Jorge Tapia

Risk factors for systemic embolism in patients with paroxysmal atrial fibrillation

The purpose of this study was to define the risk factors for systemic embolism in patients with recently diagnosed paroxysmal atrial fibrillation. We therefore studied 63 consecutive patients with symptomatic nonvalvular paroxysmal atrial fibrillation and performed a clinical and noninvasive cardiac, peripheral vascular, and neurologic evaluation that included two-dimensional echocardiography, 24-hour Holter monitoring, and computed tomographic brain scan. Patients with predisposing clinical conditions for systemic embolism (valvular heart or coronary artery disease) or paroxysmal atrial fibrillation (sick sinus disease, preexcitation, or thyroid dysfunction) were excluded. At entry 34 patients had idiopathic paroxysmal atrial fibrillation and 29 had hypertension. Fourteen patients had a recent systemic embolic complication: nine had a recent occlusive nonlacunar cerebrovascular accident, two had transient ischemic attacks, and three had peripheral systemic emboli that required surgery. In addition, five patients had evidence of old cerebrovascular accident on the computed tomographic scan (group 1). Forty-four patients had no systemic embolism (group 2). Results of univariate analysis showed that patients in group 1 were older (72 +/- 9 vs 63 +/- 13 years, p less than 0.05), had a higher incidence of hypertension (70% vs 35%, p less than 0.01), and had an increased left atrial diameter (4.1 +/- 0.7 vs 3.6 +/- 0.5 cm, p less than 0.05). Multiple stepwise logistic regression analysis showed that a history of hypertension and left atrial enlargement on two-dimensional echocardiography were significant independent risk factors for systemic embolism in patients with symptomatic nonvalvular paroxysmal atrial fibrillation.

C-Reactive Protein as a Prognostic Marker After Lacunar Stroke Levels of Inflammatory Markers in the Treatment of Stroke Study

Background and Purpose— Inflammatory biomarkers predict incident and recurrent cardiac events, but their relationship to stroke prognosis is uncertain. We hypothesized that high-sensitivity C-reactive protein (hsCRP) predicts recurrent ischemic stroke after recent lacunar stroke. Methods— Levels of Inflammatory Markers in the Treatment of Stroke (LIMITS) was an international, multicenter, prospective ancillary biomarker study nested within Secondary Prevention of Small Subcortical Strokes (SPS3), a phase III trial in patients with recent lacunar stroke. Patients were assigned in factorial design to aspirin versus aspirin plus clopidogrel, and higher versus lower blood pressure targets. Patients had blood samples collected at enrollment and hsCRP measured using nephelometry at a central laboratory. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs) for recurrence risks before and after adjusting for demographics, comorbidities, and statin use. Results— Among 1244 patients with lacunar stroke (mean age, 63.3±10.8 years), median hsCRP was 2.16 mg/L. There were 83 recurrent ischemic strokes (including 45 lacunes) and 115 major vascular events (stroke, myocardial infarction, and vascular death). Compared with the bottom quartile, those in the top quartile (hsCRP >4.86 mg/L) were at increased risk of recurrent ischemic stroke (unadjusted HR, 2.54; 95% CI, 1.30–4.96), even after adjusting for demographics and risk factors (adjusted HR, 2.32; 95% CI, 1.15–4.68). hsCRP predicted increased risk of major vascular events (top quartile adjusted HR, 2.04; 95% CI, 1.14–3.67). There was no interaction with randomized antiplatelet treatment. Conclusions— Among recent lacunar stroke patients, hsCRP levels predict the risk of recurrent strokes and other vascular events. hsCRP did not predict the response to dual antiplatelets. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT00059306.

Morphological classification of penetrating artery pontine infarcts and association with risk factors and prognosis: The SPS3 trial

Background Pontine infarcts are common and often attributed to small vessel disease (“small deep infarcts”) or basilar branch atherosclerosis (“wedge shaped”). A well-described morphological differentiation using magnetic resonance images has not been reported. Furthermore, whether risk factors and outcomes differ by morphology, or whether infarct morphology should guide secondary prevention strategy, is not well characterized. Methods All participants in the Secondary Prevention of Small Subcortical Strokes Study with magnetic resonance imaging -proven pontine infarcts were included. Infarcts were classified as well-circumscribed small deep (small deep infarct, i.e. lacunar), paramedian, atypical paramedian, or other based on diffusion-weighted imaging, T2/fluid-attenuated inversion recovery, and T1-magnetic resonance images. Inter-rater reliability was high (90% agreement, Cohen’s kappa = 0.84). Clinical and radiologic features independently associated with small deep infarct versus paramedian infarcts were identified (multivariable logistic regression). Differences in stroke risk and death were assessed using Cox proportional hazards. Results Of the 3020 patients enrolled, 644 had pontine infarcts; 619 images were available: 302(49%) small deep infarct, 245 (40%) paramedian wedge, 35 (6%) atypical paramedian, and 37 (6%) other. Among vascular risk factors, only smoking (OR 2.1, 95% CI 1.3–3.3) was independently associated with small deep infarct versus paramedian infarcts; on neuroimaging, old lacunes on T1/fluid-attenuated inversion recovery (OR 1.8, 1.3–2.6) and intracranial stenosis (any location) ≥50% (OR 0.62, 0.41–0.96). Small deep infarct versus paramedian was not predictive of either recurrent stroke or death, and there was no interaction with assigned treatment. Conclusions Pontine infarcts can be reliably classified based on morphology using clinical magnetic resonance images. Few risk factors differed between small deep infarct and paramedian infarcts with no differences in recurrent stroke or mortality. There was no difference in response to different antiplatelet or blood pressure treatment strategies between these two groups. Registration http://www.clinicaltrials.gov/NCT00059306.

Enfermedad cerebrovascular y trombofilia

La trombofilia es una condicion que se debe tener presente en las enfermedades cerebrovasculares (ECV) isquemicas. Si bien se considera que es la causa de un bajo porcentaje de ellas, dada la alta incidencia de las ECV isquemicas, el numero de pacientes con esta condicion pasa a ser significativo. La mayoria de las trombofilias ha sido descrita en los ultimos 20 anos, por lo que es posible que esta condicion explique un porcentaje importante de las ECV isquemicas sin causa aparente. Un 8 a 15% de las ECV isquemicas bajo los 50 anos son secundarias a trombofilia. Con frecuencia la trombofilia coexiste con otro factor de riesgo de ECV isquemica. De las trombofilias, la hiperhomocisteinemia y la presencia de anticuerpos antifosfolipidos se relaciona con obstruccion de vasos encefalicos tanto arteriales como venosos. En cambio, las trombofilias hereditarias (deficiencia de antitrombina III, proteina C y S, mutacion del factor II y V) se relacionan mas bien con trombosis de venas encefalicas. Se revisan los diferentes tipos de trombofilia, su cuadro clinico, forma de estudio y tratamiento. Se recomienda investigar trombofilia en todos los casos de trombosis venosa encefalica y, en aquellos por obstruccion arterial encefalica de causa desconocida, en los pacientes menores de 50 anos, en los con historia personal de flebotrombosis o familiar de trombosis, y cuando se detectan anormalidades en las pruebas rutinarias de coagulacion

Charles Miller Fisher, un grande de la neurología

C. Miller Fisher MD, one of the great neurologists in the 20th century, died in April 2012. Born in Canada, he studied medicine at the University of Toronto. As a Canadian Navy medical doctor he participated in World War II and was a war prisoner from 1941 to 1944. He did a residency in neurology at the Montreal Neurological Institute between 1946 and 1948, and later on was a Fellow in Neurology and Neuropathology at the Boston City Hospital. In 1954 he entered the Massachusetts General Hospital as a neurologist and neuropathologist, where he remained until his retirement, in 2005. His academic career ended as Professor Emeritus at Harvard University. His area of special interest in neurology was cerebrovascular disease (CVD). In 1954 he created the first Vascular Neurology service in the world and trained many leading neurologists on this field. His scientific contributions are present in more than 250 publications, as journal articles and book chapters. Many of his articles, certainly not restricted to CVD, were seminal in neurology. Several concepts and terms that he coined are currently used in daily clinical practice. The chapters on CVD, in seven consecutive editions of Harrisons Internal Medicine textbook, are among his highlights. His death was deeply felt by the neurological community.

Prevención secundaria de la trombosis en pacientes con síndrome antifosfolípido

Antiphospholipid syndrome is very heterogeneous and is therefore of interest to various medical specialties. The neurologist will see it in cases of ischemic cerebrovascular disease. Retrospective clinical series suggest that treatment with high levels of anticoagulants (INR of 3 to 4.5), rather than at the usual levels (INR 2 to 3), decreases its recurrence. Crowther et al. published in the New England Journal of Medicine (2003; 349: 1133-8), the first prospective, randomized study evaluating the effectiveness and safety of oral anticoagulation at the two levels mentioned to prevent the recurrence of cerebral thrombosis. The authors conclude that a high-level use of anticoagulants does not give better results than a moderate-level use (INR 2 to 3). These results are crucial for neurologists, since the most serious complication arising from the use of anticoagulants is intracranial hemorrhage, whose primary risk factors are the level of anticoagulation and previous infarction. This study allows us to manage ischemic events in antiphospholipid antibody syndrome, with usual levels of anticoagulation