Prevalence of stroke in Argentina: A door-to-door population-based study (EstEPA).

BACKGROUND: Stroke burden is highest and is still rising in low- and middle-income countries. Epidemiologic stroke data are lacking in many of these countries. Stroke prevalence in Argentina has been unexplored for almost three decades. AIM: This population-based study aims to determine prevalence of stroke in a representative sample of the Argentinean population. METHODS: We performed a door-to-door survey of randomly selected households in a city of 18,650 inhabitants. A structured questionnaire screening for potential stroke cases was used. All subjects screened positive were then evaluated by stroke neurologists for final adjudication. Data about stroke subtypes, neurological status, vascular risk factors, medications, and diagnostic tests were also collected. RESULTS: Among 2156 surveys, 294 were screened positive for a possible stroke. After neurological evaluation, there were 41 confirmed cases. The adjusted stroke prevalence was 1,974/100,000 inhabitants older than 40 years, and it was higher in men than in women (26.3‰ vs 13.2‰, p<0.01). Prevalence of ischemic stroke, intracranial hemorrhage, and transient ischemic attack were 15.8‰, 2.93‰, and 2.93‰, respectively. The most prevalent vascular risk factors in stroke survivors were hypertension, obstructive sleep apnea, and dyslipidemia. CONCLUSION: Approximately 2 in every 100 subjects older than 40 years in this population are stroke survivors. Stroke prevalence in Argentina has remained stable over the last 30 years; it is higher than in most Latin American countries and similar to western populations.

Fall in the Proportion of Atherothrombotic Strokes During the Last Decade.

OBJECTIVE: To determine the proportion of subtypes of ischemic strokes, vascular risk factors and treatment prior to stroke between 1997 and 2018 in a single institution in Argentina. METHODS: Demographics, risk factors, medications and TOAST subtypes were assessed and compared in ischemic stroke patients admitted during two periods of time, 1997-2007 (P1) and 2008-2018 (P2). RESULTS: There were 2747 patients (64% men, aged 67 ±15 years), 920 subjects in P1 and 1827 in P2. Age and gender distribution did not change over time. Proportion of large artery atherothrombotic strokes decreased from 29% in P1 to 14% in P2 (p <0.0001) and small vessel strokes from 15% to 11% (p <0.05). Cardioembolic and undetermined strokes increased from 17 to 25% (p <0.0001) and from 30% to 41% (p <0.0001), respectively. There were no changes in stroke of other etiologies (9% in both periods). Detection of atrial fibrillation increased from 14% to 19% (p<0.001). Use of medications prior to stroke increased for aspirin from 27% to 45% (p <0.0001), for antihypertensive drugs from 26% to 62% (p <0.0001), for statins from 14% to 42% (p<0.0001) and for anticoagulants from 4% to 9% (p<0.0001). CONCLUSIONS: The proportion of strokes associated to large and small vessel atherosclerosis is declining in our population with an increase in the proportion of cardioembolic and undetermined strokes. Better management of risk factors and higher prevalence and/or better screening for atrial fibrillation could explain, at least in part, these findings.

Clinical and imaging features distinguishing Susac syndrome from primary angiitis of the central nervous system.

INTRODUCTION: To assess clinical and/or imaging features useful to distinguish between Susac syndrome (SuS) and primary angiitis of central nervous system (PACNS). METHODS: Multicenter retrospective analysis of two cohorts of Argentine patients diagnosed with SuS and PACNS. RESULTS: 13 patients diagnosed with SuS (6 women and 7 men, mean age 35 ±â€¯10 years) and 15 with PACNS (10 women and 5 men, mean age 44 ±â€¯18 years) were analyzed. Cognitive impairment (11 out of 13 patients vs. 5 out of 15, p = .006), ataxia (7 out of 13 vs. 2 out of 15, p = .042) and auditory disturbances (7 out of 13 vs. 0 out of 15, p = .003) were more frequent in SuS patients; whereas seizures were more frequent in PACNS patients (8 out of 15 vs. 1 out of 13, p = .035). On MRI, corpus callosum (CC) involvement was observed more often in SuS, with abnormalities in CC genu, in 13 out of 13 SuS patients vs. only 2 out of 15 PACNS patients (p < .001); in CC body these were present in 13 out of 13 SuS patients vs. 1 out of 15 PACNS patients, (p < .001); and in CC splenium in 12 out of 13 Sus patients vs. 1 of 15 PACNS, p < .001). Cortical lesions were more frequent in PACNS patients (10 out of 15 vs. 3 out of 13 SuS patients, p = .02), as were hemorrhages (5 out of 15 vs. 0 out of 13 SuS, p = .04) and multiple basal ganglia infarcts (7 out of 15 vs. 1 out of 13 Sus, p = .037). CONCLUSION: Specific clinical and/or MRI findings may help distinguish SuS from PACNS with potential therapeutic implications.

Strategies to improve recovery in acute ischemic stroke patients: Iberoamerican Stroke Group Consensus.

Stroke is not only a leading cause of death worldwide but also a main cause of disability. In developing countries, its burden is increasing as a consequence of a higher life expectancy. Whereas stroke mortality has decreased in developed countries, in Latin America, stroke mortality rates continue to rise as well as its socioeconomic dramatic consequences. Therefore, it is necessary to implement stroke care and surveillance programs to better describe the epidemiology of stroke in these countries in order to improve therapeutic strategies. Advances in the understanding of the pathogenic processes of brain ischemia have resulted in development of effective therapies during the acute phase. These include reperfusion therapies (both intravenous thrombolysis and interventional endovascular approaches) and treatment in stroke units that, through application of management protocols directed to maintain homeostasis and avoid complications, helps to exert effective brain protection that decreases further cerebral damage. Some drugs may enhance protection, and besides, there is increasing knowledge about brain plasticity and repair mechanisms that take place for longer periods beyond the acute phase. These mechanisms are responsible for recovery in certain patients and are the focus of basic and clinical research at present. This paper discusses recovery strategies that have demonstrated clinical effect, or that are promising and need further study. This rapidly evolving field needs to be carefully and critically evaluated so that investment in patient care is grounded on well-proven strategies.

[Antiphospholipid antibodies in patients with vestibular manifestations. A study of 16 cases]. / Anticuerpos antifosfolipídicos en pacientes con manifestaciones vestibulares. Un estudio de 16 casos.

INTRODUCTION: Antiphospholipid antibodies lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) play a role in promoting arterial and venous thrombosis in several vascular territories. Acute vestibular syndromes are a common complaint in general and neurology practice. Approximately 9% of cases are due to central nervous system vestibular areas lesions, often associated with vascular disorders. OBJECTIVE: Define the potential relationship between these antibodies and central or peripheral vestibular failure. PATIENTS AND METHODS: We report the presence of antiphospholipid antibodies in 16 patients with central vestibular symptoms. All patients were seen in the Neuro otology and Vascular Neurology clinics at the Institute for Neurological Research in Buenos Aires. Magnetic resonance imaging (MRI) and ancillary neuro otologic tests were used to determine the etiology of vestibular manifestations. Determinations of LA and aCL were done using standard criteria. RESULTS: We evaluated 16 patients (13 women and 3 men), aged 44 4 years (21 65). Thirteen patients did not have stroke risk factors. MRI lesions were found in 11 subjects (1 cerebellar infarct, 3 pontine ischemic changes, and 9 white matter abnormalities). All patients had signs consistent with dysfunction of vestibulo cerebellar structures or the vestibular nuclei. All patients had positive LA and 4 of them had also elevated aCL. CONCLUSION: Our findings suggest a potential association between the presence of a prothrombotic state and central vestibular dysfunction of vascular etiology. To the best of our knowledge, this is the first report of such an association in the absence of clinically evident autoimmune disease.

Infection and risk of ischemic stroke: differences among stroke subtypes.

BACKGROUND AND PURPOSE: Although prior studies have demonstrated that 25% to 35% of stroke patients have had a recent infection, the role of infection as a risk factor remains unclear. Our aim was to characterize the effect of infectious/inflammatory syndromes on stroke risk. METHODS: Case-control and crossover analyses of 233 cases and 363 controls aged 21 to 89 years were performed. Cases were patients hospitalized with a first ischemic stroke at a Los Angeles, California, medical center. Controls were outpatients in the hypertension, diabetes, and general medical clinics. All subjects were administered a neurological examination, an infection/inflammation (I/I) examination, and an interview to elicit recent I/I history at baseline (within several days of stroke onset) and again approximately 2 months later. Three physicians classified subjects by the presence or absence of I/I within 1 month of the index dates, based on findings of the I/I examination, the interview report, and laboratory results. RESULTS: Infections, either total or specific, were not found more frequently in cases than controls. However, patients with a recent respiratory tract infection suffered more often from large-vessel atherothromboembolic or cardioembolic stroke than did patients without infection (48% vs 24%, P=0.07). The age- and sex-adjusted relative risk estimate for these subtypes was 1.75 (95% CI, 0.86 to 3.55). The risk was notably high for those without stroke risk factors: 4.15 (95% CI, 1.22 to 14.1) for normotensives, 2.71 (95% CI, 1.04 to 7.06) for nondiabetics, and 1.74 (95% CI, 0.74 to 4.07) for nonsmokers. Patients with a recent respiratory infection also had a more severe neurological deficit on admission than those without infection (P=0.05). CONCLUSIONS: Our results suggest that respiratory tract infection may act as a trigger and increase the risk of large-vessel and/or cardioembolic ischemic stroke, especially in those without vascular risk factors.

[Neuroprotection in acute ischemic stroke. Practicability of guidelines for treatment]. / Neuroprotección en el ictus isquémico agudo. Factibilidad de un protocolo terapéutico.

INTRODUCTION: Fibrinolytic agents are effective in the treatment of acute ischemic stroke. However, logistic and clinical factors limit their use. Neuroprotective drugs pose less risks and can be used even before performance of computed tomography of the brain as they are not detrimental in hemorrhagic stroke. These aspects, in theory, will allow the use of neuroprotective drugs in larger number of patients. OBJECTIVE: To evaluate the feasibility of a neuroprotection protocol and the potential usefulness of citicoline in acute ischemic stroke. PATIENTS AND METHODS: Thirty seven patients admitted with a clinical diagnosis of acute ischemic stroke (later confirmed with computed tomography) received, within 12 hours of onset of symptoms, citicoline 500 mg intravenously in a single bolus daily for 7 days. Neurological outcome in this group was compared with a group of 37 patients admitted during the 6 month period before the initiation of the trial and not treated with citicoline. Groups were matched by National Institute of Health Stroke Scale (NIHSS) on admission. RESULTS: Patients treated with citicoline (aged 69+/-14 years) improved on their NIHSS from admission (5.7+/-4.2) to discharge (4.7+/-4.5), p= 0.015. The control group (aged 60+/-17 years) did not change between admission (5.7+/-4.3) and discharge (5.2+/-3.5), ns. Patients treated within 6 hours of admission (n= 12) had more substantial improvement, from 5.4+/-2.3 on admission to 3.9+/-2.9 at discharge, p= 0.008. There were no differences in vascular risk factor profile between the groups. Citicoline was well tolerated in every subject. CONCLUSIONS: A protocol of acute stroke management using neuroprotective agents presents clear logistic advantages allowing the inclusion of larger number of patients. Citicoline appears as a safe and potentially effective option.

Detection of Helicobacter pylori in human carotid atherosclerotic plaques.

BACKGROUND AND PURPOSE: Several lines of evidence point toward a relationship between infection and atherosclerotic vascular disease. Thus, infection and inflammation often precede ischemic neurological events. Transient alterations in coagulation and direct arterial invasion by certain microorganisms have been reported. Helicobacter pylori infection is the major cause of peptic ulcer disease and appears to be a risk factor for ischemic cerebrovascular disease. However, in contrast to other chronic infectious agents, H pylori has not been consistently isolated from atherosclerotic lesions. METHODS: We investigated the presence of H pylori in 38 atherosclerotic plaques obtained at carotid endarterectomy by using morphological and immunohistochemical techniques and a highly sensitive polymerase chain reaction method. We performed immunohistochemical detection of intercellular adhesion molecule-1, a marker related to inflammatory cell response. We also examined 7 carotid arteries obtained at autopsy from subjects without carotid atherosclerosis. RESULTS: H pylori DNA was found in 20 of 38 atherosclerotic plaques. Ten of the H pylori DNA-positive plaques also showed morphological and immunohistochemical evidence of H pylori infection. None of 7 normal carotid arteries was positive for H pylori. Intercellular adhesion molecule-1 was expressed in 75% of H pylori-positive plaques and in 22% of H pylori-negative plaques. The presence of the microorganism was associated with male sex but was independent of age, vascular risk factor profile, and prior neurological symptoms. CONCLUSIONS: H pylori is present in a substantial number of carotid atherosclerotic lesions and is associated with features of inflammatory cell response. This study provides additional evidence of the relationship between H pylori infection and atherosclerotic disease.

[The treatment of cerebrovascular disorders with anticoagulants and platelet aggregation inhibitors]. / Tratamiento de la enfermedad cerebrovascular con anticoagulantes y antiagregantes plaquetarios.

INTRODUCTION: The use of anticoagulants and platelet anti-aggregants is one of the basic features of the management of patients with cerebrovascular disease. DEVELOPMENT: The indications for the use of these agents have evolved from initial empirical use based on anecdotic evidence to current recommendations following multi-centre trials. Aspirin, ticlopidine, clopidogrel and warfarin are drugs of choice for secondary prevention of ischemic stroke (IS). Anticoagulants are used more in patients with IS of cardio-embolic origin. The use of anti-aggregants/anticoagulation in acute IS has not been shown to be clearly effective and its use is limited to particular cases in which fibrinolytic treatment cannot be used. For satisfactory use of these drugs it is essential to correctly identify the type of IS and its progress over time. This article reviews the criteria established for the use of such treatment and describes the developing areas of multi-centre clinical trials.

Precipitants of brain infarction. Roles of preceding infection/inflammation and recent psychological stress.

BACKGROUND AND PURPOSE: Antecedent febrile infection and psychological stress are described as predisposing risk factors for brain infarction. We examined the temporal relationship between preceding infection/inflammation and stroke onset as well as the role of recent psychological stress as a potential precipitant for brain infarction. METHODS: In this case-control study, a standardized evaluation including a signs/symptoms-based questionnaire was used to characterize the prevalence and timing of recent prior (< 1 month) infectious and inflammatory syndromes in 37 adults with acute brain infarction, 47 community control subjects, and 34 hospitalized nonstroke neurological patient controls. Recent psychological stress was measured with scales of stressful life events and negative affect. RESULTS: The prevalence of infection/inflammation was significantly higher in the stroke group only within the preceding 1 week compared with either community control subjects (13/37 versus 6/47, P < .02) or hospitalized neurological patient controls (3/34, P < .02). Upper respiratory tract infections constituted the most common type of infection. A substantial proportion of stroke patients with preceding (< 1 week) infection/inflammation (5/13) had no accompanying fever or chills. There were no significant differences between the stroke and control groups in the levels of stressful life events within the prior 1 month or in negative-affect scale scores within the prior 1 week. CONCLUSIONS: Our data suggest that both febrile and nonfebrile infectious/inflammatory syndromes may be a common predisposing risk factor for brain infarction and that the period of increased risk is confined within a brief temporal window of less than 1 week. Results of this study argue against a role for recent psychological stress as a precipitant for cerebral infarction.

Impairments of the protein C system and fibrinolysis in infection-associated stroke.

BACKGROUND AND PURPOSE: Infection/inflammation appears to be an important predisposing risk factor for brain infarction, but little is known regarding underlying molecular mechanisms. We examined the hypothesis that patients with brain infarction preceded by infection/inflammation within 1 week could be identified by a distinctive procoagulant laboratory profile characterized by abnormalities in the protein C system and endogenous fibrinolysis. METHODS: We performed a case-control study examining the relationship between preceding systemic infectious/inflammatory syndromes and selected immunohematologic variables in 36 patients with acute brain infarction and 81 control subjects (community control subjects [n = 47] and hospitalized nonstroke neurological patient controls [n = 34]). RESULTS: The stroke group had a lower mean level of the circulating antithrombotic enzyme activated protein C (APC) (4.33 +/- 0.34% [log-transformed percentage of control value, mean +/- SD]) than community control subjects (4.51 +/- 0.27%, P < .02) or hospitalized neurological patient controls (4.57 +/- 0.31%, P < .005). The lowest circulating APC levels were found in the stroke group with antecedent infection/inflammation within 1 week preceding index brain infarction (4.23 +/- 0.4%, n = 12). Within the stroke group, circulating APC levels were inversely related to IgG isotype anticardiolipin antibody titers (r = -.55, P < .001). Only the stroke group with infection/inflammation within 1 week had elevated plasma C4b binding protein compared with control subjects (141 +/- 61% versus 112 +/- 44%, P < .05). Stroke patients with antecedent infection/inflammation had a distinctively lower ratio of active tissue plasminogen activator to plasminogen activator inhibitor (0.11 +/- 0.04, n = 9) than other stroke patients (0.19 +/- 0.06, n = 9, P < .01) and control subjects (0.22 +/- 0.16, n = 17, P < .02). CONCLUSIONS: Impairments in the protein C pathway and endogenous fibrinolysis may contribute to the increased risk for brain infarction after recent (< or = 1 week) infection/inflammation. A decrease in the circulating anticoagulant APC may be related to elevated antiphospholipid antibody titers.

Activated protein C resistance in ischemic stroke not due to factor V arginine506-->glutamine mutation.

BACKGROUND AND PURPOSE: Resistance to activated protein C (APC), a natural plasma anticoagulant, is the most common identifiable risk factor for venous thromboembolic disease. One point mutation in coagulation factor V that renders it APC-resistant is found in >90% of APC-resistant venous thrombosis patients. To determine the prevalence of APC resistance and of this factor V mutation in stroke, we screened a group of ischemic stroke patients. METHODS: Hispanic ischemic stroke patients were screened using two different activated partial thromboplastin time-based assays. One assay using neat patient plasma determined APC resistance, and the other assay using patient plasma diluted into factor V-deficient plasma determined APC-resistant factor V, including the Arg506-->Gln mutation. Results were compared with those in 31 Hispanic control subjects of similar ages. RESULTS: Six of 63 (9.5%) stroke patients had APC resistance compared with none of 31 (0%) control subjects. No patient or control subject had APC-resistant factor V, ie, the factor V Arg506-->Gln mutation. CONCLUSIONS: In Hispanic patients with ischemic stroke, the incidence (approximately 10%) of APC resistance is not caused by the factor V Arg506-->Gln mutation. APC resistance not caused by this factor V mutation may be a risk factor for ischemic stroke in this population.

Morning reduction of cerebral vasomotor reactivity.

We measured cerebral vasomotor reactivity during normoventilation, hyperventilation (hypocapnia), and breathing of 6% CO2 (hypercapnia) in 20 normal subjects during the hours of 6 to 8 AM, 1 to 3 PM, and 7 to 9 PM. Cerebral vasomotor reactivity was calculated, using transcranial Doppler, as percent change in the mean blood flow velocity of the middle cerebral artery per mm Hg change in end-tidal CO2 during hypocapnia and hypercapnia. Vasomotor reactivity during hypercapnia was lower in the morning (1.72 +/- 0.66 %/mm Hg) than in the afternoon (2.34 +/- 0.74 %/mm Hg, p < 0.01) and evening (2.31 +/- 0.56 %/mm Hg, p < 0.001). Vasomotor reactivity during hypocapnia did not vary significantly during the three periods (2.34 +/- 0.59 %/mm Hg in the morning, 2.43 +/- 0.51 %/mm Hg in the afternoon, and 2.26 +/- 0.52 %/mm Hg in the evening). This reduced morning response to hypercapnia suggests diminished vasodilator reserve during this period, and may be related to the increased stroke risk during the morning hours.

Arterial oxygen content and age are determinants of middle cerebral artery blood flow velocity.

BACKGROUND AND PURPOSE: Transcranial Doppler blood flow velocities are inversely related to age and hematocrit, but the relative importance of age, oxygenation, and hemorheological factors has not previously been examined. We evaluated the relative contributions of these factors to middle cerebral artery blood flow velocity in adults with chronic renal failure, a population subject to significant fluctuations in hematologic profile. METHODS: Twenty-six subjects were studied, with arterial shunt blood sampled at the time of transcranial Doppler before dialysis. Twenty subjects from the original cohort were studied twice to examine the effects of intraindividual changes in blood oxygenation and rheology on Doppler velocities. RESULTS: Age (r = -.61, P < .001), high-shear viscosity (r = -.46, P < .02), and arterial oxygen content (r = -.44, P < .05) were all inversely related to middle cerebral artery blood flow velocity. Age was the strongest velocity predictor, accounting for 37% of variance by simple regression analysis. Intraindividual change in arterial oxygen content explained most (54%) of the middle cerebral artery blood flow velocity variation between studies (r = -.74, P < .001). Multiple regression analysis showed that inclusion of additional variables could not account for more velocity variation than change in arterial oxygen content alone. CONCLUSIONS: In this population, age and arterial oxygen content were the most important determinants of interindividual middle cerebral artery blood flow velocity variance and intraindividual middle cerebral artery blood flow velocity variation, respectively.

Hematogenous factors and prediction of delayed ischemic deficit after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Delayed ischemic deficits contribute to the high morbidity and mortality rates associated with subarachnoid hemorrhage. We evaluated the potential usefulness of measuring coagulation and hemorheological variables and cardiolipin antibodies for prediction of delayed ischemic deficit after subarachnoid hemorrhage. METHODS: Consecutive patients with subarachnoid hemorrhage were studied. Coagulation and hemorheological variables and cardiolipin antibodies were measured on admission, within 7 days of subarachnoid hemorrhage. A subset of patients was studied on admission and at two subsequent occasions. RESULTS: Sixty-nine patients were studied. Sixty-one of these were without clinical manifestations of vasospasm at admission, and 16 developed delayed ischemic deficit during their hospitalization. None of the laboratory variables measured were significantly different between patients with or without later development of delayed ischemic deficit. Elevation of the fibrin fragment D-dimer was found in the group of eight patients admitted with ischemic symptoms and in 49% (34 of 69) of all patients, but this was not associated with delayed ischemic deficit. Sixteen patients were studied on three occasions; this group showed a significant decrease in hematocrit, an increased white blood cell count, and no change in fibrinogen concentration. Fibrin D-dimer levels rose significantly after surgery (from 5.01 +/- 0.69 to 5.53 +/- 0.58 ln-ng/ml, p less than 0.025) and after onset of delayed ischemic deficit (from 4.71 +/- 0.64 to 5.84 +/- 0.34 ln-ng/ml, p less than 0.01). CONCLUSIONS: Hemostatic measurements, hemorheological variables, and cardiolipin immunoreactivity did not predict delayed ischemic deficit in this population.

Nimodipine and the evolution of hemorheological variables after acute ischemic stroke.

We studied the effects of the calcium channel antagonist nimodipine on the evolution of hemorheological variables during the first 3 weeks following ischemic stroke. We studied 13 patients and found that, compared to baseline levels, plasma fibrinogen concentration and low-shear whole-blood viscosity rose significantly in patients receiving placebo but not in those receiving nimodipine. Red blood cell aggregation rose in both groups but less so in nimodipine-treated patients. Hematocrit, high-shear whole-blood viscosity, and red blood cell deformability did not change significantly in either group. In conclusion, the use of nimodipine appears to alter the evolution of some hemorheological variables following acute ischemic stroke.

The Effect of Hemorheologic Factors on Middle Cerebral Artery Blood Flow Velocity in Young Individuals.

Analysis of the effect of hemorheologic factors on middle cerebral artery (MCA) blood flow velocity in 55 healthy individuals aged 18 to 30 years demonstrated an inverse association between mean MCA blood flow velocity and hematocrit (r = -0.27, p < 0.05). This association was largely explained by the effect of whole-blood viscosity. Neither fibrinogen concentration nor plasma viscosity were significantly associated with MCA blood flow velocity in this group; this lack of a fibrinogen association is in contrast to results previously obtained in elderly individuals where an inverse association was observed. These findings thus demonstrate age-dependent differences in the relationship between fibrinogen and MCA blood flow velocity.

Atrial Fibrillation, Congestive Heart Failure, and the Middle Cerebral Artery.

Atrial fibrillation and congestive heart failure are risk factors for ischemic stroke usually attributed to cardiac embolism. To define potential alternative mechanisms, patients with atrial fibrillation and congestive heart failure were investigated by transcranial Doppler. Middle cerebral artery (MCA) blood flow velocities were analyzed in neurologically asymptomatic patients with nonvalvular (n = 10) and valvular (n = 13) atrial fibrillation, patients in normal sinus rhythm with congestive heart failure (n = 13), and control subjects (n = 11). Compared to patients in sinus rhythm with congestive heart failure and to control subjects, patients in both atrial fibrillation groups had significantly greater beat-to-beat variation in peak, mean, and diastolic velocities and in pulsatility index. Peak, mean, and diastolic MCA velocities in patients with atrial fibrillation and those with congestive heart failure were significantly less than those in control subjects. Patients with nonvalvular atrial fibrillation had a higher pulsatility index compared to each of the other three groups. These findings demonstrate substantial nonemboligenic alterations of the intracranial circulation associated with atrial fibrillation and congestive heart failure, and also provide an intracranial hemodynamic profile that may distinguish valvular from nonvalvular atrial fibrillation.

Immunohematologic characteristics of infection-associated cerebral infarction.

We evaluated 50 consecutive patients with acute ischemic stroke to assess the prevalence of systemic infection preceding the neurological event. We analyzed the immunohematologic characteristics of patients with and without signs and/or symptoms of a preceding infectious process. Patients were examined less than or equal to 7 days after cerebral infarction and evaluated for fibrinogen, anticardiolipin antibodies, fibrin D-dimer (a fragment of cross-linked fibrin), plasminogen activator inhibitor-1, and protein S. Of the 50 patients, 17 had symptoms of infection beginning less than or equal to 1 month before the stroke (11 had upper respiratory tract infections, three urinary tract infections, two subacute bacterial endocarditis, and one pneumonia). Compared with patients without infection, patients with infection had significant increases in fibrin D-dimer concentration (5.3 +/- 1.1 versus 4.7 +/- 0.9 log-transformed ng/ml, p less than 0.05) and cardiolipin immunoreactivity, IgG isotype (1.8 +/- 1.3 versus 1.1 +/- 0.9 log-transformed phospholipid units, p less than 0.04), and, when studied less than or equal to 2 days after the stroke, increased fibrinogen levels (459 +/- 126 versus 360 +/- 94 mg/dl, p less than 0.05). In conclusion, infection-associated cerebral infarction is common and is associated with substantial immunohematologic abnormalities.