Cardiogenic Embolism Research Articles

全国脳卒中データバンク構築に向けて

There is only a few evidence for stroke management has been reported from Japan. It is necessary to make a data bank of acute stroke patients as infrastructure to make evidence for standardization of stroke management. We made Japan standard stroke registry study (JSSRS) supported by ministry of health and welfare from 1999 to 2002. We completed computerized registry system and accumulated about 8, 000 acute stroke cases from 45 stroke center hospitals. This system is also functioning as a stroke database for each hospital. From the analysis of the distribution of stroke subtype, the incidence of atherothrombotic infarction and cardiogenic embolism was similar to lacunar infarction as shown in Figure 1. Furthermore, the 38% of ischemic stroke patients admitted within 3 hours. Thrombolytic therapy was performed in 15% of the patients who admitted within 3 hours and their initial severity were NIHSS 6-29. The outcome of the patients treated with thrombolytic therapy was significantly better than those without it. These data indicate that the stroke data bank should be useful tool to make verification of the guideline and planning a clinical trial for EBM in near future.

Cardiac morphology and physiology predisposing to thrombus formation

Cardiogenic neurologic embolism accounts for approximately 15‐20% of stroke cases. Various diseases and therapeutic interventions may predispose a patient to intra-cardiac thrombus formation and subsequent embolism. General risk factors for intra-cardiac thrombus include an abnormal endocardium, loss of atrial contraction, arrhythmias, cardiac chamber dilatation and impaired left ventricular function. The present review addresses the pathophysiological mechanisms that underlie these risk factors and their relationship to thrombus formation.

Hypoperfusion-related cerebral ischemia and cardiac left ventricular systolic dysfunction

Background: Cardiomyopathy and low ejection fraction (EF) are associated with cardiac thrombi and cardiogenic embolism but may also be risk factors for hypoperfusion-related cerebral ischemia (HRCI). Current stroke subtype criteria do not include an HRCI category. Method: To look for evidence of HRCI, we compared mean infarct volume between serial patients with EF ≤35% and high-grade (≥ 70%) carotid stenosis and serial patients with normal EF and high-grade carotid stenosis. We matched serial stroke patients with EF ≤35% with stroke patients with normal EF and compared the number and type of ischemic lesion (symptomatic or asymptomatic) and mean infarct volume on magnetic resonance imaging. We blindly compared stroke subtype in these groups using modified Trial of ORG 10172 in Acute Stroke Treament (TOAST) criteria, including an HRCI category. Results: In patients with carotid stenosis, ipsilateral infarct volume was greater with EF ≤ 35% (74.7mL, 95% CI, 17.3-132.1 mL) than in controls (17.1mL, 95% Cl, 9.4-24.8 mL) (P<.05). There was no difference in the mean number of HRCI-compatible infarcts on computed tomography scan between patients with low EF and controls. Symptomatic HRCI occurred in 4 of 15 patients with low EF and in 0 of 15 controls. Conclusions: Symptomatic HRCI occurs in patients with low EF. Severe arterial stenosis may interact with left ventricular systolic dysfunction to cause cerebral hypoperfusion. Modification of the TOAST criteria to include an HRCI subtype is feasible and HRCI should be included as a stroke subtype. Copyright © 2001 by National Stroke Association

Clinical impact of transesophageal echocardiography in patients with stroke without clinical evidence of cardiovascular sources of emboli.

The purpose of this study is to evaluate the impact of transeophageal echocardiography on management of patients at low-risk for cardiogenic embolism to prevent new potential cardiovascular sources of emboli. We studied 69 patients with ischemic stroke at low-risk for cardiogenic embolism. Transeophageal echocardiography was performed to access: left atrium enlargement; communication or aneurysm of the interatrial septum; patent foramen ovale; spontaneous echo contrast or intracavitary thrombi; the presence of intraaortic atherosclerotic plaques or thrombi; significant valvar morphologic alteration or dysfunction; left ventricle enlargement, hypertrophy, or contractile abnormality. Transesophageal echocardiography altered clinical management, and we adopted anticoagulant therapy or another procedure apart from the use of acetylsalicylic acid. Transeophageal echocardiography detected at least one abnormality in 40 cases (58%). Clinical conduct was adjusted after the performance of transesophageal echocardiography in 11 patients (15.9%); anticoagulation was added in 10 cases and surgical correction in one patient. Transeophageal echocardiography was a very useful tool in the secondary prevention for stroke in patients at low risk for cardiogenic embolism.

Large middle cerebral artery infarctions and the hyperdense middle cerebral artery sign in patients with atrial fibrillation

Purpose: Strokes in patients with atrial fibrillation are often due to large middle cerebral artery (MCA) infarctions, caused by cardiogenic emboli. The purpose of this study was to characterise the large MCA infarctions and to describe the prevalence and prognostic value of the hyperdense middle cerebral artery sign (HMCAS) in patients with atrial fibrillation. Material and Methods: The patient material comprised all 449 patients included in a randomised clinical trial of low molecular-weight heparin versus aspirin in patients with acute ischaemic stroke and atrial fibrillation. Patients with Scandinavian Stroke Scale score &amp;lt;8 were excluded. CT was performed on admission and at day 7, and was evaluated blinded to clinical data. The CT findings on admission were related to functional outcome at 14 days and 3 months, and incidence of cerebral haemorrhage within 7 days. Results: Altogether 66/449 (15%) of the patients had large MCA infarctions. These patients had poorer clinical outcomes, and a higher frequency of haemorrhage on control CT within 7 days (15/59, 26% vs. 43/368, 12%). The HMCAS was found in 32/449 (7%) of the patients. It was significantly more frequent in patients with large MCA infarctions (17/66, 26% vs. 15/383, 4%), and was found most frequently within the first few hours following stroke onset. The HMCAS was associated with poor clinical outcomes and a higher frequency of cerebral haemorrhage, but these effects were partially explained by a preponderance of other risk factors in the HMCAS group. Conclusion: Large MCA infarction is a frequent finding in patients with atrial fibrillation. These patients have a high prevalence of the HMCAS, which is an early infarction sign and a marker of a poor prognosis.

LARGE MIDDLE CEREBRAL ARTERY INFARCTIONS AND THE HYPERDENSE MIDDLE CEREBRAL ARTERY SIGN IN PATIENTS WITH ATRIAL FIBRILLATION

Strokes in patients with atrial fibrillation are often due to large middle cerebral artery (MCA) infarctions, caused by cardiogenic emboli. The purpose of this study was to characterise the large MCA infarctions and to describe the prevalence and prognostic value of the hyperdense middle cerebral artery sign (HMCAS) in patients with atrial fibrillation. The patient material comprised all 449 patients included in a randomised clinical trial of low molecular-weight heparin versus aspirin in patients with acute ischaemic stroke and atrial fibrillation. Patients with Scandinavian Stroke Scale score <8 were excluded. CT was performed on admission and at day 7, and was evaluated blinded to clinical data. The CT findings on admission were related to functional outcome at 14 days and 3 months, and incidence of cerebral haemorrhage within 7 days. Altogether 66/449 (15%) of the patients had large MCA infarctions. These patients had poorer clinical outcomes, and a higher frequency of haemorrhage on control CT within 7 days (15/59, 26% vs. 43/368, 12%). The HMCAS was found in 32/449 (7%) of the patients. It was significantly more frequent in patients with large MCA infarctions (17/66, 26% vs. 15/383, 4%), and was found most frequently within the first few hours following stroke onset. The HMCAS was associated with poor clinical outcomes and a higher frequency of cerebral haemorrhage, but these effects were partially explained by a preponderance of other risk factors in the HMCAS group. Large MCA infarction is a frequent finding in patients with atrial fibrillation. These patients have a high prevalence of the HMCAS, which is an early infarction sign and a marker of a poor prognosis.

Appendix TOAST Abstraction Manual TOAST Medical Record Abstraction Manual

Appendix TOAST Abstraction Manual TOAST Medical Record Abstraction Manual

Cardiogenic embolism as the main cause of ischemic stroke in a city hospital: an interdisciplinary study.

It is essential to understand the pathogenesis of ischemic stroke to ensure rational acute therapy and secondary prevention. We wanted to know the distribution of pathogenesis in patients of a city hospital and the differences in risk factors, neurologic deficits, disability, and delay in clinical admittance. During a period of one year, 222 patients (mean age 76.6 years; 59% women) with complete acute ischemic stroke were admitted and underwent complete clinical and diagnostic procedures: CCT/MRI; Doppler- and color-coded duplex and transcranial sonography; echocardiography; use of the NINCDS stroke scale and the Oxford disability scale; study of risk factors, and exploration of delay in admittance. The following percentages of etiologies were evident: 31% cardiogenic embolism (60% with atrial fibrillation), 13% microangiopathy, 9% macroangiopathy, 11% cerebellar or brain stem infarction, 18% more than one cause and 18% no cause found. The patients with cardiogenic embolism showed significantly the highest scores on the stroke scale and the disability scale and had the shortest delay in admittance (57% were admitted within 3 hours). In a city hospital, cardiogenic embolism is the main cause of ischemic stroke. These patients suffer significantly the most severe neurologic deficits, dependence, and requirement of daily nursing care. These patients have the shortest delay in clinical admittance and the best chance of benefitting from acute therapy and early secondary prevention.

Distribution of artificially-produced microembolic signals into the cerebral circulation

According to clinical observations, cardiogenic embolism occurs more often in the anterior than in the posterior cerebral circulation. An ultrasound (US) contrast agent was used to artificially produce microembolic signals (MES) to imitate the intracranial distribution of systemic emboli. Systemic microemboli were simulated by IV administered US agent (Levovist® 300 mg/mL as bolus). A total of 20 patients were monitored by means of transcranial Doppler sonography (TCD), 3 min after the injection, with a 2-MHz transducer simultaneously at 50 mm (middle cerebral artery, MCA, on one side) and 90 mm (basilar artery, BA). Four 3-min recordings were done (two of the right MCA, two of the left MCA, with the BA, respectively). Three observers and an automatic detection system independently performed an off-line analysis. A total of 160 recordings were analyzed. The mean numbers of detected high-intensity transient signals (HITS) were 34.5 ± 28.2 in the right MCA (simultaneously registered HITS in the BA: 9.4 ± 16.8) and 39.1 ± 34.2 in the left MCA (simultaneously registered HITS in the BA: 12.2 ± 14.5). Only 21.4 to 23.7% of all HITS were recorded in the BA. Microembolic signals artificially produced by means of US contrast agent made it possible to mimic the physiologic distribution of small embolic particles. In future, these might help to investigate the distribution of systemic emboli in different vascular territories in various pathologic conditions of the cerebral blood flow. (E-mail: Saskia.M. Meves@ruhr-unibochum.de)

Atrial septal aneurysm as a cardioembolic source in adult patients with stroke and normal carotid arteries. A multicentre study.

Atrial septal aneurysm has been considered a potential source of cardiogenic embolism for many years. The present study evaluated the prevalence and characteristics of atrial septal aneurysm in a patient population with stroke and normal carotid arteries compared to a control population without stroke. A total of 606 patients were enrolled between November 1990 and December 1996. The study group included 245 patients who had experienced cerebral ischaemic attack but had normal carotid arteries. The control group included 316 age- and sex-matched patients undergoing transoesophageal echocardiography for indications other than a search for a cardiac source of embolism. The prevalence and morphological characteristics of atrial septal aneurysm were evaluated and compared. Results We reported a higher prevalence of atrial septal aneurysm in the group with cerebral ischaemia; 68 patients (27.7%) vs 36 patients (9.9%) from the control group; P<0.001. A patent foramen ovale was detected with contrast injection in 69.2% of the patients with atrial septal aneurysm. Atrial septal aneurysm predicted the presence of a patent foramen ovale (odds ratio of patent foramen ovale 4.2; 95% CI 1.03-9.8). Multivariate analysis showed that atrial septal aneurysm was an independent predictor of an embolic event. In the 95% of patients with atrial septal aneurysm and cerebral ischaemia aged less than 45 years, transoesophageal echocardiography did not detect a source of embolism other than an associated patent foramen ovale. The prevalence of atrial septal aneurysm in patients with cerebral ischaemia and normal carotid arteries was 27.7%, higher than the control group. Atrial septal aneurysm was frequently associated with patent foramen ovale. In patients less than 45 years old, atrial septal aneurysm was the only potential cardiac source of embolism detected with transoesophageal echocardiography.

Antithrombotic and Thrombolytic Therapy for Ischemic Stroke

Ischemicstroke is a syndrome of multiple etiologies and protean clinicalmanifestations. The optimal use of antithrombotic therapies for stroketreatment or prevention is guided by the specific pathogenesis (Fig 1,2) and clinical features. Patients who are at increased risk for ischemicstroke can be identified (Fig 3). Atherosclerosis of the arteries, large and small, that supply thebrain is the most common cause of ischemic stroke. Atherosclerosis ofthe proximal aorta is also a source of atherogenic brain emboli. Largeartery atherosclerotic infarction occurs when there is an impediment tonormal perfusion, usually caused by a severe arterial stenosis orocclusion due to atherosclerosis and coexisting thrombosis orartery-to-artery embolism. Microatheroma, lipohyalinosis, and otherocclusive diseases of the small penetrating brain arteries are the mostfrequent causes of small, subcortical “lacunar” infarcts. About20% of ischemic strokes are due to cardiogenic embolism, most commonlyfrom atrial fibrillation. A variety of other arterial occlusivedisorders may be the primary cause or variably contribute to strokepathogenesis. Overall, about 30% of ischemic strokes remaincryptogenic despite a reasonably thorough evaluation. Cerebralangiography done within a few hours of cryptogenic stroke often revealsocclusions of intracranial arteries. Most of these occlusions resolvewithin a few days, suggesting transient embolic or thromboticobstruction. Thus, the specific pathogenesis of stroke in individualpatients is sometimes difficult to elucidate, and determining theoptimal choice of antithrombotic therapy for prevention of strokeworsening or recurrence is challenging. Figure 2A classification of stroke by mechanism withestimates of the frequency of various categories of abnormalities.Approximately 30% of ischemic strokes are cryptogenic. View Large Image Figure Viewer Figure 3Annual risk of stroke or vascular death amongpatients in various high-risk subgroups. Adapted from Wilterdink and Easton. 160 Wilterdink JL Easton JD Vascular event rates in patients with atherosclerotic cerebrovascular disease. Arch Neurol. 1992; 49: 857-863 Crossref PubMed Google Scholar View Large Image Figure Viewer

Instability of anticoagulation intensity contributes to occurrence of ischemic stroke in patients with non-rheumatic atrial fibrillation.

The efficacy of anticoagulation in reducing the risk of cardiogenic embolism has been demonstrated in patients with atrial fibrillation (AF), but there are few prospective studies assessing the influence of anticoagulation stability on ischemic stroke in such patients. Accordingly, the present study investigated prospectively whether an instability of the anticoagulation intensity would affect the efficacy of the therapy in a total of 156 patients with non-rheumatic AF (NRAF) who received oral anticoagulation with warfarin. During a 2-year follow-up period, the annual event rate of ischemic stroke was 2.1%. In patients without a history of prior stroke, no ischemic stroke occurred at a higher international normalized ratio (INR> or =2.0). In contrast, patients who had had a prior stroke had no INR-dependent reduction of incidence. The coefficient of variation (CV) of measured INRs was significantly greater in patients with ischemic stroke than in those without. By multivariate analysis, only greater CV (> or =0.3) of INRs was an independent risk for ischemic stroke, although New York Heart Association functional class > or =II and treatment with diuretics were of borderline significance by univariate analysis. The present results suggest that stability of anticoagulation intensity is important to protect thromboembolic events in patients with NRAF.

Antithrombotic treatments in acute ischemic stroke.

Ischemic stroke results most commonly from cerebral arterial thrombosis. Antithrombotic agents can reduce the incidence of cerebral embolic events or the extent of tissue injury and neurological outcome. The antiplatelet agents aspirin, ticlopidine, and the combination of dipyridamole and aspirin are associated with a significant reduction in second focal cerebral ischemic events. Oral anticoagulants have a role to reduce the incidence of cardiogenic emboli in patients with mechanical cardiac valves or nonvalvular atrial fibrillation. Both antithrombotics are untested in the acute setting. The recombinant tissue plasminogen activator rt-PA has been shown to significantly increase the number of stroke patients with no or minimal deficit when treated within 3 hours of symptom onset. Additional studies of this and other plasminogen activators by both intravenous and intra-arterial delivery have highlighted limitations to this approach, but also support its role in acute intervention. The risk of intracerebral hemorrhage attends the use of all antithrombotic agents, most notably plasminogen activators. Strategies to decrease this risk are likely to add to beneficial outcome.

Integrated Backscatter Assessment of Left Atrial Spontaneous Echo Contrast in Chronic Nonvalvular Atrial Fibrillation: Relation with Clinical and Echocardiographic Parameters

Integrated backscatter (IB) provides the quantitative assessment of left atrial spontaneous echo contrast (SEC). The IB intensity of the left atrial cavity relative to the left ventricular cavity is related to atrial thrombus in patients with atrial fibrillation (AF) or sinus rhythm. However, little is known about the relation between the quantitative SEC value of the left atrial cavity and variables implying thromboembolism in nonvalvular AF. To examine this relation, we performed transesophageal echo-cardiography with IB analysis in 65 patients with chronic nonvalvular AF. The quantitative SEC value of the left atrial cavity was defined as the difference between atrial IB intensity and ventricular IB intensity (corrected IB intensity). The corrected IB intensity was correlated with the left atrial dimension (r = 0.25, P =.049), the left atrial appendage velocity (r = –0.41, P <.001), and the duration of AF (r = 0.23, P =.023). The corrected IB intensity was higher in patients who had a history of hypertension (3.2 ± 2.2 dB versus 2.0 ± 1.6 dB, P =.018), SEC (3.9 ± 1.9 dB versus 1.4 ± 1.1 dB, P =.002), and left atrial thrombus (4.5 ± 2.7 dB versus 2.2 ± 1.7 dB, P <.001) when compared with those who did not have these abnormalities. The corrected IB intensity was significantly lower in patients with significant mitral regurgitation than in those without it (1.1 ± 1.2 dB versus 2.7 ± 2.0 dB, P =.036). When the cutoff value of the corrected IB intensity was set at ≥2.0 dB, the sensitivity for left atrial thrombus was 78% and the specificity was 55%. In patients with chronic nonvalvular AF, the quantitative SEC value of the left atrial cavity depends on the duration of AF as well as the left atrial dimension and appendage velocity. Although IB may be capable of identifying patients with higher risk of cardiogenic embolism, a large-scale prospective study is needed to actually establish this. (J Am Soc Echocardiogr 2000;13:666-73.)

Lipoprotein(a), Other Lipoproteins and Hemostatic Profiles in Patients with Ischemic Stroke: The Relation to Cardiogenic Embolism

Lipoprotein and hemostatic profiles including coagulation inhibitors were determined in 136 patients with acute ischemic stroke. Based on clinical examination, cerebral computed tomography, Doppler ultrasonography of precerebral arteries and transthoracic echocardiography, the strokes were classified as cardioembolic (n = 38), non-cardioembolic (n = 92), and mixed cardioembolic/hypertensive (n = 6). Patients with cardioembolic stroke were older than patients with non-cardioembolic stroke. Lipoprotein(a) was higher in the cardioembolic than in the non-cardioembolic group. Lipoprotein(a) was not significantly correlated to the other lipid levels and may represent an independent lipid risk factor. The non-cardioembolic group had higher levels of total cholesterol, triglycerides, total cholesterol/high-density lipoprotein cholesterol ratio, low-density lipoprotein cholesterol, apolipoprotein A1, and apolipoprotein B. The cardioembolic group had higher concentrations of fibrinogen and D-dimer, and lower levels of antithrombin, protein C, protein S and heparin cofactor 2 than the non-cardioembolic group. The differences in the hemostatic profile are consistent with thrombosis due to activated coagulation being more involved in the pathogenesis of cardioembolic than of non-cardioembolic stroke. Lipoprotein(a) seems to be more associated with coagulation markers of thrombosis than with atherosclerosis, whereas the other lipids mainly seem to be risk factors for atherosclerosis.

Transient ischaemic attack in a young woman

A 35-year-old woman was admitted in March, 1997 because of sudden onset of right-sided weakness. Her medical history was unremarkable. Physical examination showed normal sinus rhythm, blood pressure 120/80 mm Hg, and a grade 2/6 systolic murmur over the precordium. The head, neck, lung, and abdomen were normal. On neurological examination, she was oriented and had upper motor neuron weakness grade 4/5 in the right upper and lower limb. Routine laboratory findings were normal. Computer tomographic scan of the brain, and transthoracic echocardiography and ultrasound of carotid arteries were normal. On the second hospital day, the patient’s power returned to normal and she was discharged taking aspirin 300 mg daily. She presented again 4 weeks later with multiple peripheral emboli of her right brachial and femoral arteries. The table shows results of laboratory tests. She underwent urgent embolectomy for the peripheral arterial occlusion, but developed bilateral cortical blindness caused by cerebral embolism. Transoesophageal echocardiography (TEE) showed a vegetation on the thickened aortic valves, which measured 0·7 cm by 1 cm. Culture of blood specimens and serological testing were negative. She was treated with intravenous antibiotics and heparin. Despite treatment with heparin, she developed multiple venous thromboses and subsequently died of massive pulmonary embolism two days later. Postmortem examination showed the presence of tumour in the right lower lobe of lung with multiple lymph nodes metastases. Multiple vegetations were found over the aortic, mitral, and tricuspid valves. Culture of vegetations was negative. History of the tumour showed poorly differentiated adenocarcinoma. Histology of the vegetations did not reveal any organism or malignant cells, which suggests the diagnosis of non-bacterial thrombotic endocarditis (NBTE). NBTE can complicate various malignant diseases, and is associated with an increase in morbidity and mortality as a result of systemic embolism. It is often not suspected until embolic events occur and is a rare antemortem diagnosis. The differential diagnosis of transient ischaemic attack in a young patient includes cardiogenic embolism due to atrial fibrillation, valvular heart disease, endocarditis and cardiac masses and tumour, and carotid artery stenosis. Rare causes are vasculitis, hypercoagulable status, primary antiphospholipid syndrome, CASE REPORT

Abstracts of Literature.

Abstracts of Literature.

Prediction of cerebral infarct sizes by cerebral blood flow SPECT performed in the early acute stage.

Cerebral infarct due to embolic stroke without recanalization was examined by cerebral blood flow (CBF) SPECT in the early acute stage, and the possibility of predicting the size it will reach in the later stages was evaluated. Twenty patients (67 +/- 13 years) were examined by CBF SPECT with 99mTc-ECD 4.5 +/- 3.1 hours after the onset of cardiogenic cerebral embolism. The ratio of the anteroposterior length of the cerebral hemisphere to that of the severe ischemic region, which was defined as an area of clear-cut severe reduction in CBF as observed by SPECT, was calculated. One week after the onset, the cerebral infarct was measured in the same manner by CT, and the relationship between the two measurements was evaluated. The CBF in the region of severe ischemia and the surrounding region was determined by the Patlak plot method, and the affected/non-affected (A/NA) ratio was calculated. In severe ischemic regions the CBF ranged from 1.7 ml/100 g/min to 20 ml/100 g/min (mean, 11 +/- 5 ml/100 g/min), whereas the A/NA ratio ranged from 4% to 45% (mean, 26 +/- 11%). On the other hand, the CBF in the surrounding regions ranged from 20 ml/100 g/min to 52 ml/100 g/min (mean, 34 +/- 8 ml/100 g/min) whereas the A/NA ratio ranged from 52% to 104% (mean, 77 +/- 11%). The coefficient of correlation between the infarct size predicted by SPECT and that measured by CT was r = 0.986, and the correlation equation was Y = 1.047X - 2.969. CBF SPECT performed in the early acute stage can be used to predict the size of cerebral infarct.

Posterior cerebral artery territory infarcts in the New England Medical Center Posterior Circulation Registry.

Infarcts in the territory of the posterior cerebral arteries (PCAs) are common. Although associated clinical symptoms and signs are known, the mechanisms of stroke and the anatomical distribution of PCA territory lesions caused by the various stroke mechanisms are less well defined. Published reports have selected only special subgroups of patients. We studied stroke mechanisms, infarct distribution, and clinical findings among 79 patients in the New England Medical Center Posterior Circulation Registry in whom brain imaging scans showed infarcts that involved 1 or more cortical territories of the PCA. Forty-eight patients (61%) had infarcts limited to the PCA territory (pure PCA), while 31 (39%) also had infarcts in other territories (PCA+). Infarcts were in the cortical territory of the PCA in 47 patients (59%) and were cortical and deep in 32 (41%). Infarcts that were cortical and deep were more common in PCA+ lesions. Stroke mechanisms were embolism of cardiac origin (32 [41%]), proximal arterial disease (25[32%]), cryptogenic embolism (8[10%]), intrinsic PCA disease (7[9%]), vasoconstriction (4[5%]), and coagulopathy (3[4%]). Patients with cardiogenic embolism and intrinsic PCA disease often had pure PCA territory infarcts, while patients with proximal arterial disease more often had PCA+ infarcts. Visual abnormalities were present in 66 patients (84%). Motor weakness, cognitive and behavioral abnormalities, and ataxia were found in 20 patients (25%); only 12 (15%) had sensory signs. The great majority of pure PCA and PCA+ territory infarcts are caused by cardiac or intra-arterial embolism. Intrinsic PCA disease, vasoconstriction, and coagulopathy are less common causes of infarction.

Atrial septal aneurysm: Is it a benign finding?

We report our clinical experience in a single centre with 7 cases of atrial septal aneurysm (ASA) diagnosed by transthoracic echocardiography (TTE) between 1989–1996. They did not present any clinical event compatible with cardiogenic embolism after a five years mean follow-up period. ASA is recognized as a potential source of cardiogenic embolism [2]based on some retrospective and selection biased studies.