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Background and purpose: paroxysmal AF is detected during follow-up in approximately 30% of ESUS. We aim to identify patterns of brain lesions suggestive of embolic events and to evaluate the incidence of AF during 4-years of follow-up. Design and method: acute ischemic stroke patients were prospectively included in a multidisciplinary secondary stroke prevention program. Cardioembolic stroke was ruled out with 12-lead ECG, 48-hour cardiac monitoring and transesophageal echocardiography. Large artery disease of intracranial and extracranial vessels was evaluated with MR or CT angiography or cervical duplex plus transcranial doppler ultrasonography. After this thorough evaluation, patients without cardioembolic or large artery disease and non-lacunar lesion on MRI were defined as ESUS. Results: 479 (34%) of 1376 ischemic strokes included from September 2009 to December 2016 were ESUS; median age 78 years (IQR 69-84), 55% female. Pre-stroke VRF profile: 80% HT, 66% dyslipidemia, 14% DM, 51% obesity, 39% smoking, 34% CKD, 3% history of paroxysmal AF, 14% CHD and 10% previous stroke or TIA. Twenty-four patients (5%) died during hospitalization or within the next 30 days. There were 25 % (CI 95% 22-29) of recurrent strokes during 4-years of follow-up after stroke. The AF was detected in 15% of patients in the first year, 28% in the second year, 38% in the third year and 41% in the fourth year. Neuroimaging findings on-admission MRI are shown in the table. Conclusion: ESUS patients with AF during follow-up had higher incidence of hemorrhagic transformation during the acute phase as well as multiple lesions in different territories of the anterior and posterior cerebral circulation. As these findings are often seen in strokes of indubitable embolic origin the presence of these features should raise the suspicion of an underling embolic source.

Background and purpose: In observational studies, patients under statin therapy at the time of stroke onset have lower likelihoods of mortality and poor functional outcome. This neuroprotective effect could be related to anti-inflammatory and antiplatelet actions of statins. Our objective was to evaluate early functional outcome in a cohort of ischemic stroke patients. Design and Method: stroke patients were included in PROTEGE-ACV, a multidisciplinary secondary prevention program aimed to improve adherence to clinical practice guidelines. Vascular risk factor (VRF) profile and control, and statin treatment in the year before stroke were collected, and functionality one-month after discharge was evaluated using modified Rankin scale. Results: 1981 ischemic stroke patients (20% TIA) were included between December 2006 and December 2015; mean age was 76±11 years with 57% females. Patients receiving statins (n 713, 38%) had a significant higher prevalence of hypertension, diabetes, dislipidemia, obesity, metabolic syndrome, coronary heart disease, peripheral artery disease, chronic renal failure and previous stroke. Both groups had similar blood pressure, and patients under statins had lower total cholesterol (182±42 vs 200±40 mg/dL, p 0.00001), LDL-c (106±36 vs 128±47, p 0.00001) with similar levels of HDL-c and triglycerides; these patients also had lower GFR (62±23 vs 67±31 mL/min, 0.0003) and higher fasting glucose levels (103±26 vs 99±21 mg/mL; p 0.0003). Predictors of bad outcome in the multivariate analysis adjusted by age and VRF are shown in the table. Conclusion: Even though patients under statin treatment before stroke had higher prevalence of vascular diseases, they have better functional outcomes one-month after the event. In our cohort, previous statin use seems to have neuroprotective effect, which could be related to modulation of inflammatory response, platelet aggregation, fibrinolysis and nitric oxide production.

Background and purpose: Hypertension is the most prevalent risk factor for acute and chronic cerebrovascular disease. As patients with resistant hypertension are a subgroup with even higher risk, we aimed to evaluate the burden of microangiopatic disease and functional outcome in subjects with stroke and difficult to treat hypertension. Design and method: acute ischemic stroke patients were prospectively included in a multidisciplinary secondary stroke prevention program. Pre-stroke vascular risk factor profile and control were obtained from electronic medical records and chronic vascular disease burden was assessed on admission MRI. Functional and cognitive evaluation were performed one-month after stroke. Results: 1327 patients (16% with resistant hypertension) were included from September 2009 and December 2015. Patients with resistant hypertension were older (80±8 vs 77±10, p 0.0004), with higher prevalence of obesity (62% vs 50%, p 0.001), metabolic syndrome (52% vs 38%, p 0.0001) and history of atrial fibrillation (27% vs 16%, p 0.0001). There was a direct relationship between resistant hypertension and the severity of chronic microvascular lesions, and also with functional and cognitive outcomes (table). Conclusion: Hypertension increases vascular events risk, even more in the setting of resistant hypertension. Requirement of a therapeutic strategy involving combination of multiple drugs generally indicates more severe underlying hypertensive disease. It is possible that mechanisms of endothelial dysfunction responsible of the neurovascular unit damage might remain active despite achieving blood pressure target.

Introduction: intracerebral hemorrhagic transformation (HT) is a multifactorial phenomenon in which ischemic brain tissue converts into a hemorrhagic lesion with blood vessel leakage, and can significantly contribute to additional brain injury after stroke. Understanding mechanisms and identifying predictors of HT may contribute to improve clinical outcomes in stroke patients. Hypothesis: to evaluate clinical predictors of HT in non-lacunar ischemic stroke patients. Methods: patients were prospectively included in a multidisciplinary secondary stroke prevention program. Pre-stroke vascular risk factor profile and control were obtained from electronic medical records. Acute SBP, DBP and PP were obtained in the emergency room and HT was evaluated with on-admission and one-week CT or MRI. Predictors of HT were identified by multivariate analysis. Exclusion criteria: TIA, lacunar stroke and patients without one-week CT or MRI. Results: 747 patients with a non-lacunar ischemic stroke (mean age 77±11 years, 61% females) were included. HT was observed in 94 patients (13%); they were older (82±8 vs 77±11; p 0.0001), had higher prevalence of hypertension (94% vs 81%; p 0.003) and AF (45% vs 20%; p 0.0001), and lower e-GFR (56±29 vs 65±27 ml/min/1.73 m2; p 0.04). They also had higher on-admission SBP (168±30 vs 146±23 mmHg; p 0.0001), DBP (88±18 vs 81±13 mmHg; p 0.0001) and PP (78±23 vs 63±21 mmHg; p 0.0001); anticoagulant therapy was more frequent in this group (27% vs 12%; p 0.0001). After adjusting by age and vascular risk factors in the multivariable analysis: the age > 80 years, PP on admission > 60 mm de Hg, e-GFR < 60 ml /min/1,73 m2 and pre-stroke AF were associated with increase of risk of HT. (table) Conclusion: predictors for HT in our cohort were also related with severe vascular disease. Identification of these high risk patients is crucial in clinical decision making regarding thrombolytic treatment and optimal timing for antithrombotic therapy initiation.

Introduction: stroke recurrence in patients with TIA is one of the most frustrating medical situations and it is very important to identify strong predictors of stroke recurrence to enable practitioners to take clinical decisions Hypothesis: to evaluate the relationship between pulse pressure (PP), a marker of vascular disease, and the risk of stroke recurrence in patients with TIA. Methods: TIA patients were prospectively included in a multidisciplinary secondary stroke prevention program. Pre-stroke vascular risk factor profile and control were obtained from electronic medical records. Stroke recurrence was analyzed after five years of follow up. For the purpose of the analysis, three groups were defined according to pre-stroke PP: < 60, 60-69 and > 70 mmHg. Results: 357 patients (mean age 75±10 years, 55% females) were included. Vascular risk factors profile: hypertension 83%, dislipidemia 74%, obesity 54%, smoking 41%, diabetes 12%, AF 12%, CKD 28%, CHD 18%. Mean SBP was 130 mmHg and DBP 80 mmHg; 78% was receiving antihypertensives, 47% statins, 43% antiplatelets and 9% anticoagulants before the event. There was a direct relationship between pre-stroke PP and stroke recurrence during follow-up (figure). Conclusion: PP is related to higher burden of vascular disease, mainly an increase in arterial stiffness, which might be a key element in clinical decision making in the setting of stroke recurrence prevention.

Introduction: chronic kidney disease (CKD) coexists with microvascular brain damage. This cerebrorenal connection is considered to involve small vessel disease in both the kidney and brain, based on their hemodynamic similarities. Hypothesis: to evaluate the relationship between microvascular brain damage (white matter hyperintensities -WMH-, microbleeds -MB- and silent brain infarcts -SBI-), and glomerular filtration rate (GFR) in a cohort of ischemic stroke patients. Methods: patients were prospectively included in a multidisciplinary secondary stroke prevention program. Pre-stroke vascular risk factor profile and control were obtained from electronic medical records and the burden of microvascular brain damage was evaluated on admission MRI. For the purpose of the analysis three groups were defined according to GFR estimated by Cockroft-Gault formula: >60, 30-60 and Results: 808 patients (mean age 77±11 years, 59% females) were included. GRF was inversely related to age (70±11, 83±6, 85±8 years; p 0.0001), female sex (48%, 69%, 66%; p 0.001), hypertension (76%, 89%, 91%; p 0.0001) and AF (16%, 21%, 34%; p 0.08) prevalence. Chronic microvascular brain damage burden was inversely related to e-GFR (table). Conclusion: decreased GFR indicates small vessel disease not only in the kidney but also in the brain. As small vessel disease is a systemic disorder, information about disease in one organ may suggest damage in the other.

Introduction: pulse pressure (PP), a marker of arterial stiffness, is a useful tool for measuring vascular aging. White matter hyperintensities (WMH), deep and periventricular, are the expression of subclinical ischemic brain damage. Hypotesis: our objective was to evaluate the relationship between pre-stroke blood pressure and the burden of WMH. Method: acute ischemic stroke patients, excluding TIA, were prospectively included in a multidisciplinary secondary stroke prevention program. Pre-stroke vascular risk factor profile and control were obtained from electronic medical records and the presence of WMH was evaluated on admission MRI. Periventricular hyperintensities (PVH) and deep white matter hyperintensities (DWMH) were classified according to Fazekas scale (0-3). A correlation analysis between different components of blood pressure and WMH was performed. Results: 808 patients (59% females, mean age 77±11 years) were included between January 2009 and December 2014. Main vascular risk factors were: hypertension (83%), dyslipemia (64%), obesity (52%), smoking (37%), metabolic syndrome (37%), diabetes (14%), AF (19%), CKD (45%), CHD (14%), stroke (10%), peripheral artery disease (12%). There was a positive correlation between PP values and the severity of PVH (R 0.93) and DWMH (R 0.95), but not with SBP (R 0.48 and R 0.50) and DBP (R 0.52 and 0.47). (figure) Conclusion: different blood pressure components may have different deleterious effects on large and small vessels. Pulse pressure, a pulsatile component mainly reflecting large artery stiffness and wave reflections, was the only component of blood pressure with a positive correlation with the burden of WMH in our cohort. As the world is aging, is mandatory to identify predictors of subclinical brain damage, which is related to increased risk of dementia, depression, stroke and gait disorders.

Background and purpose: hypertension is the vascular risk factor most commonly related to stroke, making antihypertensive treatment a cornerstone of stroke prevention. Achieving targets of clinical practice guidelines could be difficult in some patients, requiring combination of drugs to maintain these goals. We aimed to evaluate the relationship between difficult-to-treat hypertension (DTTH) and stroke outcomes. Methods: acute ischemic stroke patients were prospectively included in PROTEGE-ACV, a multidisciplinary secondary stroke prevention program. Demographic data, vascular risk factors (VRF) profile and control, and stroke outcome (disability, mortality and stroke recurrence) were evaluated 30 days after stroke. Difficult-to-treat hypertension was defined as those requiring more than two drugs in hypertension management. Results: we analyzed data of the 1194 stroke patients included between December 2006 and December 2013. We found 186 DTTH patients, who had higher burden of VRF and poorer pre-stroke control (table); they had higher admission blood pressure (0 drugs 146/82 mmHg, 1 drug 151/84, 2 drugs 154/83, 3 drugs 153/83, 4 drugs 169/88; p 0.001 for SBP, 0.26 for DBP) and pulse pressure (63 mmHg, 66 mmHg, 70 mmHg, 67 mmHg, 81 mmHg respectively; p 0.0006). These patients had also worst 30-day outcome: m-Rankin >1 (24% in no-DTTH vs 54% in DTTH, 0.0001), mortality (1% vs 16%, p 0.001), composite disability + all cause death (44% vs 73%, p 0.001). We found no difference in early stroke recurrence. Conclusion: the number of drugs necessary to treat hypertension could be useful to identify barriers to achieve blood pressure targets for vascular disease prevention, as vascular aging, hemodynamic changes, adherence to medication and healthy lifestyle. This indicator is easy to collect and could help to decision making in daily clinical practice.

Background: women who have ischemic strokes are on average older than men.Several studies, however, show that stroke outcomes are worse in women even after adjusting for age, and the specific conditions that contribute to this outcome are poorly known. Our objective was to evaluate post-stroke disability and mortality after ischemic stroke in women. Methods: acute ischemic stroke patients were prospectively included in a multidisciplinary secondary stroke prevention program. Pre-stroke vascular risk factor profile and control were obtained from electronic records; disability (modified Rankin scale) were evaluated one month after stroke. Results: fifty seven percent of the 1194 ischemic stroke patients prospectively included between December 2006 and December 2013 were women. They were older, more probably hypertensive, dislipidemic and diabetic, and had higher incidence of atrial fibrillation, while men had higher prevalence of obesity, metabolic syndrome, smoking, and history of coronary heart disease and peripheral artery disease. Pre-stroke vascular risk factor control and management are shown in table 1. Women had worst outcome than men: mRankin >1 (66% women vs 52% men, p 0.0001), 30-day mortality (4% women vs 2% men, p 0.04), composite disability + mortality (52% women vs 36% men, p 0.0001). After adjusting by age women still had higher risk of disability and mortality: m-Rankin >1 (OR 1.40, 95%CI 1.05-1.87; p 0.02); mortality (OR 1.64, 95%CI 0,98-2,74), and composite disability + mortality (OR 1.59, 95%CI 1.22-2.07; p 0.004). Conclusion: in our cohort women have worst post-stroke outcome, even though they have higher burden of vascular risk factors they have lower prevalence of vascular disease in other vascular beds previous to stroke. This difference persists after adjusting by age, raising the possibility of specific gender risk factors influencing on ischemic stroke outcomes.

Background and purpose: previous studies had found that pre-stroke antiplatelet use reduces stroke severity. Our objective was to evaluate this issue in a cohort with good levels of pre-stroke vascular risk factors control. Methods: ischemic stroke patients were prospectively included in PROTEGE-ACV, a multidisciplinary prevention program. Demographic data, vascular risk factor profile and control before stroke were obtained from electronic records. Patients with functional impairment (Rankin ≥ 4), dementia or life expectancy less than three years were excluded. One month after discharge, the following tests were performed: MMSE adjusted by age and educational status, clock drawing test CDT (normal or abnormal), Barthel index, modified Rankin scale (≥3 functional impairment). Mortality and recurrence were evaluated after a mean follow-up of 2 years. Results: between December 2006 and April 2013, 1090 patients (55% female, mean age 75± 11 years) were included, 44% (n=472) were using antiplatelet drugs in the year before the stroke. This group had higher prevalence of major vascular risk factors (with good level of control in both groups) and burden of disease in other vascular beds. Stroke outcomes were worse in patients receiving antiplatelet drugs before stroke (Table). This lack of effect on functional outcomes persisted after a multivariate analysis including statins and antihpertensives. Conclusion: in contrast to published data, we did not found a beneficial effect of using of antiplatelet drugs before stroke on functionality and cognition, neither on recurrence and mortality prevention in our cohort.

Background and purpose: similarities in renal and vascular beds could explain the relationship between impaired glomerular filtration rate (iGFR) and leukoaraiosis, white matter hiperintensities (WMH), and lacunar infarcts. We evaluated the association between microbleeds (MB) and impaired kidney function in patients with acute ischemic stroke. Methods: acute ischemic stroke patients were prospectively included. Pre-stroke vascular risk factors were obtained and the presence of MB and WMH were evaluated on admission MRI and analyzed as dichotomous variables. Results: MB were present in 128 (19%) of the 663 patients evaluated.. Table shows risk factors and comorbidities associated with MB in the univariate analysis. Only leukoaraiosis (OR 3.3; CI 95% 1.5-3.3; p 0.0001), age older than 80 years (OR 1.90; CI 95% 1.10-2.8; p 0.01), WMH (OR 9.4; CI 95% 5.6-15.6; p 0.0001) and iGFR (OR 2.2; CI 95% 1.3-3.3; p 0.01) were associated with the presence of MB in the multivariate analysis. Conclusion: Besides age and WMH, well-known risk factors for MB, impaired kidney function doubles the risk these lesions in a cohort of ischemic stroke patients, reassuring the hypothesis of a common pathophysiological pathway for renal and cerebral microvascular damage.

Background and purpose: Mounting evidence suggests that the presence of chronic kidney disease (CKD) predicts poor clinical outcomes in ischemic stroke patients. However few reports are available about the association of CKD and cognitive impairments (CI) after stroke. The aim of this study was evaluate the presence of CKD in patients with CI after stroke. Methods: all patients included in PROTEGE ACV, a stroke secondary prevention stroke program, were evaluated. Demographic data, vascular risk factors profile and control, CI (abnormal clock drawing test (CDT) or MMSE, adjusted by age and educational level) and CKD (estimated glomerular filtration rate -e-GFR- < 60 ml/min/1.73 m 2 or 24 hours microalbuminuria). Results: 668 (54% female) ischemic stroke patients were included; mean age 75 ± 10 years.. The main vascular risk factors were hypertension (81%), dyslipemia (70%), metabolic syndrome (48%), obesity (42%) and smoking (41%). Pre-stroke hypertension control was good and 74% were under pharmacological treatment. Post-stroke CI were associated with hypertension (OR 1.65, 95% CI 1-2.59), impaired eGFR (OR 2.51, 95% CI 1,6-3,8), female sex (OR 2.23 95% CI 1.5-3.2) and cardioembolic stroke (OR 2.32, 95% CI 1.5-3.4) in the univariate analysis. In the logistic regression model adjusted by age, sex and main vascular risk factors, age older than 80 years, female sex, cardioembolic stroke and impaired e-GFR were predictors of CI (figure). No relationship was found between CI and microalbuminuria ≥ 20 mg/24hs. Conclusions: cognitive function is negatively affected by impaired e-GFR. Optimal pre-stroke hypertension control could be an explanation for the small number of patients with high microalbuminuria in our cohort.

Background and purpose: detection of atrial fibrillation (AF) after ischemic stroke is crucial, because anticoagulation is mandatory in order to decrease recurrence risk. However, there is no agreement regarding the optimal method to detect paroxysmal AF after the event. The aim of this study was to evaluate predictors for delayed detection of AF after ischemic stroke (IS) and transient ischemic attack (TIA). Methods: PROTEGE-ACV is a multidisciplinary stroke quality improvement program coordinated by internists and neurologists within a Buenos Aires healthcare system aimed to optimize secondary stroke preventive care after IS or TIA. Demographic data, vascular risk factors profile control and management were evaluated at the inclusion visit, and IS was categorized according to TOAST classification. Results: From 01/2007 to 04 /2012, 872 ischemic stroke patients were included; mean age was 75 ± 10 years-old and 55% were female. Twenty two percent were cardioembolic and 7% undetermined with more than one mechanism with AF as one of them; 14% of patients had history of AF or diagnosis at hospitalization. Incident AF was diagnosed in 101 (21%) of 473 patients with two or more years of follow-up.. Diagnosis of AF was associated with age older than 80 years (OR 1.96 95% CI 1.25-3), history of hypertension (OR 2.4 95% CI 1.25-4.8), chronic renal failure (OR 2.65 95% CI 1.54-4.55) and stroke recurrence (OR 2.96 95% CI 1.66-5.26). Conclusion: delayed diagnosis of AF was common in this cohort of patients with IS or TIA. Identification of risk factors is important in order to perform a close follow-up of these patients and to determine the best method for this purpose, in order to reduce recurrence risk.

Background: benefits of interventional procedures for the treatment of asymptomatic carotid stenosis (ACS) are still under debate. Our objective was to evaluate the risk of vascular events in a cohort of patients with ACS under optimal medical treatment. Methods: patients with ACS ≥50% were prospectively evaluated. Data on demographic and vascular risk factor profile and control under pharmacological treatment were collected. Severity of carotid stenosis was confirmed by at least two methods (Doppler ultrasonography, angioresonance, angiotomography or digital angiography) and evolution over time was evaluated by Doppler ultrasonography performed by the same operator, blinded to clinical data. Primary end-points were coronary events and ispsilateral ischemic stroke (IIS). Results: ninety two patients were included between January 2007 and December 2010. Mean age was 72±8 years, 35% were women. Mayor vascular risk factors were: hypertension (97%), dyslipidemia (90%), obesity (40%), diabetes (30%), smoking or former smoking (51%), history of coronary heart disease (37%) and peripheral vascular disease (32%). Average follow-up was 667±509 days (range 180-1870 days). Table 1 shows vascular risk factor control during follow-up. One IIS (1.08%; 95% CI 0.19-5.9; 5.8/1000 person/year) and 2 acute myocardial infarction (2.17%; 95% CI 0.6-7.5; 11.73/1000 person/year) were observed. Eighteen percent of patients had stenosis 50-70%, 68% between 70-90% and 13% ≥ 90%. After one year most of patients showed no changes in stenosis severity (76%), 5.56% had progression and 6.52% had regression; 14.1% had no control. Conclusion: optimal pharmacological treatment was related to a very low incidence of vascular events. These data reassert the efficacy of intensive medical treatment in delaying atherosclerotic plaque progression and carotid disease complications.

Background and Purpose— Increasing evidence links infections to atherosclerosis. Case–control and cohort studies have found that infections, especially respiratory and dental, are associated with coronary heart disease. However, data on the association of infections with cerebrovascular disease are limited, especially beyond Europe and the United States. We assessed the relationship between recent infections and atherothrombotic disease in a South American cohort. Methods— We conducted a case–control study of 105 cases and 354 control subjects in a Buenos Aires healthcare system matched by age (mean age, 73.2±12.3 and 72.9±12.8 years), sex, and major cardiovascular risk factors. Cases were patients hospitalized with atherothrombotic ischemic stroke from December 2006 to October 2007. Control subjects were randomly assigned from an electronic outpatient database. Data from the preceding year on inpatient and ambulatory respiratory, urinary and abdominal infections as well as peripheral white blood cell count were collected. Results— Infections were more frequent in cases than control subjects (29% versus 13%; OR, 2.6; 95% CI, 1.4 to 4.5; P =0.0004); however, this was driven by community-acquired respiratory tract infections (19% versus 6%; OR, 3.9; 95% CI, 1.9 to 8; P P P P =0.01). Conclusion— In this South American cohort, recent respiratory tract infections were significantly associated with atherothrombotic stroke, suggesting that prompt identification and treatment of individuals with or at risk for these infections may mitigate the burden from this type of stroke.