Are serum thyrotropin levels within the reference range associated with endothelial function?

AIMS: High serum thyrotropin (TSH) levels within the reference range might be associated with an increased cardiovascular risk. In the present study, we investigated the association between serum TSH levels and flow-mediated dilation (FMD) as a measure of endothelial dysfunction. METHODS AND RESULTS: The study population comprised 1364 subjects (670 women) aged 25-85 years with serum TSH levels between 0.25 and 2.12 mIU/L recruited from 5-year follow-up of the Study of Health in Pomerania. No interventions were performed. Measurements of FMD and nitrate-mediated dilation (NMD) were performed in the supine position using standardized ultrasound techniques. FMD and NMD values below the median of each distribution were considered decreased. Analyses adjusted for age, sex, smoking, and systolic and diastolic blood pressure revealed a non-significant inverse trend between serum TSH levels and FMD (P = 0.130). Subjects with serum TSH levels above the highest quartile had lower median FMD values relative to subjects with serum TSH levels below the lowest quartile (4.86 vs. 5.43%, P < 0.05). A linear inverse trend between serum TSH levels and decreased FMD barely missed statistical significance (P = 0.138). Subjects with high serum TSH levels had higher odds of decreased FMD relative to subjects with low serum TSH levels (odds ratio 1.42; 95% confidence interval 1.02; 1.96; P < 0.05). These associations were more pronounced in men than in women. There were no such associations for NMD. CONCLUSION: Serum TSH levels within the upper reference range are associated with impaired endothelial function. Our findings contribute to the discussion on whether the upper TSH reference limit should be redefined.

Early achievement of mild therapeutic hypothermia and the neurologic outcome after cardiac arrest.

BACKGROUND: Mild therapeutic hypothermia (MTH) achieved by endovascular cooling has emerged as a new treatment strategy to reduce hypoxic brain injury after cardiac arrest (CA). It remains to be established how the time interval between CA and MTH impacts the neurologic outcome. We hypothesized that a more rapid achievement of MTH (time to target temperature [TTT], time to coldest temperature [TCT]) improves the outcome after CA. METHODS: Forty-nine consecutive patients successfully resuscitated from CA were enrolled. MTH with a body core temperature between 32.0 and 34.0 degrees C (target temperature: 33.0 degrees C) over 24 h was achieved using a closed-loop endovascular system. Based on the neurologic outcome at discharge, the patient group was dichotomized into good (no/mild cerebral disability) and poor (severe disability, coma/vegetative state, brain death) outcomes. Serum neurone specific enolase (NSE) as biochemical marker of brain damage was sampled at 24, 48, and 72 h after CA. RESULTS: Twenty-eight patients were discharged with a good outcome. Multivariate stepwise regression showed TTT (odds ratio for every h TTT: 0.69 [95% confidence interval: 0.51-0.98]) or, if entered into the model, TCT (odds ratio for every h TCT: 0.72 [95% confidence interval: 0.56-0.94]) to be independent predictors for good outcome. Further independent determinants were age, BMI, asystole as presenting rhythm, and thrombolysis during resuscitation. However, TCT was the only variable to correlate with maximum NSE values after CA (r=0.32, P<0.05). CONCLUSIONS: Early achievement of MTH by endovascular cooling appears to reduce hypoxic brain injury and to favour a good neurologic outcome after CA.

Relation of self-reported sleep duration with carotid intima-media thickness in a general population sample.

OBJECTIVES: An association of sleep with cardiovascular disease has been suggested. We analyzed the association of sleep duration with carotid intima-media thickness (IMT) as measure of generalized atherosclerosis. METHODS: IMT of the common carotid arteries was measured in 2437 participants of the Study of Health in Pomerania (SHIP). Participants indicated their daily sleep duration as sum of night and afternoon sleep. RESULTS: There was a J-shaped association of sleep duration (5 to 11/12h) with IMT. In this association, IMT values were lowest among subjects with an average sleep duration of 7-8h (0.76+/-0.15 and 0.79+/-0.16 mm, respectively) but increased with shorter and, still more so, with longer sleep duration. Subjects with only 5h sleep showed age- and sex-adjusted differences of 0.042 mm IMT (95% confidence interval 0.008-0.076 versus 8h sleep). IMT values were still greater among subjects with 11-12h sleep (adjusted differences versus 8h sleep 0.084 mm [0.040-0.128] IMT). Further adjustment for lifestyle indicators, socioeconomic determinants, and biological variables attenuated these differences, but they remained significant. CONCLUSIONS: Both longer and shorter sleep duration is associated with an increased risk of atherosclerosis. These findings support the hypothesis that sleep is related to cardiovascular disease.

MARS dialysis in decompensated alcoholic liver disease: a single-center experience.

Acute decompensation of chronically stable alcoholic liver disease (ALD) is the most common cause of terminal liver failure in developed countries. Molecular adsorbent recirculation system (MARS) is increasingly used as artificial liver support to facilitate spontaneous organ recovery. However, the experience to date and the evidence to justify this therapeutic strategy in acutely decompensated ALD are still insufficient. We report our clinical experience with MARS in 14 patients with acutely decompensated ALD (6 male subjects; median age [interquartile range], 51 [47-56] years; Child-Pugh score, 12 [10-13]; Acute Physiology and Chronic Health Evaluation (APACHE) II score, 20 [18-24]) and severely impaired liver function whose disease was unresponsive to conventional supportive care. At least 3 sessions were applied in any patient (48 sessions in total). Under MARS treatment, the following levels decreased: bilirubin (544 [489-604] to 242 [178-348] micromol/L; P<0.001), creatinine (212 [112-385] to 91 [66-210] micromol/L; P=0.002), cholestatic parameter gamma-glutamyl transpeptidase (5.9 [1.8-13.1] to 4.6 [1.8-8.3] micromol/L) (P<0.001), blood urea nitrogen (56 [32-91] to 34 [21-68] mmol/L; P=0.044), and platelet count (176 [85-241] to 84 [31-145] Gpt/L; P=0.004). In contrast, MARS failed to improve daily urine output (P=0.846), ammonia levels (P=0.340), or thromboplastin time (P=0.775). Only 3 patients survived the hospital stay (mortality 78.6%). Although MARS improved laboratory parameters of hepatic detoxification and renal function in patients with acutely decompensated ALD, the patients' mortality remained unsatisfactorily high. Our experience does not support the indiscriminative use of MARS in acutely decompensated ALD without further controlled studies.

Impaired peripheral endothelial function in severe idiopathic pulmonary hypertension correlates with the pulmonary vascular response to inhaled iloprost.

BACKGROUND: Pulmonary endothelial function is known to be impaired in subjects with idiopathic pulmonary arterial hypertension (IPAH), but peripheral endothelial dysfunction and its predictive value for pulmonary vasoreactivity have not been previously investigated. METHODS: Measurements of peripheral endothelium-dependent and endothelium-independent vasoreactivity using flow-mediated dilation (FMD) and nitroglycerin-mediated dilation of the brachial artery were performed in 18 patients with severe IPAH (15 women; mean age 50 years [95% confidence interval 46-55 years], mean pulmonary artery pressure [PAP] 51 mm Hg [43-59 mm Hg], pulmonary vascular resistance [PVR] 1239 dyn s cm(-5) [861-1618 dyn s cm(-5)] at baseline) and in 36 age- and sex-matched controls. In patients with IPAH, acute pulmonary vasoreactivity was measured as pulmonary vascular response to inhaled iloprost (PVRII) during pulmonary catheterization. RESULTS: Compared to controls, patients with IPAH demonstrated impaired peripheral endothelial function (FMD, 0.19 [0.07-0.31] vs 0.38 [0.30-0.44] mm among controls; P =.002). No such impairment was observed for nitroglycerin-mediated dilation (0.34 [0.23-0.46] vs 0.36 [0.20-0.51] mm among controls; P = .679). Among patients with IPAH, iloprost lowered mean PAP by 8.2 mm Hg (2.0-14.5 mm Hg) (P = .001) and PVR by 395 dyn s cm(-5) (109-680 dyn s cm(-5)) (P < .001). Subsequent analysis of the association between peripheral endothelial function and PVRII disclosed a correlation of FMD with the percent decrease in mean PAP (r = .65, P = .003) and PVR (r = 0.67, P = .002), in which patients with IPAH with the greatest PVRII also exhibited the highest FMD values. CONCLUSIONS: Idiopathic pulmonary arterial hypertension is associated with peripheral endothelial dysfunction. Peripheral endothelium-dependent vasoreactivity correlates with the PVRII. It remains to be established if FMD has the potential as a clinical tool for noninvasive estimation of pulmonary vasoreactivity in IPAH.

Severe septic inflammation as a strong stimulus of myocardial NT-pro brain natriuretic peptide release.

BACKGROUND: Septic shock (SS) has recently been identified as stimulus of N-terminal pro-brain natriuretic peptide (NT-proBNP) release. We tested whether SS mediates NT-proBNP release through cardiomyocyte necrosis. Moreover, the discriminative value of NT-proBNP for the distinction between SS and non-septic shock (NSS) was assessed. METHODS: The study included 50 ICU patients with SS (n=25) and NSS (n=25), 40 patients with acute coronary syndrome and elevated troponin-I (ACStrop+) and 16 patients with unstable angina and normal troponin-I (UAtrop-). Eleven subjects without inflammation or cardiac disease served as controls. NT-proBNP levels of coronary patients were measured on admission, those of ICU patients 48 h after onset of shock symptoms. RESULTS: ACStrop+ (1525 [25th-75th percentile: 790-3820] pg/L) and NSS (687 [254-1552]) patients showed increased NT-proBNP levels above those of UAtrop- patients (107 [43-450], p<0.001) and controls (52 [42-99], p<0.001), but SS patients exhibited still higher levels (11,335 [4716-25,769], p<0.001 vs all others). Among ICU patients with shock symptoms, NT-proBNP discriminated SS and NSS with high sensitivity and specificity (area under ROC curve: 0.946 [95% confidence interval, 0.872-1.019]). NT-proBNP correlated with troponin-I, as marker of cardiomyocyte damage, among ACStrop+ (p<0.001) and SS patients (p=0.013). But, whereas SS patients showed the greatest NT-proBNP values, ACStrop+ patients had higher troponin-I levels (p<0.001), suggesting different mechanisms by which myocardial ischemia and SS mediate NT-proBNP release. CONCLUSIONS: SS is a more potent stimulus of NT-proBNP release than myocardial ischemia. NT-proBNP reliably distinguishes SS from other forms of shock. SS-related NT-proBNP release appears to involve cardiomyocyte damage but not genuine cardiomyocyte necrosis.

Cerivastatin reduces cytokine-induced surface expression of ICAM-1 via increased shedding in human endothelial cells.

Activation of endothelial cells is an incipient process in atherogenesis and leads to induction of the cellular adhesion molecules ICAM-1 and VCAM-1. Their expression can be induced by cytokines as well as other inflammatory mediators. The effects of HMG-CoA reductase inhibitors (statins) include mediation of anti-inflammatory properties. The aim of this study was the comparison of cerivastatin and simvastatin-mediated effects on inflammation-induced ICAM-1 and VCAM-1 expression in human umbilical venous endothelial cells (HUVEC). In HUVEC, TNF-alpha induced ICAM-1 and VCAM-1 mRNA and surface expression. Co-incubation with cerivastatin, but not simvastatin reduced TNF-alpha-induced up-regulation of ICAM-1 surface expression whereas both statins reduced VCAM-1 surface expression; all reductions in surface expression correlated with an increase in the soluble forms of ICAM-1 and VCAM-1 in cell culture supernatants. Mevalonate and nonsteroidal isoprenoids significantly reversed protein expression and shedding. Both statins caused an aggravation of TNF-alpha-induced ICAM-1 and VCAM-1 mRNA expression which was dependent on RNA synthesis. The statin-mediated increase in ICAM-1 and VCAM-1 mRNA expression correlated with the degradation of IkappaBa. Nuclear translocation of p65 was not significantly affected by statin-treatment of cytokine-treated cells. We conclude that cerivastatin and simvastatin reduce TNF-alpha-induced up-regulation of ICAM-1 and VCAM-1 surface expression via increased protein shedding mediated by HMG-CoA reductase inhibition and subsequent isoprenoid depletion.

Acute reversible cardiomyopathy with cardiogenic shock in a patient with Addisonian crisis: a case report.

A 42 year-old female, admitted to the ICU, with Addisonian crisis developed acute cardiopulmonary failure after hydrocortisone therapy was initiated. An echocardiogram showed severe reduction in the left-ventricular ejection fraction. Additionally, profound ECG abnormalities with diffuse ST-elevation and decreased QRS-amplitudes occurred, whereas Troponin-I was only moderately increased. Chest X-ray displayed bilateral pulmonary edema. The patient's condition culminated in respiratory failure and cardiogenic shock requiring catecholamines and ventilatory support. After a week, she had recovered uneventfully.

Thyroid function and serum ferritin levels: the study of health in Pomerania.

OBJECTIVE: Serum ferritin levels are assumed to be an atherosclerotic risk factor. Ferritin production is increased in individuals with activated liver production, which has been shown in hyperthyroid conditions. An association between subclinical hyperthyroidism and serum ferritin levels would add an explanation to the relation between low serum thyrotropin levels and mortality. The aim of the present analysis was to investigate an association between thyroid function and serum ferritin levels. We hypothesized low serum thyrotropin to be related to high serum ferritin levels. DESIGN: The Study of Health in Pomerania (SHIP) is a population-based study comprising male and female adults aged 20 to 79 years. Data of 4111 subjects (2071 females) were available for the present analysis. Serum ferritin levels were determined by an immunoturbidimetric assay. Multivariable analyses were performed to investigate an independent relation between thyroid function and serum ferritin levels. MAIN OUTCOME: Age-adjusted and gender-stratified analyses revealed no association between thyroid function and serum ferritin levels, neither in females nor in males. This finding remained stable after adjustment for potential confounders and in sensitivity analyses. CONCLUSION: There was no association between thyroid function and serum ferritin levels. We conclude that serum ferritin levels do not account for the relation between subclinical hyperthyroidism and vascular mortality.

Seropositivity for anti-Borrelia IgG antibody is independently associated with carotid atherosclerosis.

BACKGROUND: Various infectious agents are associated with atherosclerosis. This analysis was performed to investigate relation between seropositivity for anti-Borrelia IgG and carotid atherosclerosis. METHODS: The cross-sectional Study of Health in Pomerania was conducted in a general community living in a region with endemic Lyme disease. A random sample of 2483 individuals aged 45-79 years was available for the present analysis. Carotid atherosclerosis was sonographically assessed as intima-media thickness of the common carotid artery and as prevalent atherosclerotic plaques in the extracranial carotid arteries. IgG antibodies to Borrelia were determined by ELISA. RESULTS: IgG antibodies to Borrelia were found positive (> 10 IU/mL) in 108 subjects (4.3%). Persons with and without positive anti-Borrelia IgG antibodies differed with respect to carotid intima-media thickness values (0.863 +/- 0.017 mm versus 0.792 +/- 0.004 mm; p < 0.001) and prevalent carotid plaques (odds ratio 2.65, 95% confidence interval 1.53-4.61; p = 0.001), respectively. Seropositivity for anti-Borrelia IgG was also associated with both atherosclerotic endpoints when age, sex and further atherogenic risk factors and confounders were included in multivariable statistical models. CONCLUSIONS: In a region with endemic Lyme disease, seropositivity for anti-Borrelia IgG antibodies is independently associated with atherosclerosis. Our findings add support to the hypothesis that exposure to infectious pathogens increases the atherosclerosis risk.

Tooth loss is independently associated with the risk of acquired aortic valve sclerosis.

BACKGROUND: Several studies have shown that periodontal disease and atherosclerosis are associated. Aortic valve sclerosis (AVS) represents the sum of processes that are similar to the development of atherosclerosis. The present analysis was performed to investigate associations between periodontal disease, tooth loss, and AVS. METHODS: The population-based SHIP was conducted in northeast Germany. A study population of 2341 individuals aged > or =45 years was available for the present analysis. Aortic valve sclerosis was determined by echocardiography. Periodontal status was assessed by attachment loss and tooth loss. RESULTS: The prevalence of AVS was 29.9%. Logistic regression analyses did not reveal attachment loss as an independent risk factor for AVS. However, a reduced number of teeth was independently associated with AVS. Other risk factors for AVS were age, history of myocardial infarction, body mass index, pulse pressure, plasma fibrinogen and lipoprotein (a) levels, and the use of drugs that act on the renin-angiotensin system. CONCLUSION: A reduced number of teeth was independently associated with the risk of AVS. This finding further strengthens the link between oral health and cardiovascular disorders.

Endothelial nitric oxide synthase Glu(298)-->Asp polymorphism, carotid atherosclerosis and intima-media thickness in a general population sample.

The Glu(298)-->Asp (E298D; 894G-->T) polymorphism of eNOS (endothelial nitric oxide synthase) has been related with cardiovascular disease. In the present study, we investigated the association of Glu(298)-->Asp with atherosclerotic plaques in different carotid vessel segments and with carotid IMT (intima-media thickness). The Glu(298)-->Asp eNOS polymorphism was determined by 5'-exonuclease assay among 2448 participants of the SHIP (Study of Health in Pomerania). Mean and maximum common carotid IMT, as well as carotid atherosclerosis, were measured by high-resolution ultrasound. The Asp/Asp(298) genotype was associated with an increased risk of atherosclerotic plaques at the level of the common carotid arteries [multivariate odds ratio, 1.57 and 95% CI (confidence interval), 1.05-2.34; P=0.025], but not in the carotid bifurcations or internal or external carotid arteries. Glu(298)-->Asp genotype was not associated with carotid IMT in the whole sample. However, the Asp/Asp(298) genotype was independently associated with both higher mean [adjusted increase by 0.046 mm (95% CI, 0.013-0.078); P=0.006] and maximum carotid IMT [0.137 mm (95% CI, 0.064-0.209); P<0.001] in the low-risk group of subjects without carotid atherosclerosis. In conclusion, the Asp/Asp(298) genotype is associated with atherosclerosis in the common carotid arteries and, in a low-risk group, also with carotid IMT. This suggests that the association of the Glu(298)-->Asp genotype with atherosclerosis in the carotid arteries is site-specific and is modified by overall cardiovascular risk.

Endothelial nitric oxide synthase Glu298Asp gene polymorphism, blood pressure and hypertension in a general population sample.

OBJECTIVE: The Glu298Asp (E/D) polymorphism of the endothelial nitric oxide synthase (eNOS) gene has been related to hypertension. Since several studies have produced contradictory results, this issue is still subject to ongoing debate. We investigated the association of the eNOS E298D polymorphism with hypertension and with blood pressure (BP) in a large population-based sample of Caucasian ethnicity. DESIGN: Cross-sectional study in a random sample of the general population. METHODS: The eNOS E298D polymorphism was determined by 5'-exonuclease assay among 4219 participants aged 20-79 years of the Study of Health in Pomerania (SHIP). RESULTS: The percentages of the EE298, ED298 and DD298 genotypes were 49.2, 42.0 and 8.8%, respectively. The D allele frequencies did not differ between the groups of normotensive and hypertensive subjects (29.7 versus 29.9%, P = 0.812). Similarly, no association could be established between E298D genotype and prevalent hypertension, neither for D allele carriership (multivariate odds ratio 0.97, 95% confidence interval 0.83-1.12) nor for DD homozygosity (multivariate odds ratio 1.10, 95% confidence interval 0.84-1.43). Likewise, genotype groups did not differ as to the distribution of systolic (ANCOVA P = 0.917) or diastolic BP values (ANCOVA P = 0.657). Nearly identical results were obtained if the analyses were repeated sex-specifically or if subjects on antihypertensive medication were excluded. CONCLUSION: In a population-based cohort of Caucasians covering a broad age range, the eNOS E298D polymorphism is neither associated with prevalent hypertension nor with systolic or diastolic BP. These results do not support the hypothesis that the E298D polymorphism contributes to the genetic susceptibility to hypertension.

Interaction between factor V Leiden and serum LDL cholesterol increases the risk of atherosclerosis.

OBJECTIVES: We investigated the association between the factor V Leiden gene variant and carotid atherosclerosis in a cross-sectional study and explored possible associations between this gene variant and coronary artery disease (CAD) in a case-control study. METHODS: The presence (n=1696) or absence (n=703) of carotid atherosclerosis were sonographically assessed among participants of the population-based Study of Health in Pomerania (SHIP). The case-control study included 1021 patients with severe CAD and 2791 healthy SHIP participants. The factor V Leiden gene variant was determined by PCR and MnlI digestion. RESULTS: Multivariable analyses revealed no independent association between the factor V Leiden gene variant per se and carotid atherosclerosis or CAD. In the cross-sectional study, there was an interaction between the factor V Leiden gene variant and serum LDL cholesterol in non-diabetics with respect to the risk of carotid atherosclerosis. In the case-control study a similar interaction was found for CAD. In both studies the atherosclerotic risk increased with rising serum LDL cholesterol concentrations in carriers of the factor V Leiden gene variant. CONCLUSION: The co-existence between the factor V Leiden gene variant and high serum LDL cholesterol is independently associated with the risk of atherosclerosis.

Relation of parity with common carotid intima-media thickness among women of the Study of Health in Pomerania.

BACKGROUND AND PURPOSE: Metabolic and hormonal changes associated with pregnancy and childbirth are assumed to contribute to the development of cardiovascular disease among women. We analyzed the association of parity with common carotid intima-media thickness (IMT), which has a predictive value of subsequent myocardial infarction and stroke. METHODS: The Study of Health in Pomerania (SHIP), an epidemiological study of the general population in the northeast of Germany, included 1195 women aged 45 to 79 years. Mean and maximum far-wall IMT of the common carotid arteries were assessed by high-resolution ultrasound. All women were comprehensively characterized as to their reproductive history as well as to socioeconomic, behavioral, and biological risk factors. RESULTS: There was a U-shaped association between the number of children (from 0 to > or =4) and mean and maximum IMT. Nulliparous women had the highest age-adjusted mean (0.81 mm [95% CI, 0.78 to 0.84]) and maximum IMT (1.04 mm [95% CI, 1.00 to 1.09]), and women with single parity the lowest (mean IMT, 0.73 [95% CI, 0.72 to 0.74]; maximum IMT, 0.91 mm [95% CI, 0.89 to 0.93]; P<0.001 versus nulliparity for both parameters). Stepwise multivariate adjustment for socioeconomic factors, lifestyle variables, and biological variables attenuated the magnitude of this association yet significance remained. CONCLUSIONS: Nulliparity and higher number of children are associated with increased carotid IMT. These findings add support to the hypothesis of a link between the reproductive history of women and cardiovascular disease.

The association of thyroid function with cardiac mass and left ventricular hypertrophy.

Decreased serum TSH levels predict cardiovascular mortality, which could be explained by left ventricular hypertrophy (LVH). The aim of this analysis was to investigate the association between thyroid function and LVH. The population-based Study of Health in Pomerania was conducted in a previously iodine-deficient area. Data of 1510 individuals at least 45 yr of age with echocardiography and without thyroid disorders were analyzed. LVH was defined as a left ventricular mass index (LVMI) exceeding 150 g/m(2) (men) or 120 g/m(2) (women). Overt hyperthyroidism was associated with LVMI (P < 0.01), whereas euthyroid subjects and those with elevated TSH levels did not significantly differ with regard to LVMI. LVH was observed in three (15.0%) subjects with elevated serum TSH levels, in 127 (10.5%) euthyroid persons, in 24 (12.5%) individuals with decreased serum TSH levels, and in four (57.1%) subjects with hyperthyroidism (P < 0.01). Logistic regression analysis identified overt hyperthyroidism as an independent risk factor for LVH (odds ratio, 13.65; 95% confidence interval, 2.83-65.75; P < 0.01). There is an association between thyroid function status, cardiac mass, and LVH. Hyperthyroidism is an independent risk factor for LVH.

Hepatitis B and C virus infection and the risk of atherosclerosis in a general population.

BACKGROUND: The development of atherosclerosis has an inflammatory component. Currently it is not clear, whether hepatitis B and C virus infections are associated with the risk of atherosclerosis. The aim of the present analysis was to investigate those relationships in a population sample. METHODS AND RESULTS: The study of health in Pomerania (SHIP) is a cross-sectional study of the adult population in the northeast of Germany. HBs antigen (HBsAg) and IgG antibodies against hepatitis B and C virus (anti-HBs and anti-HCV) were determined by enzyme linked immunosorbent assays. Fifteen subjects (0.4%) were positive for HBsAg, and 21 subjects (0.5%) were positive for anti-HCV. Among the persons who had no history of anti-hepatitis B vaccination, 213 individuals (5.0%) were found to be as positive for anti-HBs. These individuals and those with prevalent anti-HCV antibodies were regarded as cases (n = 233). The control group comprised of 4033 individuals. Multivariable analyses revealed that there was no independent association between anti-HBs and anti-HCV antibody seropositivity and atherosclerotic end-points such as prevalent myocardial infarction, stroke, carotid intima-media thickness (IMT), carotid plaques and stenoses. CONCLUSION: There is no association between serological markers for hepatitis B and C virus infection and the risk of atherosclerosis in this population sample.

Association between high serum ferritin levels and carotid atherosclerosis in the study of health in Pomerania (SHIP).

BACKGROUND AND PURPOSE: Several studies have provided evidence for a relationship between body iron load and cardiovascular disease. We analyzed the association of serum ferritin levels with carotid atherosclerosis. METHODS: We assessed intima-media thickness and plaque prevalence in the carotid arteries by high-resolution ultrasound among 2443 participants (1200 women; age, 45 to 79 years) in the Study of Health in Pomerania (SHIP), a population-based study in northeast Germany. RESULTS: In multivariate analysis, serum ferritin levels were not independently associated with carotid intima-media thickness among women or men. In contrast, the relationship between serum ferritin levels and carotid plaque prevalence was significant among men (odds ratio per 1-SD increase of serum ferritin levels, 1.33; 95% confidence interval, 1.08 to 1.44) yet not among women (odds ratio, 1.29; 95% confidence interval, 0.98 to 1.75). However, both men and women showed a dose-response relation between serum ferritin levels and carotid atherosclerosis in which higher serum ferritin levels were associated with greater odds ratios for carotid plaque prevalence. Additionally, there was an interaction of serum ferritin levels with low-density lipoprotein (LDL) cholesterol (P=0.039) among men in which the association of serum ferritin levels with carotid plaque prevalence became stronger with increasing LDL cholesterol levels. CONCLUSIONS: Our study identified a relationship between serum ferritin levels and carotid atherosclerosis that was potentiated by LDL cholesterol. This relationship adds support to the hypothesis of a link between iron and cardiovascular disease.

Candidate genetic markers and the risk of restenosis after coronary angioplasty.

The aim of the present study was to test for possible associations between candidate gene polymorphisms and the risk of restenosis and recurrent restenosis after percutaneous transluminal coronary angioplasty (PTCA) without stenting. We followed up 511 PTCA patients, and restenosis and recurrent restenosis were defined according to angiographical criteria. Genotyping of the beta-fibrinogen -455 G/A, glycoprotein (GP) IIIa PlA1/PlA2, plasminogen activator inhibitor-1 (PAI-1) 4G/5G, factor V Leiden 1691 G/A, tumour necrosis factor alpha (TNFalpha) -238 G/A, TNFalpha -308 G/A, interleukin (IL)-1alpha -889 C/T, IL-1beta -511 C/T, methylenetetrahydrofolate reductase (MTHFR) 677 C/T and endothelial nitric oxide synthase (eNOS) 4 b/a gene polymorphisms was performed by PCR and restriction-fragment-length-polymorphism-based techniques. One hundred and sixty patients (31.3%) developed restenosis and in 130 of these patients, of whom 123 were available for analysis, a second PTCA without stenting was performed. Of these patients, 35 (28.5%) developed recurrent restenosis. None of the investigated genotypes were associated with the risk of restenosis or recurrent restenosis after PTCA. The degree of stenosis before and immediately after PTCA and the severity of the lesion were independent predictors for restenosis after PTCA. In conclusion, there was no association between the beta-fibrinogen -455 G/A, GP IIIa PlA1/A2, PAI-1 4G/5G, factor V Leiden 1691 G/A, TNFalpha -238 G/A, TNFalpha -308 G/A, IL-1alpha -889 C/T, the IL-1beta -511 C/T, MTHFR 677 C/T and eNOS 4 b/a gene polymorphisms and the risk of restenosis after PTCA as well as recurrent restenosis after repeated PTCA.