Cardiogenic Brain Embolism Research Articles

Clinical Features of Very Elderly Patients Aged 90 Years or Above with Acute Ischemic Stroke: A Study by Using Diffusion Weighted Brain Magnetic Resonance Imaging

We investigated the diffusion weighted magnetic resonance imaging (DWI) features of 76 very elderly patients aged 90 years or above with acute ischemic stroke. Stroke subtypes were classified into five types according to the Trial of Org 10172 in Acute Stroke Treatment (TOAST) and the Japanese Stroke Databank. The incidence rates of atherothrombotic brain infarction (ATBI), atherothrombotic brain embolism (ATBE), lacunar infarction (LI), cardiogenic brain embolism (CBE) and undetermined type of brain infarction (UTBI) were 2.6%, 17.1%, 10.5%, 50.0% and 19.8%, respectively. We estimated that the incidence of acute ischemic stroke in women was 3.5-fold higher than that in men. This is likely because survival rate of females is higher than that of males in populations aged 90 years or above. The prevalence of atrial fibrillation (AF) was 46.1% in patients with brain infarctions, and 92.1% in patients with CBE. The frequency of multiple infarctions is 52.6% and that of single infarction is 47.4%. In DWI of lesions, the frequencies of territorial infarction in the cerebral hemisphere, borderzone infarction, and vertebrobasilar infarction were 85.5%, 13.2% and 17.1%, respectively. The frequencies of massive territorial infarction and cerebellar infarction were 23.7% and 13.2%, respectively. With regard to the relationship between DWI lesion topography and stroke subtypes, superficial infarctions in the cerebral hemisphere were seen in patients with ATBE, CBE and UTBI. Single infarctions deep in the cerebral hemisphere were seen in all patients with any of the five stroke subtypes. Massive territorial infarctions with infarctions in other sites of the cerebral hemisphere or vertebrobasilar region were seen only in patients with CBE, and single pontine infarction was seen only in patients with LI. (Received November 19, 2015; Accepted July 3, 2017; Published November 1, 2017).

心原性か大動脈原性かの脳塞栓症診断に苦慮した1例

心原性か大動脈原性かの脳塞栓症診断に苦慮した1例

Scorpion Stings: Focus on Cerebrovascular Complications of Envenoming

Dear editor, Scorpion stings kills thousands of people every year (1). Clinical picture of envenoming is dominated by local pain, weakness, arterial hypertension, cardiac arrhythmias, myocarditis, or pulmonary oedema. These manifestations occur as the result of massive release of catecholamines into the bloodstream or due to direct toxicity of the venom (2). Cerebrovascular complications occur in up to 8% of severely envenomed scorpion sting victims, particularly after the sting of Mesobuthus thalamus (Indian red scorpion). Intracranial haemorrhages occur in the setting of acute increases in blood pressure related to sympathetic overstimulation, and cerebral infarctions are related to cerebral hypoperfusion, consumption coagulopathy, vasculitis, intracranial vessels spasm, or cardiogenic brain embolism (3,4). A PubMed search revealed 23 well-documented cases of stroke following scorpion stings (mean age 25 years; 71% men). Fifteen patients (65%) had ischaemic and eight had haemorrhagic strokes. Infarctions were located in the middle cerebral artery territory (six patients), watershed areas between major cerebral arteries (three patients), the cerebellum (two patients), multiple arterial territories (two patients), and the posterior cerebral artery territory and the pons (one patient each). Pathogenetic mechanisms responsible for the infarction were suspected in 13 patients, six of whom had cerebral hypoperfusion (related to systemic hypotension), four had disseminated intravascular coagulation, two had vasculitis, and one had spasm of intracranial arteries. Haemorrhagic strokes were located in the basal ganglia in four cases, the subcortical white matter in two, and the ventricular system in one. The remaining patient had multiple intracranial haemorrhages. In seven cases, the cause of the haemorrhage was an increase in arterial blood pressure occurring as part of the ‘autonomic storm’ observed in scorpion sting victims. Prompt management of these patients reduces stroke morbidity and mortality. Prazosin reverses the overstimulation of peripheral a1-adrenergic receptors and reduces the risk of cardiac and pulmonary complications. While the use of antivenom has been questioned due to allergic reactions, combination therapy with antivenom plus prazosin was more effective than prazosin alone for enhancing recovery in a recent trial (5).

Differences in Diffusion-Weighted Image and Transesophageal Echocardiographical Findings in Cardiogenic, Paradoxical and Aortogenic Brain Embolism

Background and Purpose: The purpose of the present study was to clarify the difference in the infarct topography on diffusion-weighted image (DWI) and cardiac and aortic findings on transesophageal echocardiography (TEE) in stroke patients with different embolic sources. Methods: We studied 270 consecutive patients with acute ischemic stroke who had DWI-documented cortical or subcortical infarcts without significant stenosis of the cerebral arteries. As embolic sources, cardiac diseases, right-to-left shunt diseases and an aortic arch atheroma ≧4.0 mm in thickness were identified using various diagnostic tools including TEE. Results: Seventy-eight (29%) patients had multiple embolic sources. Large infarcts were common in patients in whom cardiac disease was the only embolic source and uncommon in patients in whom aortic atheroma was the only embolic source (p < 0.0001). Vertebrobasilar infarcts were relatively common in patients only having aortic atheromas. Atrial septal aneurysms were more common in patients with a right-to-left shunt than in those with a shunt plus other embolic sources (p = 0.0036). Unique characteristics of the arch atheroma (mobile plaque, extension to branches, or ulcer formation; p < 0.0001) as well as small or moderate-sized infarcts (p = 0.0004) were more common in patients with arch atheromas as the only embolic source than in those with atheromas plus other embolic sources. Conclusions: Embolic stroke patients often have multiple embolic sources. The present study suggests the possibility that embolic stroke has unique clinical features depending on its source. DWI and TEE findings might be helpful in characterizing cardiogenic, paradoxical and aortogenic brain embolism.

Specific cardiological evaluation after focal cerebral ischemia.

Purpose of this study was to define a subgroup of TIA/stroke patients who should be examined by transthoracal and transesophageal echocardiography or Holter-electrocardiography to identify those with cardiogenic brain embolism reliably; 300 consecutive patients with acute focal brain ischemia underwent a standardized diagnostic protocol for the evaluation of the etiology including, clinical examination by a cardiologist and routine electrocardiography, Holter-electrocardiography, transthoracal and transesophageal echocardiography. 188 patients had a potential cardiac source of embolism. In particular echocardiography was diagnostic in 163 patients, and Holter-electrocardiography 10; 159 of these 188 patients (84.6%) had competitive etiologies, predominantly large vessel atherosclerosis. In 136 patients cardiogenic brain embolism was assumed as quite definite or possible. To identify these patients reliably, transthoracal and transesophageal echocardiography would have been necessary in 89% of the entire group of patients (all with clinically cardiological abnormalities, pathological routine ECG, without vascular risk factors, or no atherosclerosis in duplex sonography), and Holter-electrocardiography in 54%.

Early outcome and recurrences after cardiogenic brain embolism.

Functional outcome and recurrence rate were evaluated retrospectively in a series of 566 consecutive patients with a cardioembolic TIA or stroke. Seventy-five patients had a TIA/RIND, 163 a minor stroke, 238 a major deficit, and 90 a fatal event. In a logistic regression analysis the probability of a disabling or fatal outcome was significantly influenced by age (p = 0.0023), a previous stroke (p = 0.0262), concomitant carotid artery disease in Doppler sonography (p = 0.0210), and the underlying heart disease (p = 0.0001). Fatal or major strokes predominated among patients with nonvalvular atrial fibrillation, prosthetic heart valves, acute or chronic myocardial infarction. Kaplan-Meier estimates revealed a cumulative risk of recurrent cerebral embolism of 2.9% within three weeks. In a proportional hazards model only the underlying heart disease was significantly linked with the risk of recurrent embolism (p = 0.021).

Cardioembolic stroke: an update.

Cardioembolic stroke accounts for approximately 15% of all strokes and is thought to be one of the more preventable types of strokes. Features that have been reported to support cardioembolism as a mechanism for ischemic stroke have included documented cardiac source of embolism, maximal neurologic deficit at onset, multiple cerebrovascular territories involved, enhanced tendency toward hemorrhagic transformation, enhanced risk of syncope or seizure associated with presentation, and lower likelihood of premonitory transient ischemic attacks. Features that tend to make cardioembolic stroke less likely include significant cerebral atherosclerosis, step-wise progression of the neurologic deficit within a finite period of time, vascular distribution such as entire internal carotid artery territory with combined middle cerebral artery and anterior cerebral artery involvement or watershed distribution, and premonitory transient ischemic attacks. A number of cardiac conditions can promote thromboembolism, and there is risk stratification reflective of the specific condition or coexistent conditions. Anticoagulant therapy generally has been found to be the most effective means of preventing cardiogenic brain embolism, but the intensity of anticoagulation needs to be optimized to reflect the risk-to-benefit ratio for the particular patient.

Patent Foramen Ovale and Recurrent Stroke

Clinical management of patients with acute stroke and the approach used for secondary prevention depends upon clarification of pathogenesis. Although most strokes are a consequence of cerebrovascular disease, ≈15% to 20% of ischemic (nonhemorrhagic) strokes have been attributed to cardiogenic embolism.1 In practice, determination of the stroke mechanism is fraught with uncertainty, particularly when the possibility of thromboembolism emanating from atherosclerotic lesions in the aorta or cervical arteries is considered. When cardiogenic embolism is suspected, cardiac ultrasound is the principal method used to identify the potential source. The finding of left atrial enlargement has been shown to bear a significant relationship to the risk of stroke in a multivariate analysis of population-based data from the Framingham Heart Study2. The most frequent confounding variable is atrial fibrillation, occurring in >2 million patients in North America and in over half of all patients with cardiogenic embolism. Criteria for selection of patients with acute ischemic stroke for transesophageal echocardiography (TEE) to search for a potential cardiac source of embolism are controversial, particularly because cardiogenic embolism is often an uncertain diagnosis that is inferred merely on the basis of the finding of potential cardiac source. Even after extensive investigation, ≈40% of ischemic stroke patients have no clearly identifiable pathogenesis (cryptogenic stroke).3 In one study, 62% of patients younger than 60 years of age without an obvious source of cerebral infarction and 23% of those with arterial lesions had potential sources of cardiogenic embolism identified by TEE ( P =0.0007 for the difference).4 See p 2625 Among the cardiac anomalies detected by TEE that have been implicated as risk factors for stroke are patent foramen ovale (PFO) and atrial septal aneurysm (ASA).5,6⇓ The foramen ovale, a remnant of the fetal circulation, remains patent through adulthood in ≈1 in 4 …

American Heart Association Prevention Conference. IV. Prevention and Rehabilitation of Stroke. Etiology of stroke.

The diagnosis of arterial stroke differentiates ischemia from hemorrhage. The former may be due to arterial occlusion or stenosis, the latter to leakage or rupture of an artery. Computed tomography (CT) and magnetic resonance imaging (MRI) have shown that this basic differentiation cannot be reliably made from the history and clinical examination alone. Of the clinical stroke syndromes, only Wallenberg’s syndrome has not been reported to be due to hemorrhage. When CT or MRI is not available for diagnosis, spinal tap is reliably positive only when the aneurysm or arteriovenous malformation has ruptured into the subarachnoid space; the results are often normal when a small hemorrhage occurs in the parenchyma. For some therapies, notably neuroprotective agents, the potential benefits for ischemia do not seem to be offset by potential harm in the case of hemorrhage. However, because fibrinolytics, antithrombotic agents, or surgery are treatment options, diagnostic certainty is essential to avoid harming the patient. Most—but not all—strokes have a sudden or rapidly evolving onset. Differential diagnosis of sudden change in focal neurological status includes seizures or postepileptic paralysis, hemorrhage into a tumor (itself a form of stroke), and migraine. Neuroimaging helps to differentiate between these and the cause of short-lived symptoms (transient ischemic attack [TIA]) usually presumed due to ischemia but possibly due to new-onset infarction or hemorrhage. More precise classification of stroke into a pathogenic subtype (embolism, thrombosis, decreased perfusion or “lacunar” infarction, leakage, or rupture) evades the best clinical skills. The classification of stroke mechanism depends on the presence of risk factors for stroke (preexisting condition or circumstance epidemiologically related to stroke) and etiologies (disease directly causing the mechanism) that implicate the cause of stroke in a given patient. However, more than one risk factor and etiology are frequently present in the same patient and may be related …

Cardioembolic stroke: results from three current stroke data banks.

About 17% of all transient ischemic attacks (TIA) and ischemic strokes were due to cardiogenic embolism in three prospective stroke registries (Berlin, Giessen, Klosterneuburg). Most of these patients can be identified by history, clinical examination, conventional ECG, and appropriate use of echocardiography. Widespread screening of stroke patients with transesophageal echocardiography, as intented in the protocol of two registries, did not appreciably increase the portion of patients with the final diagnosis of cardiogenic embolism, although, in many cases, minor-risk embolic sources can be identified. Prognosis for death or early recurrence after cardiogenic brain embolism was not worse than assumed previously.

Acute prognosis and differentiation of various cerebral infarct groups in comparison with cerebral hemorrhage

For clinical trials classification of stroke should be possible at the bedside by simple methods that are available every where. In this study are 1105 patients with every first ischaemic strokes and 130 patients with intracerebral haemorrhages. The differences between severity of clinical symptoms, outcome and risk factors of intracerebral haemorrhages, ischaemic stroke caused by cerebral microangiopathy, ischaemic stroke combined with extracranial carotid stenosis, cardiogenic brain embolism and atherothrombotic stroke, were analysed. Intracerebral haemorrhages show the poorest outcome of all groups (mortality 23.8%), due to increased intracranial pressure. Cardiogenic brain embolism is more frequent in older women (mean age 77.8 y.). Main risk factor is atrial fibrillation with absolute arrhythmia. The outcome of this group is the worst of all subgroups of ischaemic stroke and survivors most often in need of institutionalization. Patients with ischaemic stroke combined with extracranial carotid stenosis are significantly younger (mean age 67.6 y.), predominantly male, and smokers. Their mortality is low (0.63%), but recovery of paresis is slower than in other subgroups. Ischaemic strokes caused by cerebral microangiopathy with hypertension as main risk factor recover most quickly but acute mortality is higher than in ischaemic stroke combined with extracranial carotid stenosis because of higher age (mean age 74.5 y.). Institutionalization is more frequent too because of higher incidence of dementia in this subgroup. The main prognostic factors of all groups are age and severity of clinical symptoms. A special subgroup are infratentorial ischaemic strokes.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral embolism in elderly patients with atrial fibrillation

Novalvular (nonrheumatic) atrial fibrillation (NVAF) is the most common cardiac condition associated with presumed embolic stroke, accounting for approximately half of the cardiogenic embolic infarctions. Of autopsied stroke patients in the Tokyo Metropolitan Geriatric Hospital, cerebral infarction was found in 75%, intracranial hemorrhage in 19%, and coexisting cerebral hemorrhage and cerebral infarction in 6%. Twenty-eight percent of the cerebral infarctions were embolic infarctions of cardiac origin, 56% of which were caused by NVAF. The incidence of cardiogenic brain embolism ranged from 6 to 23% of the ischemic strokes, and NVAF is the most frequent substrate for brain embolism. Atrial fibrillation increases in its incidence with increasing age. Chronic AF was observed in 10%, and paroxysmal AF in 7% of the autopsied elderly patients. Most of them were nonrheumatic AF. Twenty-two percent of the AF patients had large cerebral infarction, and 15% had medium-sized cortical infarction at the autopsy. NVAF is a very important cause of fatal massive cerebral infarction in the elderly. Of 56 patients with fatal massive cerebral infarction who died within 2 weeks after the strokes, 25 (45%) had embolic stroke associated with NVAF. Anticoagulant therapy prevents recurrent cerebral embolism of cardiac origin. The proper time to initiate anticoagulant therapy following cardiac brain embolism is controversial. Immediate initiation of anticoagulant therapy can reduce the early recurrence, but can result in secondary brain hemorrhage or hemorrhatic transformation. Patients with NVAF may have a lower risk of recurrence during the first 2 to 4 weeks following the initial embolic stroke compared with other cardioembolic sources. Cerebral embolism with NVAF can recur during a long period.(ABSTRACT TRUNCATED AT 250 WORDS)

Antithrombotic Therapy for Cerebrovascular Disorders

Stroke remains the most common and disabling neurologic disorder of the elderly. As estimated 500,000 people suffer stroke each year in the United States, and there are over 2,000,000 stroke survivors alive with varying neurologic sequelae. While the mortality from stroke has declined in recent decades, the incidence of stroke appears to be stable or perhaps even increasing, 1 Broderick JP Phillips SJ Whìsnent JP et al. Incidence of stroke rates in the eighties: the end of the decline in stroke?. Stroke. 1989; 20: 577-582 Crossref PubMed Scopus (327) Google Scholar which may reflect the expanding elderly population who have survived myocardial infarction and cancer to an age more vulnerable for stroke. Most strokes are the result of ischemic brain infarction, and antithrombotic therapy is an important aspect of management. Our previous reports reviewed the status of antithrombotic therapy in cerebrovascular disorders; 2 Cerebral Embolism Task Force. Cardiogenic brain embolism. Arch Neurol 1986; 43:71-84 Google Scholar ,3 Sherman DG Dyken ML Fisher M et al. Antithrombotic therapy for cerebrovascular disorders. Chest. 1989; 95: 140-155 Abstract Full Text Full Text PDF PubMed Google Scholar we now summarize new information available since our prior review.

'Spectacular shrinking deficit'

We studied the clinical features of a major hemispheric stroke syndrome with rapid recovery ("spectacular shrinking deficit" [SSD]) compared with stroke patients with the same major initial manifestations but without rapid recovery (non-SSD). There were 118 patients with an initial major hemispheric syndrome; 14 patients (12%) had SSD. All but one SSD patient met criteria for cardiogenic brain embolism. Angiographic examination within 24 hours after stroke onset demonstrated that the occlusion sites in SSD differed from those in non-SSD and suggested that rapid embolus migration had occurred in all SSD patients but in only five of 39 non-SSD. Infarcts in SSD were smaller and often scattered over the cortices and deeper structures. Hemorrhagic transformation was less frequent in SSD. In patients with a potential cardiac source of emboli, SSD was more likely to occur in nondiabetic men less than 60 years of age.

Epileptic seizures following ischaemic cerebral infarction

Clinical, CT and EEG findings of 100 consecutive patients suffering from epileptic seizures following hemispheric cerebral infarction were evaluated retrospectively. All patients were followed up for an average of 49 months. Twelve patients suffered from cardiogenic brain embolism, 20 had an occlusive disease of the internal cerebral artery. Forty-seven patients had a single middle cerebral artery infarct, 6 each a posterior cerebral artery or watershed infarct. CT showed lacunes in only 6 cases, 8 had multiple larger infarcts and 27 were normal. Seventy-six patients suffered from generalized seizures, 54 from partial fits, predominantly focal motor seizures. Seventy-one patients had their first seizure within the 1st year after stroke, 30 within 2 weeks after the infarct. The interval between stroke and the first epileptic fit exceeded 1 year in the remaining 29 cases. If the first fit occurred in the acute phase after stroke, the risk of further ones was significantly lower than when the first fit occurred in the chronic stage. The frequency of fits mainly depended on the occurrence of epileptic potentials in the EEG and the interval between stroke and the first seizure. During follow-up 27 patients suffered a recurrent stroke, and 52 patients died. Cardiac failure was the predominant cause of death; only 4 patients died as a consequence of an epileptic fit.

Cardiogenic brain embolism and lupus anticoagulant

The lupus anticoagulant, an acquired immunoglobulin associated with an increased tendency for thrombosis, has been linked to the occurrence of cerebral ischemia presumably related to in situ thrombosis. Cardioembolic cerebral ischemic events have rarely been reported. We encountered 2 patients with focal cerebral ischemia, substantial mitral valvular masses, and a circulating lupus anticoagulant. In each, diagnostic evaluation supported a cardioembolic etiology. These findings illustrate the need for evaluating patients with cerebral ischemic events for a cardioembolic source when a circulating lupus anticoagulant is present.

Cardiogenic Brain Embolism

Cardiogenic Brain Embolism

Stroke: Pathophysiology, Diagnosis, and Management.

Section I: Pathophysiology of Stroke. Epidemiology of Stroke. Atherosclerosis. Vascular Biology of Cerebral Arteries. Neurochemistry and Molecular Biology. Pathophysiology of White Matter Anoxic/Ischemic Injury. Positron Emission Tomography. Functional Magnetic Resonance Imaging. Pathology. Basic Science of Fibrinolysis: Coronary and Cerebral Thrombolysis. Section Ii: Diagnostic Studies for Stroke. Overview of Laboratory Studies. Computed Tomography Scanning. Magnetic Resonance Scanning. Cerebral Angiography. Ultrasound Imaging and Doppler Sonography. Single-Photon Emission Computed Tomography. Section Iii: Clinical Manifestations of Stroke. Classification of Ischemic Stroke. Internal Carotid Artery Disease. Anterior Cerebral Artery Disease. Middle Cerebral Artery Disease. Posterior Cerebral Artery Disease. Choroidal Artery Disease. Vertebrobasilar Occlusive Disease. Lacunes. Cerebral Venous Thrombosis. Intracerebral Hemorrhage. Intracranial Aneurysms. Brain Vascular Malformations. Spinal Cord Ischemia. Section Iv: Specific Medical Diseases and Stroke. Dissections and Trauma of Cervicocerebral Arteries. Stroke in the Setting of Collagen Vascular Disease. Moyamoya Disease. Cerebrovascular Fibromuscular Dysplasia. Migraine and Stroke. Hypertensive Encephalopathy. Multi-Infarct Dementia. Atherosclerotic Disease of the Aortic Arch. Binswanger's Disease. Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (Cadasil). Cerebral Amyloid Angiopathy. Coagulation Abnormalities in Stroke. Stroke and Substance Abuse. Stroke in Young Adults. Patent Foramen Ovale and Ischemic Stroke. Section V: Stroke Therapy. Principles of Hemostasis and Antithrombotic Therapy. Platelet Function and Antiplatelet Agents. Antithrombotic Therapy in Diseases of the Cerebral Vasculature. Pharmacologic Modification of Acute Cerebral Ischemia. Cardiogenic Brain Embolism: Incidence, Varieties, And Treatment. Medical Complications of Stroke. The Intensive Care of the Stroke Patient. Thrombolytic and Defibrino

Cardiogenic Brain Embolism

Cardiogenic Brain Embolism

Cere bral Emboli of Cardiac Origin

To the Editor. —Martin and Biller 1 anticoa gulated 59 consecutive patients with presumed cardiogenic brain embolism, and no patient experienced brain hemorrhage. This experience contrasts markedly with the recent reports of secondary brain hemorrhage in 14% 2 and 16% 3 of consecutive anticoagulated patients who had suffered embolic strokes. This striking discrepancy in rates of hemorrhagic complications suggests that either differences in the patient population (eg, infarct size) or anticoagulation practice (eg, timing of initiation of anticoagulation) were operative. It has been suggested that infarct size and interval from stroke onset to initial, nonhemorrhagic computed tomography (CT) may predict risk of brain hemorrhage in this setting. 4,5 Would Drs Martin and Biller provide further information on estimated infarct size (percentage with large infarcts) and interval from stroke onset to initial CT (mean interval, percentage less than 24 hours)? While we fully agree with their conclusions and recommendations, additional information