Independent Predictor Of Cardiovascular Disease Research Articles

The PR interval and QRS duration could be predictors of renal function decline

ObjectivePrevious studies have implicated PR interval (iPR) and QRS duration (dQRS) obtained by electrocardiography in independent predictors of cardiovascular disease, which often precedes renal dysfunction. The aim of this study was to examine whether iPR or dQRS could be a predictor of renal function decline in a community-based cohort. MethodsWe enrolled 1149 healthy subjects, and retrospectively evaluated the relationships between iPR or dQRS and renal function decline, observation period of which was 3 years, and assessed whether iPR or dQRS could predict renal function decline. ResultsThe iPR (r = −0.102, p = 0.0006) or dQRS (r = −0.097, p = 0.0010) was negatively associated with a rate of decline in estimated glomerular filtration rate (eGFR). Multiple regression analyses revealed that iPR (β = −0.095, p = 0.0023) or dQRS (β = −0.069, p = 0.0351) was an independent determinant of the rate of decline in eGFR after adjustment for covariates. Logistic regression analyses demonstrated that the longest iPR (odds ratios (OR), 2.03; 95% confidence intervals (CI), 1.49 to 2.76; p < 0.0001) or dQRS (OR, 1.62; 95% CI, 1.16 to 2.25; p = 0.0043) tertile showed an increased OR for prevalence of the rate of decline in eGFR ≤ 1 ml/min/1.73 m2/year compared to the shortest iPR or dQRS tertile after adjustment for covariates. ConclusionThe iPR and dQRS could be independent predictors of renal function decline in healthy subjects.

To Study Insulin Resistance in Type 2 Diabetes Mallitus by Homa-IR Score

Introduction: Insulin resistance precedes and strongly predicts the development of type 2 diabetes mellitus, estimation of insulin resistance was helpful in detection of early complications and selecting the treatment options, hence the present study was planned. HOMA estimated insulin resistance is an independent predictor of cardiovascular disease in type-2 diabetic subjects Materials and Methods: A case control study was carried out in the Department of Medicine comprising 50 newly diagnosed type 2 diabetes mellitus patients and 50 healthy controls. The HOMA IR method was used in the present study for estimation of insulin resistance as it is simple and appropriate. Results: median value of fasting plasma insulin in cases was 7.45µU/ml with mean 10.53 ± 9.42µU/ml while in control was 7.19 with mean 7.43 ± 2.26µU/ml (p value 0.025856) and of fasting plasma glucose was 146 mg/dl with mean 164.12 + 54.43mg/dl and controls had median 112 with mean 110.6 + 7.07mg/dl (p value 0.000000). The median value of HOMA IR score is 2.91 in cases with mean value of 4.15 ± 3.56 and controls of 1.97, mean 2.03 + 0.64 (p value .000072). The most prevailing complications were retinopathy 26%(13,p<0.01) and neuropathy26%(13,P<0.01). Conclusion: HOMA-IR score in present study was higher, it indicates that IR was higher in Patient of T2 DM in Gwalior Chambal zone as compared to other countries and high score is associated with increase risk of diabetic retinopathy, neuropathy, nepropathy, CAD, Peripheral vascular disease.

Complication characteristics between young-onset type 2 versus type 1 diabetes in a UK population

BackgroundIn the UK, the care of young people with diabetes has focused predominantly on type 1 diabetes (T1D). However, young-onset T2D has become increasingly prevalent. At present, it is unclear...

Abstract W P395: Aging Alters Vascular Stiffness in the Posterior Cerebral Artery in C57bl/6 Mice

Aging is a major risk factor for cardiovascular disease in part as a result of dysfunctional arteries. Arterial stiffening with age is considered to be an independent predictor of cardiovascular disease. Age-related artery remodeling in large conduit arteries increases the risk of stroke and dementia. Atherosclerotic elderly mice exhibit aorta outward remodeling compared to young mice. Also, peripheral resistance arteries remodel with age. Less is known on how aging alters the morphology of cerebral arteries. Historically young mice have been used in many stroke studies, however the STAIR criteria for preclinical testing clearly states that potential neuroprotective drugs need to be tested in aged mice. It is therefore important to understand how aging affects cerebral artery structure. The effects of aging have not been investigated in the posterior cerebral artery (PCA). The PCAs provide blood flow support when the middle cerebral artery is occluded or when blood flow to the brain is decreased by carotid artery stenosis. We hypothesized that aging would increase the PCA lumen diameter and wall thickness in C57BL/6 mice. PCAs were collected from 5 month (n=7) and 24 month (n=7) old mice for assessment of vessel structure by pressure myography. All results are presented as mean ± SEM, young vs old. The old mice weighed significantly more than the young mice (28.85±0.36 vs 33.27±1.04 grams p&lt;0.05). Surprisingly, aging caused limited changes to the structure of the PCA. Statistically significant changes in the outer diameter (126.9± 2.5 vs 141.6 ± 3.3μm, ANOVA p &lt;0.05) and lumen diameter (100.9± 2.4 vs 115.8± 3.2μm ANOVA p &lt;0.05) where only observed at an intralumenal pressure of 20mmHg. Changes observed at such a low intralumenal pressure are unlikely to be physiologically relevant. Aging had no effect on the wall-to-lumen ratio, wall thickness, or distensibility. Aging did increase artery stiffness assessed by calculating the slope of the individual stress strain curves (beta coefficient: 5.13± 0.42 vs 6.71± 0.42, t-test p &lt;0.05). Increased artery stiffness is associated with an increased risk of cardiovascular disease. In the absence of a change in the wall thickness this increased stiffness is likely to be due to changes in extracellular matrix deposition.

Myeloperoxidase-mediated oxidation targets serum apolipoprotein A-I in diabetic patients and represents a potential mechanism leading to impaired anti-apoptotic activity of high density lipoprotein

BackgroundIt is demonstrated that levels of protein-bound chlorotyrosine, nitrotyrosine and myeloperoxidase (MPO), a protein that catalyzes generation of chlorinating and nitrating oxidants, serve as independent predictors of cardiovascular disease. MethodsImmunoprecipitation and Western blot were used to analyze protein concentration, nitration and chlorination. LC-MS/MS was used to identify nitrated and chlorinated sites of Tyr from immunoprecipitated serum proteins. ResultsApolipoprotein A-I (apoA-I), the primary protein constituent of high density lipoprotein (HDL), was identified as a selective target for MPO-catalyzed nitration and chlorination in patients with type 2 diabetes. The serum proteins from diabetic subjects showed that the levels of apoA-I nitration and chlorination were clearly increased, whereas apoA-I concentration and cholesterol efflux activity were significantly decreased. MPO as a likely mechanism for oxidative modification of apoA-I in vivo was apparently facilitated by MPO binding to apoA-I. Subsequently, it was found that Tyr 192 was the major nitration and chlorination site in apoA-I from diabetic serum. Further studies in vitro revealed that besides the classic inhibition in cholesterol efflux activities, MPO-catalyzed oxidation could result in a loss of anti-apoptotic activity of lipoprotein. ConclusionsApoA-I undergoes MPO-mediated oxidation in serum from diabetic patients compared to non-diabetic subjects and MPO-catalyzed modification may impair the anti-apoptotic properties of HDL in vitro.

Carbohydrate intake and nonalcoholic fatty liver disease: fructose as a weapon of mass destruction.

Excessive accumulation of triglycerides (TG) in liver, in the absence of significant alcohol consumption is nonalcoholic fatty liver disease (NAFLD). NAFLD is a significant risk factor for developing cirrhosis and an independent predictor of cardiovascular disease. High fructose corn syrup (HFCS)-containing beverages were associated with metabolic abnormalities, and contributed to the development of NAFLD in human trials. Ingested carbohydrates are a major stimulus for hepatic de novo lipogenesis (DNL) and are more likely to directly contribute to NAFLD than dietary fat. Substrates used for the synthesis of newly made fatty acids by DNL are primarily glucose, fructose, and amino acids. Epidemiological studies linked HFCS consumption to the severity of fibrosis in patients with NAFLD. New animal studies provided additional evidence on the role of carbohydrate-induced DNL and the gut microbiome in NAFLD. The excessive consumption of HFCS-55 increased endoplasmic reticulum stress, activated the stress-related kinase, caused mitochondrial dysfunction, and increased apoptotic activity in the liver. A link between dietary fructose intake, increased hepatic glucose transporter type-5 (Glut5) (fructose transporter) gene expression and hepatic lipid peroxidation, MyD88, TNF-α levels, gut-derived endotoxemia, toll-like receptor-4, and NAFLD was reported. The lipogenic and proinflammatory effects of fructose appear to be due to transient ATP depletion by its rapid phosphorylation within the cell and from its ability to raise intracellular and serum uric acid levels. However, large prospective studies that evaluated the relationship between fructose and NAFLD were not performed yet.

Carotid pulse wave velocity by magnetic resonance imaging is increased in middle-aged subjects with the metabolic syndrome.

Arterial pulse wave velocity (PWV), an independent predictor of cardiovascular disease, physiologically increases with age; however, growing evidence suggests metabolic syndrome (MetS) accelerates this increase. Magnetic resonance imaging (MRI) enables reliable noninvasive assessment of arterial stiffness by measuring arterial PWV in specific vascular segments. We investigated the association between the presence of MetS and its components with carotid PWV (cPWV) in asymptomatic subjects without diabetes. We assessed cPWV by MRI in 61 individuals (mean age, 55.3 ± 14.1 years; median age, 55 years): 30 with MetS and 31 controls with similar age, sex, body mass index, and LDL-cholesterol levels. The study population was dichotomized by the median age. To remove the physiological association between PWV and age, unpaired t tests and multiple regression analyses were performed using the residuals of the regression between PWV and age. cPWV was higher in middle-aged subjects with MetS than in those without (p = 0.001), but no differences were found in elder subjects (p = 0.313). cPWV was associated with diastolic blood pressure (r = 0.276, p = 0.033) and waist circumference (r = 0.268, p = 0.038). The presence of MetS was associated with increased cPWV regardless of age, sex, blood pressure, and waist (p = 0.007). The MetS components contributing independently to an increased cPWV were hypertension (p = 0.018) and hypertriglyceridemia (p = 0.002). The presence of MetS is associated with an increased cPWV in middle-aged subjects. In particular, hypertension and hypertriglyceridemia may contribute to early progression of carotid stiffness.

Abstract 11002: Anemia Plays a Role in Pre-Clinical Myocardial Damage and Cardiovascular Mortality in General Population

Background: Anemia is an independent risk factor for morbidity and mortality in patients with cardiovascular disease. However, the impact of anemia on pre-clinical cardiac damage has not yet fully determined in apparently healthy subjects. The aim of the present study was to investigate whether anemia is associated with pre-clinical cardiac damage and cardiovascular mortality in general population. Methods and Results: A cohort study was conducted with subjects who participated in a community-based annual health check in Takahata, Japan, from 2004 through 2006. We examined blood count, serum levels of brain-type natriuretic peptide (BNP) and heart-type fatty acid binding protein (H-FABP) in participants and prospectively followed them (n = 3,509). Anemia was defined as hemoglobin &lt; 13 g/dl for men; &lt; 12 g/dl for women. Four hundred subjects (11.4%) had anemia. In both gender, BNP levels were higher in subjects with anemia than in those without. H-FABP levels were also higher in male subjects with anemia than in those without, while anemia was not associated with H-FABP levels in female subjects. During follow-up period of 7 years, 40 subjects died of cardiovascular diseases. Kaplan-Meier analysis demonstrated that subjects with anemia had higher cardiovascular mortality than those without. Further, subjects those with macrocytic anemia, defined as anemia with mean corpuscular volume (MCV) ≥ 100 fl, had the highest levels of BNP and H-FABP and the highest event rate among subjects with anemia. Multivariate Cox proportional hazard analysis revealed that anemia was an independent predictor of cardiovascular diseases after adjusting age, gender, smoking index, estimated glomerular filtration rate, and BNP (HR: 2.307; 95% CI, 1.032 - 4.808). Conclusions: Anemia, especially macrocytic anemia, was associated with pre-clinical myocardial damage and cardiovascular mortality in general population.

Simplicity is the ultimate sophistication. PR electrocardiographic intervals for smart forecasting of decline in renal function

Simplicity is the ultimate sophistication. PR electrocardiographic intervals for smart forecasting of decline in renal function

Lp-PLA2 levels in HIV-infected patients.

IntroductionHIV-infected patients show an increased risk of cardiovascular disease (CVD). In the general population, lipoprotein-associated phospholipase A2 (Lp-PLA2) appears to be an independent predictor of CVD. We aimed to study associations between Lp-PLA2 plasma levels and other risk factors for CVD in HIV patients.Materials and MethodsA cross-sectional, comparative study of two series of cases (HIV patients, n=116 and age-matched non-HIV healthy controls, n=113) was conducted. Eighty-seven percent HIV patients on antiretroviral therapy (ART), 72.4% with HIV-1 viral load <50 cop/mL. Inflammatory biomarkers (CRP, Lp-PLA2) and internal carotid intima-media thickness (IMT) were measured and CVD risk (Framingham and SCORE algorithms) was calculated. Univariate and multivariable associations between these variables were performed.ResultsHIV patients presented higher Lp-PLA2 levels [276.81 ng/mL (209.71–356.58)] than uninfected healthy controls [220.80 ng/mL (172.70–256.90)], p≤0.01. In univariate analysis of the global sample, only cigarette smoking was associated with higher Lp-PLA2 levels, p≤0.001. In HIV group, female and smoker patients showed higher Lp-PLA2 levels, p≤0.05. No significant association was found between Lp-PLA2 levels and another CVD risk factors, carotid IMT, Framingham and SCORE algorithms, ART, HIV-1 viral load neither and CD4+ T lymphocyte count. In multivariate analysis, cigarette smoking remained significantly associated with Lp-PLA2 levels [β=64.8 (95% CI 10.8–118.9) ng/mL, p=0.020].ConclusionsHIV-infected patients present higher Lp-PLA2 levels than healthy controls, and in this population, tobacco smoking is significantly associated with increased Lp-PLA2 levels. Smoking cessation should be a priority in CVD prevention in HIV-infected patients.

Serum lipoprotein(a) concentrations do not change significantly in the immediate seven-day period post myocardial infarction.

Lipoprotein(a) is an independent predictor of cardiovascular disease and its variability after myocardial infarction was assessed in this study. Lipoprotein(a) was analysed by a size insensitive latex immunoturbidimetric end point assay in samples from days 0 to 7 in 31 patients admitted with myocardial infarction. Median lipoprotein(a) changed by -0.9%, -0.1% and 9.6% on days 1, 2-3 and 4-7, respectively, and was not statistically significant. Median total cholesterol reduced by 8.7%, 9.1%, 14.5% and C-reactive protein increased by 68.4%, 510%, 502% over days 1, 2-3, 4-7, respectively. Unlike total cholesterol and C-reactive protein, lipoprotein(a) does not demonstrate significant variability for up to seven days after myocardial infarction and measurements made during this period after myocardial infarction are physiologically meaningful.

Left ventricular hypertrophy and cardiovascular disease risk prediction and reclassification in blacks and whites: The Atherosclerosis Risk in Communities Study

Left ventricular hypertrophy (LVH) is a major independent predictor of cardiovascular disease (CVD) survival and is more prevalent in blacks than whites. In a large biracial population, we evaluated the ability of electrocardiography (ECG)-determined LVH (ECG-LVH) to reclassify CVD/coronary heart disease (CHD) events beyond traditional risk factors in blacks and whites. The analysis included 14,489 participants (mean age 54 ± 5.7 years; 43.5% men; 26% black) from the ARIC cohort, with baseline (1987-1989) ECG, followed up for 10 years. Predicted risk for incident CVD and CHD were estimated using the 10-year Pooled Cohort and Framingham risk equations (base models 1A/1B), respectively. Models 2A and 2B included respective base model plus LVH by "any" of 10 traditional ECG-LVH criteria. Net reclassification improvement (NRI) was calculated, and the distribution of risk was compared using models 2A and 2B versus models 1A and 1B, respectively. There were 792 (5.5%) 10-year Pooled Cohort CVD events and 690 (4.8%) 10-year Framingham CHD events. Left ventricular hypertrophy defined by any criteria was associated with CVD and CHD events (hazard ratio [95% CI] 1.62 [1.38-1.90] and 1.56 [1.32-1.86], respectively]. Left ventricular hypertrophy did not significantly reclassify or improve C statistic in models 2A/B (C statistics 0.767/0.719; NRI = 0.001 [P = not significant]), compared with the base models 1A/B (C statistics 0.770/0.718), respectively. No racial interactions were observed. In this large cohort of black and white participants, ECG-LVH was associated with CVD/CHD risk but did not significantly improve CVD and CHD events risk prediction beyond the new Pooled Cohort and most used Framingham risk equations in blacks or whites.

Biological correlates of blood pressure variability in elderly at high risk of cardiovascular disease.

Visit-to-visit variability in blood pressure is an independent predictor of cardiovascular disease. This study investigates biological correlates of intra-individual variability in blood pressure in older persons. Nested observational study within the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER) among 3,794 male and female participants (range 70-82 years) with a history of, or risk factors for cardiovascular disease. Individual visit-to-visit variability in systolic and diastolic blood pressure and pulse pressure (expressed as 1 SD in mm Hg) was assessed using nine measurements over 2 years. Correlates of higher visit-to-visit variability were examined at baseline, including markers of inflammation, endothelial function, renal function and glucose homeostasis. Over the first 2 years, the mean intra-individual variability (1 SD) was 14.4mm Hg for systolic blood pressure, 7.7mm Hg for diastolic blood pressure, and 12.6mm Hg for pulse pressure. After multivariate adjustment a higher level of interleukin-6 at baseline was consistently associated with higher intra-individual variability of blood pressure, including systolic, diastolic, and pulse pressure. Markers of endothelial function (Von Willebrand factor, tissue plasminogen activator), renal function (glomerular filtration rate) and glucose homeostasis (blood glucose, homeostatic model assessment index) were not or to a minor extent associated with blood pressure variability. In an elderly population at risk of cardiovascular disease, inflammation (as evidenced by higher levels of interleukin-6) is associated with higher intra-individual variability in systolic, diastolic, and pulse pressure.

Lack of association between serum gamma-glutamyltransferase and carotid atherosclerosis: The Namwon study

Objectives: There is little evidence for an association between gamma-glutamyltransferase (GGT) and carotid atherosclerosis, an independent predictor of cardiovascular disease. We examined the association between serum GGT and carotid atherosclerotic parameters, including carotid intima-media thickness (IMT) and plaques, in a large general population. Methods: The study population consisted of community-dwelling adults who participated in the baseline survey of the Namwon Study. A total of 9120 subjects aged 45–74 years were included in the analyses. High-resolution B-mode ultrasound was used to measure carotid IMT and to evaluate the presence of carotid plaques. A mean carotid IMT of ≥1.0 mm was classified as ‘high carotid IMT’. Results: Serum GGT levels were classified into quartiles. In a fully adjusted model, we found no linear trend between GGT quartile and mean carotid IMT (P for trend = 0.167). Compared with the first quartile (the reference category), the odds ratios (ORs) and 95% confidence intervals (CIs) for high carotid IMT were 0.89 (0.68–1.16), 1.10 (0.84–1.43), and 0.97 (0.71–1.33) for the second, third, and fourth quartiles (P for trend = 0.754), respectively. The ORs (95% CIs) for carotid plaques were 0.89 (0.77–1.02), 0.95 (0.82–1.10), and 0.94 (0.79–1.11) for the second, third, and fourth quartiles, respectively, in the fully adjusted model (P for trend = 0.644). Conclusions: No significant association of GGT concentration with carotid IMT or plaques was found in this large cross-sectional study. Further longitudinal studies are needed to confirm our findings.

Early renal abnormalities as an indicator of cardiovascular risk in type 2 diabetes.

Accurate assessment of cardiovascular (CV) risk is a prerequisite for devising effective therapeutic strategies in patients with type 2 diabetes (T2DM) as it allows to refine prognosis and treatment targets as well as the cost-benefit ratio for specific pharmacological interventions. The presence of subclinical vascular organ damage plays a well known role in determining overall risk and a wider use of low cost, easy to perform diagnostic tools to stratify CV risk is very much needed. Besides their well known prognostic value for progression to end stage renal disease (ESRD), subclinical renal abnormalities such as microalbuminuria and/or a slight reduction in estimation of glomerular filtration rate (eGFR), have been shown to be powerful, independent predictors of CV diseases in patients with T2DM. Through the combined evaluation of these two biomarkers of chronic kidney disease (CKD), clinicians can usefully and reliably get a perspective on global and CV outcome of their diabetic patients.

Non-invasive markers of atherosclerosis and their correlation with Framingham risk score in Indian patients with type 2 diabetes mellitus

Background : India has been referred as the capital of the world”. Diabetes mellitus (DM) is widely accepted as a vascular disease leading to substantive increase in cardiovascular disease (CVD). Recently, there has been much interest in the relationship between arterial stiffness and cardiovascular disease. So this study was conducted to assess the risk of atherosclerosis in patients with DM. Aim : To investigate the relationship between non-invasive oscillometric methods that assesses subclinical atherosclerosis, and Framingham Risk Score (FRS), an independent predictor of CVD, in patients with type 2 DM, and age-matched hypertensive and healthy controls. Methods : The four study groups consisted of group A I; patients with diabetes mellitus (>5 years) along with hypertension (n=55), group A II; newly diagnosed patients with DM without hypertension (n=28), group B I; patients with hypertension (n=31) and group B II; healthy controls (n=30). The participants were subjected to oscillometric measurements like arterial stiffness index (ASI), pulse wave velocity (PWV), and augmentation index (AIx). All these parameters were correlated with FRS. Results : The PWV, ASI, AIx as well as FRS of 30 yr risk of CVD were elevated in patients with DM compared to healthy controls. A significant correlation was observed between FRS, and PWV, ASI, and AIx. Conclusion : This study reveals that non-invasive oscillometric markers can be useful in early detection of early atherosclerosis in patients with type 2 DM. Key Words : Diabetes; atherosclerosis; arterial stiffness index; pulse wave velocity; augmentation index; Framingham risk score

Platelet-lymphocyte ratio is an independent predictor for cardiovascular disease in obstructive sleep apnea syndrome.

There is a strong relationship between obstructive sleep apnea syndrome (OSAS) and cardiovascular disease (CVD). Chronic intermittent hypoxia, inflammation, oxidative stress, and endothelial dysfunction may constitute etiologic mechanisms, linking OSAS to CVD. Inflammation play an important role in the development of CVD. Platelet-lymphocyte ratio (PLR) is a new biomarker showing inflammation. No previous study has ever investigated the association between PLR, CVD and OSAS severity in patients with OSAS. This study was designed to investigate the association between PLR and CVD in patients with OSAS, and relationship between severity of OSAS, polysomnographic parameters and PLR. This was a cohort study in which patients who had undergone a full night polysomnoraphy for diagnosis of OSA were recruited. Patients were divided according to their apnea-hypopnea index (AHI) scores into OSAS negative (Group 1: AHI < 5), mild (Group 2: AHI, 5-15), moderate (Group 3:AHI,15-30), and severe OSAS (Group 4: AHI > 30) groups. The presence of heart failure, coronary artery disease or arrhythmia was defined as CVD. A total of 424 patients were included in this study. There were 57, 93, 82, and 192 patients in Groups 1, 2, 3, and 4, respectively. PLR were significantly different between groups (Group 1: 87.38; Group 2: 95.07; Group 3: 97.01, Group 4: 126.9, P < 0.05). PLR were significantly correlated with AHI, oxygen desaturation index, average and minimum O2 saturation values (P < 0.05). Values of PLR were significantly higher in patients with CVD compared with those without. Multiple regression analysis demonstrated that PLR is an independent predictor of CVD. PLR cut-off value for demonstrating the presence of CVD is higher than 108.56. In the light oh findings, PLR is strongly associated with the severity of OSAS and cardiovascular disease in OSAS patients. PLR might be used as a biomarker to predict CVD in OSAS patients.

Lipoprotein(a) Levels in Familial Hypercholesterolemia: An Important Predictor of Cardiovascular Disease Independent of the Type of LDL Receptor Mutation

The aim of this study was to determine the relationship between lipoprotein(a) [Lp(a)] and cardiovascular disease (CVD) in a large cohort of patients with heterozygous familial hypercholesterolemia (FH). Lp(a) is considered a cardiovascular risk factor. Nevertheless, the role of Lp(a) as a predictor of CVD in patients withFH has been a controversial issue. A cross-sectional analysis of 1,960 patients with FH and 957 non-FH relatives recruited for SAFEHEART (Spanish Familial Hypercholesterolemia Cohort Study), a long-term observational cohort study of a molecularly well-defined FH study group, was performed. Lp(a) concentrations were measured in plasma using an immunoturbidimetric method. Patients with FH, especially those with CVD, had higher Lp(a) plasma levels compared with their unaffected relatives(p< 0.001). A significant difference in Lp(a) levels was observed when the most frequent null and defective mutations in LDLR mutations were analyzed (p< 0.0016). On multivariate analysis, Lp(a) was an independent predictor of cardiovascular disease. Patients carrying null mutations and Lp(a) levels >50 mg/dl showed the highest cardiovascular risk compared with patients carrying the same mutations and Lp(a) levels<50 mg/dl. Lp(a) is an independent predictor of CVD in men and women with FH. The risk of CVD is higher in those patients with an Lp(a) level >50 mg/dl and carrying a receptor-negative mutation in the LDLR gene compared with other less severe mutations.

Framingham score and LV mass predict events in young adults: CARDIA study

BackgroundFramingham risk score (FRS) underestimates risk in young adults. Left ventricular mass (LVM) relates to cardiovascular disease (CVD), with unclear value in youth. In a young biracial cohort, we investigate how FRS predicts CVD over 20years and the incremental value of LVM. We also explore the predictive ability of different cut-points for hypertrophy. MethodsWe assessed FRS and echocardiography-derived LVM (indexed by body surface area or height2.7) from 3980 African–American and white Coronary Artery Risk Development in Young Adults (CARDIA) participants (1990–1991); and followed over 20years for a combined endpoint: cardiovascular death; nonfatal myocardial infarction, heart failure, cerebrovascular disease, and peripheral artery disease. We assessed the predictive ability of FRS for CVD and also calibration, discrimination, and net reclassification improvement for adding LVM to FRS. ResultsMean age was 30±4years, 46% males, and 52% white. Event incidence (n=118) across FRS groups was, respectively, 1.3%, 5.4%, and 23.1% (p<0.001); and was 1.4%, 1.3%, 3.7%, and 5.4% (p<0.001) across quartiles of LVM (cut-points 117g, 144g, and 176g). LVM predicted CVD independently of FRS, with the best performance in normal weight participants. Adding LVM to FRS modestly increased discrimination and had a statistically significant reclassification. The 85th percentile (≥116g/m2 for men; ≥96g/m2 for women) showed event prediction more robust than currently recommended cut-points for hypertrophy. ConclusionIn a biracial cohort of young adults, FRS and LVM are helpful independent predictors of CVD. LVM can modestly improve discrimination and reclassify participants beyond FRS. Currently recommended cut-points for hypertrophy may be too high for young adults.

Uric acid is a risk factor for ischemic stroke and all-cause mortality in the general population: a gender specific analysis from The Tromsø Study

BackgroundThe role of serum uric acid as an independent predictor of cardiovascular disease and death is uncertain in the general population. Adjustments for additional cardiovascular risk factors have not been consistent. We examined the association of serum uric acid with all-cause mortality, ischemic stroke and myocardial infarction in a prospective population based study, with several traditional and non-traditional risk factors for cardiovascular disease included in the model.MethodsA population-based prospective cohort study was performed among 2696 men and 3004 women. Endpoints were all-cause mortality after 15 years, and fatal or non-fatal myocardial infarction (MI) and ischemic stroke after 12 years.Results1433 deaths, 659 MIs and 430 ischemic strokes occurred during follow-up. Fully adjusted Cox regression analyses showed that per 1 SD (87 μmol/L) increase in serum uric acid level, the risk of all-cause mortality increased in both genders (hazard ratios, HR men; 1.11, 95% CI 1.02-1.20, women; 1.16, 1.05-1.29). HRs and 95% CI for stroke were 1.31, 1.14-1.50 in men, 1.13, 0.94-1.36 in women, and 1.22 (1.09, 1.35) in the overall population. No independent associations were observed with MI.ConclusionSerum uric acid was associated with all-cause mortality in men and women, even after adjustment for blood pressure, estimated GFR, urinary albumin/creatinine ratio, drug intake and traditional cardiovascular risk factors. After the same adjustments, serum uric acid was associated with 31% increased risk of stroke in men.