Cause Of Cerebral Embolism Research Articles

Mitral valve endocarditis presenting as a stroke in a young lady: A case report

Left-sided infective endocarditis is a recognized but less common cause of cerebral embolism. When the causative organism is Methicillin- resistant Staphylococcus aureus, the rate of embolic phenomena increases. In such cases, surgical interventions should be considered when indicated. We present a case of a 20-year-old girl who presented with acute onset aphasia, and found to be having multifocal acute cerebral infarctions in brain imaging, which do not fall into a single vascular territory. Her echocardiogram confirmed mitral valve endocarditis while blood cultures were positive for Methicillin- resistant Staphylococcus aureus. She responded poorly to antibiotics and ultimately ended up with metallic prosthetic mitral valve replacement.

Mechanical Thrombectomy for Acute Ischemic Stroke due to Thrombus in the Pulmonary Vein Stump after Left Pulmonary Lobectomy: A Case Series.

Cerebral embolic stroke caused by a thrombus in the pulmonary vein stump after left pulmonary lobectomy is a serious complication. We retrospectively analyzed four patients who underwent mechanical thrombectomy for large-vessel occlusion after left pulmonary lobectomy between January 2014 and March 2022. Two cases occurred after left upper lobectomy and the others occurred after left lower lobectomy. All patients presented with cerebral embolic stroke from the day after surgery to the 9th postoperative day, and successful reperfusion was achieved in all cases. Two patients had good outcomes at 90 days. Thrombus in the pulmonary vein stump is the probable cause of cerebral embolism, and mechanical thrombectomy is effective. Further studies are required to establish preventive measures and perioperative management strategies.

Clinical case of an ischemic stroke of the patient with non-bacterial thrombotic endocarditis

Ischemic stroke in oncological diseases occurs as a result of the prothrombotic effect caused by cancer. Besides that, it is associated with antitumor therapy. In the first instance, cardioembolism should be ruled out for recurrent systemic embolism in patients with a tumor history. In most cases, the cause of cerebral embolism in oncological diseases is non-bacterial thrombotic endocarditis. Its diagnosis preferably based on transesophageal echocardiography. This article presents a clinical case of ischemic stroke developed by marantic endocarditis, methods of its verification and treatment.

D-dimer and C-reactive Protein as Potential Biomarkers for Diagnosis of Trousseau's Syndrome in Patients with Cerebral Embolism

BackgroundDifferentiating stroke due to Trousseau's syndrome from other types of cerebral embolism is challenging, especially in patients with occult cancer. The current study aimed to determine predicting factors and biomarkers of stroke due to Trousseau's syndrome. MethodsThis retrospective study comprised 496 consecutive patients with acute cerebral embolism, including 19, 85, 310, and, 82 patients with stroke due to Trousseau's syndrome, artery-to-artery embolism, cardioembolic stroke, and embolic stroke with undetermined source, respectively. All patients were evaluated within 72 hours of onset. The clinical characteristics, laboratory findings, and patterns on diffusion-weighted magnetic resonance imaging (DWI) were compared among the groups. ResultsPlasma D-dimer and C-reactive protein (CRP) levels were significantly higher in the Trousseau's syndrome than in the other causes of cerebral embolism. Multivariate analyses demonstrated that female sex, multiple lesions on DWI, high D-dimer and CRP levels, and low platelet and low brain natriuretic peptide levels were independent predictors that could distinguish Trousseau's syndrome from the other causes of cerebral embolism. The cutoff values of D-dimer and CRP to identify stroke due to Trousseau's syndrome was 2.68 µg/mL fibrinogen equivalent units and .29 mg/dL, respectively. ConclusionsThe elevated D-dimer and CRP levels on admission in addition to specific clinical features may be useful for diagnosis of Trousseau's syndrome in patients with cerebral embolism.

Small, smooth, nonmobile cardiac myxoma detected by transesophageal echocardiography following recurrent cerebral infarction: a case report

BackgroundCardiac myxoma is known to cause repeated events of cerebral embolism. Soft and irregularly shaped myxomas with high mobility are associated with a higher occurrence of cerebral embolism. In contrast, nonmobile cardiac myxomas with a round regular shape are rarely considered to be a cause of cerebral embolism. In this case, we present a patient with recurrent cerebral embolism associated with a small and nonmobile cardiac myxoma of round regular shape.Case presentationA 76-year-old Japanese man presented to our hospital with weakness in his right upper extremity. He had a history of right frontal lobe infarction in the previous month. T2-weighted magnetic resonance imaging revealed an area of hyperintensity in the left precentral gyrus, indicating acute cerebral infarction. Transthoracic echocardiography revealed normal left ventricular function and no abnormalities. However, transesophageal echocardiography showed a small and nonmobile left atrial tumor with round regular shape attached to the ostium secundum of the atrial septum. Based on these findings, we diagnosed recurrent cerebral infarction due to embolization caused by left atrial myxoma, and cardiac tumor extraction was performed on hospitalization day 36. The excised tumor measured 0.6 × 0.6 × 0.5 cm and was diagnosed as cardiac myxoma by histologic examination.ConclusionsEven small and nonmobile cardiac myxomas with a round regular shape may cause recurrent cerebral infarction. The diagnosis of this type of atrial myxoma is elusive and transesophageal echocardiography was an effective method of detection. In a clinical situation, this type of cardiac myxoma may be overlooked as a cause of cerebral infarction.

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.

Risk factors for left atrial thrombus from transesophageal echocardiography findings in ischemic stroke patients.

To identify the cause of cerebral embolism, we performed transesophageal echocardiography (TEE) in patients suspected of embolic brain infarction including transient ischemic attack (TIA). We analyzed TEE findings and investigated factors associated with left atrial thrombus (LAT) detected by TEE. We enrolled 98 consecutive patients who underwent TEE and had acute brain infarction or TIA that was possibly due to embolism. We assessed age, sex, presence of atrial fibrillation (AF), days from admission to TEE and TEE findings, including the prevalence of LAT, spontaneous echo contrast (SEC), left atrial appendage (LAA) slow flow velocity, patent foramen ovale (PFO), atrial septal aneurysm and aortic plaque (ASA). LAT was detected with TEE in 20 patients (20%). The factors that were significantly associated with the presence of LAT were male sex (unadjusted odds ratio (OR), 3.94; 95% confidence interval (CI), 1.07-14.58; p=0.037), presence of AF (unadjusted OR, 9.58; 95% CI, 2.58-35.50; p< 0.001), SEC (unadjusted OR, 8.48; 95% CI, 2.57-28.00; p< 0.001) and LAA slow flow velocity (unadjusted OR, 5.18; 95% CI, 1.59-16.91; p=0.005). Multivariate logistic regression analysis revealed that male sex (adjusted OR, 5.30; 95% CI, 1.09-25.71; p=0.039), presence of AF (adjusted OR, 8.97; 95% CI, 1.10-73.20; p=0.041) and SEC (adjusted OR, 10.87; 95% CI, 1.001-118.0; p=0.049) were independently associated with LAT, but LAA slow flow velocity was not. SEC is an important risk factor associated with LAT in patients suspected of embolic brain infarction that is independent of AF.

Optimized 3D bright blood MRI of aortic plaque at 3 T

To evaluate the feasibility of an optimized bright blood MRI protocol at 3 T in combination with contrast agent administration for the detection and characterization of aortic high-risk plaques for the improved workup of acute stroke patients. ECG synchronized T1-weighted 3D gradient echo MRI was performed in 45 acute stroke patients. Data were acquired with high near isotropic spatial resolution (approximately 1 mm(3)) covering the entire thoracic aorta. To compensate for breathing and vessel motion artifacts, images were collected using respiratory navigator gating in combination with short diastolic data acquisition windows adjusted on a patient-by-patient basis. In patients with aortic plaques > or =3 mm in thickness, gadolinium contrast agent was administered and both pre- and post-contrast T1-weighted 3D measurements with identical vessel coverage were performed. Bright blood 3D MRI detected 33 high-risk plaques with an average maximum plaque thickness of 4.2+/-1.0 mm in 23 of 45 acute stroke patients. The availability of pre- and post-contrast images acquired within the same session enhanced the identification of calcified plaque components in 77% of all analyzed plaques: post-contrast MRI clearly improved the delineation of hypointense plaque cores in 23 of 30 cases and assisted in the classification of core shape and of core fraction. 3D bright blood MRI at 3 T was feasible for the detection of aortic high-risk sources and may help to improve the detection of causes of cerebral embolism in acute stroke patients.

Early cardiac involvement in senile systemic amyloidosis: a case report

Senile systemic amyloidosis (SSA) is caused by the deposition of wild-type transthyretin (TTR)-derived amyloid fibrils. This type of amyloidosis is not rare in elderly individuals over the age of 80 and is usually detected on postmortem microscopic examination of myocardium. We report a 67-year-old male patient who was clinically diagnosed as having SSA with cardiac involvement. The initial event was cerebral infarction conceivably due to cardiac embolism. Endomyocardial biopsy was performed twice, which led to a definitive diagnosis of amyloidosis at the second biopsy. This amyloid was immunolabeled by an anti-TTR antibody and direct DNA sequencing of the TTR gene did not detect any mutation. Clinical confirmation of SSA in individuals before the age of 70 is infrequent and cardiac amyloidosis associated with this disease might have been the cause of cerebral embolism in our patient. Additionally, it is important to distinguish cardiac amyloidosis of SSA from that of primary immunoglobulin light chain (AL)-derived amyloidosis, because the treatment and prognosis differ considerably from those of primary AL amyloidosis.

Aortic Atherosclerotic Disease and Stroke

In the 1940s, most strokes were attributed to cerebral vasospasm, a mechanism that is not given a great deal of credence today. It was not until the early 1950s that Harvard neurologist C. Miller Fisher1 stressed the importance of carotid artery atherosclerosis as a major cause of cerebral infarction. Later that decade, the importance of atrial fibrillation as a cause of cerebral embolism began to be stressed,2 and the presence of a left atrial thrombus was first seen on angiocardiography in 1965.3 Despite the established importance of these 2 causes of stroke, carotid disease and atrial fibrillation, nearly half of strokes were listed as “of undetermined cause” in a large stroke registry as recently as 1989.4 In this series, 40% of 1273 cerebral infarctions in the Stroke Databank of the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) were thought to be cryptogenic (from the Latin crypticus , meaning secret or mysterious). The clinical syndrome in those patients, as well as the angiographic and computed tomographic (CT) findings, could be reclassified as embolic; however, because no source of embolus could be identified, the authors kept these strokes in the undetermined cause category. In 1990, a third leading cause of embolic stroke was identified on transesophageal echocardiography (TEE), namely severe atherosclerotic plaques in the aortic arch.5 The 3 patients described in that initial report were a 68-year-old woman with dysarthria and an embolus to the foot, a 77-year-old woman with a cerebellar infarction after cardiac catheterization, and a 70-year-old man with staggering, diplopia, and a visual field cut. All 3 had severe plaque in the aortic arch on TEE. In addition, freely mobile projections were seen superimposed on the plaques, making it seem likely that these findings were the reason for the patients’ embolic …

Predictive value of inflammatory and hemostatic parameters, atherosclerotic risk factors, and chest x-ray for aortic arch atheromatosis.

Aortic arch atheromatosis (AAA) is a common cause of cerebral embolism. Transesophageal echocardiography (TEE) shows not only the extension of atherosclerotic plaques but also the mobility of superimposed thrombi. In most cases AAA is only detected after the embolic event. This study was therefore designed to identify predictive factors for AAA. One hundred seven consecutive patients referred for routine TEE were included in the study. Patients on warfarin therapy, with a history of recent surgery, or with any signs of infectious, immunological, or malignant diseases were excluded. Diabetes mellitus carried the highest risk for AAA (odds ratio, 3.0), followed by hyperlipidemia (2.5) and arterial hypertension (2.3). Age >70 years was accompanied with a 1.8-fold increased risk. Patients with aortic calcifications on standard chest x-ray had a 4.6-fold higher prevalence. Severe AAA was associated with higher levels of C-reactive protein (14.6+/-14.1 versus 4.9+/-7.2 mg/L), fibrinogen (4.20+/-1.22 versus 3.45+/-1.29 mg/L), plasmin/antiplasmin complexes (728+/-297 versus 453+/-243 microg/L), and D-dimers (980+/-652 versus 444+/-349 microg/L). AAA is accompanied by elevation of inflammatory and hemostatic parameters. Patients with classic cardiovascular risk factors and aortic calcifications on chest x-ray have a higher prevalence. Further prospective studies are now warranted to establish a risk score to identify patients in whom TEE screening should be undertaken.

Cardiac Causes of Stroke.

At least 20% of all ischemic strokes are cardioembolic. Cardiac conditions that cause cerebral embolism are classified as major or minor depending on whether the causal link has or has not been fully established between the underlying cardiac condition and the stroke. Atrial fibrillation, acute myocardial infarction, valvular heart disease, infective endocarditis, nonbacterial thrombotic endocarditis, and atrial myxoma are the main cardiac causes of cerebral embolism. Patent foramen ovale, atrial septal aneurysm, mitral valve prolapse, mitral annular calcification, calcific aortic stenosis, and mitral valve strands are cardiac conditions with a potential causal link to cerebral embolism, but until now, either they have been found to be poor predictors of recurrent stroke or their risk of recurrent stroke is unknown. The management of patients with a stroke of cardiac source is twofold: 1) treatment of the acute phase of stroke and 2) prophylactic treatment of recurrent thromboembolism. When possible, primary prevention of cerebral embolism should be recommended, particularly in cardiac conditions with known high risk of stroke (eg, atrial fibrillation, mitral stenosis, or presence of mechanical prosthetic heart valves).

Cerebral Embolism as a Cause of Stroke and Transient Ischemic Attack.

The most frequent cause of stroke and transient ischemic attacks is cerebral embolism. Cardiogenic cerebral embolization is common among patients with any cause of atrial fibrillation (AF) but particularly in AF resulting from rheumatic and arteriosclerotic heart disease. Rare causes of cerebral embolism include fat entering the bloodstream after trauma, tumor cells arising from atrial myxomata, and gas embolism. Cerebral embolic infarctions and their sources of origin can now be confirmed during life by many invasive (I) and noninvasive (NI) procedures including computerized tomography (CT) scanning (NI), magnetic resonance imaging (MR) (NI), contrast angiography (I), digital subtraction angiography (I), magnetic resonance angiography (NI), carotid Doppler and transcranial Doppler (NI), and echocardiography (NI) without and with contrast. These tests visualize the following: embolic occlusions of small and large cerebral arteries, resultant cerebral infarctions in appropriate vascular territories, plaques within the aorta, subclavian, vertebral, and carotid arteries, and mural thrombi located within the heart and aortocephalic arteries. Transcranial Doppler monitoring of the middle cerebral artery detects both small (asymptomatic) and large (symptomatic) cerebral emboli, as well as transseptal cardiac shunting, which is a cause of paradoxical embolization. Holter monitoring detects episodic cardiac dysrhythmias not apparent during routine ECG. CT or MRI identify cerebral infarctions resulting from virtually all large cerebral emboli. Early recognition and identification of types of cerebral embolism are important because of the availability of effective prophylactic therapies. (ECHOCARDIOGRAPHY, Volume 13, September 1996)

Diagnosis of cardiac thrombosis in patients with atrial fibrillation in the absence of macroscopically visible thrombi

Cardiac thrombosis due to atrial fibrillation (AF) has been recognized as the most common cause of cerebral embolism. However, sometimes no macroscopic thrombus is found at autopsy in the heart of a victim of this type of cerebral embolism. We investigated morphological changes in the left atrial endocardium of 31 patients (including 21 cases with AF) who had died of cerebral embolism. "Rough endocardium" (RE) seen macroscopically provided evidence for the existence of atrial thrombosis. The RE that appeared in AF cases was due to a granular and wrinkled appearance of the endocardium associated with oedematous and fibrous thickening. Fibrin-thread deposits were also always distinguishable. Mural thrombi and oedema with neutrophil infiltration in the subendocardium could be seen under the microscope. Small areas of endothelial denudation and thrombotic aggregations were commonly observed by scanning electron microscopy (SEM). These SEM lesions were significantly more frequent in cases with AF than in controls (P < 0.001). The diagnostic success rate for atrial thrombosis among cases with AF increased from 33.3% to 81% when thrombi proven by histological investigation of the areas with RE were added. Left atrial RE may be an anatomically relevant finding for the existence of atrial thrombosis with AF, when the thrombosis cannot be detected upon gross observation at autopsy.

Cerebrovascular disease in north-west India: a study of necropsy material.

The pattern of cerebrovascular disease in North-West India has been studied in a necropsy series of 362 cases over a 14 year period. One hundred and thirty eight cases of intracranial haemorrhage were found, 89 of cerebral embolism, 101 of cerebral arterial thrombosis and 34 of cerebral venous thrombosis. Nearly 37% of the affected patients were below 40 years of age. Cerebral embolism and cerebrovenous thrombosis were important causes of stroke in the young. Rheumatic heart disease and infective endocarditis formed the major causes of cerebral embolism. Cerebral venous thrombosis associated with pregnancy and puerperium was relatively more common in our series than has been reported in the West.

Atrial septal aneurysm as a cause of cerebral embolism in young patients.

Atrial septal aneurysm as a cause of cerebral embolism in young patients.

Nonhemorrhagic cerebral infarction in young adults.

We evaluated 144 patients (81 males and 63 females) aged 15 to 45 years who had nonhemorrhagic cerebral infarction. Atherosclerotic cerebral infarction was diagnosed in 38 patients. Potential cardiac causes of cerebral embolism were found in 33 patients. Only three events could be attributed to mitral valve prolapse. Hematologically related disorders were diagnosed in 21 patients, while 38 patients had nonatherosclerotic vasculopathies. Young patients with cerebral infarction are a heterogeneous group. A potential cause can be found in most patients. We found more than 40 possible etiologies among our patients. Mitral valve prolapse apparently is not a common cause of cerebral infarction among young adults. Cerebral infarction should not be ascribed to oral contraceptives or migraine until other possible causes have been eliminated.

The epidemiology of stroke in an urban black population.

Hospital admissions for acute stroke were monitored over a twelve month period. Only patients age 20 and over were studied. Out of a population at risk of 114931 there were 116 cases, giving an overall incidence of 1.01 admissions per 1000 population per year over age 20. Cerebral hemorrhages were present in 32.8%, large artery thromboses in 31.9%, cerebral embolism in 13.8% and lacunar infarctions in 20.7% of cases. Atrial fibrillation was the presumed cause of cerebral embolism in 6.9% of patients. Hypertension was present in 69.8% of patients. Further studies are needed to establish the characteristics of stroke in the Third World.

Cerebral Embolism in Cancer Patients

Sudden neurological deterioration suggesting embolism in a patient with a history of cancer should alert the physician to the possibility of a non-metastatic, and therefore potentially reversible, cause of cerebral embolism before cerebral metastasis is implicated. During a four year period, we have observed eight cases of acute cerebral embolism among 3000 cancer patients seen in a department of medical oncology. Five patients had features post mortem of non-bacterial thrombotic endocarditis, and in one, the diagnosis had been made antemortem, but treatment with heparin did not prevent further emboli. Two patients had radiation related carotid vascular disease, and one patient post lymphangiographic embolism. The literature reporting these uncommon causes of cerebral embolism is reviewed. Post-lymphangiographic embolism carries a uniformly good prognosis. In selected cases of post-irradiation cerebral embolism, surgical intervention may prevent a neurological catastrophe. Non-bacterial thrombotic endocarditis and mucin embolism are of uncertain aetiology and natural history; long-term survival is uncommon, and treatment does not appear to influence the clinical course or outcome.