Evaluation of von Willebrand factor in COPD patients

OBJECTIVE:

To compare the absolute serum von Willebrand factor (vWF) levels and relative serum vWF activity in patients with clinically stable COPD, smokers without airway obstruction, and healthy never-smokers.

METHODS:

The study included 57 subjects, in three groups: COPD (n = 36); smoker (n = 12); and control (n = 9). During the selection phase, all participants underwent chest X-rays, spirometry, and blood testing. Absolute serum vWF levels and relative serum vWF activity were obtained by turbidimetry and ELISA, respectively. The modified Medical Research Council scale (cut-off score = 2) was used in order to classify COPD patients as symptomatic or mildly symptomatic/asymptomatic.

RESULTS:

Absolute vWF levels were significantly lower in the control group than in the smoker and COPD groups: 989 ± 436 pg/mL vs. 2,220 ± 746 pg/mL (p < 0.001) and 1,865 ± 592 pg/mL (p < 0.01). Relative serum vWF activity was significantly higher in the COPD group than in the smoker group (136.7 ± 46.0% vs. 92.8 ± 34.0%; p < 0.05), as well as being significantly higher in the symptomatic COPD subgroup than in the mildly symptomatic/asymptomatic COPD subgroup (154 ± 48% vs. 119 ± 8%; p < 0.05). In all three groups, there was a negative correlation between FEV₁ (% of predicted) and relative serum vWF activity (r² = −0.13; p = 0.009).

CONCLUSIONS:

Our results suggest that increases in vWF levels and activity contribute to the persistence of systemic inflammation, as well as increasing cardiovascular risk, in COPD patients.     

Microalbuminuria,von Willebrand factor and fibrinogen levels as markers of the severity in COPD exacerbation

In COPD, the systemic effects of the disease reflect the structural and/or biochemical alterations occurring in the structures or organs other than the lungs in relation to the characteristics of the primary disease. The disorders of endothelial structures due to COPD may lead vascular pathologies, such as ischemic heart disease, stroke, to occur more commonly in those with COPD. On consideration of the fact that the vascular endothelium is a major site in which the systemic effect of the inflammation occurs, should von Willebrand Factor, a clotting factor of endothelium origin, and the plasma level of fibrinogen vary with the severity of the disease in COPD, the variability of arterial blood gas values, and the stability or exacerbation of the disease? Considering the fact that microalbuminuria is an indirect manifestation of the renal endothelial permeability and/or renal perfusion; should there be an association between microalbuminuria and the severity of COPD? Therefore, in order to assess the effect of the systemic inflammation in COPD on the vascular endothelium, we compared the levels of the plasma vWF, fibrinogen, 24-h urine microalbuminuria of those with stable COPD (33 patients) and exacerbation of COPD (26 patients) with those of the controls (16 healthy subjects). The mean age was 63.42 ? 10.29, 68.00 ? 9.77 and 59.63 ? 14.10 years in SCOPD, COPDAE, and CG, respectively. The level of microalbuminuria was found to increase significantly in COPDAE group, compared to that of the controls (P = 0.004). When we investigated the relation between smoking burden and microalbuminuria, vWF, fibrinogen levels, the amount of consumption and positive relationship were found significant. (r = 0.336, P = 0.003 between smoking pack-years and vWF, r = 0.403, P = 0.001 between smoking pack-years and fibrinogen, and r = 0.262, P = 0.02 between smoking pack-years and microalbuminuria). The levels of vWF and fibrinogen are AECOPD > SCOPD > CG, with the highest being in AECOPD, and the difference among the groups was statistically significant. The relationship between the level of hypoxemia and microalbuminuria, fibrinogen and vWF was found to be significant (r = ?0.360, P = 0.005 between oxygen saturation and microalbuminuria, r = ?0.359, P = 0.005 between the level of PaO₂ and fibrinogen, and r = ?0.336, P = 0.009 between PaO₂ and vWF). In conclusion, the levels of plasma vWF, fibrinogen, and microalbuminuria may be helpful in grading the severity of COPD exacerbation. The related increase in these markers may represent a possible pathophysiological mechanism behind the increased vascular morbidity of patients with COPD and detecting indirectly the endothelial dysfunction as a manifestation of systemic outcomes due to COPD and in detecting earlier the cases in which the risk for developing the associated complications are higher. We suggest that further studies are necessary to investigate the impact of antithrombotic treatment on microalbuminuria, plasma vWF and fibrinogen as markers of endothelial dysfunction coexisting COPD exacerbation.     

Haemorheological, platelet and endothelial indices in relation to global measures of cardiovascular risk in hypertensive patients: a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial

INTRODUCTION AND METHODS: We tested the hypothesis that there was a significant relationship between haemorheological markers [white blood cell count (WCC), plasma viscosity (PV), haematocrit (HCT) and fibrinogen], as well as plasma von Willebrand factor (vWf, an index of endothelial damage/dysfunction) and soluble P-selectin (sP-sel, an index of platelet activation), to five global measures of cardiovascular risk [i.e. Framingham coronary heart disease (CHD), stroke and cardiovascular death score, the Pocock cardiovascular risk score and the sum of individual risk factors]. RESULTS: Men with a high (> or = median, n = 156) Framingham 10-year CHD risk score had higher levels of WBC (P = 0.027), fibrinogen (P = 0.012) and vWF (P = 0.002) than 153 men with results < median. Men with a high 10-year stroke risk score had significantly higher levels of fibrinogen (P = 0.01) and vWF (P < 0.0001). In stepwise linear regression analysis in men, vWF and fibrinogen were independent predictors of the number of risk factors (P < 0.0001), whilst WCC, vWF and fibrinogen emerged as independent predictors of Framingham CHD risk (P < 0.0001), and fibrinogen and vWF predicted Framingham stroke risk (R(2) = 0.089, P < 0.0001). vWF, PV and fibrinogen were predictors of Pocock cardiovascular death risk (P < 0.0001) but vWF was the only independent predictor of Framingham cardiovascular death risk (P = 0.001). CONCLUSIONS: Abnormal haemorheological factors (particularly high plasma fibrinogen levels) and endothelial damage/dysfunction (high vWF), but not platelet activation (sP-sel), are related to established cardiovascular and death risk scores. This relationship was most evident amongst male 'high-risk' hypertensive subjects.     

Concordance between Doppler and pulsed-wave Doppler tissue imaging in estimation of the degree of left ventricular dysfunction and correlating it to the degree of chronic obstructive pulmonary disease

Objective

As a consequence of leftward shift of the interventricular septum and of pericardial restraint, related to the degree of right ventricular dilation, alveolar hypoxia and related pulmonary vascular changes, left ventricular function is influenced by chronic obstructive pulmonary disease (COPD). The aim of this study was to assess the prevalence of echocardiographic abnormalities by conventional echocardiography and Doppler tissue imaging (DTI) in COPD patients according to the degree of disease severity.

Methods

We enrolled forty consecutive patients with COPD and twenty matched control. Twenty of the patients were suffering from mild form of COPD, twenty were suffering from severe form of COPD as decided by pulmonary function test and arterial blood gases and twenty apparently healthy non COPD control persons were subjected to echocardiographic assessment to left ventricular diastolic and systolic functions by conventional echocardiography and DTI at the mitral annulus.

Results

There were no significant statistical difference between the three groups as regards the age and the gender. There were significant statistical differences between the patients and the control as regards the diastolic functions of the left ventricle. E and A waves obtained by conventional Doppler and by DTI showed significant statistical difference between mild, severe forms of COPD and control subjects. The degree of diastolic dysfunction increased significantly with increase of the severity of COPD.

Conclusion

Left ventricular diastolic function is significantly affected in patients with COPD and the degree of affection is related to the severity of COPD.     

Changes of HMGB1 and sRAGE during the recovery of COPD exacerbation

Background

Acute exacerbation of chronic obstructive pulmonary disease is associated with increased airway and systemic inflammation. However, the correlation between acute exacerbation/convalescence of chronic obstructive pulmonary disease (COPD) and simultaneous changes of high mobility group protein B1 (HMGB1) and soluble RAGE (sRAGE) levels has not been clearly clarified. The aim of this study was to assess these issues.

Methods

A total of 44 COPD patients were recruited. Following a structured interview, plasma levels of HMGB1, sRAGE, fibrinogen and serum level of high-sensitivity C-reactive protein (hsCRP) were measured in patients with acute exacerbation of COPD (AECOPD) within 24 h of hospitalization and pre-discharge (convalescence). All patients were examined with spirometry in convalescence of COPD.

Results

There was a significant decline in plasma HMGB1 (P<0.01), sRAGE (P<0.05), fibrinogen (P<0.01) and serum hsCRP (P<0.01) levels from acute exacerbation to convalescence phase of COPD. Changes of sRAGE was significantly correlated with changes of HMGB1 (r=0.4, P=0.007). COPD disease status correlated with the ratio of HMGB1/sRAGE, but not gender, age, course of disease, smoking history and FEV1% pred. Levels of HMGB1 and sRAGE were the highest in the current smoker group, and significantly decreased in ex-smoker group in both acute exacerbation and convalescence phase of COPD, however, their levels in never smoker group were higher than ex-smoker group in either phase of COPD.

Conclusions

HMGB1 and sRAGE levels were dynamically changed between exacerbation and convalescence phase of COPD, HMGB1 and sRAGE were likely not only a potential marker in COPD exacerbation but also a therapeutic target for COPD treatment.     

Chronic HCV infection is a risk factor of ischemic stroke

Objectives

Cerebrovascular diseases are leading cause of death worldwide. Plaque rupture and embolization account for one-third of ischemic stroke. The causes are not fully known, but inflammation plays a pathogenic role. Recently, HCV infection has been identify as risk of atherosclerosis. HCV replicates within carotid plaques and brain endothelia cells; moreover, HCV patients showed higher levels of inflammation. Thus, we hypothesized that subjects carrying HCV are at higher risk of stroke. Accordingly, we evaluated prevalence and role of HCV infection in patients with stroke.

Methods

A priori sample size was calculated. Overall, 820 consecutive patients were enrolled, 123 with stroke and, as control, 697 age- and gender-matched (295 with COPD; 402 with diseases other than HCV-associated). Patients were evaluated for HCV and conventional risk of stroke.

Results

Prevalence of HCV was higher in patients with stroke than that observed in control (26.8% vs. 6.6%, p = 0.0001). An analysis of stroke patients showed that those HCV positive were younger (p = 0.017) had lower serum levels of cholesterol (p = 0.001), triglycerides (p = 0.045), and higher serum levels of inflammation markers (ESR, p = 0.001; CRP, p = 0.0001; fibrinogen, p = 0.012). A multivariate analysis showed that HCV infection was an independent risk factor of stroke (O.R. 2.04, 95% C.I. 1.69–2.46; p = 0.0001). A secondary analysis showed that HCV patients had higher (p = 0.031) prevalence of past ischemic heart disease.

Conclusions

HCV infected patients are at higher and earlier risk of stroke. Inflammation is a key mediator. Clinicians in clinical practice and researchers in future trials should take into account these new findings.     

Hypertension and diabetes mellitus as a predictive risk factors for stroke

Background

Stroke is becoming a major challenge in healthcare systems, and this has necessitated the study of the various risk factors. As the number of people with hypertension, diabetes mellitus and obesity increases, the problem is expected to worsen. This review paper evaluates what can be done to eliminate or reduce the risk of stroke.

Baseline vWF factor predicts the development of elevated pulmonary artery pressure in systemic sclerosis

Objectives. This study aims to examine the utility of von Willebrand factor (vWF) as a biomarker in lcSSc, in particular the ability of vWF to predict the future development of disease manifestations in this disease. Methods. vWFAg concentrations were measured in the serum of patients with lcSSc at baseline and at 3 years, during the QUINs trial [Prevention of Vascular Damage in Scleroderma with Angiotensin-Converting Enzyme (ACE) Inhibition]. %DL(CO), %KCO, %FVC, pulmonary artery pressure (PAP) estimation by echocardiography, Raynaud's attack frequency, Raynaud's severity, digital ulcer frequency, urinary protein excretion, estimated glomerular filtration rate (eGFR), modified Rodnan skin score and Medsger disease activity score were also measured at baseline and 3 years. Results. Baseline serum vWF concentrations were related to concurrent Medsger disease activity score, %DL(CO), %FVC, urinary protein excretion, eGFR and PAP >30?mmHg. In logistic regression models, baseline serum vWF concentrations were able to predict the future development of elevated PAP by echocardiography (PAP >40?mmHg, P?=?0.001). Conclusions. Pulmonary artery hypertension is a life-threatening complication of lcSSc. vWF is a marker of endothelial cell activation. Raised serum concentrations of vWF in lcSSc increase the risk of developing subsequent elevation in PAP. Therefore screening patients with lcSSc for vWF may identify a group at risk of developing PAH. These patients could potentially be targeted with agents that stabilize the endothelium, e.g. statins.     

Differences in cardiovascular risk factors and socioeconomic status do not explain the increased risk of death after a first stroke in diabetic patients: results from the Swedish Stroke Register

Aims/hypothesis

This study compared survival rates and causes of death after stroke in diabetic and non-diabetic patients in Sweden. We hypothesised that differences in cardiovascular risk factors, acute stroke management or socioeconomic status (SES) could explain the higher risk of death after stroke in diabetic patients.

Methods

The study included 155,806 first-ever stroke patients from the Swedish Stroke Register between 2001 and 2009. Individual patient information on SES was retrieved from Statistics Sweden. Survival was followed until 2010 (532,140 person-years) with a median follow-up time of 35 months. Multiple Cox regression was used to analyse survival adjusting for differences in background characteristics, in-hospital treatment, SES and year of stroke. Causes of death were analysed using cause-specific proportional hazard models.

Results

The risk of death after stroke increased in diabetic patients (HR 1.28, 95% CI 1.25, 1.31), and this risk was greater in younger patients and in women. Differences in background characteristics, cardiovascular risk factors, in-hospital treatment and SES did not explain the increased risk of death after stroke (HR 1.35, 95% CI 1.32, 1.37) after adjustments. Diabetic patients had an increased probability of dying from cerebrovascular disease and even higher probabilities of dying from other circulatory causes and all other causes except cancer.

Conclusions/interpretation

Differences in cardiovascular risk factors, acute stroke management and SES do not explain the lower survival after stroke in diabetic compared with non-diabetic patients. Diabetic patients are at higher risk of dying from cardiovascular causes and all other causes of death, other than cancer.     

Metabolic syndrome and carotid intima-media thickness in chronic obstructive pulmonary disease

Background

The aim of this study is to investigate the prevalence of metabolic syndrome (MetS), carotid intima media thickness (IMT), and serum C-reactive protein (CRP) levels in patients with chronic obstructive pulmonary disease (COPD), and the possible relationships among them.

Methods

Fifty stable COPD patients and 40 healthy controls were included in the study. The participants were further divided into four groups according to their smoking status. Pulmonary function tests were performed in COPD patients. Anthropometric measurements and blood chemistry analysis, serum CRP levels and carotid intima-media thickness (IMT) measurements were performed in all the study population.

Results

Prevalence of metabolic syndrome was 43% in COPD patients and 30% in the control group (p?=?0.173). FEV₁% and FEV₁/FVC were higher in COPD patients with MetS (p?=?0.001 and p?=?0.014, respectively) compared to those without MetS. Prevalence of MetS was significantly different among the COPD patients with different stages (p?=?0.017) with the highest value in stage 2 (59%). Carotid IMT was significantly higher in COPD patients than in control group (1.07?±?0.25 mm and 0.86?±?0.18 mm, respectively; p?<?0.001). Serum CRP levels were not different in COPD patients and controls, however they were higher in individuals with MetS compared to those without MetS regardless of COPD presence (p?=?0.02).

Conclusions

Early markers of atherogenesis, in terms of carotid IMT, were found to be higher in COPD patients than in healthy controls. MetS prevalence was observed to decrease as the severity of airflow obstruction increased. Therefore, screening COPD patients for these cardiovascular risk factors would be a novel approach even in absence of symptoms.

     

Heart Failure and Stroke

Purpose

Ischemic stroke significantly contributes to morbidity and mortality in heart failure (HF). The risk of stroke increases significantly, with coexisting atrial fibrillation (AF). An aggravating factor could be asymptomatic paroxysms of AF (so-called silent AF), and therefore, the risk stratification in these patients remains difficult. This review provides an overview of stroke risk in HF, its risk stratification, and stroke prevention in these patients.

Recent Findings

Stroke risk stratification in HF patients remains an important issue. Recently, the CHA₂DS₂-VASc score, originally developed to predict stroke risk in AF patients, had been reported to be a predictive for strokes in HF patients regardless of AF being present. Furthermore, there are several independent risk factors (e.g., hypertension, diabetes mellitus, prior stroke) described.

Summary

Based on the current evidence, HF should be considered as an independent risk factor for stroke. The CHA₂DS₂-VASc score might be useful to predict stroke risk in HF patients with or without AF in clinical routine. However, there is only a recommendation for the oral anticoagulation use in patients with concomitant HF and AF, while in patients with HF and no AF, individualized risk stratification is preferred. Current guidelines recommend to prefer non-vitamin Kantagonist anticoagulants over warfarin.

     

A cross-sectional and diurnal study of thrombogenesis among patients with chronic atrial fibrillation

OBJECTIVES

First, we sought to determine whether there is diurnal variation in hemostatic factors related to thrombogenesis and hypercoagulability among patients with chronic atrial fibrillation (AF). Second, we sought to determine whether levels of soluble thrombomodulin (sTM), a marker of endothelial function, or soluble P-selectin (sP-sel), an index of platelet activation, are altered in patients with AF as compared with subjects in sinus rhythm.

BACKGROUND

Atrial fibrillation is associated with an increased risk of stroke and thromboembolism and is known to confer a hypercoagulable state, with abnormalities of thrombosis, platelet activation and endothelial cell function. Many cardiovascular events, such as acute myocardial infarction, have thrombosis as an underlying process, and they undergo diurnal variation.

METHODS

Fifty-two patients (45 men, mean [±SD] age 66 ± 6 years) with chronic AF, none of whom received antithrombotic therapy, were studied. Baseline levels of fibrinogen, sP-sel, sTM and von Willebrand factor (vWF) were compared to those levels in matched healthy control subjects in sinus rhythm. In a subgroup of 20 patients, five venous blood samples were collected through an indwelling cannula at 6-h intervals from 12 to 12 the following day and were analyzed for the same markers.

RESULTS

Patients with chronic AF had higher plasma sP-sel, sTM, vWF and fibrinogen levels as compared with control subjects in sinus rhythm. Significant correlations were found between fibrinogen and sP-sel in patients with AF (r = 0.567 [Spearman], p < 0.001) and in control subjects (r = 0.334, p = 0.016). There was no significant diurnal variation in plasma levels of sP-sel, sTM, vWF or fibrinogen over the 24-h study period (repeated measures analysis of variance, p = NS).

CONCLUSIONS

There is no circadian or diurnal variation in the hypercoagulable state seen in AF, as assessed by plasma fibrinogen and markers of platelet (sP-sel) and endothelial function (vWF and sTM). The persistent hypercoagulable state, together with the loss of diurnal variation in various hemostatic markers, in chronic AF may contribute to the high risk of stroke and thromboembolic complications in these patients.     

Incidence and characteristics of stroke during 90-day follow-up in patients stabilized after an acute coronary syndrome

Background

Stroke is a rare but serious event that complicates the course of patients with acute coronary syndromes (ACS). The type, outcome, and risk factors of stroke occurring in stabilized patients with ACS have not been previously reported.

Methods

We evaluated stroke incidence, subtypes, and outcomes, in addition to demographics and clinical risk characteristics associated with stroke among patients enrolled in the Sibrafiban versus Aspirin to Yield Maximum Protection from Ischemic Heart Events Post-acute Coronary Syndromes (SYMPHONY) and 2nd SYMPHONY trials.

Results

Of 15,904 stabilized patients with ACS, 113 (0.71%) had a stroke over a median follow-up of 90 days. The majority of strokes occurred within 30 days of presentation, and the time course for stroke occurrence paralleled that of myocardial (re)infarction. Most strokes were ischemic (78%), and 52% resulted in moderate or severe disability or death. Patients with stroke were older and more often had hypertension, diabetes, peripheral vascular disease, and atrial fibrillation. Among patients with stroke who had cardiac catheterization, percutaneous coronary intervention, or coronary artery bypass grafting, stroke occurred predominantly after the procedure. No difference in occurrence or type of stroke was observed in the assigned treatment groups. In multivariable modeling age, heart failure, prior stroke, left bundle branch block, and systolic blood pressure predicted the occurrence of stroke.

Conclusions

In patients stabilized after presenting with a spectrum of ACS and treated with sibrafiban and/or aspirin, stroke occurred in fewer than 1% within 90 days but carried a significant mortality and morbidity risk.     

A prospective study of plasma fibrinogen levels and the risk of stroke among participants in the bezafibrate infarction prevention study.

PURPOSE: Plasma fibrinogen has emerged as an important predictor of cardiovascular disease, but few data are available on its association with stroke. We sought to determine if plasma fibrinogen is a marker of increased risk or a direct causative risk factor for stroke. SUBJECTS AND METHODS: Patients from the Bezafibrate Infarction Prevention Study, a placebo-controlled, randomized clinical trial of secondary prevention of coronary heart disease by lipid modification with bezafibrate retard (400 mg daily), were studied. Plasma fibrinogen levels were measured at baseline and yearly thereafter. Stroke, a prospectively monitored endpoint, was systematically assessed regarding stroke type, subtype, and functional outcome. RESULTS: Mean baseline fibrinogen levels were significantly higher in patients subsequently having a cerebrovascular event (140 strokes, 36 transient ischemic attacks; mean follow-up, 6.2 years) than in patients who did not (375 vs. 349 mg/dL, P <0.0001). Fibrinogen levels did not differ significantly by the type, subtype, or severity of the cerebrovascular event. Risk of ischemic stroke increased from 3.3% in the lowest tertile (baseline fibrinogen <314 mg/dL) to 7.% in the middle tertile (fibrinogen 314 to 373 mg/dL) to 10% in the upper tertile (fibrinogen >373 mg/dL, P <0.001). Adjusting for age, blood pressure, and other covariates, fibrinogen levels in the upper tertile were associated with more than a twofold increase in risk of ischemic stroke compared with in the lowest tertile (hazard ratio = 2.6; 95% confidence interval: 1.5 to 4.3). We did not find fibrinogen change from baseline to be related to subsequent ischemic stroke events. CONCLUSION: Plasma fibrinogen is a strong predictor of, rather than a direct causative factor for, subsequent stroke among patients at increased risk owing to manifest coronary heart disease.     

Meta-analysis of stroke after transradial versus transfemoral artery catheterization

Background

Transradial (TR) catheterization is gaining popularity due to its association with lower bleeding and access site complications, improved patient comfort, and lower costs compared to transfemoral (TF) catheterization; however, there is concern that TR catheterization may be associated with an increased risk of neurological complications. New randomized data has emerged since the publication of the last meta-analysis evaluating the risk of stroke between TR and TF catheterization in 2009.

Methods

We conducted a meta-analysis of randomized studies published until 2013 reporting risk of stroke in TR vs. TF catheterization.

Results

Data from 11,273 patients in 13 studies were collated. The majority of patients were men, and 8987 (79.7%) were enrolled in acute coronary syndrome trials. Very few patients had a history of prior coronary artery bypass grafting, and approximately 2/3 of patients underwent percutaneous coronary intervention. Stroke occurred in 25 of 5659 patients in the TR group, vs. 24 of 5614 patients in the TF group. There was no difference in stroke rates between the TR and TF groups (risk difference 0.00%, 95% confidence interval − 0.29%–0.25%, p = 0.88).

Conclusions

TR catheterization is not associated with a significant increase in stroke compared to TF catheterization.     

Stroke complicating percutaneous coronary intervention in patients with acute myocardial infarction.

BACKGROUND: Stroke associated with percutaneous coronary intervention (PCI) is a tragic complication. Despite advances in the practice of PCI, the incidence of stroke complicating PCI has not changed over the decades. The objective of the present study was to evaluate incidence and correlates of stroke occurring in patients with myocardial infarction (MI) undergoing PCI. METHODS AND RESULTS: Stroke was defined as the presence of any new focal neurological deficit lasting > or =24 h that occurred anytime during or after PCI until discharge. In 2,281 consecutive patients with PCIs for non-ST-elevation MI, or ST-elevation MI (STEMI), 20 strokes were identified (0.88%). Strokes were ischemic in 95%. On multivariate analyses, ejection fraction < or =30% (odds ratio =4.3, p=0.003) was the only independent predictor for stroke. In patients who developed stroke within 24 h of PCI, PCI of vein grafts was more frequent, and use of glycoprotein IIb/IIIa inhibitor was less frequent. Those patients tended to present late in the course of MI. Stroke found more than 24 h after PCI was related to diabetes, higher serum creatinine, lower ejection fraction, anterior wall STEMI and emergency use of intra-aortic balloon pumps. CONCLUSIONS: Low ejection fraction was the only independent predictor for stroke, but risk factors for periprocedural stroke are different from those of stroke occurring more than 24 h after PCI. Upstream use of glycoprotein IIb/IIIa inhibitor might decrease the risk of periprocedural stroke.     

Platelet Count Affects Efficacy of Folic Acid in Preventing First Stroke

Background

The role of platelets and important effect modifiers on the risk of first stroke is unknown.

Endothelial damage and hemostatic markers in patients with uncomplicated mild-to-moderate hypertension and relationship with risk factors.

Endothelial damage, high fibrinogen levels, and platelet activity are the important accelerating factors for the development of hypertension (HT). von Willebrand factor (vWF; endothelial damage marker), fibrinogen levels, and platelet aggregability were compared between patients with uncomplicated, mild-to-moderate hypertension and healthy subjects. The relationship between traditional cardiovascular risk factors and endothelial damage and prothrombotic state was evaluated. One hundred sixty-nine (54 males, 115 females) patients with untreated and uncomplicated mild-to-moderate HT, and age, gender, and body mass index-matched 124 (58 males, 83 females) healthy subjects were enrolled in this study. Plasma vWF, fibrinogen levels, adenosine diphosphate-induced platelet aggregability, insulin, glucose, serum lipids, and uric acid were measured. Patients with HT had significantly increased fibrinogen, vWF, platelet number and aggregability induced by adenosine diphosphate, triglycerides, total/HDL-C, glucose, uric acid levels, and insulin resistance than control group. vWF and hemostatic markers were comparable between smoker and nonsmoker subjects. Platelet aggregability was positively related to systolic and diastolic blood pressure, and vWF. Fibrinogen was positively associated with body mass index (BMI), systolic and diastolic blood pressure, total cholesterol (TC), uric acid, vWF, and insulin resistance. vWF was significantly related to age, systolic blood pressure, TC, LDL-C, and total/HDL-C. Systolic blood pressure was independently related to vWF. vWF and diastolic blood pressure were significant predictors for adenosine diphosphate-induced platelet aggregability. Systolic blood pressure and vWF were independent predictors for fibrinogen levels. Uncomplicated mild-to-moderate HT had endothelial damage and is associated with a prothrombotic state. Traditional cardiovascular risk factors such as age, BMI, dyslipidemia, and insulin resistance are important contributors to the development of endothelial damage and a prothrombotic state. Therefore, it is important to control these cardiovascular risk factors along with proper treatment of HT for preventing target organ damage in mild-to-moderate HT.     

First-ever atrial fibrillation documented after hemorrhagic or ischemic stroke: the role of the CHADS(2) score at the time of stroke

Background:

The CHADS₂ score (C, congestive heart failure [CHF]; H, hypertension [HT]; A, age ≥75 y; D, diabetes mellitus; S₂, prior stroke or transient ischemic attack) is used to assess the risk of ischemic stroke in patients with atrial fibrillation (AF). However, its role in patients without documented AF is not well explored.

Hypothesis:

The goal of the current study was to explore if the incidence of hospitalization with first‐ever AF after stroke increased with increasing CHADS₂ score.

Methods:

We identified 57636 patients with nonfatal stroke and no documented AF in the Swedish Stroke Register (Riks‐Stroke) during 2001–2004 and followed them for a mean of 2.2 years through record linkage to the Inpatient and Cause of Death registers. Cox regression hazard models were used to estimate the relative risk (RR) of new AF following stroke and its association with different CHADS₂ scores.

Results:

Overall, 2769 patients were hospitalized with new AF (4.8%, 21.7 per 1000 person‐years). The incidence increased from 9.6 per 1000 person‐years in CHADS₂ score 0 to 42.7 in CHADS₂ score 6, conferring a RR of 4.2 (95% confidence interval [CI]: 2.5–6.8). For CHADS₂ scores 3–5, the RRs were approximately 3 (vs CHADS₂ score 0). Adjusted RRs were 1.9 (95% CI: 1.7–2.1) for CHF, 1.4 (95% CI: 1.3–1.5) for HT, 2.1 (95% CI: 2.0–2.3) for age ≥75 years, 0.9 (95% CI: 0.8–1.0) for diabetes, and 1.0 (95% CI: 0.91–1.07) for previous stroke. The risk of AF was higher in ischemic than in hemorrhagic stroke.

Conclusions:

In this retrospective register study, the incidence of AF following stroke was strongly influenced by higher CHADS₂ scores where age ≥75 years, CHF, and HT were the contributing CHADS₂ components. © 2011 Wiley Periodicals, Inc. Riks‐Stroke is funded by the National Board of Health and Welfare and the Swedish Association of Local Authorities and Regions. S. Åsberg has received a research scholarship from the National Association for Stroke Patients in Sweden. All authors have independent affiliations with universities in Sweden. B. Farahmand and K. Henriksson are employees of AstraZeneca R&D, Sweden. A. Terént has received funding from AstraZeneca. N. Edvardsson serves as medical advisor to AstraZeneca R&D, Sweden. The authors have no other funding, financial relationships, or conflicts of interest to disclose.     

The association baseline NIH Stroke Scale score with ABO blood-subtypes in young patients with acute ischemic stroke

Objectives

The presence of the A and B blood group antigens has been associated with risk of arterial thrombosis. The aim of the current study was to design a new simpler form of National Institutes of Health Stroke Scale (NIHSS) for use on admission, and assess the association of blood groups with NIHSS score in young stroke patients.

Methods

We conducted this study in 1311 young Chinese adults with acute ischemic cerebral stroke. The outcome measures included a composite favorable outcome (defined as a modified Rankin Scale (mRS) of 0 or 2) and poor outcome (defined as a modified Rankin Scale score of 3 or 6) at discharge; a minor strokes (NIHSS scores 0–5) and severe strokes (NIHSS scores ≥6). Logistic regression analyses were used to determine the association between ABO blood groups and stroke severity.

Results

Regression analysis confirmed in relative to patients with AB subtype, Oxfordshire community stroke project classification (OCSP) subtype and serum white blood cell (WBC) were the major predictors for stroke severity. Meanwhile, diabetes, serum triglyceride and uric acid levels were determined as independent indicators of stroke severity in A, B and O blood subtype respectively. The optimal cutoff score of the baseline NIHSS was ≤5 for patients with non-O subtype, the optimal cutoff score of the baseline NIHSS was ≤7 for patients with blood O subtype.

Conclusions

Our analysis provide compelling information regarding the ABO blood groups differences in predictors of stroke severity and the different validity of NIHSS scores in predicting prognosis at discharge between O subtype and non-O subtype.