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Valsalva Sinus Thrombosis in a HeartMate 3 Patient: A Case Report
Session:
CASOS CLÍNICOS DE INSUFICIÊNCIA CARDÍACA E CUIDADOS INTENSIVOS
Speaker:
Rafael Viana
Congress:
CPC 2025
Topic:
E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
Theme:
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Subtheme:
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Session Type:
Sessão de Casos Clínicos
FP Number:
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Authors:
Rafael Viana; Marta Paralta de Figueiredo; Rita Louro; António Almeida; Rita Rocha; Diogo Brás; Bruno Piçarra
Abstract
<p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Introduction: <span style="color:#1f1f1f">Valsalva sinus thrombosis is a rare complication of </span></span></span><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif"><span style="color:#1f1f1f">left ventricular assist device</span></span></span><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif"><span style="color:#1f1f1f"> (LVAD)<span style="font-size:10.0pt"><span style="background-color:white"><span style="font-family:"Arial",sans-serif"><span style="color:#1b1b1b">. Thrombosis may occur due to persistent closure of the aortic valve and stasis of blood in the aortic sinus. </span></span></span></span><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Heartmate 3 (HM3) has a reduced thrombotic risk compared to other LVAD due to its broad blood flow passages and lack of mechanical bearings, resulting in a frictionless environment. Here we present a case of a Valsalva aortic thrombosis in a patient with HM3.</span></span></span></span></span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Case Report: Male, 65 years old, with a history of HM3 implantation as a bridge to heart transplant due to pulmonary hypertension and dilated cardiomyopathy. Patient (pt) also underwent Mitraclip implantation, and implantable cardioverter-defibrillator after an acute myocardial infarction (AMI). </span></span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Pt went to emergency department due to syncope and chest pain radiating to the left upper limb and cervical region. Electrocardiogram showed new right bundle branch block with T waves congruent in V1-V6 leads. A transthoracic echocardiogram (TTE) was performed, limited by poor acoustic window, revealing severely decreased left ventricular ejection fraction (LVEF), being impossible to assess segmental changes. An anterior AMI was assumed an coronary angiography preformed, which revealed dissection of the left coronary sinus. After catheterization, angioCT showed partial thrombosis of the left valsava sinus involving the left main branch, corroborated by transoesophageal echocardiogram and unfractionated heparin was started.</span></span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">During hospitalization, an episode of ventricular tachycardia treated with amiodarone was registered. Due to hypotension, norepinephrine and dobutamine were initiated, with episodes of non-sustained ventricular tachycardia and rapid ventricular response atrial fibrillation leading to dobutamine discontinuation.</span></span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">After a week, the patient underwent heart transplantation. Post-transplant, endomyocardial biopsy did not reveal any changes suggesting rejection and the TTE showed preserved LVEF and right ventricle systolic function was impaired. On the fifty-first day of hospitalization, a marked elevation of NTproBNP was observed, prompting a TTE that showed severely decreased LVEF. Rejection was suspected, and immunosuppressive treatment was intensified, leading to recovery of LVEF.</span></span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Other complications included left thalamic ischemic stroke, CMV viremia and use of renal replacement therapy due to worsening of chronic kidney disease.</span></span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">At discharge, given the prolonged hospitalization and associated myopathy, he was referred to a Convalescence Unit for intensive motor rehabilitation.</span></span></span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><span style="font-size:10.0pt"><span style="font-family:"Arial",sans-serif">Conclusion: <span style="background-color:white"><span style="color:#1b1b1b">The number of LVAD patients is increasing. V</span></span>alsalva aortic thrombosis is a known complication of LVAD. Treatment options include systemic anticoagulation, percutaneous or surgical thrombectomy and, in refractory pt, emergent heart transplantation may be considered. </span></span></span></span></p>
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