Central Retinal Artery Occlusion In Patient Research Articles

Association Between Hospital-Ascertained Atrial Fibrillation And Central Retinal Artery Occlusion: A Study Of 12 Million Patients (P2-9.003)

<h3>Objective:</h3> To determine whether hospital-ascertained atrial fibrillation (AF) is associated with subsequent central retinal artery occlusion (CRAO). <h3>Background:</h3> Atrial fibrillation is a major risk factor for cerebral ischemic stroke. However, it is not known whether AF predicts the development of central retinal artery occlusion. <h3>Design/Methods:</h3> A retrospective cohort study was undertaken using data from the California Healthcare Cost and Utilization Project (HCUP) State Inpatient and State Emergency Department Datasets (SID/SEDDs). Patients 18 years and older discharged from non-federal hospitals between 2005 and 2011 who did not have a history of CRAO were analyzed. AF and CRAO were identified using validated ICD-9-CM diagnosis codes. Association between AF and CRAO was modeled using a Fine-Gray method with death as a competing risk with adjustment for age, biological sex, race, and vascular comorbidities. <h3>Results:</h3> A total of 12,181,778 patients were included, 806,397 with AF and 11,375,381 without AF. In total, 309 patients had CRAO. In an unadjusted analysis, there was a higher risk of CRAO in patients with versus without AF (HR 2.24 (95% CI: 1.51 to 3.32)). After adjustment for pre-specified covariates, there appeared to be a lower hazard of CRAO in patients with AF (aHR 0.61 (95% CI: 0.45 to 0.98)). Further analyses including cerebral ischemic stroke (aHR 1.16 (95% CI: 1.14 to 1.18)) and specifically embolic stroke (aHR 4.29 (95% CI 4.10–4.48)) as positive controls argued against overadjustment bias. We present sensitivity analyses including CRAO identified in any position of the ICD list, using different ascertainment windows for AF and using broader categories of retinal ischemia. <h3>Conclusions:</h3> The incidence of CRAO was higher in patients with AF than those without AF, but the hazard of CRAO was not higher for patients with AF after adjustment for measured covariates. Endpoint and exposure ascertainment may have been limited by inclusion only of inpatient and emergency department encounters. <b>Disclosure:</b> Mr. Lusk has received research support from American Heart Association. The institution of Ms. Song has received research support from Research to Prevent Blindness. Ms. Unnithan has nothing to disclose. Dr. Al-Khalidi has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Medpace. Dr. Al-Khalidi has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for CSL Behring . The institution of Dr. Al-Khalidi has received research support from NIH/NHLBI. Jonathan Piccini has nothing to disclose. Dr. Xian has nothing to disclose. Dr. O’Brien has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for Boehringer Ingelheim. The institution of Dr. O’Brien has received research support from Pfizer. The institution of Dr. O’Brien has received research support from BMS. Dr. Mac Grory has nothing to disclose.

Abstract 30: Association Between Hospital-ascertained Atrial Fibrillation And Central Retinal Artery Occlusion: A Study Of 12 Million Patients

Introduction: Atrial fibrillation (AF) is a major risk factor for cerebral ischemic stroke. However, it is not known whether AF predicts the development of central retinal artery occlusion (CRAO), a form of ischemic stroke affecting the retina. Methods: A retrospective cohort study was undertaken using data from the California Healthcare Cost and Utilization Project (HCUP) State Inpatient and State Emergency Department Datasets (SID/SEDDs). Patients 18 years and older discharged from non-federal hospitals between 2005 and 2011 who did not have a history of CRAO were analyzed. The exposure variable was AF and the endpoint was CRAO, each identified using validated ICD-9-CM diagnosis codes. Association between AF and CRAO was modeled using a Fine-Gray method with death as a competing risk with adjustment for age, biological sex, race, and vascular co-morbidities. Results: A total of 12,181,778 patients were included, among these 806,397 with AF and 11,375,381 without AF. In total, 309 patients had CRAO. In an unadjusted analysis, there was a higher risk of CRAO in patients with versus without AF (HR 2.24 (95% CI: 1.51 to 3.32)). After adjustment for pre-specified covariates, there appeared to be a lower hazard of CRAO in patients with AF (aHR 0.61 (95% CI: 0.45 to 0.98)). Further analyses including cerebral ischemic stroke (aHR 1.16 (95% CI: 1.14 to 1.18)) and specifically embolic stroke (aHR 4.29 (95% CI 4.10-4.48)) as positive controls argued against overadjustment bias. We present sensitivity analyses including CRAO identified in any position of the discharge ICD list, using different ascertainment windows for AF and using broader categories of retinal ischemia. Conclusion: The incidence of CRAO was higher in patients with AF than those without AF, but the hazard of CRAO was not higher for patients with AF after adjustment for measured covariates. Endpoint and exposure ascertainment may have been limited by inclusion only of inpatient and emergency department encounters.

Central retinal artery occlusion in a patient with ANCA-negative Churg-Strauss syndrome

Ocular involvement in Churg-Strauss syndrome is infrequent. We describe the case of a 54-year-old woman with eosinophilia and involvement of the respiratory tract, skin, and peripheral nervous system, fulfilling the American College of Rheumatology criteria for Churg-Strauss syndrome. The patient presented with acute, painless vision loss in her right eye. Central retinal artery occlusion (CRAO) without accompanying retinal vasculitis was diagnosed by angiographic findings and funduscopic findings of retinal whitening with a cherry-red spot. Although her antineutrophil cytoplasmic antibody (ANCA) status was negative, CRAO was thought to be an ocular manifestation of Churg-Strauss syndrome, and appropriate treatment was planned. She was treated with high-dose corticosteroids and anticoagulant therapy. Her macular edema improved, but visual recovery was poor. Specific therapy to alter inflammation, blood coagulation, and rheology reportedly plays an important role in ANCA-positive patients with Churg-Strauss syndrome who develop CRAO. Regardless of ANCA status, high-dose corticosteroids should be considered for CRAO in patients with Churg-Strauss syndrome, as discussed in this case.

Association of Protein Z Deficiency with Retinal Artery and Vein Occlusion.

Central retinal vein occlusion (CRVO) and central retinal artery occlusion (CRAO) are common disorders mainly associated with traditional risk factors for atherosclerosis. There is no clear correlation between thrombophilia and CRVO. However it was suggested that hyperhomocysteinemia and the presence of antiphospholipid antibodies are risk factors for the development of CRAO. Protein Z is a vitamin K dependent cofactor for the inactivation of activated factor X (Xa) by the protein Z dependent protease inhibitor (ZPI). Protein Z deficiency presumably promotes thrombosis, in particular arterial thrombosis, as suggested by an association between low plasma protein Z levels and ischemic stroke. The similarity between risk factors for ischemic stroke and CRVO / CRAO and the fact that low protein Z levels are associated with an increased risk for ischemic stroke has led us to assess protein Z levels in patients with CRVO and CRAO. Plasma samples from 29 patients with CRVO and 7 patients with CRAO (total study group= 36, mean age 60±11) were screened for protein Z levels by ELISA. Study group was also screened for the presence of lupus anticoagulant (LAC) by the kaolin clotting time (KCT) index and the dilute Russells' viper venum test (DRVVT), for activated protein C resistance (APCR) and anticardiolipin antibodies (ACA). Levels of protein Z were compared with a control group of 42 healthy individuals (mean age 43±11). Patients with CRAO and history of ischemic stroke or an embolic source were excluded. Thirty patients in the study group had traditional risk factors for atheroscalerosis including hypertension, diabetes mellitus, hyperlipidemia and smoking and 6 patients had none. There was no significant difference in protein Z levels between the whole study group patients and controls (1995±810 vs. 2010±603 ng/ml p=0.922). However, patients with no risk factors for CRVO/CRAO had significantly lower protein Z levels than controls (1379±682 vs. 2010±603 ng/ml p=0.022) and patients with risk factors (1379±682 vs. 2118±785 ng/ml p=0.04). In the study group three patients had abnormal APCR and 6 had positive LAC. There was no correlation between low protein Z levels and the presence of LAC, APCR or ACA, or a correlation between low protein Z levels and the specific diagnosis (CRVO or CRAO) or age. The data show that low protein Z levels may be an additional risk factor for CRVO and CRAO in patients without traditional risk factors for these disorders. The association should be explored in a larger group of patients.