Treatment with Mannitol is Associated with Increased Risk for In-Hospital Mortality in Patients with Acute Ischemic Stroke and Cerebral Edema.

BACKGROUND: Current guidelines state that osmotic therapy is reasonable in patients with clinical deterioration from cerebral infarction-related cerebral edema. However, there are limited data on the safety and efficacy of this therapy. We aimed to evaluate the effect of mannitol on the outcome of ischemic stroke-related cerebral edema. METHODS AND RESULTS: We prospectively studied 922 consecutive patients admitted with acute ischemic stroke. Patients who showed space-occupying brain edema with tissue shifts compressing the midline structures received mannitol. The outcome was assessed with dependency rates at discharge (modified Rankin Scale grade 2-5) and in-hospital mortality. Rates of dependency were higher in patients treated with mannitol (n = 86) than in those who were not (97.7 and 58.5%, respectively; p < 0.001). Independent predictors of dependency were age, history of ischemic stroke and National Institutes of Health Stroke Scale (NIHSS) score at admission. Rates of mortality were higher in patients treated with mannitol than in those who were not (46.5 and 5.6%, respectively; p < 0.001). Independent predictors of in-hospital mortality were diastolic blood pressure [relative risk (RR) 1.05, 95% confidence interval (CI) 1.02-1.08, p < 0.001], NIHSS score at admission (RR 1.19, 95% CI 1.14-1.23, p < 0.001) and treatment with mannitol (RR 3.45, 95% CI 1.55-7.69, p < 0.005). CONCLUSIONS: Administration of mannitol to patients with ischemic stroke-related cerebral edema does not appear to affect the functional outcome and might increase mortality, independently of stroke severity.

Effect of antihypertensive treatment on the long-term outcome of patients discharged after acute ischemic stroke.

We aimed to evaluate the effects of the five main classes of antihypertensive agents on the long-term outcome of 313 consecutive patients discharged after acute ischemic stroke (36.4% males, age 78.5 ± 6.3 years). One year after discharge, the functional status [evaluated with the modified Rankin scale (mRS)], the occurrence of cardiovascular events, and vital status were recorded. Patients prescribed angiotensin receptor blockers (ARBs) had lower mRS than patients not prescribed ARBs (1.7 ± 2.0 vs. 2.9 ± 2.5, respectively; p = 0.006). The rates of adverse outcome (mRS 2-6) and cardiovascular events did not differ between patients prescribed each one of the major classes of antihypertensive agents and those not prescribed the respective class. Patients who were prescribed ARBs had lower risk of death during follow-up than patients who did not receive ARBs (9.4 and 26.9%, respectively; p < 0.05). In binary logistic regression analysis, the only independent predictor of all-cause mortality during follow-up was the mRS at discharge (relative risk 1.69, 95% confidence interval 1.25-2.28; p < 0.001). In conclusion, in patients discharged after acute ischemic stroke, administration of ARBs appears to have a more beneficial effect on long-term functional outcome and all-cause mortality than treatment with other classes of antihypertensive agents.

Stress hyperglycemia and acute ischemic stroke in-hospital outcome.

BACKGROUND AND AIMS: Stress hyperglycemia is frequent in patients with acute ischemic stroke. However, it is unclear whether stress hyperglycemia only reflects stroke severity or if it is directly associated with adverse outcome. We aimed to evaluate the prognostic significance of stress hyperglycemia in acute ischemic stroke. METHODS: We prospectively studied 790 consecutive patients who were admitted with acute ischemic stroke (41.0% males, age 79.4±6.8years). The severity of stroke was assessed at admission with the National Institutes of Health Stroke Scale (NIHSS). Stress hyperglycemia was defined as fasting serum glucose levels at the second day after admission ≥126mg/dl in patients without type 2 diabetes mellitus (T2DM). The outcome was assessed with adverse outcome rates at discharge (modified Rankin scale between 2 and 6) and with in-hospital mortality. RESULTS: In the total study population, 8.6% had stress hyperglycemia. Patients with stress hyperglycemia had more severe stroke. Independent predictors of adverse outcome at discharge were age, prior ischemic stroke and NIHSS at admission whereas treatment with statins prior to stroke was associated with favorable outcome. When the NIHSS was removed from the multivariate model, independent predictors of adverse outcome were age, heart rate at admission, prior ischemic stroke, log-triglyceride (TG) levels and stress hyperglycemia, whereas treatment with statins prior to stroke was associated with favorable outcome. Independent predictors of in-hospital mortality were atrial fibrillation (AF), diastolic blood pressure (DBP), serum log-TG levels and NIHSS at admission. When the NIHSS was removed from the multivariate model, independent predictors of in-hospital mortality were age, AF, DBP, log-TG levels and stress hyperglycemia. CONCLUSION: Stress hyperglycemia does not appear to be directly associated with the outcome of acute ischemic stroke. However, given that patients with stress hyperglycemia had higher prevalence of cardiovascular risk factors than patients with normoglycemia and that glucose tolerance was not evaluated, more studies are needed to validate our findings.

Prognostic significance of major lipids in patients with acute ischemic stroke.

Although dyslipidemia increases the risk for ischemic stroke, previous studies reported conflicting data regarding the association between lipid levels and stroke severity and outcome. To evaluate the predictive value of major lipids in patients with acute ischemic stroke. We prospectively studied 790 consecutive patients who were admitted with acute ischemic stroke (41.0 % males, age 79.4 ± 6.8 years). The severity of stroke was assessed at admission with the National Institutes of Health Stroke Scale (NIHSS). Moderate/severe stroke was defined as NIHSS ≥5. The outcome was assessed with dependency rates at discharge (modified Rankin scale between 2 and 5) and with in-hospital mortality. Independent predictors of moderate/severe stroke were age (relative risk (RR) 1.05, 95 % confidence interval (CI) 1.02-1.08, p < 0.001), atrial fibrillation (RR 1.71, 95 % CI 1.19-2.47, p < 0.005), heart rate (RR 1.02, 95 % CI 1.01-1.04, p < 0.001), log-triglyceride (TG) levels (RR 0.24, 95 % CI 0.08-0.68, p < 0.01) and high-density lipoprotein cholesterol (HDL-C) levels (RR 0.97, 95 % CI 0.95-0.98, p < 0.001). Major lipids did not predict dependency at discharge. Independent predictors of in-hospital mortality were atrial fibrillation (RR 2.35, 95 % CI 1.09-5.04, p < 0.05), diastolic blood pressure (RR 1.05, 95 % CI 1.02-1.08, p < 0.001), log-TG levels (RR 0.09, 95 % CI 0.01-0.87, p < 0.05) and NIHSS at admission (RR 1.19, 95 % CI 1.14-1.24, p < 0.001). Low-density lipoprotein cholesterol levels were not associated with stroke severity or outcome. Lower TG and HDL-C levels are associated with more severe stroke. Lower TG levels also appear to predict in-hospital mortality in patients with acute ischemic stroke.

Treatment with Clopidogrel Prior to Acute Non-Cardioembolic Ischemic Stroke Attenuates Stroke Severity.

BACKGROUND: Clopidogrel reduces the risk of non-cardioembolic ischemic stroke, but it is unclear whether it affects the severity and outcome of stroke. We aimed at evaluating the effect of prior treatment with clopidogrel on acute non-cardioembolic ischemic stroke severity and in-hospital outcome. METHODS: We prospectively studied 608 consecutive patients (39.5% males, age 79.1 ± 6.6 years) who were admitted with acute ischemic stroke. The severity of stroke was assessed at admission with the National Institutes of Health Stroke Scale (NIHSS). Severe stroke was defined as NIHSS ≥21. The outcome was assessed using the dependency rates that prevailed at the time of discharge (i.e. modified Rankin scale between 2 and 5) and with in-hospital mortality. RESULTS: At admission, 397 patients did not have atrial fibrillation or heart valve disease. Among these 397 patients, 69 were receiving monotherapy with clopidogrel prior to stroke, 69 were receiving monotherapy with aspirin and 236 patients were not on any antiplatelet treatment. The prevalence of severe stroke was lower in patients who were receiving clopidogrel than in patients who were receiving aspirin and patients who were not on antiplatelets (1.4, 13.0 and 11.0%, respectively; p < 0.05). Independent predictors of severe stroke at admission were male gender (relative risk (RR) 0.31, 95% CI 0.12-0.78, p < 0.05) and treatment with clopidogrel prior to stroke compared with no antiplatelet treatment (RR 0.13, 95% CI 0.02-0.97, p < 0.05). Treatment with aspirin prior to stroke did not predict severe stroke compared with no antiplatelet treatment (RR 1.24, 95% CI 0.51-2.98, p = NS). The rate of dependency at discharge did not differ between patients who were receiving clopidogrel, patients who were receiving aspirin and those who were not on antiplatelets (57.9, 47.8 and 59.7%, respectively; p = NS). Independent predictors of dependency at discharge were age (RR 1.12, 95% CI 1.05-1.19, p < 0.001) and NIHSS at admission (RR 1.67, 95% CI 1.46-1.92, p < 0.001). In-hospital mortality rate also did not differ between patients who were receiving clopidogrel, patients who were receiving aspirin and those who were not on antiplatelets (4.3, 4.3 and 5.0%, respectively; p = NS). The only independent predictor of in-hospital mortality was NIHSS at admission (RR 1.22, 95% CI 1.14-1.30, p < 0.001). CONCLUSIONS: Treatment with clopidogrel prior to acute non-cardioembolic ischemic stroke attenuates the severity of stroke at admission but does not appear to affect the functional outcome at discharge or the in-hospital mortality of these patients.

Adequacy of preadmission oral anticoagulation with vitamin K antagonists and ischemic stroke severity and outcome in patients with atrial fibrillation.

It is unclear whether vitamin K antagonists affect stroke severity and outcome in patients with atrial fibrillation (AF). We aimed to evaluate this association. We prospectively studied 539 consecutive patients admitted with acute ischemic stroke (41.2 % males, age 78.9 ± 6.6 years). The severity of stroke was assessed at admission with the National Institutes of Health Stroke Scale (NIHSS). The outcome was assessed with dependency rates at discharge (modified Rankin scale 2-5) and with in-hospital mortality. 177 patients had a history of AF. The median NIHSS at admission did not differ between patients on acenocoumarol with INR 2.0-3.0, on acenocoumarol with INR < 2.0, on single antiplatelet treatment, on dual antiplatelet treatment, or on no treatment [4 (range 0-26), 13 (0-39), 8 (0-33), 3 (2-23) and 7 (0-33), respectively; p = 0.433]. Dependency rates were lower in patients on acenocoumarol with INR 2.0-3.0 or on dual antiplatelet treatment than in those on acenocoumarol with INR < 2.0, single antiplatelet treatment, or no treatment (20.0, 22.2, 61.5, 58.7 and 68.0 %, respectively; p = 0.024). Independent predictors of dependency were age, NIHSS at admission and history of ischemic stroke. In-hospital mortality did not differ between patients on acenocoumarol with INR 2.0-3.0, on acenocoumarol with INR < 2.0, on single antiplatelet treatment, on dual antiplatelet treatment, or on no treatment (7.7, 18.2, 16.1, 16.7 and 22.2 %, respectively; p = 0.822). In conclusion, optimally anticoagulated patients with AF have more favorable functional outcome after stroke and a trend for less severe stroke whereas patients with subtherapeutic anticoagulation have similar stroke severity and outcome with those on no treatment.

Acenocoumarol vs. low-dose dabigatran in real-world patients discharged after ischemic stroke.

The aim of this study was to compare the efficacy of dabigatran 110 mg twice daily and acenocoumarol in patients with atrial fibrillation discharged after ischemic stroke. We prospectively studied 436 consecutive patients who were discharged after acute ischemic stroke (39.2% males, age 78.6 ±â€Š6.7 years). Approximately 1 year after discharge, the functional status was assessed with the modified Rankin scale (mRS). Adverse outcome was defined as mRS between 2 and 6. The occurrence of ischemic stroke, myocardial infarction (MI) and death during the 1-year follow-up was also recorded. At discharge, 142 patients had atrial fibrillation. Acenocoumarol and dabigatran 110 mg twice daily were prescribed to 52.1 and 6.3% of these patients, respectively. At 1 year after discharge, there was a trend for patients treated with acenocoumarol to have lower mRS than patients prescribed dabigatran (2.3 ±â€Š2.4 and 4.1 ±â€Š2.2, respectively; P = 0.060). Adverse outcome rates and the incidence of stroke during follow-up did not differ between the two groups. The incidence of MI was almost three times higher in patients prescribed dabigatran than in those prescribed acenocoumarol, but this difference did not reach significance (11.1 and 4.0%, respectively; P = 0.254). The incidence of cardiovascular death was also almost three times higher in the former, but again this difference was not significant (33.3 and 12.2%, respectively; P = 0.237). In real-world patients with acute ischemic stroke, dabigatran 110 mg twice daily is as effective as acenocoumarol in preventing stroke but appears to be associated with worse long-term functional outcome and higher incidence of MI.

No Association Observed Between Blood Pressure Variability During the Acute Phase of Ischemic Stroke and In-Hospital Outcomes.

BACKGROUND: Recent data suggest that blood pressure (BP) variability confers increased cardiovascular risk independently of BP. We aimed to evaluate the association between BP variability during the acute phase of ischemic stroke and the in-hospital outcome. METHODS: We prospectively studied 608 consecutive patients admitted with acute ischemic stroke (39.5% males, age: 79.1±6.6 years). Variability in BP was assessed with the SD and with the coefficient of variation of systolic (SBP) and diastolic BP (DBP) during the first 2 and the first 3 days of hospitalization. The outcome was assessed with dependency rates at discharge and with in-hospital mortality. RESULTS: Patients who were dependent at discharge did not differ from patients who were independent in any index of BP variability. Independent predictors of dependency at discharge were age (relative risk (RR) 1.17, 95% confidence interval (CI) 1.09-1.25, P < 0.001), history of prior ischemic stroke (RR 2.08, 95% CI 1.02-4.24, P = 0.04), and National Institutes of Health Stroke Scale (NIHSS) at admission (RR 1.64, 95% CI 1.44-1.86, P < 0.001). Patients who died during hospitalization did not differ in any index of BP variability from patients who were discharged. DBP at admission was independently and directly associated with in-hospital mortality (RR 1.06, 95% CI 1.03-1.09, P < 0.001). Other independent predictors of in-hospital mortality were history of atrial fibrillation (RR 3.30, 95% CI 1.46-7.49, P = 0.004) and NIHSS at admission (RR 1.18, 95% CI 1.13-1.23, P < 0.001). CONCLUSIONS: Our data do not support the hypothesis of an association between BP variability and in-hospital outcomes among patients admitted for ischemic stroke.

Comparative effects of more versus less aggressive treatment with statins on the long-term outcome of patients with acute ischemic stroke.

BACKGROUND AND AIMS: There are no studies that compared the effects of different intensities of statin treatment on the long-term outcome of patients with recent ischemic stroke. We aimed to evaluate these effects. METHODS: We prospectively studied 436 consecutive patients who were discharged after acute ischemic stroke (39.2% males, age 78.6 ± 6.7 years). Statin treatment was categorized in equipotent doses of atorvastatin. One year after discharge, the functional status was assessed with the modified Rankin scale (mRS). Adverse outcome was defined as mRS between 2 and 6. The occurrence of ischemic stroke, myocardial infarction and death was recorded. RESULT: Adverse outcome rates were lower in patients treated with atorvastatin 20 mg/day or more potent doses of statins than in patients treated with atorvastatin 10 mg/day (63.5, 38.2 and 48.2%, respectively; p = 0.004). In binary logistic regression analysis, independent predictors of adverse outcome were the mRS at discharge (relative risk (RR) 2.33, 95% confidence interval (CI) 1.77-3.07, p < 0.001) whereas more aggressive treatment with statins independently predicted favorable outcome (atorvastatin 20 vs. 10 mg/day, RR 0.30, 95% CI 0.11-0.87, p = 0.026; atorvastatin 40 mg/day or more potent dose of statins vs. atorvastatin 10 mg/day, RR 1.66, 95% CI 0.62-4.44, p = NS). The incidence of cardiovascular events and all-cause mortality showed a trend for being lower in patients treated with atorvastatin 40-80 mg/day or rosuvastatin 10-40 mg/day than in those treated with less potent doses of statins. CONCLUSION: More aggressive statin treatment improves the long-term functional outcome of patients with acute ischemic stroke more than less aggressive treatment.

Prior treatment with dipeptidyl peptidase 4 inhibitors is associated with better functional outcome and lower in-hospital mortality in patients with type 2 diabetes mellitus admitted with acute ischaemic stroke.

It is unclear whether prior antidiabetic treatment affects stroke severity and outcome. To evaluate this association, we prospectively studied all patients who were admitted in our Department with acute ischaemic stroke (n = 378, mean age = 78.8 ± 6.5 years). The severity of stroke was assessed at admission with the National Institutes of Health Stroke Scale. The outcome was assessed with the modified Rankin Scale at discharge and with in-hospital mortality. A total of 123 patients had type 2 diabetes mellitus. At admission, there was a trend for lower National Institutes of Health Stroke Scale in patients treated with dipeptidyl peptidase 4 inhibitors compared with patients treated with other antidiabetic agents (6.1 ± 7.5 vs 10.0 ± 9.2, respectively; p = 0.079). At discharge, patients treated with dipeptidyl peptidase 4 inhibitors had lower modified Rankin Scale than patients treated with other antidiabetic agents (2.1 ± 1.9 vs 3.2 ± 2.1, respectively; p < 0.05). Patients treated with dipeptidyl peptidase 4 inhibitors also had lower in-hospital mortality than patients treated with other antidiabetic agents (0.0% vs 15.1%, respectively; p < 0.05). In conclusion, prior treatment with dipeptidyl peptidase 4 inhibitors in patients with acute ischaemic stroke appears to be associated with better functional outcome and lower mortality risk.

Clinical relevance of clopidogrel-proton pump inhibitors interaction.

Clopidogrel is a widely used antiplatelet agent for the secondary prevention of cardiovascular events in patients with stable coronary heart disease, acute coronary syndromes and ischemic stroke. Even though clopidogrel is safer than aspirin in terms of risk for gastrointestinal (GI) bleeding, the elderly, and patients with a history of prior GI bleeding, with Helicobacter pylori infection or those who are also treated with aspirin, anticoagulants, corticosteroids or nonsteroidal anti-inflammatory drugs are at high risk for GI complications when treated with clopidogrel. Accordingly, proton pump inhibitors are frequently administered in combination with clopidogrel to reduce the risk for GI bleeding. Nevertheless, pharmacodynamic studies suggest that omeprazole might attenuate the antiplatelet effect of clopidogrel. However, in observational studies, this interaction does not appear to translate into increased cardiovascular risk in patients treated with this combination. Moreover, in the only randomized, double-blind study that assessed the cardiovascular implications of combining clopidogrel and omeprazole, patients treated with clopidogrel/omeprazole combination had reduced risk for GI events and similar risk for cardiovascular events than patients treated with clopidogrel and placebo. However, the premature interruption of the study and the lack of power analysis in terms of the cardiovascular endpoint do not allow definite conclusions regarding the cardiovascular safety of clopidogrel/omeprazole combination. Other proton pump inhibitors do not appear to interact with clopidogrel. Nevertheless, given the limitations of existing observational and interventional studies, the decision to administer proton pump inhibitors to patients treated with clopidogrel should be individualized based on the patient's bleeding and cardiovascular risk.

Effects of different classes of antihypertensive agents on the outcome of acute ischemic stroke.

It is unclear whether antihypertensive treatment before stroke affects acute ischemic stroke severity and outcome. To evaluate this association, the authors studied 482 consecutive patients (age 78.8±6.7 years) admitted with acute ischemic stroke. Stroke severity was assessed at admission with the National Institutes of Health Stroke Scale (NIHSS). The outcome was assessed with rates of adverse outcome (modified Rankin scale at discharge ≥2). Independent predictors of severe stroke (NIHSS ≥16) were female sex and atrial fibrillation. Treatment with diuretics before stroke was associated with nonsevere stroke. At discharge, patients with adverse outcome were less likely to be treated before stroke with ß-blockers or with diuretics. Independent predictors of adverse outcome were older age, higher NIHSS at admission, and history of ischemic stroke. Treatment with diuretics before stroke appears to be associated with less severe neurologic deficit in patients with acute ischemic stroke.

Elevated diastolic but not systolic blood pressure increases mortality risk in hypertensive but not normotensive patients with acute ischemic stroke.

BACKGROUND: The relationship between blood pressure (BP) at admission for acute ischemic stroke and outcome is controversial. We aimed to assess whether only systolic BP (SBP), only diastolic BP (DBP), both or neither predict outcome and whether these associations differ between patients with and without a history of hypertension. METHODS: We prospectively studied all patients who were admitted with acute ischemic stroke (n = 415; 39.5% males, age 78.8 ± 6.6 years). The severity of stroke was assessed at admission with the National Institutes of Health Stroke Scale (NIHSS). The outcome was evaluated with dependency at discharge (modified Rankin scale between 2 and 5) and in-hospital mortality. RESULTS: In the total study population, independent predictors of dependency at discharge were age, history of prior ischemic stroke, and NIHSS score at admission. Independent predictors of in-hospital mortality were DBP at admission and NIHSS score at admission. In patients with a history of hypertension (n = 343), independent predictors of dependency at discharge were age and NIHSS score at admission whereas independent predictors of in-hospital mortality were DBP at admission and NIHSS score at admission. In patients without a history of hypertension (n = 72), the only independent predictor of dependency at discharge and in-hospital mortality was the NIHSS score at admission. CONCLUSIONS: Higher DBP at admission predict in-hospital mortality in patients with acute ischemic stroke whereas SBP in the acute phase is not associated with short-term outcome. The relationship between DBP at admission and outcome appears to be more prominent in hypertensive patients.

Type 2 diabetes is associated with a worse functional outcome of ischemic stroke.

AIM: To assess whether ischemic stroke severity and outcome is more adverse in patients with type 2 diabetes mellitus (T2DM). METHODS: Consecutive patients hospitalized for acute ischemic stroke between September 2010 and June 2013 were studied prospectively (n = 482; 40.2% males, age 78.8 ± 6.7 years). T2DM was defined as self-reported T2DM or antidiabetic treatment. Stroke severity was evaluated with the National Institutes of Health Stroke Scale (NIHSS) score at admission. The outcome was assessed with the modified Rankin scale (mRS) score at discharge and with in-hospital mortality. Adverse outcome was defined as mRS score at discharge ≥ 2 or in-hospital death. The length of hospitalization was also recorded. RESULTS: T2DM was present in 32.2% of the study population. Patients with T2DM had a larger waist circumference, higher serum triglyceride and glucose levels and lower serum high-density lipoprotein cholesterol levels as well as higher prevalence of hypertension, coronary heart disease and congestive heart failure than patients without T2DM. On the other hand, diabetic patients had lower low-density lipoprotein cholesterol levels and reported smaller consumption of alcohol than non-diabetic patients. At admission, the NIHSS score did not differ between patients with and without T2DM (8.7 ± 8.8 and 8.6 ± 9.2, respectively; P = NS). At discharge, the mRS score also did not differ between the two groups (2.7 ± 2.1 and 2.7 ± 2.2 in patients with and without T2DM, respectively; P = NS). Rates of adverse outcome were also similar in patients with and without T2DM (62.3% and 58.5%, respectively; P = NS). However, when we adjusted for the differences between patients with T2DM and those without T2DM in cardiovascular risk factors, T2DM was independently associated with adverse outcome [relative risk (RR) = 2.39; 95%CI: 1.21-4.72, P = 0.012]. In-hospital mortality rates did not differ between patients with T2DM and those without T2DM (9.0% and 9.8%, respectively; P = NS). In multivariate analysis adjusting for the difference in cardiovascular risk factors between the two groups, T2DM was again not associated with in-hospital death. CONCLUSION: T2DM does not appear to affect ischemic stroke severity but is independently associated with a worse functional outcome at discharge.

Increased augmentation index is paradoxically associated with lower in-hospital mortality in patients with acute ischemic stroke.

OBJECTIVE: To evaluate the association between arterial stiffness and stroke severity and in-hospital outcome in patients admitted with acute ischemic stroke. METHODS: We prospectively studied 415 consecutive patients who were admitted with acute ischemic stroke (39.5% males, age 78.8 ± 6.6 years). On the third day of hospitalization, the following markers of arterial stiffness were recorded: central systolic blood pressure (cSBP), diastolic BP (cDBP), mean pressure (cMP), pulse pressure (cPP), augmentation index (AIx) and pulse wave velocity (PWV). The severity of stroke was assessed on admission with the National Institutes of Health Stroke Scale (NIHSS) score. The outcome was evaluated with rates of dependency at discharge (modified Rankin scale score between 2 and 5) and in-hospital mortality. RESULTS: None of the markers of arterial stiffness showed significant correlation with the NIHSS score on admission. However, there was a trend for an inverse correlation with AIx (r = -0.142, p = 0.064) and for a positive correlation with PWV (r = 0.235, p = 0.054). None of the markers of arterial stiffness differed between patients who were dependent at discharge and those who were independent. Patients who died during hospitalization had higher cDBP and cMP but lower cPP and AIx than patients who were discharged. In binary logistic regression analysis, independent predictors of in-hospital mortality were NIHSS score on admission (relative risk (RR) 1.16, 95% confidence interval (CI) 1.08-1.25, p < 0.001), presence of atrial fibrillation (RR 6.41, 95% CI 1.37-29.93, p = 0.018) and AIx (RR 0.94, 95% CI 0.89-0.99, p = 0.030). CONCLUSIONS: Increased AIx appears to be associated with lower in-hospital mortality rates in elderly patients with acute ischemic stroke. Other markers of arterial stiffness do not appear to be associated with short-term outcome in this population.

Association between nonalcoholic fatty liver disease and acute ischemic stroke severity and outcome.

AIM: To evaluate the association of nonalcoholic fatty liver disease (NAFLD) with acute ischemic stroke severity and in-hospital outcome. METHODS: We prospectively studied all patients who were admitted in our Department with acute ischemic stroke between September 2010 and August 2012 (n = 415; 39.5% males, mean age 78.8 ± 6.6 years). The severity of stroke was assessed with the National Institutes of Health Stroke Scale (NIHSS) score at admission. NALFD was defined as serum alanine aminotransferase and/or aspartate aminotransferase levels above the upper limit of normal in the absence of other causes of elevated aminotransferases levels [chronic hepatitis B or C, drug toxicity, increased alcohol consumption (> 21 and > 14 drinks per week in men and women, respectively), cholestatic diseases or rhabdomyolysis]. The outcome was assessed with the modified Rankin scale (mRS) score at discharge and in-hospital mortality. Adverse outcome was defined as mRS score at discharge ≥ 2. Dependency at discharge was defined as mRS score between 2 to 5. RESULTS: NAFLD was present in 7.7% of the study population. Patients with NAFLD had lower serum high-density lipoprotein cholesterol and higher triglyceride levels than patients without NAFLD (P < 0.05 for both comparisons). Demographic data, the prevalence of other cardiovascular risk factors and the prevalence of established CVD did not differ between the two groups. At admission, the NIHSS score did not differ between patients with and without NAFLD (6.3 ± 6.4 and 8.8 ± 9.6, respectively; P = NS). At discharge, the mRS score did not differ between the two groups (1.9 ± 2.2 and 2.6 ± 2.2 in patients with and without NAFLD, respectively; P = NS). Rates of dependency at discharge were also similar in patients with and without NAFLD (36.8% and 55.0%, respectively; P = NS) as were the rates of adverse outcome (42.9% and 58.6%, respectively; P = NS). In-hospital mortality rates also did not differ between the 2 groups (8.0% and 7.0% in patients with and without NAFLD, respectively; P = NS). CONCLUSION: The presence of NAFLD in patients admitted for acute ischemic stroke does not appear to be associated with more severe stroke or with worse in-hospital outcome.

Potential treatment of human nonalcoholic fatty liver disease with long-chain omega-3 polyunsaturated fatty acids.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder in the Western world. Its prevalence has increased with the growing obesity epidemic, yet no definitive treatment has been developed, and optimal management remains a clinical challenge. Long-chain omega-3 polyunsaturated fatty acids (PUFAs) have recently been proposed as a potential treatment for liver inflammation associated with fat accumulation. PubMed literature and the ClinicalTrials.gov database were reviewed for the effects of omega-3 PUFA treatment on NAFLD, from mechanisms to the results of preclinical studies, human studies, and unreported ongoing clinical trials, using terms such as NAFLD, nonalcoholic steatohepatitis, omega-3 fatty acids, and fish oil. Articles published over the last 3-4 years were emphasized, and relevancy was ensured by scanning their abstracts. Preliminary studies have confirmed an ameliorative effect, yet the translation of promising early data into therapeutic interventions will have to await the results of larger, properly conducted, ongoing clinical trials.