Cerebral Embolism In Patients Research Articles

Prognostic impact of cerebral embolism in patients with active infective endocarditis and therapeutic strategies. A retrospective real world study in a surgical centre

Abstract Purpose Infective endocarditis still has high mortality and invalidating complications, such as cerebral embolism. The best strategies to prevent and to manage neurologic complications remain uncertain. This study aimed to identify predictors of septic cerebral embolism and to evaluate the role of surgery in these patients, in a real-world surgical center. Methods We retrospectively analyzed 551 consecutive patients admitted to our department with a definite diagnosis of non-device-related infective endocarditis; of these, 126 (23%) presented a neurologic complication. Results Cerebral embolism was significantly more frequent in patients with large vegetations (p=0.001), mitral valve infection (p=0.001), and Staphylococcus aureus infection (p=0.025). At multivariable analysis, only vegetation length was an independent predictor of cerebral embolism (HR 1.057, 95% CI 1.025–1.091, p 0.001), with a best predictive threshold of 10 mm at ROC curve analysis (AUC 0.54, p=0.001). Patients with neurologic complications were more often excluded from surgery despite an indication to it (16% vs 8%, p=0.001). If eligible, they were treated within two weeks from diagnosis in similar proportion as patients without cerebral embolism with similar survival rate. Predictors of mortality were hemorrhagic lesions (p=0.018), a GCS<14 (p=0.001) or a severe degree of disability (p=0.001) at presentation. The latter was the only independent predictor of mortality at multivariable analysis (HR 2.3, 95% CI 1.43–3.80, p=0.001). Conclusions The present study highlights the prognostic value of clinical functional presentation and the safety of cardiac surgery, when feasible, in patients with septic cerebral embolism. Funding Acknowledgement Type of funding sources: None.

Relationship between D-dimer levels and infarct pattern in acute ischemic stroke patients with non-valvular atrial fibrillation

Background: Cerebral embolism in patients with non-valvular atrial fibrillation (NVAF) is mainly caused by thrombus formation in the left atrial appendage. D-dimer is known to reflect the thrombogenic activity of the left atrium in NVAF patients. This study aimed to investigate the relationship between D-dimer levels and infarct pattern in ischemic stroke patients with NVAF. Methods: We enrolled 255 patients who developed cardioembolic stroke caused by NVAF and presented to the hospital within 7 days. We divided the infarct pattern into two groups: single lesions (SL) and multiple lesions (ML). The infarct pattern was also classified into two groups: ischemic lesions involving a single vascular territory (ST) and multiple vascular territories (MT). We analyzed the relationship between the infarct pattern and D-dimer levels. Results: Of the 255 patients, 79 (31.0%) and 176 (69.0%) were in the SL and ML groups, respectively. In addition, 207 (81.2%) and 48 (18.8%) patients were classified into the ST and MT groups, respectively. Compared with the SL group, a higher D-dimer level was observed in the ML group (p=0.006). Similarly, the MT group had higher D-dimer levels than the ST group (p=0.001). Logistic regression analysis showed that elevated D-dimer levels were significantly and independently associated with the presence of multiple ischemic lesions (p=0.021) and the involvement of multiple vascular territories (p=0.020). Conclusions: This study showed that elevated D-dimer levels were independently associated with multiple ischemic lesions involving multiple vascular territories in ischemic stroke patients with NVAF.

Cerebral embolism in patients with systemic lupus erythematosus caused by Libman-Sacks endocarditis

Cerebral embolism in patients with systemic lupus erythematosus caused by Libman-Sacks endocarditis

Etiology of Cryptogenic Stroke

Ischemic stroke is a heterogeneous syndrome with a plurality of potential etiological factors. The routine diagnosis does not always allow the cause of acute cerebrovascular accident to be found, in such cases we talk about cryptogenic ischemic stroke, which incidence is 20-40%. The category of patients with cryptogenic stroke was first characterized and assigned to a separate group in the database of the National Institute of Neurological Diseases and Stroke in the USA, and later in the TOAST study. The diagnosis of cryptogenic stroke is usually based on the exclusion of well-known causes of acute cerebrovascular accidents, such as atherosclerosis, cardiac arrhythmias, arterial hypertension. Due to the considerable variability of concepts for cryptogenic stroke, the term ESUS (Embolic Stroke of Undetermined Source) appeared in 2014 and formulated criteria which accurately characterized these patients: non-lacunar cerebral infarction by CT and/or MRI, no atherosclerotic lesion stenosing a stroke-associated artery of more than 50%, no sources of high-risk cardioembolism, no other causes of stroke such as dissection of the artery supplying the area of infarction in the brain, migraine, arteritis. Among the potential causes and sources of cerebral embolism in patients with cryptogenic stroke are heart, veins of lower extremities and pelvis, nonstenosing atherosclerosis of brachiocephalic artery, atheroma of aortic arch, paradoxical embolism non-atherosclerotic vasculopathy, monogenic diseases, hypercoagulable states, and others. We should note that there is a lot of studies on the possible causes of cryptogenic stroke in the available literature, but no common approach to classification of etiologic factors and examination algorythms were developed. The high incidence of cryptogenic stroke, the significant heterogeneity of its etiopathogenetic mechanisms and the need for differentiated approaches to the secondary prevention of this type of acute cerebrovascular accident determine the relevance of further studies in this field.

Cholesterol Crystals in Embolic Debris are Associated with Postoperative Cerebral Embolism after Carotid Artery Stenting

Object: We investigated possible associations among the presence of cholesterol crystals in embolic debris, the proportions of debris components, and postoperative cerebral embolism in patients undergoing carotid artery stenting (CAS). Methods: Sixty-seven consecutive procedures were performed for internal carotid artery stenosis with CAS at our hospital between November 2015 and February 2018. Procedures for emergency CAS for stroke in evolution or crescendo transient ischemic attack were excluded (n = 12). The embolic debris from remaining procedures (n = 55) was stained with hematoxylin-eosin and the red blood cells, white blood cells, and fibrin were quantified by color-based segmentation. Cholesterol crystals and calcification were examined histopathologically. Diffusion-weighted imaging (DWI) was performed 1–3 days after CAS, and the images were used to classify procedures according to the presence of new lesions. Results: Of the 55 CAS procedures, new DWI lesions were identified after 32. One patient had symptomatic cerebral embolism. Higher proportions of patients with cholesterol crystals in embolic debris (17 vs. 78%, p < 0.001) and higher proportion of white blood cells (mean 2.3 [0–9.9] vs. 4.2% [0–29.9%], p < 0.01) were observed in the embolic debris of procedures with and without new DWI lesions. Conclusions: Cholesterol crystals were common in the embolic debris from patients with postoperative ischemic lesions after CAS. These results suggest that inflammatory destabilization of the intraplaque lipid component is related to postprocedural DWI lesions.

Frequency and clinical course of cerebral embolism in patients undergoing transcatheter left atrial appendage closure.

The aim of this study was to assess silent and clinically apparent cerebral embolic events in patients undergoing transcatheter left atrial appendage closure. In this prospective single-centre study, 28 patients underwent percutaneous closure of the left atrial appendage. In all patients, a diffusion-weighted magnetic resonance imaging (DW-MRI) study was performed before, the day after the procedure, and during routine follow-up after 45 days. All patients underwent neurological assessment at the time of DW-MRI. Additionally, transcranial Doppler ultrasound monitoring (TCD) for the detection of microembolic material during the procedure was performed. The procedure was successfully completed in all patients. New embolic lesions were detected in nine patients (32%) after the procedure, of which three (33%) were detectable as gliotic lesions at follow-up. One (3.6%) new lesion was observed at 45-day follow-up. Neurological assessment showed no neurological deficits. We observed no relationship between the numbers of microembolic signals on TCD monitoring and the occurrence of cerebral infarctions on DW-MRI. New cerebral embolic events occur after transcatheter closure of the left atrial appendage. However, most of the lesions demonstrate no gliotic transformation at follow-up. In all patients, the cerebral lesions were clinically unapparent.

Transesophageal Echocardiographic Guidance for Septal Puncture and Balloon Mitral Commissurotomy

Interatrial septal puncture has become more and more important in the era of percutaneous intervention for structural heart diseases. Some arrhythmia ablation procedures may also require septal puncture. However, septal puncture is probably one of the most risky percutaneous intervention techniques. It may inadvertently perforate the atrial wall or the ascending aorta, leading to cardiac tamponade or even death. Online guidance with TEE can dramatically reduce the risk. Selection of optimal bicaval plane is of paramount importance. The Brockenbrough puncture needle within the Mullin sheath should be managed so that the typical tenting sign can appear on this plane before protruding the puncture needle. Online TEE is also very convenient for guiding balloon commissurotomy in patients with mitral stenosis. It can provide immediate post-dilatation hemodynamic information through Doppler measurements, and reveal flail mitral valve if the chordae have ruptured. It can reduce the risk of cerebral embolism in patients with isolated immobile appendageal thrombus, if they decide to undergo balloon commissurotomy after anticoagulation for more than three months. Importantly it can detect life-threatening complications such as pericardial tamponade promptly and reliably. Indeed, mastering the technique of online TEE guidance is truly rewarding for balloon mitral commissurotomy.

Cardiovascular diseases in patients 65 years and younger with non-cardiogenic stroke.

IntroductionApproximately 10–15% of patients with stroke are under 65 years of age. The aim of the study was to determine types of stroke In people below 65. We analysed the incidence and types of associated cardiovascular diseases in patients with non-cardiogenic stroke.Material and methodsIn this prospective study patients (aged ≤ 65) with stroke underwent physical examination, computed tomography of the head, blood tests, electrocardiogram, echocardiography, and transcranial and carotid artery ultrasound. Classification of stroke was performed according to the ASCOD scale. Analysis considered the incidence of heart diseases in patients with non-cardiogenic stroke and the incidence of heart diseases recognised as a cause of cerebral embolism in patients with cardiogenic stroke.ResultsThe study included 611 patients with stroke at the age of 27–65 (mean: 57.2 ±6.7; M/F 380/231). Stroke of heterogeneous aetiology was observed in 321 patients, cardiogenic stroke in 78, and stroke caused by small vessel and carotid artery disease in 73 and 72 patients, respectively. The most common heart diseases in non-cardiogenic stroke patients included persistent foramen ovale, coronary heart disease and past myocardial infarction. The most common causes of cardiogenic embolism were cardiomyopathy, atrial fibrillation and interatrial septal defect.ConclusionsAetiologically heterogeneous stroke and cardiogenic stroke are the most commonly observed among young stroke patients. Cardiomyopathy and atrial fibrillation are the most common sources of cerebral embolism in young patients with cardiogenic stroke. Nearly 1/5 of patients with a non-cardiogenic stroke have congenital or acquired structural changes in the heart.

Paradoxical Air Microembolism Induces Cerebral Bioelectrical Abnormalities and Occasionally Headache in Patent Foramen Ovale Patients With Migraine

BackgroundAlthough controversial, paradoxical embolism via patent foramen ovale (PFO) may account for some of the migraine attacks in a subset of migraine with aura (MA) patients. Induction of MA attacks with air bubble injection during transcranial Doppler ultrasound in MA patients with PFO supports this view. It is likely that cerebral embolism in patients with right-to-left shunt induces bioelectrical abnormalities to initiate MA under some conditions.Methods and ResultsWe investigated changes in cerebral bioelectrical activity after intravenous microbubble injection in 10 MA patients with large PFO and right-to-left cardiac shunt. Eight PFO patients without migraine but with large right-to-left shunt and 12 MA patients without PFO served as controls. Four MA patients with PFO were reexamined with sham injections of saline without microbubbles. Bioelectrical activity was evaluated using spectral electroencephalography and, passage of microbubbles through cerebral arteries was monitored with transcranial Doppler ultrasound. Microbubble embolism caused significant electroencephalographic power increase in MA+PFO patients but not in control groups including the sham-injected MA+PFO patients. Headache developed in 2 MA with PFO patients after microbubble injection.ConclusionsThese findings demonstrate that air microembolism through large PFOs may cause cerebral bioelectrical disturbances and, occasionally, headache in MA patients, which may reflect an increased reactivity of their brain to transient subclinical hypoxia–ischemia, and suggest that paradoxical embolism is not a common cause of migraine but may induce headache in the presence of a large PFO and facilitating conditions.

Clinical and pharmacological properties of new oral anticoagulants for the prevention of cerebral thromboembolism: Factor Xa and thrombin inhibitors

Vitamin K antagonists, such as warfarin and phenprocoumon, are the first-line oral anticoagulants for primary and secondary prevention of cerebral embolism in patients with atrial fibrillation. Although vitamin K antagonists can significantly decrease the risk of stroke, their use is limited by several important drawbacks, such as a narrow therapeutic window, the risk of intracranial and gastrointestinal bleeding, interactions with a number of drugs and nutrients, and the need for regular laboratory tests for therapy adjustment. Currently, new oral anticoagulants, such as direct thrombin inhibitors (e.g., dabigatran) and direct factor Xa inhibitors (e.g., apixaban, rivaroxaban), are being developed and tested in clinical trials. Dabigatran and rivaroxaban were recently approved for prevention of cerebral embolism in patients with atrial fibrillation. The advantages of dabigatran in comparison to warfarin are a lower rate of major bleedings with dabigatran 110 mg bid, a better efficacy with dabigatran 150 mg bid, no clinically relevant interactions with other drugs and no need for routine coagulation monitoring. The disadvantages are the absence of antidote and the absence of routine laboratory tests for precise measurements of anticoagulant effect of direct thrombin/ factor Xa inhibitors. This review will focus on thrombin and factor Xa inhibitors, which are new and promising oral anticoagulants for the prevention of cerebral embolism. We will discuss their pharmacological and clinical properties and provide the most recent updates on their clinical trials.

Anticoagulation Should Not Be Used in Most Patients With Stroke With Infective Endocarditis

One of the most worrisome consults to the stroke service is the patient with neurological symptoms in the setting of infective endocarditis (IE). Stroke is the main neurological complication of IE and in 50% to 75% is the presenting feature. The most effective strategy for the prevention of a first or recurrent stroke is the prompt institution of appropriate antibiotic therapy, which reduces the risk to 1% to 3% within the first week.1 Ischemic stroke is 3-fold more common than hemorrhagic stroke. Embolic patterns are seen on diffusion-weighted MR in 92% of patients with stroke or encephalopathy. Initiating anticoagulation may seem reasonable to prevent embolization of infected or bland platelet–fibrin valvular vegetations—perhaps enhanced in the presence of antiphospholipid antibodies—and it is the standard of care for most cardioembolic stroke; however, the stroke risk is similar in the presence or absence of anticoagulants at onset of IE. The most compelling reason to avoid anticoagulation in Staphylococcus aureus IE is the predominance of early …

Prominence of the Eustachian valve in paradoxical embolism

to investigate the relationship between Eustachian valve (EV) length and degree of atrial septal movement in patients with patent foramen ovale (PFO) and presumed paradoxical cerebral embolism. PFO is a well-established risk factor for cryptogenic stroke. However, due to the high prevalence of PFO, many of these are bystanders rather than true pathological entities. Other studies have sought to define which patients with PFO are particularly at risk of cryptogenic stroke by measuring various parameters of right atrial anatomy. We investigated the relationship between EV length and atrial septal movement. measurements of EV length and atrial septal movement were made prospectively from 72 consecutive patients referred to our centre for PFO closure following presumed cryptogenic stroke, by intracardiac phased array echocardiography. The most significant finding from this study was that patients with fewer than 10 mm atrial septal movement had significantly longer EVs than those in whom there was >10 mm septal movement (P = 0.003). The mean EV length with >10 mm septal movement is 6.35 mm, and 13.33 mm with fewer than 10 mm movement. The prevalence of septal movement beyond 10 mm was significantly less in our series than in previously published papers. we propose that while a large degree of atrial septal movement significantly increases propensity to cerebral embolism in patients with PFO, its absence does not negate this risk. We have shown that long EV may function independently from atrial septal movement to potentiate paradoxical embolism.

Relation between intracranial artery calcifications and aortic atherosclerosis in ischemic stroke patients

We previously demonstrated a strong relation between carotid atherosclerosis (defined as carotid artery stenosis > or =50%) and intracranial artery calcification (IAC) in ischemic stroke patients. The purpose of this study was to evaluate the relation between aortic atherosclerosis and IAC. Four hundred fifty-four patients with ischemic stroke were included. Complex aortic plaques (CAP) were assessed by transesophageal echocardiography (TEE) and defined as plaques > or =4 mm thick or with mobile components in the proximal aorta. IAC were assessed in the seven major cerebral arteries and a semiquantitative score system was applied, ranging from 0 (no calcification) to 7. Forty-two patients (9.3%) had CAP. Patients with CAP were older compared with patients without CAP (73.6 vs. 63.6 years, p < 0.001), had more vascular risk factors, more significant carotid artery atherosclerosis (p < 0.001), more chronic kidney disease (p < 0.001), and a higher IAC score (3.0 vs. 1.8; p < 0.001). Stepwise logistic regression selected the following independent factors for CAP: previous stroke or TIA (OR 3.3; 95%CI 1.5-7.0; p = 0.002), carotid artery stenosis > or =50% (OR 3.7; 95%CI 1.7-8.0; p = 0.001), chronic kidney disease (OR 3.8; 95%CI 1.9-7.8; p < 0.001), and IAC score (OR 1.5; 95%CI 1.2-1.9; p = 0.002). IAC was present in 100% of patients with CAP. Moreover, IAC had a high sensitivity (100%) and negative predictive value (100%) for the presence of CAP. In ischemic stroke patients, the absence of IAC strongly points to the lack of CAP. However, these results warrant confirmation in prospective studies before concluding the non-utility of the use of TEE to exclude CAP as a potential source of cerebral embolism in patients without IAC.

Silent Cerebral Infarcts in Patients With Pulmonary Embolism and a Patent Foramen Ovale

Pulmonary embolism is thought to be associated with a small but definite risk of paradoxical embolism in patients with a patent foramen ovale (PFO). Although neurological complications are infrequent, the incidence of clinically silent brain infarction is unknown. We assessed the rate of clinically apparent and silent cerebral embolism in patients with pulmonary embolism in relation to the presence or not of a PFO. We used diffusion-weighted MRI in patients hospitalized for a pulmonary embolism to assess cerebral embolic events. Sixty consecutive patients were evaluated at diffusion-weighted MRI. All patients underwent neurological assessment before diffusion-weighted MRI and a contrast echocardiography to detect PFO the next day. Diffusion-weighted MRI showed bright lesions in 6 patients among the 60 consecutive patients with pulmonary embolism in a pattern consistent with embolic events. There was only one patient with a neurological deficit. After contrast echocardiography, a PFO was diagnosed in 15 patients (25%). The frequency of silent brain infarcts in patients with a PFO was significantly higher than in patients without PFO (5 [33.3%] of 15 versus one [2.2%] of 45 patients, P=0.003). By logistic regression analysis, PFO was identified as an independent predictor of silent brain infarcts (OR, 34.9 [3.1 to 394.3]; P=0.004). In pulmonary embolism, cerebral embolic events are more frequent than the apparent neurological complication rate. The prevalence of silent brain infarcts is closely related to the presence of a PFO suggesting a high incidence of unsuspected paradoxical emboli in those patients.

Fatal Cerebral Emboli in the Absence of a Cardiac Arterial-Venous Shunt: Case Report

Cerebral embolism in patients undergoing total joint arthroplasty has an incidence rate of 0.5%. In those cases where cerebral emboli were confirmed, a venous-to-arterial circulation shunt, most commonly a patent foramen ovale, was identified. We report a case of severe cerebral fat emboli during cementless total hip arthroplasty in the absence of an intracardiac defect.

Is Unprotected Carotid Stenting Safe?

Background and Purpose: So far, there is no proof that protection systems reduce the risk of cerebral embolism in patients undergoing stent-assisted angioplasty of the carotid artery. However, there is increased pressure on interventionalists to use protection devices, arguing that the use of protection devices is mandatory for a safe performance of the procedure. In order to answer this question, we prospectively evaluated all carotid stenting procedures performed in our institution. We did not use protection devices at all. Methods: Between November 2001 and March 2006 we treated 56 patients with 59 stenoses. 42 out of 59 stenoses were neurologically symptomatic (71%). In all patients the indication of therapy was established by interdisciplinary discussion. Only stenoses above 70% (NASCET) were treated, provided there were contra-indications against surgery. We did not use any protection device. Preprocedural medication was ASS, Clopidogrel and Heparin. Pre- and post-interventional diffusion-weighted MRI and independent neurological examination were done. Results: In all 59 procedures a Carotid Wallstent® was implanted successfully without significant residual stenosis. There were no neurological complications. Diffusion-weighted MRI 24 hours after the procedure showed isolated small signal increases in six out of 59 procedures (10.2%). Despite anticoagulation with ASS, Clopidogrel and Heparin there were no local complications owing to a vessel closure system. Conclusion: Carotid stenting in our patient sample with our method does not require protection systems against cerebral embolism. In our interdisciplinary selected patient group which included only patients with risks higher than the average, there were no complications. In our opinion peri-interventional anticoagulation is more important than using protection systems which have their intrinsic complication rate.

Atrial Thrombi—A Prospective Follow‐up Study over 3 Years with Transesophageal Echocardiography and Cranial Magnetic Resonance Imaging

Patients with atrial fibrillation (AF) and atrial thrombi have an increased risk for cerebral embolism. However, there is little knowledge about the long-term fate of atrial thrombi and the incidence of cerebral embolism in patients under oral anticoagulation. Consecutive patients with persistent or permanent AF and left atrial (LA) thrombi were included in the study. We performed serial and prospective transesophageal echocardiography, cranial magnetic resonance imaging, and clinical examinations during a period of 3 years. Oral anticoagulation was continued or initiated in all patients. A target INR of 2.5 was intended in all patients. Forty-three patients with LA thrombi and persistent or permanent AF were included. During the follow-up period 31(72%) of the thrombi disappeared. Patients with disappearance of thrombi had significantly smaller thrombi (P < 0.01), a lower echogenicity of thrombi (P < 0.01), and a lower LA volume (P = 0.02). Twenty-two (51%) patients suffered from cerebral embolism and/or death during the observation period. Five patients died due to embolic events. The only independent predictors of cerebral embolism were an elevated peak emptying velocity of the LA appendage (P < 0.001) and a history of previous thromboembolism (P < 0.01). Patients with persistent or permanent AF and atrial thrombi have a high long-term risk of cerebral embolism and/or death (51%) even despite the oral anticoagulation therapy. Thrombus size may predict thrombus resolution under continued anticoagulation.

Fate of left atrial thrombi in patients with atrial fibrillation determined by transesophageal echocardiography and cerebral magnetic resonance imaging

Patients with atrial fibrillation (AF) and atrial thrombi have an increased risk for cerebral embolism. However, there is little knowledge about the long-term fate of atrial thrombi and the incidence of cerebral embolism in patients receiving continued oral anticoagulation. Forty-three consecutive patients with AF and atrial thrombi were enrolled in the study. Serial and prospective transesophageal echocardiographic studies, cranial magnetic resonance imaging (MRI), and clinical examinations were performed during a period of 12 months. Oral anticoagulation was continued or initiated in all patients. An international normalized ratio of 2.0 to 3.0 was regarded as effective. During follow-up, 56% of the thrombi disappeared (7 [16%] at 1 month, 18 [42%] at 3 months, 21 [49%] at 6 months, and 24 [56%] at 12 months). Patients with the disappearance of thrombi had significantly smaller thrombi compared with patients with persistent thrombi (1.5 +/- 0.8 cm in length and 0.8 +/- 0.5 cm in width vs 1.9 +/- 0.6 cm in length and 1.3 +/- 0.4 cm in width, p = 0.04), reduced echogenicity of thrombi (46% vs 89%, p <0.01), and smaller left atrial (LA) volume (83 +/- 27 vs 116 +/- 55 cm(3)). Seven patients (16%) had embolic lesions during follow-up MRI. Six of these patients (86%) had clinically apparent embolisms, and 1 died from stroke. The only independent predictors of cerebral embolism were an elevated peak emptying velocity of the LA appendage (p <0.01) and previous thromboembolic events (p = 0.02). Patients with AF and atrial thrombi have a large likelihood of cerebral embolism (16%) and/or death despite oral anticoagulation therapy. Thrombus size may predict thrombus resolution under continued anticoagulation.

A02-4 Incidence of cerebral embolism in patients with atrial fibrillation and cardioversion

A02-4 Incidence of cerebral embolism in patients with atrial fibrillation and cardioversion

A02-4 Incidence of cerebral embolism in patients with atrial fibrillation and cardioversion

A02-4 Incidence of cerebral embolism in patients with atrial fibrillation and cardioversion