SPC365

Aortic atherosclerotic plaques: the role of anticoagulation

Session: Posters - G. Aortic Disease, Peripheral Vascular Disease, Stroke
Speaker: Ana Beatriz Garcia

Congress: CPC 2021
Topic: G. Aortic Disease, Peripheral Vascular Disease, Stroke
Theme: 22. Aortic Disease
Subtheme: 22.4 Aortic Disease - Treatment
Session Type: Posters
FP Number: ---
Authors: Ana Beatriz Garcia; Margarida Martins; Catarina Oliveira; Beatriz Silva; Pedro Alves da Silva; Joana Brito; Pedro Silvério António; Sara Couto Pereira; Nelson Cunha; Tiago Rodrigues; Cláudio David; Daniel Caldeira; Fausto j. Pinto; Ana Almeida

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Introduction: </strong></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Aortic atherosclerotic plaques (AAPs) are one of the major causes of spontaneous and iatrogenic stroke and peripheral emboli, carrying an high morbidity and mortality. Transesophageal echocardiography (TEE) plays a key rule on detecting AAP. The therapeutic approach of this patients (pts) is not well stablished.&nbsp;</span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Purpose:</strong></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"> To evaluate the impact of anticoagulation (ACO) therapy on major events in asymptomatic pts with AAP detected in TEE.&nbsp;</span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Methods: </strong></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Single-center retrospective study of consecutive patients submitted to TEE between 2010 and 2019 with documentation of AAP. Plaques were described as (1) complex (&gt;4mm), (2) ulcerated and (3) mobile thrombi. The plaque location was also documented. We consulted pts data charts for clinical characterization and events recording during the follow up. Major events were defined as stroke, bleeding, hospital admissions (either cardiovascular (CV) and non-CV) and death. Statistical analysis was performed using Cox regression and Chi-square tests.&nbsp;</span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Results: </strong></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">We enrolled 177 pts with a mean age of 70&plusmn;10.5 years, 63.8% males, 31.1% diabetic, 73.4% hypertensive, 54.2% with dyslipidemia, 62.7% obese, 25.4% with peripheral arterial disease, 25.9% with previous stroke and 55.4% with supraventricular arrhythmia. Most of pts had complex plaques (80.8%), mobile thrombi in 11.9% and ulcerated plaques in 7.3%; most of the plaques were located in proximal descending aorta (50.3%) and aortic cross (38.4%). Regarding baseline therapy, 52% were under ACO and 50.3% under statin. The main indication of ACO was atrial fibrillation (45.8%).</span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">During follow up (mean time: 1613&plusmn;1255 days), 61.5% pts died (10.7% from CV causes, 13% with unknown cause), 17.5% had a stroke, 5.7% had other embolic event (lower limbs emboli, unilateral amaurosis and ischemic colitis). Bleeding occurred in 18.3% pts; 47% pts were hospitalized (28.3% from CV cause).&nbsp;</span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">Adjusting for age and comorbidities, there were no significant differences between the group with and without ACO. ACO therapy prevented death from any cause, being also an </span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>independent predictor </strong></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">(p=0.08, OR 0.489, IC 95% 0.288-0.831) when adjusted for comorbidities and age. ACO was associated with bleeding events (p=0.003), but not with stroke or hospitalization from any cause (p=NS).&nbsp;</span></span></span></p>

<p style="text-align:justify"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000"><strong>Conclusion: </strong></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="color:#000000">In this subset of pts, ACO therapy prevented death from any cause in pts with AAP. This may have therapeutic implications when approaching this pts, although larger studies to confirm this results are needed.</span></span></span></p>