulant therapy, as well as imagistic monitoring for the progression of the aneurysmal dilated ascending aorta and aortic dissection.

CONCLUSION
The association of pulmonary embolism and aortic dissection remains uncommon, especially in emergen-cy situations. The main therapeutic problem is the use of anticoagulant with maximal benefit but, meanwhile, trying to minimize the increased bleeding risk. Management of such patients represents a continuous challenge in everyday clinical practice.
Conflicts of interest: none declared.

References
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6. Lee F-Y, Chen W-K, Chiu C-H et al. Increased risk of deep vein thrombosis and pulmonary thromboembolism in patients with aor-tic aneurysms: A nationwide cohort study. PLoS ONE 2017; 12(6): e0178587.
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