SESSION TYPE: Cardiovascular Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Giant ascending aortic aneurysm is a rare finding, defined as an aneurysm in the ascending aorta that is more than 10 cm in diameter. Etiological factors include atherosclerosis, Marfan's syndrome, giant cell arteritis, tuberculosis, syphilis, HIV-associated vasculitis, hereditary hemorrhagic telengectasia, and medial agenesis. We report a unique case of giant dissecting aortic aneurysm discovered in an asymptomatic outpatient.

CASE PRESENTATION:

A 33-year old asymptomatic Brazilian male with no significant prior medical history was referred to our institution for an outpatient 2D Echocardiogram after his primary physician heard a diastolic murmur on a routine office visit. To our surprise, the transthoracic echocardiogram revealed a severely dilated proximal ascending aorta with effacement of aortic valve and aortic root. An immediate transesophageal echocardiogram was performed that revealed a proximal ascending aortic aneurysm of 13.0 cm in maximal diameter with well-defined dissection flaps on either side causing severe aortic insufficiency (Fig 1). However, aortic arch and descending aorta dimensions were within normal limits with preserved left ventricular systolic function. Findings were confirmed with CT angiography. Retrospectively when interviewed, patient endorsed family history significant for Marfan's in his mother. On physical examination, the patient was noted to have some Marfanoid features like buffalo hump and long arm span. On physical examination , there was a diastolic murmur, 3/6 in intensity in the aortic area. Rest of the examination was normal. The patient was then admitted to the hospital and underwent successful Bentall procedure constituting reconstruction of ascending aorta, aortic valve replacement and re-implantation of coronaries (Fig 2).

DISCUSSION:

The average rate of growth of thoracic aneurysms is 0.1-0.2 cm/year. Giant aneurysms can have varied presentation. The most feared complications include dissection and rupture. The risk of rupture depends on the size and the rate of growth of the aneurysm. However, an asymptomatic giant thoracic aneurysm in a young patient is extremely rare. Conservative treatment is reserved for asymptomatic aneurysms less than 6 cm in diameter. However surgery is the modality of choice for larger aneurysms.

CONCLUSIONS:

We report a unique case of an asymptomatic dissecting giant ascending aortic aneurysm in a young patient with Marfanoid features.1) Agarwal V, et al. Giant Ascending Aortic Aneurysm-A case report and review. Heart, Lung and Circulation. 2007;16(5):385-388.2) Kitami Y, et al. Giant Unruptured Aneurysm of the Thoracic Aorta: A case report. Angiology. 1999;50(10):865-869.DISCLOSURE: The following authors have nothing to disclose: Nishant Gupta, Naser Mohammad, Sharad Bajaj, Priyank Shah, Mahesh Bikkina, Fayez ShamoonNo Product/Research Disclosure InformationSt. Joseph's Regional Medical Center, Paterson, NJ.

SESSION TYPE: Critical Care Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Aortic dissections commonly extend beyond the renal arteries with varying effects ranging from asymptomatic to renal failure. We report a case of aortic dissection with initial renal compromise, which was continuously monitored utilizing direct renal oximetry for evaluation of real-time renal perfusion and function.

CASE PRESENTATION:

A 65 year-old female with a long history of uncontrolled hypertension presented with acute retrosternal chest pain radiating to the back for 12 hours. She was in stable condition except for a serum creatinine of 1.6mg/dl. Magnetic resonance angiography (MRA) demonstrated a type A dissection extending from the aortic root to the left common iliac artery. The only vessel originating from the false lumen was the left renal artery. The patient was emergently taken to the operating room for aortic root repair with graft. She sustained no intra-operative complications and underwent standard post-operative care. Due to initial elevation in serum creatinine and false lumen perfusion of the left kidney, FORE-SIGHT oximetry monitoring was placed on each kidney utilizing pre-operative imaging. Absolute renal tissue oxygen saturation was recorded for 3 consecutive days post-operatively. The right kidney spent a total 1858 minutes (89%) at greater than 60% saturation while the left kidney spent 1915minutes (92%) (Figure 1). Neither kidney recorded saturations below 52% and serum creatinine cleared to baseline of 1.0 mg/dl. Computed tomography (CT) angiography confirmed perfusion in both kidneys.

DISCUSSION:

Distal organ perfusion can be a difficult assessment to make in the setting of aortic dissection. The laser technology utilized by FORE-SIGHT implements precise and narrow wavelengths proven to provide more accurate and absolute oxygen saturation values.[1] By utilizing FORE-SIGHT oximetry in conjunction with imaging for precise placement, our group was able to accurately monitor renal perfusion in real time as opposed to waiting for contrast CT scan or traditional secondary markers such as serum creatinine and urine output. Saturations were maintained at expected levels throughout the post-operative course and renal function improved. This novel approach may serve a role in adjusting for renal oxygenation and subsequent perfusion in order to prevent renal failure in variety of settings from aortic injury to open cardiac procedures.

CONCLUSIONS:

Renal oximetry may serve as an additional tool in evaluating, and potentially preventing, renal injury in the setting of aortic dissection.1) Fischer W, Gregory. Recent advances in application of cerebral oximetry in adult cardiovascular surgery. Seminars in Cardiothoracic and Vascular Anesthesia. 2008;12(1):60-69.DISCLOSURE: The following authors have nothing to disclose: Philip Batista, NIcholas Cavaricchi, Hitoshi HiroseDIscuss the use of oximetry monitoring utilized in cerebral oxygenation and applying to a new purpose for evaluation of renal perfusionThomas Jefferson University, Philadelphia, PA.

SESSION TYPE: Cardiovascular Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Eisenmenger syndrome (ES) is frequently associated with hemoptysis and sudden death. We describe a patient with ES presenting with chest pain and hemoptysis due to pulmonary artery (PA) dissection with subsequent death from rupture.

CASE PRESENTATION:

A 44-year-old man with ES was transferred to our facility for further evaluation of hemoptysis and chest pain. Past history included a large muscular ventricular septal defect with ineffective PA banding at ten months of age and subsequent irreversible pulmonary vascular disease and cyanosis. He had a known large PA aneurysm and one prior episode of massive hemoptysis requiring coil embolization of pulmonary collaterals. He had been treated with bosentan but had been noncompliant at times and was lost to follow-up for six years prior to presentation. He presented to an outside hospital with left-sided pleuritic chest pain and fevers. Despite antibiotics, he had persistent chest pain and had four episodes of hemoptysis. At the time of transfer, oxygen saturation was 71%, heart rate 118 bpm, and blood pressure 113/62. Chest x-ray revealed a large left pleural effusion and dilatation of the pulmonary arteries. Thoracentesis yielded one liter of bloody fluid. Transthoracic echo showed severe right ventricular enlargement and an estimated right ventricular systolic pressure of 120 mmHg. Computed tomography (CT) showed massive dilatation of the main PA and a dissection flap extending from the intimal disruption caused by the pulmonary band. The patient experienced pulseless electrical activity arrest and resuscitation was unsuccessful. Autopsy revealed a ruptured main PA which was massively dilated with chronic dissection present. The rupture occurred in the outer wall of the dissection channel and migration of the PA band through the vessel wall was also noted.

DISCUSSION:

PA dissection is a rare complication of pulmonary hypertension and is usually fatal. Dissection and rupture are more common with PA aneurysms, which occur more often in patients with ES due to increased pulmonary blood flow. In contrast to aortic dissection which develops a re-entry tear, in PA dissections the false lumen is more likely to rupture (1). In this case, the patient was likely more prone to dissection due to the PA band that had migrated through the wall of the vessel. Surgical repair of PA dissection has been reported but the overall prognosis remains poor (2).

CONCLUSIONS:

PA dissection or rupture is a rare complication in patients with ES, is often fatal, and should be suspected in patients presenting with hemoptysis.1) Khattar RS, Fox DJ, Alty JE, Arora A. Pulmonary artery dissection: an emerging cardiovascular complication in surviving patients with chronic pulmonary hypertension. Heart 2005; 91:142-145.2) Senbaklavaci O, Kaneko Y, Bartunek A, et al. Rupture and dissection in pulmonary artery aneurysms: incidence, cause, and treatment-review and case report. J Thorac Cardiovasc Surg 2001;121(5):1006-1008.DISCLOSURE: The following authors have nothing to disclose: Crystal Bonnichsen, Martha Grogan, Richard OecklerNo Product/Research Disclosure InformationMayo Clnic, Rochester, MN.

SESSION TYPE: Cardiovascular Student/Resident Case Report Posters IIPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

Acute syndromes involving the ascending aorta are typically emergently surgically repaired [1]. We describe a case presenting with spinal ischemia where aortic intervention was delayed in order to perform spinal cord rescue.

CASE PRESENTATION:

64 year old female with past medical history of hypertension presented with acute onset of total lower extremity flaccid paralysis, chest and back pain. CT revealed acute type A intramural hematoma (IMH) extending from the aortic root to the iliac bifurcation. TEE showed maximal ascending aortic diameter at 4.8cm with 1.2cm IMH thickness, and no aortic insufficiency or pericardial effusion. A lumbar drain was emergently inserted and spinal cord perfusion was optimized by maintaining high hematocrit and elevated systemic perfusion pressures. In the following days, she regained 4/5 strength of her bilateral lower extremities and lumbar drain was removed on hospital day 5. On day 13, CTA showed her ascending aorta had increased to 5.4cm and echo showed new aortic insufficiency and pericardial effusion. She underwent planned aortic valve resuspension, ascending and extended hemiarch replacement with pre-operative lumbar drain insertion. Intraoperative findings were significant for a ruptured plaque in the proximal to mid aortic arch, which was excised. Postoperatively she initially had 3/5 bilateral lower extremity strength but by 1 year, she was ambulatory with cane. CT at 1 year showed small amount of residual arch hematoma.

DISCUSSION:

Spinal involvement in acute ascending aortic syndromes is likely secondary to the sheering effects of the intramural hematoma on the intercostals. In this setting, emergent proximal repair will not likely revascularize the spinal cord, but it may be rescued by optimization of spinal perfusion and delayed aortic repair as we demonstrate.

CONCLUSIONS:

Purposeful surgical delay [1, 2] with medical optimization of comorbidities, including neurologic complications [3], may be utilized in the management of acute type A IMH.1) Song JK, Yim JH, Ahn JM, Kim DH, Kang JW, Lee TY, Song JM, Choo SJ, Kang DH, Chung CH, Lee JW, Lim TH. Outcomes of patients with acute type A aortic intramural hematoma. Circulation. 2009; 120: 2046-2052.2) Estrera A, Miller C 3rd, Lee TY, De Rango P, Abdullah S, Walkes JC, Milewicz D, Safi H. Acute type A intramural hematoma: analysis of current management strategy. Circulation. 2009 Sep 15;120(11 Suppl):S287-91.3) Augoustides JG, Szeto WY, Desai ND, Pochettino A, Cheung AT, Savino JS,Bavaria JE. Classification of acute type A dissection: focus on clinical presentation and extent. Eur J Cardiothorac Surg. 2011 Apr;39(4):519-22.DISCLOSURE: The following authors have nothing to disclose: Nishtha Sodhi, Joseph Bavaria, Nimesh DesaiNo Product/Research Disclosure InformationThe Cleveland Clinic Foundation, Cleveland, OH.

SESSION TYPE: Miscellaneous Student/Resident Case Report PostersPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION:

An aberrant right subclavian artery (ARSA) is the most common anatomical abnormality of the aortic arch, found in 0.5-1.8% of autopsies. Fistula formation between a non-aneurysmal retro-esophageal ARSA and the esophagus is exceptionally rare. (1)

CASE PRESENTATION:

A 44 year-old woman with history of hypertension, GERD, presented to the Emergency Department with rapidly progressive dyspnea and coffee-ground emesis. Initial findings included hypothermia (36.3 C), hypotension (97/43), tachypnea (respiratory rate 28) and hypoxemia (oxygen saturation 90% on room air). Chest radiograph showed a right lower lobe infiltrate with pleural effusion. Within hours the patient required intubation and mechanical ventilation with a high level of positive end-expiratory pressure (25 cmH2O). During her ICU stay the patient failed many weaning attempts and underwent tracheostomy. Two weeks after tracheostomy placement, the patient acutely developed copious bleeding from the mouth, nose, and tracheostomy tube. Coagulation parameters and platelet count were within normal limits (INR: 1.2, aPTT: 32 Second). The oral cavity was packed with Kerlix with transient control of bleeding. Bleeding continued and the patient was brought emergently to the operating room. A median sternotomy was performed and dissection was extended along the ascending aorta to the 1st branch that was noted to be a bicarotid trunk. The patient underwent emergent computed tomography scan with contrast that confirmed the diagnosis of Abarrent right subclavian artery- Esophageal Fistula and returned to the operating room where she had a cardiac arrest and failed resuscitative measures.

DISCUSSION:

Only 10% of adult patients with ARSA have symptoms. Patients usually complain of compressive symptoms, particularly dysphagia (2). The main diagnostic criterion in intensive care patients is occurrence of abrupt, massive arterial bleeding several days after placement of an endotracheal or nasogastric tube. The mechanism underlying the development of a fistula involves the induction of limited necrosis of the digestive and arterial walls by pulsatile compression of the esophageal wall between the retro-esophageal subclavian artery and rigid intubation catheter. This leads to thrombosis of the vasa vasorum as well as to ischemia of the digestive wall and with time, this leads to a fistula formation (1). The prognosis of Arterioesophegeal fistula is highly unfavorable with high mortality. (2)

CONCLUSIONS:

Aberrant right Subclavian Artery- Esophageal fistula should be considered in any patient who has a hematemesis of bright red blood several days after placement of an endotracheal or nasogastric tube.1) Patrick Feugier, MD,et al. Arterioesophageal Fistula: A Rare Complication of Retroesophageal Subclavian Arteries. Ann Vasc Surg. 2003 May;17(3):302-5.2) Delap TG,MD. El al. Aneurysm of an aberrant right subclavian artery presenting as dysphagia lusoria. Ann Otol Rhinol Laryngol 109:231-234, 2000.DISCLOSURE: The following authors have nothing to disclose: Ahmed Al-Badri, Wael NasserNo Product/Research Disclosure InformationMedStar Health Research Institute, Washington, DC.

Thoracic aortic endografting has been successfully implemented to treat aneurysmal disease of the distal aortic arch and descending thoracic aorta. Although there are reports of ascending aortic endovascular interventions, the total endovascular repair of a ruptured ascending aorta secondary to a Type A dissection has not been described. We report the case of a 77-year-old patient who presented with a ruptured ascending aortic aneurysm secondary to degeneration of a Stanford type A aortic dissection. His surgical history was significant for orthotropic heart transplant 19 years prior. The dissection, aneurysm, and rupture occurred in the native aorta distal to the ascending aortic suture line. At presentation, he was hemodynamically unstable with a right hemothorax. We placed 3 Medtronic Talent Thoracic Stent Graft devices (Medtronic Inc, Minneapolis, MN) across the suture line in the ascending aorta, excluding the rupture. The patient survived and has been followed to 25 months.

BACKGROUND:

This study attempts to explore the clinical features, possible mechanisms and prognosis of the neurologic complications in patients with acute aortic dissection (AD).

METHODS:

Medical records of 278 consecutive patients with AD (165 with type A and 113 with type B dissection) over 11.5 years were retrospectively analyzed for clinical history, CT findings, neurologic complications and outcome. Neurologic complications were classified into early-onset or delayed-onset complications. Independent t-test or Chi-square test (or Fisher exact test) was used for comparing the different groups. Multivariable logistic regression analysis was performed to determine the independent association between variables.

RESULTS:

The mean age of the included patients (145 male and 133 female) was 59.4 years (range 19--91 years). 41 patients (14.7%) had a neurologic complication, which included 21 with early-onset complication and 23 with delayed-onset complication, including 3 with both. Advanced age and classic type of dissection were independently associated with the neurologic complication in patients with type A dissection. The most frequent manifestation was ischemic stroke (26 patients, 9.4%), followed by hypoxic encephalopathy (9, 3.2%), ischemic neuropathy (5, 1.8%), spinal cord ischemia (5, 1.8%), seizure (2, 0.7%), hoarseness (1, 0.4%) and septic encephalopathy (1, 0.4%). Overall in-hospital mortality was 10.1%, whereas the complicated group had a mortality rate of 43.9%. Renal impairment, pulse deficit, neurologic complication and nonsurgical treatment were independent variables for determining in-hospital mortality in patients with type A dissection.

CONCLUSIONS:

The dominance of neurologic symptom in the early stage of AD may make its early diagnosis difficult. Besides chest pain and widened mediastinum in chest x-ray, variable neurologic symptoms including left hemiparesis with asymmetric pulse and hypotension may suggest underlying AD.

OBJECTIVE:

Dysregulated angiotensin II (Ang II) signaling induces local vascular interleukin-6 (IL-6) secretion, producing leukocyte infiltration and life-threatening aortic dissections. Precise mechanisms by which IL-6 signaling induces leukocyte recruitment remain unknown. T-helper 17 lymphocytes (Th17) have been implicated in vascular pathology, but their role in the development of aortic dissections is poorly understood. Here, we tested the relationship of IL-6-signal transducer and activator of transcription-3 signaling with Th17-induced inflammation in the formation of Ang II-induced dissections in C57BL/6 mice. APPROACH AND

RESULTS:

Ang II infusion induced aortic dissections and CD4(+)-interleukin 17A (IL-17A)-expressing Th17 cell accumulation in C57BL/6 mice. A blunted local Th17 activation, macrophage recruitment, and reduced incidence of aortic dissections were seen in IL-6(-/-) mice. To determine the pathological roles of Th17 lymphocytes, we treated Ang II-infused mice with IL-17A-neutralizing antibody or infused Ang II in genetically deficient IL-17A mice and found decreased aortic chemokine monocytic chemotactic protein-1 production and macrophage recruitment, leading to a reduction in aortic dissections. This effect was independent of blood pressure in IL-17A-neutralizing antibody experiment. Application of a cell-permeable signal transducer and activator of transcription-3 inhibitor to downregulate the IL-6 pathway decreased aortic dilation and Th17 cell recruitment. We also observed increased aortic Th17 infiltration and IL-17 mRNA expression in patients with thoracic aortic dissections. Finally, we found that Ang II-mediated aortic dissections occurred independent of blood pressure changes.

CONCLUSIONS:

Our results indicate that the IL-6-signal transducer and activator of transcription-3 signaling pathway converges on Th17 recruitment and IL-17A signaling upstream of macrophage recruitment, mediating aortic dissections.