Case Presentation: 46-year-old male with past medical history of nicotine dependence was seen in the emergency department as code neuro with chief complaints of right arm/leg weakness and numbness which started 2 hours ago while he was playing video games. Physical exam showed right sided facial droop with power 0/5 in right upper extremity and 3/5 in right lower extremity and loss of right arm and leg sensations. NIH stroke scale on presentation was 12. Computerized Tomography (CT) head showed no evidence of acute infarction or hemorrhage. CT angiogram of head and neck didn’t show any significant hemodynamic stenosis of bilateral carotid arteries and cerebral arteries. Patient met criteria for thrombolysis and received tenecteplase with resolution of right sided weakness and improvement in numbness during hospital course. MRI of the brain showed moderate acute cortical infarction involving the left temporal and parietal lobes. Transthoracic Echocardiogram confirmed normal left ventricle function and ruled out patent foramen ovale with negative bubble study. Work up of cryptogenic stroke in younger population was initiated. Hemoglobin A1c was 5.2 and lipid panel showed hypertriglyceridemia with undetectable LDL. Inflammatory markers ESR and CRP were normal and hypercoagulable work-up did not show any acute abnormalities. Syphilis and HIV serology was negative. Transesophageal echocardiogram showed a small mobile echogenic structure on the anterior mitral valve leaflet suspicious for Lambl’s Excrescence (LE). Zio patch ordered at discharge did not show any arrhythmias. Neurology consult was taken and recommended lifelong anticoagulation to be started five days after initial presentation of stroke. Patient was discharged home on high intensity statin and rivaroxaban with outpatient follow up with cardiothoracic surgery.
Discussion: Lambl’s Excrescences originally named after a Bohemian Physician Lambl are tiny filiform strands originating on the line of valve closure that hypothetically result from valvular wear and tear. Patients may remain asymptomatic or present with embolic phenomenon to distant organs including cerebral and coronary vasculature. Diagnosis is mostly based on Transesophageal Echocardiogram(TEE). Currently here are no consensus guidelines for treatment however patients presenting with first stroke episode are usually managed with anticoagulation and surgical options are reserved for patients with large symptomatic LE who present with recurrent strokes and/or fail anticoagulation. LE is a rare cause of cardioembolic stroke however incidence is underreported due to non availability and/or non utilization of TEE.
Conclusions: Clinicians should have a high clinical suspicion especially in younger patients without classical risk factors who present with recurrent stroke or TIA for timely diagnosis and management. Further studies are required to fully understand the pathophysiology of LE so that management guidelines for medical and surgical treatment can be formulated.