Plaque rupture in the carotid artery is localized at the high shear stress region: a case report.

BACKGROUND AND PURPOSE: Cerebrovascular events are related to atherosclerotic disease in the carotid arteries and are frequently caused by rupture of a vulnerable plaque. These ruptures are often observed at the upstream region of the plaque, where the wall shear stress (WSS) is considered to be highest. High WSS is known for its influence on many processes affecting tissue regression. Until now, there have been no serial studies showing the relationship between plaque rupture and WSS. Summary of Case- We investigated a serial MRI data set of a 67-year-old woman with a plaque in the carotid artery at baseline and an ulcer at 10-month follow up. The lumen, plaque components (lipid/necrotic core, intraplaque hemorrhage), and ulcer were segmented and the lumen contours at baseline were used for WSS calculation. Correlation of the change in plaque composition with the WSS at baseline showed that the ulcer was generated exclusively at the high WSS location. CONCLUSIONS: In this serial MRI study, we found plaque ulceration at the high WSS location of a protruding plaque in the carotid artery. Our data suggest that high WSS influences plaque vulnerability and therefore may become a potential parameter for predicting future events.

Correlation between carotid intraplaque hemorrhage and clinical symptoms: systematic review of observational studies.

BACKGROUND AND PURPOSE: We sought to investigate the association between carotid intraplaque hemorrhage (IPH) and ipsilateral symptoms of cerebral ischemia. METHODS: A search was performed for clinical observational studies comparing the incidence of IPH between symptomatic and asymptomatic patients. Odds ratios (ORs) for IPH as a factor in the pathogenesis of neurologic events were calculated and combined by a meta-analysis. Interstudy heterogeneity, estimated effects, and methodologic quality of the studies were assessed. RESULTS: Thirty-one studies were included for analysis. The reported ORs varied widely. Overall, the incidence of IPH in the symptomatic groups was significantly higher than in the asymptomatic group. However, there was an apparent trend for heterogeneity (P<0.00001) between studies. The random-effects summary estimator of ORs was 2.25 (95% CI, 1.57 to 3.22; P<0.00001). To identify potential sources of heterogeneity, subgroup analyses were performed. The pooled ORs varied greatly by stratification. Major heterogeneity was found among studies with low quality, microscopic methods of examination, significant effects, small sizes, early publication, and unequal severity of carotid stenosis in both groups. Large, recent, macroscopic, or high-quality studies, as well as studies with equal degrees of stenosis, tended to yield insignificant associations. The methods in defining and evaluating hemorrhage were very heterogeneous. Characterizations of the age, size, number, and location of hemorrhages were poorly reported and highly variable. In addition, a lack of control of confounders and selection bias were frequently identified among studies. CONCLUSIONS: Statistical inferences have suggested a plausible role in the production of cerebral ischemia; however, reliable interpretation was strongly undermined by poor methodologic quality, substantial heterogeneity, and suspicious publication bias. To preciously estimate the underlying correlation, a well-designed study with uniformity in definition and evaluation for IPH might be warranted.

Frequent atrial premature beats predict paroxysmal atrial fibrillation in stroke patients: an opportunity for a new diagnostic strategy.

BACKGROUND AND PURPOSE: For patients having suffered ischemic stroke, the current diagnostic strategies often fail to detect atrial fibrillation as a potential cause of embolic events. The aim of the study was to identify paroxysmal atrial fibrillation in stroke patients. We hypothesized that patients with frequent atrial premature beats (APBs) recorded in 24-hour ECG will show more often atrial fibrillation when followed by repeated long-term ECG recordings than patients without or infrequent APBs. METHODS: 127 patients with acute ischemic stroke and without known AF were enrolled in a prospective study to detect paroxysmal AF. Patients were stratified according to the number of APBs recorded in a 24-hour ECG (> or =70 APBs versus <70 APBs). Subsequently, they all underwent serial 7-day event-recorder monitoring at 0, 3, and 6 months. RESULTS: Serial extended ECG monitoring identified AF in 26% of patients with frequent APBs but only in 6.5% when APBs were infrequent (P=0.0021). A multivariate analysis showed that the presence of frequent APBs in the initial 24-hour ECG was the only independent predictor of paroxysmal AF during follow-up (odds ratio 6.6, 95% confidence intervals 1.6 to 28.2, P=0.01). CONCLUSIONS: In patients with acute ischemic stroke, frequent APBs (> or = 70/24 hours) are a marker for individuals who are at greater risk to develop or have paroxysmal AF. For such patients, we propose a diagnostic workup with repeated prolonged ECG monitoring to diagnose paroxysmal AF.

Role of elevated alpha2-macroglobulin revisited: results of a case-control study in children with symptomatic thromboembolism.

OBJECTIVE: alpha(2)-Macroglobulin (alpha2MG) is a broad-spectrum protease inhibitor that is known to neutralize alpha-thrombin, plasmin, and activated protein C, which suggests that it has anticoagulant as well as procoagulant properties. The present study was conducted to evaluate the role of alpha2MG in children with venous thromboembolism [VTE: paradoxical embolism causing ischemic stroke (IS) or deep-vein thrombosis (DVT)]. METHODS: alpha2MG levels measured after acute VTE onset in white patients were compared with data obtained from age- and gender-matched healthy controls. In addition, to compare the rate of elevated alpha2MG and prothrombotic risk factors [factor V G1691A, prothrombin G20210A, raised lipoprotein (a)] between patients and controls and to evaluate the interaction between elevated alpha2MG levels and other thrombophilias, odds ratios (ORs) together with 95% confidence intervals (CIs) were estimated using a logistic regression model. The model was adjusted for age and fibrinogen. RESULTS: alpha2MG levels were significantly higher in patients than in controls (320/139-524 vs. 302/109-406; P = 0.005). In the group of patients (IS n = 103; DVT n = 92), the risk of symptomatic thromboembolism was significantly increased with elevated alpha2MG levels, with a gradual increase per mg dL(-1). In addition, when elevated alpha2MG levels > 90th percentile were compared with values below the cut-off, including established prothrombotic risk factors in the multivariate analysis, patients had a significantly increased OR/95% CI for fibrinogen-adjusted alpha2MG levels (IS, 5.9/1.9-18.3; DVT, 7.2/2.1-24.4). CONCLUSIONS: The procoagulant properties of elevated alpha2MG levels independently increase the odds of stroke and DVT in white children.

Cerebral protection during retrograde carotid artery stenting for proximal carotid artery stenosis: technical note.

Carotid artery stenting for carotid bifurcation stenosis usually uses the transfemoral approach. However, in patients with proximal common carotid artery (CCA) stenosis, the guiding catheter is difficult to introduce into the narrow origin of the CCA without risking cerebral embolization before activation of the protection device. A technique of cerebral protection by internal carotid artery (ICA) clamping with or without simultaneous external carotid artery (ECA) clamping was used to treat patients with proximal CCA stenosis by the retrograde direct carotid approach. The carotid bifurcation was surgically exposed and retrograde catheterization was performed to approach the stenosis. The ICA was clamped during angioplasty and stenting to avoid cerebral embolization. The ECA was clamped simultaneously if any extracranial-intracranial anastomosis was present. None of five patients treated with this technique experienced ischemic complications attributable to this technique.

Incidence of new brain lesions after carotid stenting with and without cerebral protection.

BACKGROUND AND PURPOSE: Diffusion-weighted imaging (DWI) may be a useful tool to evaluate the efficacy of cerebral protection devices in preventing thromboembolic complications during carotid angioplasty and stenting (CAS). The goals of this study were (1) to compare the frequency, number, and size of new DWI lesions after unprotected and protected CAS; and (2) to determine the clinical significance of these lesions. METHODS: DWI was performed immediately before and within 48 hours after unprotected or protected CAS. Clinical outcome measures were stroke and death within 30 days. RESULTS: The proportion of patients with any new ipsilateral DWI lesion (49% versus 67%; P<0.05) as well as the number of new ipsilateral DWI lesions (median=0; interquartile range [IQR]=0 to 3 versus median=1; IQR=0 to 4; P<0.05) were significantly lower after protected (n=139) than unprotected (n=67) CAS. The great majority of these lesions were asymptomatic and less than 10 mm in diameter. Although there were no significant differences in clinical outcome between patients treated and not treated with protection devices (7.5% versus 4.3%, not significant), the number of new DWI lesions was significantly higher in patients who developed a stroke (median=7.5; IQR=1.5 to 17) than in patients who did not (median=0; IQR=1 to 3.25; P<0.01). CONCLUSIONS: The use of cerebral protection devices significantly reduces the incidence of new DWI lesions after CAS of which the majority are asymptomatic and less than 10 mm in diameter. The frequent occurrence of these lesions and their close correlation with the clinical outcome indicates that DWI could become a sensitive surrogate end point in future randomized trials of unprotected versus protected CAS.

Frequency of atrial septal aneurysms in patients with cerebral ischemic events.

BACKGROUND: Atrial septal aneurysm (ASA) is a putative risk factor for cardioembolism. However, the frequency of ASA in the general population has not been adequately determined. Therefore, the frequency in patients with cerebral ischemic events, compared with the frequency in the general population, is poorly defined. We sought to determine the frequency of ASA in the general population and to compare the frequency of ASA in patients with cerebral ischemic events with the frequency in the general population. METHODS AND RESULTS: The frequency of ASA in the population was determined in 363 subjects, a sample of the participants in the Stroke Prevention: Assessment of Risk in a Community study (control subjects), and was compared with the frequency in 355 age- and sex-matched patients undergoing transesophageal echocardiography in search of a cardiac source of embolism after a focal cerebral ischemic event. The proportion with ASA was 7.9% in patients versus 2.2% in control subjects (P=0.002; odds ratio of ASA, 3.65; 95% CI, 1.64 to 8.13, in patients versus control subjects). Patent foramen ovale (PFO) was detected with contrast injections in 56% of subjects with ASA. The presence of ASA predicted the presence of PFO (odds ratio of PFO, 4.57; 95% CI, 2.18 to 9.57, in subjects with versus those without ASA). In 86% of subjects with ASA and cerebral ischemia, transesophageal echocardiography did not detect an alternative source of cardioembolism other than an associated PFO. CONCLUSIONS: The prevalence of ASA based on this population-based study is 2.2%. The frequency of ASA is relatively higher in patients evaluated with transesophageal echocardiography after a cerebral ischemic event. ASA is frequently associated with PFO, suggesting paradoxical embolism as a mechanism of cardioembolism. In patients with cerebral ischemia and ASA, ASA (with or without PFO) commonly is the only potential cardioembolic source detected with transesophageal echocardiography.

Atrial fibrillation activates platelets and coagulation in a time-dependent manner: a study in patients with paroxysmal atrial fibrillation.

OBJECTIVES: To determine whether atrial fibrillation (AF) alone affects the fibrinocoagulation system, we examined the relation between fibrinocoagulation activity and duration of AF in patients with paroxysmal AF (PAF). BACKGROUND: Patients with chronic AF are at higher risk for stroke and a hypercoagulative state. It is not clear whether this hypercoagulative state is attributable to AF alone or to the underlying disease. There are no reports on the fibrinocoagulation properties in PAF. METHODS: Fibrinocoagulation variables in 21 patients with PAF were measured during AF and 7 days after recovery of sinus rhythm. There were positive correlations between the duration of AF and beta-thromboglobulin, platelet factor 4, thrombin-antithrombin III complex and fibrinogen. These variables increased significantly 12 h after the occurrence of PAF; thus, patients were classified into two groups according to the duration of PAF: PAF-I group (< 12 h, n = 10), PAF-II group (> or = 12 h, n = 11). Nine age-matched, healthy subjects formed the control group. RESULTS: Levels of beta-thromboglobulin and platelet factor 4 were significantly higher (p < 0.001) by two-way repeated measures analysis of variance (ANOVA), and thrombin-antithrombin III complex and fibrinogen levels tended to be but were not significantly higher (p = 0.06, ANOVA), in the PAF-II group than in the PAF-I group. There were no significant differences between groups in activated partial thromboplastin time, D-dimer or plasmin inhibitor complex. CONCLUSIONS: These results indicate that AF itself enhances platelet aggregation and coagulation, which are influenced by the duration of AF. The acceleration of platelet activity and coagulability occurred 12 h after the occurrence of AF.

Aortic and mitral valve incompetence: long-term follow-up (10 to 19 years) of patients treated with the Starr-Edwards prosthesis.

The long-term course (mean 15 years) of 336 patients with valvular incompetence who underwent Starr-Edwards ball valve implantation between 1962 and 1971 was reviewed. Eighteen patients (10%) with aortic valve replacement and 24 (16%) with mitral valve replacement died early postoperatively. Mortality remained high (31%) in the first 3 years after aortic valve replacement; it was highest (13%) in the first year after mitral valve replacement and then approached the normal rate. The most common mode of death was sudden death after aortic and cardiac failure after mitral valve replacement. At follow-up, 76% of survivors had improved symptomatically. Three instances of primary valve malfunction occurred. The probability of freedom from thromboembolism at 15 years postoperatively was 56% for aortic valve replacement and 52% for mitral valve replacement. The Starr-Edwards valve prosthesis is durable over prolonged follow-up period, but thromboembolism remains a persistent problem. Survival may be normal for patients surviving the early postoperative years.

Improved morphologic characterization of atrial septal aneurysm by transesophageal echocardiography: relation to cerebrovascular events.

Transthoracic and transesophageal echocardiography was performed in 23 consecutive adult patients with an atrial septal aneurysm. In three patients with a cerebrovascular event the diagnosis was established by the transesophageal approach only. Interatrial shunting on transthoracic imaging with use of echocardiographic contrast imaging or Doppler color mapping, or both, was detected in 7 (41%) of 17 patients. On performing contrast imaging in combination with color flow mapping during transesophageal echocardiography, positive shunting was demonstrated in 15 (83%) of 18 patients. Echocardiographic identification of multiple fenestrations (n = 4) and thrombus within the aneurysm (n = 2) could be achieved for the first time by transesophageal ultrasound application. Cerebrovascular events occurred in 12 (52%) of 23 patients and were regarded as being definitely thromboembolic in 10 (43%); 8 (67%) of the 12 patients had repeated cerebral events. Except for mitral valve prolapse in one patient, no other potential cardiac source of embolism could be identified despite the use of transesophageal echocardiography. A thickening of the aneurysmal membrane greater than or equal to 5 mm was found in 9 (75%) of 12 patients with versus 3 (27%) of 11 patients without a cerebrovascular event (p less than 0.05); this proved to be the only significant difference between the two patient groups. The mechanism of embolization may be both primary thrombus formation within the aneurysm and paradoxic embolization through an interatrial communication as demonstrated by the findings in two patients. It is concluded that atrial septal aneurysm is a cardiac abnormality with thromboembolic potential. In patients with this lesion and a history of an embolic event, long-term anticoagulant therapy is indicated.

Transesophageal echocardiographic demonstration of distinct mechanisms for right to left shunting across a patent foramen ovale in the absence of pulmonary hypertension.

The optimal visualization of the atrial septum and fossa ovalis by transesophageal echocardiography was utilized to demonstrate saline contrast transit across the atrial septum and to relate it to the motion of the flap valve (septum primum) of the fossa ovalis. In three cases, three distinct mechanisms of right to left interatrial shunting in the absence of right ventricular systolic hypertension were identified: 1) transient spontaneous reversal of the left to right atrial pressure differential with each cardiac cycle; 2) sustained elevation of right atrial pressure above left atrial pressure induced by respiratory maneuvers; and 3) aberrant flow redirection across the foramen ovale due to a large right atrial mass. Any of these three mechanisms may be operative during paradoxic embolism in the absence of elevation of right ventricular pressures.

The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events.

OBJECTIVES: The impact of infection-associated antiphospholipid antibodies (APA) on endothelial cell activation, blood coagulation and fibrinolysis was evaluated in patients with infective endocarditis with and without major embolic events. BACKGROUND: An embolic event is a common and severe complication of infective endocarditis. Despite the fact that APAs are known to be associated with infectious diseases, their pathogenic role in infective endocarditis has not been clearly defined. METHODS: The relationship among the occurrence of major embolic events, echocardiographic vegetation size, endothelial cell activation, thrombin generation, fibrinolysis and APA was examined in 91 patients with definite infective endocarditis, including 26 patients with embolic events and 65 control subjects without embolic events. RESULTS: Overall, 14.3% of patients exhibited elevated APA levels. Embolic events occurred more frequently in patients with elevated levels of APA than in patients without (61.5% vs. 23.1%; p = 0.008). Patients with elevated levels of APA showed higher levels of prothrombin-fragment F1 +2 (p = 0.005), plasminogen-activator inhibitor 1 (p = 0.0002), von Willebrand factor (p = 0.002) and lower levels of activated protein C (p = 0.001) than patients with normal levels of APA. Thrombin generation and endothelial cell activation were both positively correlated with levels of APA. The occurrence of elevated APA levels was frequently associated with structural valve abnormalities (p = 0.01) and vegetations >1.3 cm (p = 0.002). CONCLUSIONS: Infection-associated elevated APA levels in patients with infective endocarditis are related to endothelial cell activation, thrombin generation and impairment of fibrinolysis. This may contribute to the increased risk for major embolic events in these patients.

Left atrial "stunning" following radiofrequency catheter ablation of chronic atrial flutter.

OBJECTIVES: This study examined the effect of radiofrequency ablation (RFA) on left atrial (LA) and left atrial appendage (LAA) function in humans with chronic atrial flutter (AFL). BACKGROUND: Atrial stunning and the development of spontaneous echocardiographic contrast (SEC) is a consequence of electrical cardioversion of AFL to sinus rhythm. This phenomenon has been termed "stunning" and is associated with thrombus formation and embolic stroke. Radiofrequency ablation is now considered to be definitive treatment for chronic AFL, but whether this procedure is complicated by LA stunning is unknown. METHODS: Fifteen patients with chronic AFL undergoing curative RFA underwent transesophageal echocardiography to evaluate LA and LAA function and SEC before and immediately, 30 minutes and 3 weeks after RFA. To control for possible direct effects of RFA on atrial function, seven patients undergoing RFA for paroxysmal AFL were also studied. In this group, RF energy was delivered in sinus rhythm and echocardiographic parameters were assessed before and immediately and 30 minutes following RFA. RESULTS: Chronic AFL: Mean arrhythmia duration was 17.2 +/- 13.3 months. Twelve patients (80%) developed SEC following RF energy application and reversion to sinus rhythm. LAA velocities decreased significantly from 54.0 +/- 14.2 cm/s in AFL to 18.0 +/- 7.1 cm/s in sinus rhythm after arrhythmia termination (p < 0.01). These changes persisted for 30 minutes. Following 3 weeks of sustained sinus rhythm, significant improvements in LAA velocities (68.9 +/- 23.6 vs. 18.0 +/- 7.1 cm/s, p < 0.01) and mitral A-wave velocities (49.8 +/- 10.3 vs. 13.4 +/- 11.2 cm/s, p < 0.01) were evident and SEC had resolved in all patients. Paroxysmal AFL: Radiofrequency energy delivered in sinus rhythm had no significant effect on any of the above indexes of LA or LAA function and no patient developed SEC following RFA. CONCLUSIONS: Radiofrequency ablation of chronic AFL is associated with significant LA stunning and the development of SEC. Left atrial stunning is not secondary to the RF energy application itself. Sustained sinus rhythm for 3 weeks leads to resolution of these acute phenomena. Left atrial stunning occurs in the absence of direct current shock or antiarrhythmic drugs, suggesting that its mechanism may be a function of the preceding arrhythmia rather than the mode of reversion.

Comparison of transesophageal echocardiographic identification of embolic risk markers in patients with lone versus non-lone atrial fibrillation.

Although transesophageal echocardiographically derived parameters, notably spontaneous echocardiographic contrast (SEC) in the left atrium or left atrial appendage (LAA), are known predictors of embolism in atrial fibrillation, their value is less well known in patients who have lone atrial fibrillation (LAF). This study describes transesophageal echocardiographic findings and identifies clinical predictors of SEC in the left atrium or LAA in a cohort of patients who had LAF. Eighty-two patients who had LAF and 289 patients who had non-LAF and underwent transesophageal echocardiography were enrolled from July 1998 to March 2002. LAA abnormality was defined as the presence of an LAA area >5 cm(2), emptying or filling LAA velocities <25 cm/s, or the presence of SEC or thrombus in the left atrium or LAA; LAA abnormalities were significantly less frequent in patients who had LAF than in those who had non-LAF. SEC in the left atrium or LAA was significantly less frequent in patients who had LAF than in those who had non-LAF (29.3% vs 49.8%, respectively, p <0.001). In patients who had LAF, SEC in the left atrium or LAA was significantly (p <0.05) less frequent in patients who were 60 years old (39.5%) and in patients who had paroxysmal LAF (5.9%) than in those who had persistent LAF (45.8%). On multivariate analysis, age and persistent LAF were the only clinical variables independently associated with SEC. Thus, transesophageal echocardiography detects thromboembolism risk markers in patients who have LAF. These abnormalities are less frequent in patients who have LAF than in those who are at low risk and have non-LAF; however, in patients who have LAF, older age and persistent atrial fibrillation are associated with these risk markers.

Interatrial block as a predictor of embolic stroke.

Interatrial block (IAB), defined as a prolonged (>/=110 ms) P wave, is remarkably prevalent in general hospital populations and is associated with an enlarged, poorly contractile left atrium. The investigators sought to determine whether there is an increased incidence of IAB in patients with embolic strokes. Patients' medical records were reviewed for evidence of embolic cerebrovascular events and IAB. One hundred four patients were identified. In 61 patients in normal sinus rhythm, 49 (80%) had IAB. This was almost twice the prevalence of 2 previous studies (41% and 47%). Therefore, IAB may represent a new risk factor for stroke.

Long-term effects of sequential cortical infarcts on scar size, brain volume and cognitive function.

Focal ischemia induces long-term pathophysiological consequences in widespread brain areas. Here we analyzed long-term effects of sequential cortical lesions on brain volume and cognitive function. Rats received either single photothrombotic lesions in the forelimb sensorimotor cortex (SL) or two lesions in sequence either immediately (DL0), 2 days (DL2), 7 days (DL7), or 10 days (DL10) after the first surgery in the homotopic contralateral area. Infarct and global brain volume were measured 7 days (SL and DL2 groups) and one month (all groups) after the last period of ischemia. In the weeks following a stroke, the single lesion shrank considerably. This shrinkage was accentuated by a further lesion received either earlier or later. Thirty-one days after obtaining the second lesion, the lesion scars on both sides had a mean volume of 5.8 +/- 2.3 mm3 in DL2 as compared to 8.5 +/- 3.5 mm3 in SL-animals. In addition, there was a super-additive loss of residual brain volume by 2.2-8.0% in each hemisphere in animals with sequential lesions. In the watermaze, this loss of brain volume corresponded to a slight but significant impairment in performance. The present study revealed a complex interaction of lesions in animals with sequential strokes associated with global reduction of brain volume and cognitive impairment indicating degenerative processes beyond the lesions itself.

Atrial fibrillation. Thromboembolic risk and indications for anticoagulation.

The risk of embolic stroke in patients with atrial fibrillation is largely related to the underlying disorders responsible for the arrhythmia. Atrial fibrillation associated with rheumatic mitral valve disease has the highest stroke risk (about 17 times greater than unaffected controls), but even with nonvalvular heart disease, the risk is increased fivefold. The stroke risk is greater with chronic than with paroxysmal atrial fibrillation, is highest in the year after onset of the arrhythmia, and is lower in younger patients with idiopathic ("lone") atrial fibrillation. Major bleeding episodes, the most important risk of anticoagulation, occur in about 5% to 10% of patients. The decision to anticoagulate a patient with atrial fibrillation depends on the cause of the arrhythmia, especially any associated cardiovascular disease, and the individual's risk from anticoagulation. Growing evidence supports the effectiveness of anticoagulation of most patients with nonvalvular, as well as valvular, cardiac disease for the prevention of both primary and recurrent strokes.

Cerebral embolization resulting from esophageal-atrial fistula.

A rare but catastrophic complication of nontraumatic esophageal perforation is the formation of an esophageal-left atrial fistula. Although surgical correction of this condition should be possible, failure to recognize it antemortem has thus far prevented such intervention. A woman with long-standing severe esophagitis, was admitted with hematemesis and acute neurologic abnormalities that progressed to coma and death. A similar picture of chronic esophagitis terminating in uppergastrointestinal-tract bleeding accompanied by neurologic signs was seen in the three previously reported cases as well. Recognition of this symptom complex should permit future cases to be diagnosed clinically, and, it is hoped, corrected.

Nonseptic cerebral emboli of cardiac origin.

There is considerable debate regarding immediate anticoagulation with heparin sodium for patients suspected of having acute cerebral embolism from a cardiac source. We studied 60 consecutive hospitalized patients suspected of having a nonseptic cardiogenic cerebral embolism who, with one exception, were treated with immediate full-dose anticoagulation. None of the patients had progression of their neurologic deficits secondary to intracranial hemorrhage or recurrent embolism, and there were no deaths secondary to anticoagulant therapy. One patient had punctate hemorrhages in the area of infarction, but remained clinically stable. In light of our experience and a review of the literature, we conclude that immediate anticoagulation is judiciously safe in selected patients after nonseptic embolic stroke of cardiac origin, provided early cranial computed tomography fails to demonstrate hemorrhagic infarction.

Hemophilus endocarditis. Two patients with complications.

Two cases of Hemophilus endocarditis were diagnosed in our hospital during a six-month period. Although both patients were in good health until the onset of their endocarditis, both had brain emboli and required emergency heart-valve surgery. Falsely low incidences of this disease have been reported, since Hemophilus sp are difficult to isolate. Additionally, these organisms are consistently associated with large vegetations and have a greater than 50% incidence of embolization. It is this higher incidence of embolization that leads us to conclude that prophylactic surgery should be considered in selected patients.