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Cardiovascular health (CVH) factors are associated with lower risk of cardiovascular disease, stroke, and mortality. We investigated the association between a modified CVH metrics score and change in cognitive functions 2 decades later in patients with pre-existing coronary artery disease. A subset of 200 men (mean age at baseline 57.3 ± 6.3 years) who previously participated in a secondary prevention trial (1990 to 1997) underwent cognitive evaluation 14.6 ± 1.9 years after baseline (mean age 72.3 ± 6.2 years, T1 evaluation), and were re-evaluated for cognitive performance 19.9 ± 1.0 years after baseline (mean age 77.2 ± 6.4 years, T2 evaluation). A CVH metrics score at baseline was calculated, including 3 health parameters and 4 health behaviors. We have scored each of these CVH metrics into best (2 points), intermediate (1 point), and poor (0 points) levels. Cognitive function was assessed using the NeuroTrax Computerized Battery. A linear mixed model was used to assess change in cognitive functions between T1 and T2 cognitive evaluations. Among the 200 patients, 68 (34.0 %) had ≤7 (bottom group), 85 (42.5%) had 8 to 9 (middle group), and 47 (23.5%) had ≥10 (top group) CVH metrics points. After adjustments, the top group of CVH score versus others was associated with slower decline in the overall cognitive performance composite z-score (0.23 ± 0.09, p = 0.009) and on tests of executive and visual spatial functions (0.23 ± 0.11, p = 0.047, and 0.49 ± 0.17, p = 0.004, respectively). In conclusion, an inverse association was observed between the score of best CVH metrics and cognitive decline. Lifestyle factors are important predictors of late-life decline in cognitive function among high-risk patients., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Unrecognized renal dysfunction, defined as an estimated glomerular filtration rate <60 mL/min/1.73 m(2) in the presence of normal serum creatinine levels, is a common comorbidity among patients with various cardiovascular conditions. The current study was aimed to evaluate the prevalence and clinical significance of unrecognized renal dysfunction in patients with acute stroke., Methods: The cohort consisted of patients with acute stroke included in the prospective National Acute Stroke ISraeli (NASIS) registry. Unrecognized renal insufficiency was defined as an estimated glomerular filtration rate <60 mL/min/1.73 m(2) in the presence of serum creatinine ≤1.2 mg/dL. The 2 primary outcomes were in-hospital mortality and the composite of in-hospital mortality or severe disability at hospital discharge., Results: Of the 7900 patients with stroke included in the study, 5571 (70.5%) had normal renal function, 1510 (19.1%) had recognized renal insufficiency, and 819 (10.4%) had unrecognized renal insufficiency. Mortality rates were higher in patients with recognized and unrecognized renal insufficiency compared with patients with normal renal function (9.9%, 9.1%, and 4.4%, respectively, P < .0001). Adjusted odds ratios (ORs) for in-hospital mortality were higher for patients with renal dysfunction recognized (OR, 2.1; 95% confidence interval [CI], 1.6-2.7; P < .001) or unrecognized (OR, 1.6; 95% CI, 1.1-2.2; P = .006) compared with patients with normal renal function. Likewise, adjusted ORs for the composite of in-hospital mortality or severe disability at hospital discharge were higher for patients with renal dysfunction recognized (OR, 1.3; 95% CI, 1.1-1.5; P = .004) or unrecognized (OR, 1.2; 95% CI, 1.01-1.5; P = .04)., Conclusions: Unrecognized renal insufficiency is common among patients with acute stroke and is associated with adverse short-term outcomes., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Although the benefit of antithrombotic therapy for stroke prevention in atrial fibrillation (AF) is well recognized, its potential effect on stroke severity and outcome is less well established. Our objective was to examine the effect of preadmission antithrombotic therapy on stroke severity and outcome in patients with AF within a large comprehensive nationwide stroke survey. The data from consecutive patients with AF admitted with acute ischemic stroke or transient ischemic attack during a 2-month period were collected. The patients were categorized into 4 groups according to the use of preadmission antithrombotic therapy: no antithrombotic therapy, antiplatelet therapy, warfarin with an admission international normalized ratio (INR) <2 and INR of > or = 2. Of 1,938 patients presenting with acute brain ischemia, 329 (17%) had AF. The age-adjusted rate of more severe stroke (baseline National Institutes of Health stroke scale score >5) stratified by antithrombotic therapy use was 70% for no antithrombotic therapy use, 55% for antiplatelet therapy use, 59% for warfarin with an INR <2, and 38% for warfarin with an INR of > or = 2 (p = 0.01). Compared to warfarin therapy with an admission INR of > or = 2, the adjusted odds ratio for more severe strokes was 4.0 (95% confidence interval [CI] 1.7 to 10.0) for no antithrombotic therapy, 2.2 (95% CI 1.0 to 9.4) for antiplatelet therapy, and 2.7 (95% CI 1.1 to 6.7) for warfarin therapy with an INR of <2. Similarly, graded associations of antithrombotic medication were observed with severe disability (modified Rankin Scale score >3) or death at discharge, with corresponding adjusted odds ratios of 4.1 (95% CI 1.8 to 9.9), 2.1 (95% CI 1.0 to 4.6), and 1.5 (95% CI 0.6 to 3.5), and 1-year mortality, with corresponding adjusted ORs of 2.4 (95% CI 0.9 to 6.7), 1.9 (95% CI 0.8 to 5.0), and 2.2 (95% CI 0.8 to 6.2). In conclusion, in addition to its established benefit for stroke prevention, effective anticoagulation therapy is associated with decreased stroke severity and better functional outcome and survival in patients with AF presenting with acute brain ischemia., (Copyright 2010 Elsevier Inc. All rights reserved.)

Low high-density lipoprotein (HDL) cholesterol is a strong independent predictor of cardiovascular risk. The present study was designed to assess the relation between the clinical response to HDL cholesterol modification and serum levels of low-density lipoprotein (LDL) cholesterol in patients with coronary artery disease (CAD). The risk for a major cardiac event (defined as nonfatal myocardial infarction or cardiac death) during a median 7.9-year follow-up period in 3,020 patients with CAD enrolled in the Bezafibrate Infarction Prevention (BIP) trial was related to changes in lipid levels during the study. Baseline LDL cholesterol levels were categorized according to National Cholesterol Education Program Adult Treatment Panel III criteria. Multivariate analysis demonstrated that the benefit of HDL cholesterol increase was most pronounced in patients with low baseline LDL cholesterol (or=160 mg/dl; hazard ratio 0.94, 95% confidence interval 0.75 to 1.17, p = 0.14). A similar relation was shown for risk reduction-associated triglyceride decrements, whereas the benefit of LDL cholesterol reduction was more pronounced in patients with baseline LDL cholesterol >or=130 mg/dl. In conclusion, these data suggest that the clinical response to HDL cholesterol and triglyceride modification is inversely related to baseline LDL cholesterol levels. Thus, combined assessment of baseline and follow-up lipid levels to direct therapeutic goals in patients with CAD may provide incremental prognostic information to secondary prevention that is based solely on LDL cholesterol modification.

Individuals involved in intense resistance training present with increased absolute left ventricular (LV) wall thickness and mass and show good systolic responses to isometric exercise. There is no consensus regarding diastolic features and no available information regarding diastolic function in athletes during isometric exertion itself. Therefore, the main aim of this study was to assess diastolic LV function at baseline and during exercise in athletes. The population consisted of 96 men (mean age 29 +/- 7 years): 48 weight lifters who trained for 15 to 20 hours/week and 48 sedentary men. All weight lifters had been active for >6 years, including the 6 months before the study. Ultrasound was performed using a commercially available Doppler echocardiographic system. Isometric exercise was performed in the supine position using a standard 2-hand bar dynamometer. The man end-diastolic volumes at rest were 97 +/- 6 ml in sedentary subjects and 101 +/- 5 ml in weight lifters, increasing to 100 +/- 6 and 118 +/- 11 ml during exercise (p = 0.06 and p <0.01, respectively). End-systolic volumes at rest were similar in the 2 groups, showing significantly greater reductions during exercise in the weight lifters. The mean absolute LV mass was 167 +/- 30 g in sedentary subjects and 202 +/- 32 g in weight lifters (p <0.0001). The mean stroke volume increased from 65 +/- 7 to 86 +/- 7 ml in sedentary subjects and from 70 +/- 6 to 107 +/- 11 ml in weight lifters (intergroup significance p = 0.05 and p <0.01, respectively). A similar pattern of response was documented for the ejection fraction (i.e., significantly greater increases during exercise in weight lifters). Regarding diastolic indexes, in the weight lifters, the mean peak early velocity at rest was 68 +/- 7 cm/s, the mean acceleration rate was 1,242 +/- 176 cm/s/s, and the mean deceleration rate was 414 +/- 44 cm/s/s. All these values were significantly higher than in sedentary subjects, with further increases during exercise (p <0.0001). In weight lifters, the mean peak atrial velocity at rest was 37 +/- 6 cm/s, the mean acceleration time was 55 +/- 4 ms, the mean isovolumic relaxation time was 63 +/- 3 ms, and the mean deceleration time was 164 +/- 4 ms; these values were lower than in sedentary subjects (p <0.0001 for all). In conclusion, intense resistance training leads to enhanced LV diastolic function at rest and during isometric exercise despite the markedly increased LV mass.

The aim of this study is to explore the impact of metabolic syndrome (MS) on the outcome of patients with non-clinically diagnosed diabetes with acute coronary syndrome (ACS) based on a comprehensive nationwide registry during a 1-year follow-up. In the ACS Israeli Survey, 1,060 consecutive patients with non-clinically diagnosed diabetes were admitted due to ACS; 359 patients with MS features on admission were compared with 701 subjects without MS. A modified National Cholesterol Education Program Adult Treatment Panel III definition of MS was used in patients who presented with > or =3 of the 5 components: (1) hyperglycemia, defined as occasional blood glucose on admission >140 mg/dl; (2) preexisting hypertension; (3) body mass index >28 kg/m(2); (4) high-density lipoprotein cholesterol < or =40 mg/dl (men) or < or =50 mg/dl (women); and (5) triglycerides > or =150 mg/dl. Patients with MS were more frequently women (27% vs 12%, p = 0.001), were in Killip > or =II on admission (19% vs 14%, p = 0.03), and had higher 30-day (5.0% vs 1.7%, p = 0.002) and 1-year (8.9% vs 4.6%, p = 0.005) crude mortality rates. Patients with hyperglycemia (glucose >140 mg/dl) and MS had higher 30-day mortality rates compared with patients with hyperglycemia without MS (8.3% vs 2.5%, p <0.05). Multivariate analysis identified MS as a strong independent predictor of 30-day and 1-year mortality with hazard ratios of 2.54 (95% confidence interval 1.22 to 5.31) and 1.96 (95% confidence interval 1.18 to 3.24), respectively. In conclusion, MS defined early at admission is a strong independent predictor of mortality and morbidity in patients with non-clinically diagnosed diabetes with ACS.

The aim of this study was to evaluate the prognostic value of interleukin-6 (IL-6) for myocardial infarction (MI) and mortality in a population with stable coronary artery disease (CAD) during a mean period of 6.3 years. IL-6 is a major proinflammatory cytokine of acute phase response; elevated levels are associated with worse prognosis in unstable angina and after acute MI. However, data regarding its long-term prognostic value in stable CAD are limited and controversial. A nested case-control study design was used. Of 3,090 patients with stable CAD, 129 with an adequate blood sample for IL-6 and who reached the end points (MI or sudden death) were randomly selected. Each case was 1:1 matched with 129 controls (alive at the end of the study and free of cardiovascular events) according to age, gender, and treatment. Of the 129 cases, 113 had a MI as the initial event, and for the other 16 the initial event was sudden death. There were 8 patients who first had a MI and later died suddenly. IL-6 was significantly higher in cases (2.34 pg/ml) than in controls (1.65 pg/ml) (p = 0.0004). IL-6 was significantly correlated with C-reactive protein (r = 0.2, p = 0.002); a borderline significance was also found for fibrinogen (r = 0.11, p = 0.07). Each increase of 1 pg/ml in IL-6 was associated with a 1.70 (range 1.23 to 2.45) increased relative odds of subsequent MI or sudden death. Events rate per 1,000 patients-years for the 5 quintiles of IL-6 were 72.26, 89.61, 79.76, 142.53, and 181.08, respectively (p <0.0001). A significantly higher risk in the upper quintile was found (odds ratio, 3.44; 95% confidence interval 1.57 to 8.13). In conclusion, elevated IL-6 levels are strongly associated with future cardiac events and mortality in a population with stable CAD during a long-term follow-up.

Purpose: White blood cell (WBC) count is a marker of inflammation and has been associated with the development of cardiovascular disease. We investigated the relationship between WBC counts and the incidence of ischemic cerebrovascular disease in a large cohort of patients with pre-existing atherothrombotic disease and defined blood lipid boundaries., Subjects and Methods: We followed up patients with documented coronary heart disease for 4.8 to 8.1 years. An extensive medical evaluation, conducted at baseline, included assessment of vascular risk factors and measures of blood lipids. Among 5435 patients with WBC counts, free of stroke, 295 developed an ischemic cerebrovascular disease (fatal and nonfatal). After review of available medical records, 186 of these cases had ischemic stroke or TIA., Results: Higher WBC counts were associated with increased risk for ischemic cerebrovascular disease. Age-adjusted hazard ratio (HR) was 1.55 with 95% confidence interval (CI) 1.16-2.07, upper WBC tertile compared with the lowest. Adjusting for clinical covariates, WBC count remained an independent predictor for ischemic cerebrovascular disease (HR = 1.39; 95% CI 1.03-1.87, upper WBC tertile compared with the lowest). A similar trend appeared for the endpoint of ischemic stroke/transient ischemic attack (TIA). Further adjustment for plasma fibrinogen did not change the association materially (HR = 1.32; 95% CI 1.01-1.80; upper tertile of WBC compared with lowest)., Conclusions: These findings support the role of WBC count as a simple inexpensive and readily available marker for risk stratification of ischemic cerebrovascular disease among patients with pre-existing atherothrombotic disease and defined blood lipid boundaries.

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.

Recently it was shown that subjects with aortic valve calcium (AVC) are at increased risk for future cardiovascular disease including stroke. We hypothesized that the increased risk of stroke may be due to an association with carotid artery atherosclerotic disease. Between 1995 and 1999 our laboratory made a diagnosis of AVC without significant stenosis in 3,949 patients. Of those, 279 patients without other cardiac structural exclusion criteria (148 men and 131 women; mean age 73 +/- 9 years, range 45 to 90) underwent carotid artery duplex ultrasound for various indications, and formed the study group. Age- and sex-matched patients without AVC (n = 277), who underwent carotid artery duplex ultrasound during the same period and for the same indications, served as the control group. Compared with the control group, the AVC group had a significantly higher prevalence of carotid stenosis (> 40% to 60%, 89% vs 78% [p < 0.001]; >60% to 80%, 43% vs 23% [p <0.001];and > 80% to 100%, 32%vs 14% [p < 0.001]). The AVC group had a similar, significantly higher prevalence of > or = 2-vessel disease and bilateral carotid stenosis (stenosis levels of > 20% to 40%, >40% to 60%, > 60% to 80%, and > 80% to 100%). In multivariate analysis, AVC, but not traditional risk factors, was the only independent predictor of severe carotid atherosclerotic disease (stenosis > 80% to 100%; p = 0.0001). Thus, there is a significant association between the presence of AVC and carotid atherosclerotic disease.

Patients with chronic CAD and a history of cerebrovascular events were compared with patients without prior cerebrovascular events to assess the effect of these events on 5-year prognosis. Despite adjustment for older age and higher comorbidity among patients who had experienced a cerebrovascular event, a history of such an event was associated with an increased risk of 1.86 for total mortality.

Purpose: The purpose of this study was to report the incidence, the antecedents, and the clinical significance of clinically recognized cerebrovascular accidents or transient ischemic attacks (CVA-TIA) complicating acute myocardial infarction., Patients and Methods: During 1981 to 1983, a secondary prevention study with nifedipine (SPRINT) was conducted in 14 hospitals in Israel among 2,276 survivors of acute myocardial infarction. During the study, demographic, historical, and medical data were collected on special forms for all patients with diagnosed acute myocardial infarction in 13 of these 14 hospitals (the SPRINT registry, n = 5,839). Mortality follow-up was completed for 99% of hospital survivors for a mean follow-up of 5.5 years (range: 4.5 to 7 years)., Results: The incidence of CVA-TIA was 0.9% (54 of 5,839). The latter rate increased significantly only with age, from 0.4% among patients up to 59 years old to 1.6% among those aged greater than or equal to 70 years. Multivariate analysis identified age, congestive heart failure, and history of stroke as predictors of CVA-TIA during the acute phase of myocardial infarction. Patients with CVA-TIA exhibited a complicated hospital course, with a 15-day mortality rate of 41%. Subsequent mortality rates in survivors at 1 and 5 years were 34% and 59%, respectively. Rates at the same time points in patients without CVA-TIA were 16%, 11%, and 29% (p less than 0.01). In a multivariate analysis that included age, gender, congestive heart failure, history of previous myocardial infarction, and hypertension, CVA-TIA was independently associated with increased 15-day mortality (covariate-adjusted odds ratio [OR] = 2.62; 90% confidence interval [CI], 1.59 to 4.32), as well as subsequent 1-year (OR = 3.29; 90% CI, 1.70 to 6.36) and long-term (mean follow-up = 5.5 years) mortality (OR = 2.46; 90% CI, 1.30 to 4.69)., Conclusion: In this large cohort of consecutive patients with myocardial infarction, CVA-TIA was a relatively infrequent complication of acute myocardial infarction. Factors independently favoring the occurrence of CVA-TIA were old age, previous CVA, and congestive heart failure. CVA-TIA occurring during acute myocardial infarction independently increased the risk of early death threefold as well as the risk of long-term mortality in early-phase survivors. (2.5-fold).