1. Cardiovocal Syndrome Secondary to Aortic Aneurysm -Case report Chien-Mei Chen 1,Pin-Zhir Chao 1, Tsung-Ming Chen 1, Wei-Hsuan Chan 1, Wei-Han Lee 1, Tsung-Wei Liu 1, Hsing-Won Wang 1,2 1 Department of Otolaryngology, Shuang Ho Hospital, Taipei Medical University, 2 Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University Introduction Case report Discussion Conclusion Reference Nobert Ortner first described hoarseness, which resulted from left recurrent laryngeal nerve palsy, in three patients with severe mitral stenosis in 1897 1. Later in 1958, Stocker & Enterline further identified that hoarseness atributable to recurrent laryngeal nerve paralysis caused by cardiovascular disease as cardiovocal syndrome 2. A 68-year-old man presented to the ENT out-patient department complained of hoarseness for more then 10 months. He denied symptoms of choking or dysphagia. He had history of coronary artery bypass graft surgery 4-5 years ago at Far-East Hospital. He had regular follow-up in another medical facility since then. Clinical exam identified left vocal palsy in the paramedian position and atrophic corditis (Fig. 1.). Laryngoplasty was planned. However, chest radiography revealed a large bulging contour overlying aorta and left hilar shadow(Fig. 2.). Aortic aneurysm was highly suspected. Constrast-enhanced chest computed tomography for further evaluation showed a broad-based aortic aneurysm at proximal descending aorta, projecting anterolaterally, just distal to left subclavian artery orifice, about 6.9cm in largest dimension with mural thrombus (Fig. 3-1.3-2.). After explaining to patient and family, they’ve decided to go to Far-East Hospital for aneurysm management. Fig. 1. Left vocal fold fixed in abduction during respiration. Fig. 2. Chest radiography revealed a large bulging contour overlying aorta nad left hilar shadow. Initially, Ortner postulated that left recurrent laryngeal nerve was compressed by enlarged left atrium against the aorta arch. Later, Fetterrolf and Norris, after autopsy studies, suggested that the distance between the aorta and pulmonary artery is only 4mm, hence, most likely responsible for palsy 4. There are reports of reversible nerve palsy after disease correction and there are reports not. Due to the limitation of case numbers, correlation of the duration of hoarseness and recovery time isn’t known. Generally, the degree and duration of neural damage is possible related. The most common cause of unilateral vocal palsy is lung cancer(42%). Iatrogenic(24%) comes the second. Ortner’s syndrome constitutes only part of the other causes(11%) 2. Ortner’s syndrome, also known as cardiovocal syndrome, refers to hoarseness due to recurrent laryngeal nerve palsy secondary to cardiovascular disease which comprises all kinds of disease such as mitral stenosis, mitral prolapse, mitral regurgitation, pulmonary artery hypertension, aortic aneurysm, aortic dissection, pulmonary embolism, left atrial enlargement…etc. There are congenital causes such as atrial septal defect, ventricular septal defect, Eisenmenger’s complex, patent ductus arteriosus…etc 3. Cardiovocal syndrome is a rare clinical presentation. While a patient with unilateral vocal palsy is encountered, one might keep in mind the possibility of cardiovocal syndrome especially in an adult with cardiovasecular disease or in an infant since the vocal palsy might be reversible after disease correction. Fig. 3-1. Transverse chest CT scan. Fig. 3-2. Coronal scan. Aortic aneurysm at proximal descending aorta (arrow). 1. Ortner N: Recurrenslahmung bei mitral stenose. Wien Klin Wochenschr 1897;10:753-755 2. Mulpuru SK, Vasavada BC, Punukollu GK, et al. Cardiovocal syndrome: a systematic review. Heart Lung Circ 2008;17:1-4 3. Loughran S, Alves C, MacGregor FB. Current aetiology of unilateral vocal fold paralysis in a teaching hospital in the West of Scotland. J Laryngol Otol 2002;116:907-10 4.Fetterolf G, Norris G. The anatomical explanation of paralysis of left recurrent laryngeal nerve found in certain case of mitral stenosis. Am J Med Sci 1911;141:625-38