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Septic embolization is a common and potentially life-threatening complication of infective endocarditis (IE), with a prevalence of 22-50%. While acute coronary syndrome secondary to septic embolism is rare, it poses significant risks. This study examines coronary embolism (CE) in left-sided IE, describing clinical characteristics and outcomes. We retrospectively analysed 649 patients with non-device-related left-sided IE treated between January 2013 and December 2023 in a high-volume surgical centre. CE was diagnosed via ECG, clinical and laboratory signs of acute coronary syndrome, and confirmed by coronary angiography or magnetic resonance imaging. All patients were treated according to current European Society of Cardiology guidelines. A structured follow-up was performed. Among patients included in the study, surgery was performed in 514 (79%) patients. Median follow-up duration was 4.7 years. CE occurred in 8 (1.2%) patients, and 6 (80%) of them were treated surgically. We found no significant differences in overall mortality rate between patients with or without CE (p = 0.65). Finally, cerebral embolism was significantly more frequent in patients with than without CE (75% vs 25%, p = 0.006, post-hoc power 87.8%). CE is a rare but severe complication of IE, significantly associated with cerebral embolism. Early recognition and treatment are crucial to improve patient outcomes. Multicentre studies with larger patient populations are needed to further elucidate risk factors and enhance prognosis for CE in IE patients.

We described a rare case of acute ischemic stroke due to calcified cerebral emboli from calcified carotid plaque (CCP). Radiological examinations revealed that the CCP had an irregular configuration containing a calcified nodule and scattered spotty calcifications, and a large calcified plate. The patient underwent carotid endarterectomy to prevent embolic recurrence. Histopathological examination confirmed the presence of an erupted plaque with a disrupted fibrous cap. Calcified nodular protrusion and spotty calcifications in CCP are predictive of a high risk of embolic stroke with plaque rupture. Thus, careful treatment strategies are crucial to prevent the CCP-related embolic recurrence.

Artery-to-artery embolism (AAE) is a common stroke mechanism in intracranial atherosclerotic disease (ICAD), associated with a considerable risk of recurrent stroke. We aimed to investigate cerebral hemodynamic features associated with AAE in symptomatic ICAD. Patients with anterior-circulation, symptomatic ICAD confirmed in CT angiography (CTA) were recruited. We classified probable stroke mechanisms as isolated parent artery atherosclerosis occluding penetrating artery, AAE, hypoperfusion, and mixed mechanisms, largely based on infarct topography. CTA-based computational fluid dynamics (CFD) models were built to simulate blood flow across culprit ICAD lesions. Translesional pressure ratio (PR = Pressure post-stenotic /Pressure pre-stenotic ) and wall shear stress ratio (WSSR = WSS stenotic-throat /WSS pre-stenotic ) were calculated, to reflect the relative, translesional changes of the two hemodynamic metrics. Low PR (PR ≤ median) and high WSSR (WSSR ≥ 4th quartile) respectively indicated large translesional pressure and elevated WSS upon the lesion. Among 99 symptomatic ICAD patients, 44 had AAE as a probable stroke mechanism, 13 with AAE alone and 31 with coexisting hypoperfusion. High WSSR was independently associated with AAE (adjusted OR = 3.90; P  = 0.022) in multivariate logistic regression. There was significant WSSR-PR interaction on the presence of AAE ( P for interaction = 0.013): high WSSR was more likely to associate with AAE in those with low PR ( P  = 0.075), but not in those with normal PR ( P  = 0.959). Excessively elevated WSS in ICAD might increase the risk of AAE. Such association was more prominent in those with large translesional pressure gradient. Hypoperfusion, commonly coexisting with AAE, might be a therapeutic indicator for secondary stroke prevention in symptomatic ICAD with AAE.

We describe a case of cerebral air embolism in a man with vascular Ehlers-Danlos syndrome. The key learning point is that cerebral air embolism can cause a florid encephalopathy and MR imaging appearance, yet the causative diagnosis may be made only by carefully scrutinising the CT scan, rather than the MRI. This patient was incorrectly diagnosed with posterior reversible encephalopathy syndrome before subsequent closer inspection of the CT scan at presentation disclosed the true diagnosis. Other diagnostic clues were the close temporal proximity to events that might introduce air into the systemic circulation (eg, thoracic procedures) or syndromes that predispose people to cerebral air embolism. The likely cause in this case was a transient bronchovenous fistula associated with vascular Ehlers-Danlos syndrome. Prompt identification of cerebral air embolism allows supportive measures to be started to prevent potentially fatal sequelae.

Cerebral air embolism infarction (CAEI) is a rare but life-threatening condition that can affect the venous or arterial blood supply to the brain. Its aetiology is mostly iatrogenic, often resulting from complications of cardiothoracic or neurosurgical procedures, as well as manipulations with peripheral or central catheters. If undiagnosed and untreated, cerebral air embolism infarction can lead to long-term neurological consequences or even death. Diagnosis relies on clinical presentation and neuroimaging findings from CT and MRI, which are time-sensitive and not well described in the current literature. We present a rare case of cerebral infarction as a complication of retrograde cerebral venous air embolism following haemodialysis catheter removal in a young patient, with management leading to a favourable outcome. The diagnosis was confirmed based on clinical manifestations and neuroimaging findings, with air emboli identified in the subarachnoid space on the CT scan, followed by characteristic MRI changes defined for cerebral air embolism infarcts. Timely diagnosis allowed for the rapid initiation of hyperbaric oxygen therapy and the rehabilitation process, resulting in positive outcomes. Timely neuroimaging-particularly CT within the first 2 hours-is critical for diagnosing CAEI. MRI findings, including cytotoxic and vasogenic oedema in a distal vascular distribution and leptomeningeal enhancement, further support diagnosis. Early identification and treatment initiation are essential for improving patient outcomes.

ObjectiveTo assess (1) the association between atrial cardiopathy (AC) and non-stenotic intracranial complicated atherosclerotic plaque (NICAP) in patients with embolic stroke of undetermined source (ESUS) or small-vessel disease (SVD), and (2) the performance of previously proposed biomarkers to identify AC as the underlying aetiology in ESUS.MethodsBased on our high-resolution MRI (HR-MRI) cohort, 403 subjects (243 ESUS and 160 SVD) were enrolled in the final analysis. All patients underwent intracranial HR-MRI to assess the presence of ipsilateral NICAP. Biomarkers of AC (ie, P-wave terminal force in lead V1 (PTFV1) on ECG, N-terminal probrain natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T and left atrial diameter) were collected within 24 hours after admission.ResultsAmong patients without ipsilateral NICAP, we found an association between the presence of AC (adjusted OR (aOR): 4.76, 95% CI 2.48 to 9.14), increased PTFV1 (aOR: 5.70, 95% CI: 2.43 to 13.39) and NT-proBNP (aOR: 1.65, 95% CI: 1.16 to 2.35) with ESUS. This association was not evident among patients with ipsilateral NICAP. The discrimination between ESUS versus SVD by AC/AC-related biomarkers was significantly improved after excluding ipsilateral NICAP. Similarly, the discrimination between ESUS and SVD by ipsilateral NICAP was notably augmented after excluding AC, PTFV1 and NT-proBNP.InterpretationAC is more prevalent in patients who had ESUS without ipsilateral NICAP compared with patients with, implying that AC and ipsilateral NICAP are two distinct, competing aetiologies of ESUS. Among the AC biomarkers studied in this analysis, PTFV1 seems to be the most informative.

A 58-year-old woman with a history of catheter ablation for atrial fibrillation (AF) 3 weeks prior presented with right middle cerebral artery syndrome and a temperature of 38°C. Her National Institutes of Health Stroke Scale (NIHSS) was 23. [...]there were local inflammatory changes revealed by the presence of soft tissue infiltration centered on the latter structures. Corresponding author:

Background High-power short-duration (HPSD) ablation strategy has emerged as a popular approach for treating atrial fibrillation (AF), with shorter ablation time. The utilized Smart Touch Surround Flow (STSF) catheter, with 56 holes around the electrode, lowers electrode-tissue temperature and thrombus risk. Thus, we conducted this prospective, randomized study to investigate if the HPSD strategy with STSF catheter in AF ablation procedures reduces the silent cerebral embolism (SCE) risk compared to the conventional approach with the Smart Touch (ST) catheter. Methods From June 2020 to September 2021, 100 AF patients were randomized 1:1 to the HPSD group using the STSF catheter (power set at 50 W) or the conventional group using the ST catheter (power set at 30 to 35 W). Pulmonary vein isolation was performed in all patients, with additional lesions at operator’s discretion. High-resolution cerebral diffusion-weighted magnetic resonance imaging (hDWI) with slice thickness of 1 mm was performed before and 24–72 h after ablation. The incidence of new periprocedural SCE was defined as the primary outcome. Cognitive performance was assessed using the Montreal Cognitive Assessment (MoCA) test. Results All enrolled AF patients (median age 63, 60% male, 59% paroxysmal AF) underwent successful ablation. Post-procedural hDWI identified 106 lesions in 42 enrolled patients (42%), with 55 lesions in 22 patients (44%) in the HPSD group and 51 lesions in 20 patients (40%) in the conventional group ( p  = 0.685). No significant differences were observed between two groups regarding the average number of lesions ( p  = 0.751), maximum lesion diameter ( p  = 0.405), and total lesion volume per patient ( p  = 0.669). Persistent AF and CHA 2 DS 2 -VASc score were identified as SCE determinants during AF ablation procedure by multivariable regression analysis. No significant differences in MoCA scores were observed between patients with SCE and those without, both immediately post-procedure ( p  = 0.572) and at the 3-month follow-up ( p  = 0.743). Conclusions Involving a small sample size of 100 AF patients, this study reveals a similar incidence of SCE in AF ablation procedures, comparing the HPSD strategy using the STSF catheter to the conventional approach with the ST catheter. Trial registration Clinicaltrials.gov: NCT04408716. Graphical Abstract AF = Atrial fibrillation, DWI = Diffusion-weighted magnetic resonance imaging, HPSD = High-power short-duration, ST = Smart Touch, STSF = Smart Touch Surround Flow.

Routine blood tests, blood lipids, glucose concentration, and electrolytes were also normal. A CT scan of the woman's brain showed a low-density strip (appendix) in the right middle cerebral artery (MCA) that was hyperintense on T1, T2, and T2 fluid-attenuated inversion recovery weighted MRIs (figure; appendix). Magnetic resonance angiography (appendix) showed an occlusion of part of the right MCA and a low-density filling defect in the initial segment of the right external carotid artery—which, on an ultrasound scan, was hyperechoic—indicative of an embolus (figure).

No patent foramen ovale was found, but a positive bubble test result suggested an underlying pulmonary venous shunt. Prognostic implications hinge on variables such as emboli dimensions, anatomical localization, and the expeditiousness of therapeutic intervention. [...]a prompt diagnosis and timely implementation of therapeutic measures are paramount given their potential to result in favorable clinical outcomes. Source of Support Open access funding provided by University of Zurich.