Risk Factor For Cardiovascular Mortality Research Articles

Similar decline in mortality rate of older persons with and without type 2 diabetes between 1993 and 2004 the Icelandic population-based Reykjavik and AGES-Reykjavik cohort studies

BackgroundA decline in mortality rates due to cardiovascular diseases and all-cause mortality has led to increased life expectancy in the Western world in recent decades. At the same time, the prevalence of type 2 diabetes, a disease associated with a twofold excess risk of cardiovascular disease and mortality, has been increasing. The objective of this study was to estimate the secular trend of cardiovascular and all-cause mortality rates in two population-based cohorts of older persons, with and without type 2 diabetes, examined 11 years apart.Methods1506 participants (42% men) from the population-based Reykjavik Study, examined during 1991–1996 (median 1993), mean age 75.0 years, and 4814 participants (43% men) from the AGES-Reykjavik Study, examined during 2002–2006 (median 2004), mean age 77.2 years, age range in both cohorts 70–87 years. The main outcome measures were age-specific mortality rates due to cardiovascular disease and all causes, over two consecutive 5.7- and 5.3-year follow-up periods.ResultsA 32% decline in cardiovascular mortality rate and a 19% decline in all-cause mortality rate were observed between 1993 and 2004. The decline was greater in those with type 2 diabetes, as illustrated by the decline in the adjusted hazard ratio of cardiovascular mortality in individuals with diabetes compared to those without diabetes, from 1.88 (95% CI 1.24-2.85) in 1993 to 1.46 (95% CI 1.11-1.91) in 2004. We also observed a concurrent decrease in major cardiovascular risk factors in both those with and without diabetes. A higher proportion of persons with diabetes received glucose-lowering, hypertensive and lipid-lowering medication in 2004.ConclusionsA decline in cardiovascular and all-cause mortality rates was observed in older persons during the period 1993–2004, in both those with and without type 2 diabetes. This decline may be partly explained by improvements in cardiovascular risk factors and medical treatment over the period studied. However, type 2 diabetes still persists as an independent risk factor for cardiovascular mortality.

GABA-induced vasorelaxation mediated by nitric oxide and GABAA receptor in non diabetic and streptozotocin-induced diabetic rat vessels

Diabetes has profound, negative effects on the function of arteries and arterioles. Hypertension is considered an independent risk factor for cardiovascular mortality in diabetic patients. The present study was designed to determine whether GABA-induced vasorelaxation in normal and streptozotocin-induced diabetic rat vessels is mediated by nitric oxide and the GABAA receptor. Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ) (60 mg/kg). Eight weeks later, superior mesenteric arteries of all groups were isolated and perfused according to the McGregor method. Baseline perfusion pressure of STZ diabetic rats was significantly higher than non-diabetic rats in both intact and denuded endothelium. In the presence of bicuculline, a selective GABAA receptor blocker, GABA-induced relaxation in intact and denuded endothelium mesenteric beds of non-diabetic and STZ diabetic rats was suppressed. But in the presence of L-NAME, a nitric oxide synthesis inhibitor, although GABA- induced vasorelaxation was not suppressed at a dose of 1 µM of GABA in all groups, this response was suppressed with the other doses of GABA. From the results of this study it may be concluded that the vasorelaxatory effect of GABA is mediated by the GABAA receptor and nitric oxide in both STZ diabetic and non-diabetic vessels.

The effects of excess weight on cardiac strain and steatosis in adults and children

Background Excess body fat is a known risk factor for cardiovascular mortality and morbidity. However, obesity, hypertension, hyperlipidaemia and insulin resistance are closely interlinked, both in their causes (eg sedentary lifestyle, social class, diet & age) and effects (endothelial function, increased left ventricular mass, increased myocardial fatty acid uptake). Thus it has been difficult to determine the exact effects of excess weight alone on myocardial function and metabolism. Myocardial triglyceride deposition and impaired strain have been clearly shown in adult diabetic cardiomyopathy. Recently, similar findings have been demonstrated in obese non-diabetic women. We set out to see if obesity alone, in the absence of other components of the Metabolic Syndrome, was also associated with cardiac steatosis and/or impaired peak circumferential strain in adults of both sexes and in adolescent boys. Methods We recruited 100 adults (44 lean, 28 overweight & 28 obese) and 22 boys aged 10-15 years (11 lean & 11 obese) by open poster advertisement. Exclusion criteria were heart failure, valvular disease, the use of any cardiovascular medications and any classical risk factors (hypertension, hyperlipidaemia, diabetes mellitus, smoking and obstructive sleep apnoea). Body mass index (BMI) and waist circumference were measured in all subjects. Left ventricular (LV) mass, volumes, function and peak circumferential strain were measured with 3T cardiac MR imaging and tagging. Myocardial triglyceride content (MTGC) was determined by ECG-gated localised proton spectroscopy to calculate the lipid : water ratio in the interventricular septum. Image and spectroscopy data were anonymised prior to analysis. Results There was a clear increase in myocardial lipid content in overweight and obese adults compared to the lean control group (Figure 1). Body mass index and waist circumference were associated with a linear increase in MTGC (a 10kg/m 2 increase in BMI was associated with a 48% increase in MTGC, p < 0.05), but gender had no impact. There was also an 11% reduction in the peak circumferential strain of obese adults compared to their lean peers (median -18.0 v -21.4, p = 0.01), despite similar LV ejection fractions. LV mass was 16% higher in overweight and 20% higher in obese adults (p <0.01). In the adolescent group, obese boys had higher mean myocardial triglyceride deposition (0.29% v 0.16%, p = 0.04) and impaired strain (-17.5 v -20.2, p < 0.01), but with no significant difference in LV mass, ejection fraction, end-diastolic volume, glucose or cholesterol (Figure 2). Conclusions Obesity in the absence of diabetes or Metabolic Syndrome is associated with significant myocardial triglyceride deposition and impaired strain in adults and children. In paediatric obesity, this data suggests that myocardial steatosis and change in strain occur before any hypertrophy. The assessment of strain and MTGC may help in the diagnosis and monitoring of obesityrelated heart disease, especially in children.

1392 – Treated diabetes mellitus in institutionalized patients with schizophrenia

Patients with schizophrenia have higher cardiovascular morbidity and mortality compared to the general population. They also have a high levels of cardiovascular mortality risk factors: hypertension, smoking, hyperglycemia, physical inactivity, obesity and dyslipidemia, However, the presence of type 2 diabetes mellitus in institutionalized patients with schizophrenia has not been well studied. To establish an association between type 2 diabetes mellitus and schizophrenia in patients living in residential homes. To confirm a high prevalence of diabetes mellitus treatment in these patients. Four residential institutions for patients with schizophrenia were chosen for the study. There were a total of 145 patients with schizophrenia. The first had 48 patients, males 30 and females 18, the second had 42 patients; 29 males 13 females, the third had 27 patients; 13 males and 14 females and the fourth had 28 patients; 15 males and 13 females. Computerized pharmacy print outs and records from the institutions and our office charts were reviewed. Of the 145 institutionalized schizophrenia patients, there were 87 males (60%) and 58 females (40%). The average age was 55.76 years. 39(27%) of 145 patients were on treatment for DM; 106(73%) had no diabetes mellitus; 18 (21%) of 87 males had DM and 69 (79%) had no DM; 23 (40%) of 58 females had DM and 35(60%) had no DM. Type II diabetes mellitus is extremely common (27%) in institutionalized patients with schizophrenia. Due to close medical monitoring, awareness and treatment is one hundred percent.

A Crucial Role for p90RSK-Mediated Reduction of ERK5 Transcriptional Activity in Endothelial Dysfunction and Atherosclerosis

Diabetes mellitus is a major risk factor for cardiovascular mortality by increasing endothelial cell (EC) dysfunction and subsequently accelerating atherosclerosis. Extracellular-signal regulated kinase 5 (ERK5) is activated by steady laminar flow and regulates EC function by increasing endothelial nitric oxide synthase expression and inhibiting EC inflammation. However, the role and regulatory mechanisms of ERK5 in EC dysfunction and atherosclerosis are poorly understood. Here, we report the critical role of the p90 ribosomal S6 kinase (p90RSK)/ERK5 complex in EC dysfunction in diabetes mellitus and atherosclerosis. Inducible EC-specific ERK5 knockout (ERK5-EKO) mice showed increased leukocyte rolling and impaired vessel reactivity. To examine the role of endothelial ERK5 in atherosclerosis, we used inducible ERK5-EKO-LDLR(-/-) mice and observed increased plaque formation. When activated, p90RSK associated with ERK5, and this association inhibited ERK5 transcriptional activity and upregulated vascular cell adhesion molecule 1 expression. In addition, p90RSK directly phosphorylated ERK5 S496 and reduced endothelial nitric oxide synthase expression. p90RSK activity was increased in diabetic mouse vessels, and fluoromethyl ketone-methoxyethylamine, a specific p90RSK inhibitor, ameliorated EC-leukocyte recruitment and diminished vascular reactivity in diabetic mice. Interestingly, in ERK5-EKO mice, increased leukocyte rolling and impaired vessel reactivity were resistant to the beneficial effects of fluoromethyl ketone-methoxyethylamine, suggesting a critical role for endothelial ERK5 in mediating the salutary effects of fluoromethyl ketone-methoxyethylamine on endothelial dysfunction. Fluoromethyl ketone-methoxyethylamine also inhibited atherosclerosis formation in ApoE(-/-) mice. Our study highlights the importance of the p90RSK/ERK5 module as a critical mediator of EC dysfunction in diabetes mellitus and atherosclerosis formation, thus revealing a potential new target for therapeutic intervention.

Chronic fluoxetine reduces autonomic control of cardiac rhythms in rats with congestive heart failure

Up to 40% of patients with heart failure develop depression, and depression is an independent risk factor for cardiovascular mortality in this patient population. Consequently, increasing numbers of patients with heart failure are treated with antidepressants. Selective serotonin reuptake inhibitors are typically the antidepressant of choice since this drug class has limited cardiovascular toxicity. However, little is known about the effects of selective serotonin reuptake inhibitors on autonomic cardiac regulation in congestive heart failure (CHF). Here, indexes of cardiac autonomic control were evaluated before and during chronic fluoxetine (FLX) treatment (20 mg·kg(-1)·day(-1), 5 wk) in rats that developed CHF after coronary artery ligation. FLX reduced the low-frequency (LF) component of heart rate variability (HRV; P < 0.01) as well as the sympathetic contribution to LF HRV (P < 0.01) in both CHF and sham-operated rats. Both FLX and CHF reduced high-frequency HRV (P < 0.01). Spontaneous baroreflex gain was decreased in CHF rats 8 wk after ligation (P < 0.01). Cross-spectral coherence between the interbeat interval and mean arterial pressure was reduced in the LF domain 3 wk after ligation in CHF rats (P < 0.01) and was further reduced after chronic FLX treatment (P < 0.01). Plasma catecholamines and LF blood pressure variability were not affected by FLX. Chronotropic responses to both efferent vagal nerve stimulation and isoproterenol administration were reduced in CHF rats and by FLX (P < 0.01), whereas inotropic responses to isoproterenol were reduced only in CHF rats (P < 0.01). These data indicate that chronic FLX reduces the responsiveness to autonomic output controlling cardiac rhythm and may further compromise autonomic regulation of cardiac function in CHF.

Evidence of a synergistic association between heart rate, inflammation, and cardiovascular mortality in patients undergoing coronary angiography

Both elevated inflammatory activity and sustained tachycardia reflect unfavourable cardiovascular risk profiles, and there is evidence to suggest the deleterious effects of inflammation are amplified by increased heart rate. The purpose of this study was to assess the interaction between resting heart rate and inflammation in cardiovascular mortality. A total of 3267 patients (2283 men), aged 18-95 years, scheduled for coronary angiography, were followed prospectively. By principle component analysis, we developed an overall multi-marker index of inflammation weighting the respective coefficients of five inflammatory markers including: interleukin-6, C-reactive protein, serum amyloid A, neutrophils, and fibrinogen. Cox proportional hazard regression models were employed to evaluate the relationship between inflammation and heart rate with cardiovascular mortality. Across 29,940 person years of follow-up, there were 546 (17%) deaths due to cardiovascular disease (CVD). Significantly, we observed a strong synergistic effect of inflammatory activity and concurrent elevated heart rate. For CVD mortality, patients in the highest quartile of inflammation had an adjusted hazard ratio (95% confidence interval) of 1.84 (1.31-2.57), P < 0.0001 if their resting heart rate was <75 b.p.m. Substantially, patients had a greater adjusted HR of 7.50 (3.21-17.50), P < 0.0001 if their resting heart rate was ≥75 b.p.m. The present analyses underline elevated inflammation as a risk factor for cardiovascular mortality. The effects of inflammation appeared to be strongly amplified by a faster resting heart rate. If confirmed by additional studies, this association may prove a useful adjunct for therapeutic approaches to alleviate symptoms and prolong survival.

Does uric acid qualify as an independent risk factor for cardiovascular mortality?

UA (uric acid) is the final product of purine metabolism in humans and is implicated in many disease conditions. Sustained hyperuricaemia has putative adverse roles in cardiovascular diseases. Despite strong evidence emerging from large epidemiological studies supporting the hypothesis that UA independently influences cardiovascular disease outcomes and mortality, a causal role is yet to be established. Serum UA is also considered as a useful biomarker for mortality in high-risk patients with acute coronary syndromes, heart failure and hypertension and in patients with Type 2 diabetes mellitus. Post-hoc analyses of clinical trial data suggest beneficial effects of reducing serum UA. However, these findings are inconclusive and are only hypothesis-generating. In the present issue of Clinical Science, Ndrepepa and co-workers have investigated the prognostic role of UA in high-risk Type 2 diabetic patients with established coronary artery disease in predicting 1-year survival and cardiovascular mortality. These results support the independent role of serum UA in predicting survival in Type 2 diabetic patients. However, long-term follow-up studies are required with serial UA measurement to establish the time-dependent association of UA with mortality outcomes.

Meal-induced blood pressure variation and cardiovascular mortality in ambulatory hypertensive elderly patients

This prospective cohort study was designed to investigate the prevalence and the prognostic value of postprandial hypotension (PPH) in ambulatory hypertensive elderly patients without overt heart diseases, an issue that has never been evaluated so far. All patients consecutively referred to our cardiologic clinic in the period from January 2005 to August 2009, were enrolled in the study and underwent a 24-h ambulatory arterial blood pressure monitoring (ABPM). PPH has been defined as a decrease in SBP of 20 mmHg within 2 h after a meal. Four hundred and one patients were enrolled (mean age 77.7 ± 11 years, males 47.7%). Hypertension was not adequately controlled in 290 (72.3%) patients. PPH was found in 292 of 401 (72.8%) patients. A value of 10 mmHg or higher of SD SBP was predictive of PPH, with a sensitivity and specificity of 87 and 57%, respectively. At each meal, patients with higher SBP readings before meal had the greatest decrease in SBP (P < 0.001). During the follow-up, 34 patients died for cardiovascular causes. Breakfast BP variation was the most predictive variable of cardiovascular mortality (B = 0.020, P = 0.04, HR 1.020, IC 1.001-1.040). In our population, PPH was common. A diurnal standard deviation of SBP of 10 mmHg or higher was suggestive of its presence. ABPM identified breakfast BP decrease as a possible new risk factor for cardiovascular mortality.

927 HYPERTENSION AS RISK FACTOR FOR CARDIOVASCULAR MORTALITY IN DIABETES MELLITUS. A MULTIPLE CAUSES ANALYSIS

Objective: To evaluate hypertension (H) as risk factor for cardiovascular mortality in diabetes mellitus (DM) in Zulia State, Venezuela, during 2006-2008 period. Methods: Observational and descriptive study. The Ministry of Health provided the data with the transcription of section I of each death certificate. The National Statistics Institute provided the population denominators. It was used the International Diseases Classification (10th-review) to select the disease codes. A multiple-cause analysis1,2 (MCA) was applied to general mortality to extract all deaths with DM as underlying cause. From this latter group, there were extracted all deaths with H registered as an associated cause of death (ACD).The presence of cardiovascular diseases (CVD) coded as other ACD, was determined using MCA and compared between DM-H and DM-non-H deaths. DM-H impact on DM mortality was estimated. DM-H mortality rates were calculated and compared between years and expressed as the period median. There were characterized the impacts of CVD as ACD on DM-H mortality and its possibility of association was quantified [odds ratio (OR)]. Results: DM-H was registered in 28.04% of DM mortality. CVD represents 52.75% of other ACD in DM-H, (OR 2.03) [X2 99.39] and 35.78% in DM-non-H mortality. DM-H mean mortality rate was 10.19 per 100,000 populations: 10.20 males and 10.17 females. The ischemic diseases represented 74.14% of CVD. Conclusions: Although H may be under registered in death certificates, 52.75% of DM-H deaths show CVD as other ACD. The possibility of CVD to appear as other ACD in DM is 2.03-fold higher when H is present. References Goodman RA, Manton KG, Nolan TF, Bregman D.J, Hinman AR. Mortality data analysis using a multiple-cause approach.JAMA.1982; 247(6): 786-796. Lindahl BI, Johansson LA. Multiple cause-of-death data as a tool for detecting artificial trends in the underlying cause statistics: a methodological study. Scand J Soc Med.1994; 22(2):145-158.[Pubmed]

832 CAROTID INTIMA-MEDIA THICKNESS AND BLOOD PRESSURE IN JAPANESE VERY ELDERLY

Background: Carotid intima-media thickness (IMT) is one of the risk factors for cardiovascular mortality and morbidity, and its relationships to the cardiovascular risk factors such as hypertension (HT), diabetes mellitus (DM), hyperlipidemia (HL), ischemic heart disease (IHD), stroke has been demonstrated. However, a little is known about its relationships in the Japanese very elderly. Methods: We measured carotid IMT of 240 patients (mean age 79 years, male/female = 114/126) who were over 70 years old, and examined the relationships between IMT, mean systolic and diastolic blood pressure of six hospital visits (mSBP and mDBP) and other cardiovascular risk factors (treatment of hypertension (HT), DM, HL, IHD and stroke). Result: IMT positively correlated with mSBP (p = 0.011, r = 0.16), and multivariate analysis revealed that IMT had a positive correlation with age, sex and mSBP. In the subjects below 80 years old (n = 129, mean age 75 years), mSBP was a significant determinant factor for IMT (p = 0.026), but we did not observed the correlation between mSBP and IMT in the subjects over 80 (n = 111, mean age 84 years). Conclusions: In the Japanese seventies, carotid IMT was correlated with SBP, but its correlation was not seen in the elderly over 80 years. These results suggested that the blood pressure control still affected atherosclerosis below 80 years, but in the Japanese elderly over 80 years, atherosclerosis did not simply reflect the blood pressure control.

Long-Term Outcome of Patients With Moderate and Severe Prosthetic Aortic Valve Regurgitation After Transcatheter Aortic Valve Implantation

Recently, moderate and severe postprocedure aortic regurgitations (ARs) have been identified as independent risk factors for short- and midterm mortality after transcatheter aortic valve implantation (TAVI). However, very few data exist on the long-term outcome of postprocedure AR. From 2008 to 2011, 198 consecutive patients with severe aortic stenosis successfully underwent TAVI with the CoreValve prosthesis (Medtronic CV, Minneapolis, Minnesota). After the procedure, patients were subdivided into groups depending on the presence of moderate/severe AR. The primary study end point was death from any cause after TAVI. The secondary end point was defined as cardiovascular death. In study patients (80 ± 6 years old, logistic European System for Cardiac Operative Risk Evaluation 22 ± 16%, left ventricular ejection fraction 53 ± 13%), moderate/severe AR occurred in 28 patients (14%). Despite similar baseline characteristics, patients with moderate/severe AR had higher 30-day and 1-year mortality rates than patients with none/mild AR (21% vs 6%, p = 0.019; 57% vs 16%, p <0.001, respectively). During a mean follow-up of 535 ± 333 days, the primary end point was reached in 54 and the secondary end point in 33 patients. Moderate/severe AR was the strongest independent risk factor of all-cause-mortality (hazard ratio 4.89, 95% confidence interval 2.78 to 8.56, p <0.001) and the strongest independent risk factor of cardiovascular mortality (hazard ratio 7.90, 95% confidence interval 3.95 to 15.81, p <0.001). In conclusion, moderate and severe postprocedure ARs are not uncommon complications after TAVI. Although long-term outcome of patients with none/mild AR is favorable, outcome of patients with moderate/severe AR is dismal.

Vitamin D: something new under the sun.

Vitamin D: something new under the sun.

Letter by Triantafyllou et al Regarding Article, “Mild Retinopathy Is a Risk Factor for Cardiovascular Mortality in Japanese With and Without Hypertension: The Ibaraki Prefectural Health Study”

To the Editor: We have read with great interest the work from Sairenchi et al in a large cohort of 87 890 individuals with a mean 14.1 years of follow-up,1 which was long awaited for the establishment of the prognostic value of mild hypertensive retinopathy in terms of actual hard clinical outcomes, including all-cause, total cardiovascular, and total stroke mortality. Given the study's findings, we acknowledge the importance attributed to mild hypertensive retinopathy as an independent risk factor for cardiovascular mortality in individuals with and without hypertension. Yet we believe that this conclusion (reproduced in the article's title) might be somewhat …

Letter by Cheung et al Regarding Article, “Mild Retinopathy Is a Risk Factor for Cardiovascular Mortality in Japanese With and Without Hypertension: The Ibaraki Prefectural Health Study”

To the Editor: The Ibaraki Prefectural Health Study shows that mild hypertensive retinopathy signs are independent predictors of cardiovascular mortality among Japanese men and women, with or without hypertension.1 Although this is the largest study to date examining the link between retinal signs and mortality, some aspects of the study merit clarification and further discussion. For instance, there are several noteworthy issues related to the methodology used for retinal grading. First, to grade hypertensive retinopathy, the authors used the Keith-Wagner-Barker classification scheme, which has known major limitations.2 Based on the strength of the reported associations between retinopathy …

Response to Letters Regarding Article, “Mild Retinopathy Is a Risk Factor for Cardiovascular Mortality in Japanese With and Without Hypertension: The Ibaraki Prefectural Health Study”

We appreciate the interest of Triantafyllou et al and Cheung et al in our recent article on retinopathy and cardiovascular mortality.1 They pointed out several issues with the article. Triantafyllou et al discussed 3 major points. First, they stated that grade 1 retinopathy did not possess a predictive role for cardiovascular mortality in normotensive individuals. However, the probability value for the trend showed significance in nonhypertensive men and women (Table 3); in addition, the multivariable (including blood pressure levels and antihypertensive medication use) adjusted hazard ratio for grade 1 retinopathy was significantly higher in all (ie, nonhypertensive and hypertensive) men and women (Table 2). These results appear to suggest the predictive role of grade 1 retinopathy. Second, the lack of information on antihypertensive drugs during the follow-up period, especially in nonhypertensive subjects, was pointed out. We excluded subjects who used antihypertensive drugs …

Activation of nuclear factor-kappa B accelerates vascular calcification by inhibiting ankylosis protein homolog expression

Vascular calcification is a major risk factor of cardiovascular mortality, particularly for patients with end-stage renal disease and diabetes. Although chronic inflammation is one of the etiologic factors, the underlying mechanism is not fully understood. To clarify this, we studied how nuclear factor-kappa B (NF-κB) induction, a mediator of inflammation, might promote vascular calcification. Activation of NF-κB by tumor necrosis factor (TNF) promoted inorganic phosphate-induced calcification in human aortic smooth muscle cells. Pyrophosphate (an inhibitor of calcification) efflux to the extracellular matrix was suppressed along with the decreased expression of ankylosis protein homolog (ANKH), a transmembrane protein that controls pyrophosphate efflux of cells. The restoration of ANKH expression in these cells overcame the decreased pyrophosphate efflux and calcification. Tristetraprolin, a downstream product of NF-κB activation, may mediate destablization of ANKH mRNA since its knockdown by shRNA increased ANKH expression and decreased calcification. Furthermore, a rat chronic renal failure model, with increased serum TNF levels, activated NF-κB and decreased ANKH levels. In contrast, the inhibition of NF-κB maintained ANKH expression and attenuated vascular calcification both in vivo and in vitro. Both human calcified atherosclerotic lesions and arteries from patients with chronic kidney disease had activated NF-κB and decreased ANKH expression. Thus, TNF-activated NF-κB promotes inflammation-accelerated vascular calcification by inhibiting ankylosis protein homolog expression and consequent pyrophosphate secretion.

Neuroticism and Cardiovascular Disease Mortality

The association between personality traits and mortality might differ as a function of socioeconomic status (SES). Our aim was to evaluate the all-cause, cardiovascular disease (CVD), and cancer mortality risk associated with neuroticism or extraversion and their interactions with SES in a representative sample of the UK adult population. A total of 5450 participants (2505 men) from the Health and Lifestyle Survey completed the Eysenck Personality Inventory at baseline and were monitored for vital status over 25 years. SES was defined as a latent variable comprising occupational social class, educational attainment, and income. A significant neuroticism-by-SES-by-sex interaction (p = .04) for CVD mortality revealed a neuroticism-by-SES interaction specific to women. Compared to women with average SES, those with both high neuroticism and low SES were at an increased risk for CVD mortality (hazard ratio = 2.02, 95% confidence interval = 1.45-2.80), whereas those with high neuroticism and high SES combined were at a decreased risk for CVD mortality (hazard ratio = 0.61, 95% confidence interval = 0.38-0.97, p for interaction = 0.003). The interaction term was not explained by health behaviors (10% attenuation) and physiological variables (11% attenuation). This interaction was not observed for all-cause and cancer mortality risks or among men for CVD mortality. High neuroticism is a risk factor for cardiovascular mortality in women with low SES, whereas in women with higher SES, it is protective. Further research is needed to replicate this finding and identify the mechanisms behind the modifying effect of SES on neuroticism.

Early and late mortality of patients with community acquired pneumonia

Community acquired pneumonia is the most frequent infective cause of severe sepsis and death. The risk of mortality in community acquired pneumonia is predictable by the "pneumonia severity index" and various biomarkers (e.g., procalcitonin, troponin-I). Quantitative testing of pneumococcal load (DNA) in blood has also become possible recently. Early death due to acute myocardial infarction is more frequent among patients with previous community acquired pneumonia. The 1-year and the 5-6 year survival is shorter among these patients. Pro-inflammatory cytokines synthesized during community acquired pneumonia accelerate chronic inflammation ongoing in atherosclerotic plaques. The pro-thrombotic condition present in atherosclerosis is also potentiated by community acquired pneumonia. These pathophysiological mechanisms may explain the epidemiologic fact that community acquired pneumonia is an independent risk factor of cardiovascular mortality.

Prevalence of hyperuricemia and its correlation with cardiovascular risk factors in Iraqi subjects of karbalaa city.

Background Uric acid an independent risk factor for cardiovascular mortality is still disputed as several studies have suggested that hyperuricemia is merely associated with cardiovascular diseases because of confounding factors such as obesity, dyslipidemia, hypertension, use of diuretics and insulin resistance .Moreover, there is still no well-established pathophysio-logical link between hyperuricemia and the development of cardiovascular complicationsObjectives: The purpose of the present study is to investigate the prevalence and the clinical correlation of hyperuricemia with cardiovascular risk factors in Karbalaa city in Iraq.Subjects and method: The investigations were performed between October 2009 and June 2010 on 130 subjects of different ages who attended the public clinic in AL- Hussainy teaching hospital in Karbala. Total cholesterol and triglycerides were determined enzymaticaly. High density lipoproteincholesterol was measured similarly after precipitation with magnesium phosphotungstate. Fasting blood glucose was obtained using enzymatic oxidation method. Uric acid was determined using enzymatic methodsResults: 19% of the subjects had the elevated level of serum uric acid. In the current study, positive correlations was found between serum uric acid levels and body mass index, plasma glucose, total and low density lipoprotein - cholesterol and triglyceride levels but a negative correlation between uric acid level and high density lipoprotein -cholesterol level.Conclusion: In conclusion, these data show that hyperuricemia is closely linked to the various components of the metabolic syndrome and independently related to coronary artery disease.