Detection of Atrial Fibrillation After Central Retinal Artery Occlusion.

Background: Central retinal artery occlusion (CRAO) causes sudden, irreversible blindness and is a form of acute ischemic stroke. In this study, we sought to determine the proportion of patients in whom atrial fibrillation (AF) is detected by extended cardiac monitoring after CRAO. Methods: We performed a retrospective, observational cohort study using data from the Optum deidentified electronic health record of 30.8 million people cross-referenced with the Medtronic CareLink database of 2.7 million people with cardiac monitoring devices in situ. We enrolled patients in 3 groups: (1) CRAO, (2) cerebral ischemic stroke, and (3) age-, sex-, and comorbidity-matched controls. The primary end point was the detection of new AF (defined as ≥2 minutes of AF detected on a cardiac monitoring device). Results: We reviewed 884 431 patient records in common between the two databases to identify 100 patients with CRAO, 6559 with ischemic stroke, and 1000 matched controls. After CRAO, the cumulative incidence of new AF at 2 years was 49.6% (95% CI, 37.4%­61.7%). Patients with CRAO had a higher rate of AF than controls (hazard ratio, 1.64 [95% CI, 1.17­2.31]) and a comparable rate to patients with stroke (hazard ratio, 1.01 [95% CI, 0.75­1.36]). CRAO was associated with a higher incidence of new stroke compared with matched controls (hazard ratio, 2.85 [95% CI, 1.29­6.29]). Conclusions: The rate of AF detection after CRAO is higher than that seen in age-, sex-, and comorbidity-matched controls and comparable to that seen after ischemic cerebral stroke. Paroxysmal AF should be considered as part of the differential etiology of CRAO, and those patients may benefit from long-term cardiac monitoring.

Cryptogenic Stroke: Diagnostic Workup and Management.

PURPOSE OF REVIEW: Cryptogenic stroke describes a subset of ischemic stroke for which no cause can be found despite a structured investigation. There are a number of putative mechanisms of cryptogenic ischemic stroke including a covert structural cardiac lesion, paroxysmal atrial fibrillation, hypercoagulable state or undiagnosed malignancy. Because many of these proposed mechanisms are embolic - and based on studies of thrombus history showing commonalities between thrombus composition between cardioembolic and cryptogenic strokes - the concept of embolic stroke of undetermined source (ESUS) (Hart et al. Lancet Neurol. 13(4):429-38, 2014; Stroke. 48(4):867-72, 2017) has been proposed to describe cryptogenic strokes that may warrant systemic anticoagulation. In this review, we discuss the phenomena of cryptogenic stroke, ESUS and a proposed management pathway. RECENT FINDINGS: 1. The concept of ESUS was proposed in 2014 as a potentially useful therapeutic entity. Two recent trials - NAVIGATE-ESUS (Hart et al. N Engl J Med. 378(23):2191-201, 2018) and RESPECT-ESUS (Diener 2018) were proposed based on this concept. They were negative for their primary endpoint and for the secondary endpoint of ischemic stroke recurrence. Post-hoc analysis of the WARSS trial (Longstreth et al. Stroke. 44(3):714-9, 2013) suggested that people with elevated pro-BNP benefited from systemic anticoagulation whereas those with a normal pro-BNP did not. This led to the hypothesis that a subgroup of patients at higher risk for embolism from the left atrium would benefit from anticoagulation, even if the WARSS trial was negative for the primary endpoint. Thus, the ARCADIA trial (Kamel et al. Int J Stroke. 14(2):207-14, 2019) was proposed - a randomized, active-control, multi-center trial comparing apixaban with aspirin for secondary stroke prevention in patients with ESUS and biomarkers of left atrial cardiopathy. This trial is actively recruiting. 2. Carotid web - an intimal form of fibromuscular dysplasia - has come to increased prominence in the literature as a cause of embolic stroke. It is a non-stenosis, non-atherosclerotic lesion in the posterior wall of the internal carotid artery that leads to pooling with stasis of blood distal to the lesion and, as a consequence, embolic stroke. It is not usually detected by a standard stroke workup as it masquerades as non-calcified atherosclerosis and does not cause hemodynamically significant stenosis. There have been two major recent papers - a meta-analysis in Stroke (Zhang et al. Stroke. 49(12):2872-6, 2018) and narrative review in JAMA Neurology (Kim et al. JAMA Neurol. 2018) - that addressed this topic. Cryptogenic stroke describes a stroke for which no cause has been found. ESUS is a more precisely-defined entity that mandates a specific workup and implicates remote embolism as a cause of stroke. In ESUS, the options for further investigation include long-term cardiac monitoring, transesophageal echocardiography, investigation for occult malignancy or arterial hypercoagulability. Options for management include anti-platelet therapy (the current standard of care), empiric anticoagulation or enrollment in to a clinical trial examining the use of NOACs compared with aspirin for secondary prevention (such as ARCADIA or ATTICUS). In a person less than 60 years old with ESUS and a patent foramen ovale the risk of a recurrent stroke is low but recent trials have suggested that percutaneous device closure reduces this risk further with an acceptable complication rate.

Anticoagulation Resumption After Stroke from Atrial Fibrillation.

The goal of this paper is to review literature on the topic of anticoagulation resumption after stroke from atrial fibrillation. Following ischemic stroke, the average annual risk of recurrent stroke in a patient with a CHADS2 score of 9 is 12.2%%, translating to an average daily risk of 0.03%%. Oral anticoagulant therapy provides a 75% relative risk reduction. However, in the 2-week period immediately following an acute stroke, this daily risk appears to be elevated. The same period is associated with an increased risk of hemorrhagic transformation of ischemic stroke due to reperfusion, impaired autoregulation, and disruption of the blood-brain barrier. Use of thrombolytics and anticoagulants, baseline infarct size, presence of microhemorrhages, and evidence of hemorrhagic transformation further increases the risk of symptomatic hemorrhagic. The decision to resume anticoagulation early after ischemic stroke from atrial fibrillation must carefully balance the risks of hemorrhagic transformation with the risk of recurrent stroke. There are currently 4 trials in progress at present (OPTIMAS, ELAN, TIMING, and START) comparing different anticoagulant resumption protocols after stroke in patients on non-vitamin K oral anticoagulants. There are a number of major limitations of the studies to date on the timing of anticoagulation resumption on stroke in atrial fibrillation. For instance, they do not explicitly account for infarct size, presence/absence of hemorrhagic transformation, recanalization via mechanical thrombectomy, and bleeding diatheses such as liver synthetic dysfunction or thrombocytopenia. These factors are crucial in personalizing a treatment decision to an individual patient.

Brugada Syndrome: Death Reveals its Perpetrator.

Rapid diagnosis of Brugada syndrome is critical to therapy, which is aimed at reversing provoking factors to suppress/terminate malignant arrhythmias. This case highlights the diagnosis and peri-operative management of patients with Brugada syndrome at high risk for sudden cardiac death. (Level of Difficulty: Beginner.).

A rare cause of constrictive pericarditis.

A 67-year-old man presented with 3 months of exertional dyspnoea and 1 week of oedema. Examination revealed elevated neck veins, pulsus paradoxus, muffled heart sounds, decreased breath sounds and pedal oedema. Transthoracic echocardiogram (TTE) demonstrated cardiac tamponade, and chest X-ray showed pleural effusion. Pericardiocentesis, thoracocentesis, laboratory investigations and CT did not elucidate an underlying aetiology. Three weeks later, he presented with recurrent cardiac tamponade and pleural effusion. Pericardial window histology was benign. Pleural and pericardial fluids were again unrevealing. Three months later, he presented with worsening congestive heart failure. TTE, cardiac catheterisation and cardiac MRI were consistent with constrictive pericarditis. Preoperative workup did not identify an underlying cause. The patient underwent subtotal pericardiectomy. Intraoperative frozen section indicated malignancy. Pathology confirmed metastatic poorly differentiated signet ring adenocarcinoma of intestinal origin. He died 4 days postoperatively from multiorgan failure.