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Background: Previous epidemiological studies regarding the association between chronic periodontitis (CP) and carotid intima‐media thickness (cIMT) and subclinical atherosclerosis have been inconclusive. Objective: The aim of this study was to determine whether CP is associated with subclinical atherosclerosis in a large population‐based cohort study conducted in northern Germany (the Hamburg City Health study). Methods: Baseline data from 5781 participants of the Hamburg City Health Study with complete oral health and carotid ultrasound data (50.7% female, mean age: 62.1 ± 8.4 years) were evaluated. A standardized duplex sonography of the carotid artery was performed with measurement of carotid intima‐media thickness (cIMT) and atherosclerotic plaques. Oral health was assessed by recording the decayed, missing, and filled teeth (DMFT) index, clinical attachment loss (CAL), bleeding on probing (BOP), and the dental plaque index (PI). Correlations were tested for statistical significance by means of descriptive statistics and multivariate regression analyses. Results: Moderate and severe CP were associated with the prevalence of cIMT ≥ 1 mm (none or mild CP: 5.1%, moderate CP: 6.1%, severe CP: 10%) and mean cIMT (none or mild CP: 0.72 mm, moderate CP: 0.75 mm, severe CP: 0.78 mm) in bivariate analyses (p <.001). Additionally, severe and moderate CP were associated with higher prevalence of carotid atherosclerotic plaques (plaque = yes: none or mild CP: 23.9%, moderate CP: 29%, severe CP: 40.2%,). After adjustment for age, sex, smoking, diabetes, hypertension, educational level, hypercholesterolemia, and hsCRP, severe CP still correlated significantly with cIMT and the prevalence of cIMT ≥1 mm and/or presence of carotid atherosclerotic plaques. Conclusion: In this study, severe CP was associated with increased cIMT and higher prevalence of carotid plaques independent of common risk factors. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to determine local control and overall survival of patients with medically inoperable early-stage non-small cell lung cancer treated with stereotactic ablative radiotherapy. Methods: A total of 35 patients [6 (17%) females and 29 (83%) males] with medically inoperable early-stage non-small cell lung cancer and who were treated with stereotactic ablative body radiotherapy by a CyberKnife robotic radiotherapy machine between 2009 and 2015 were evaluated retrospectively. Results: Amyloidal inflammatory disease patients demonstrated a significantly greater carotid IMT (0.71±0.8 mm) compared with the non-amyloidal inflammatory disease patients (0.56±0.1 mm; p<0.001) and the healthy controls (0.43±0.4 mm; p<0.001). The patients with amyloidal inflammatory disease had a significantly greater CRP level (5.7±2.5 mg/L) than the other groups (3.7±3.1 mg/L, 1.5±1.2 mg/L; p<0.001). Conclusion: Increased carotid arterial wall thickness was associated with the presence of amyloidosis, perhaps due to an increase in atherosclerotic changes related to chronic lowlevel inflammation. [ABSTRACT FROM AUTHOR]

Background and aims Increased proinsulin relative to insulin levels have been associated with subclinical atherosclerosis (measured by carotid intima-media thickness (cIMT)) and are predictive of future cardiovascular disease (CVD), independently of established risk factors. The mechanisms linking proinsulin to atherosclerosis and CVD are unclear. A genome-wide meta-analysis has identified nine loci associated with circulating proinsulin levels. Using proinsulin-associated SNPs, we set out to use a Mendelian randomisation approach to test the hypothesis that proinsulin plays a causal role in subclinical vascular remodelling. Methods We studied the high CVD-risk IMPROVE cohort (n = 3345), which has detailed biochemical phenotyping and repeated, state-of-the-art, high-resolution carotid ultrasound examinations. Genotyping was performed using Illumina Cardio-Metabo and Immuno arrays, which include reported proinsulin-associated loci. Participants with type 2 diabetes (n = 904) were omitted from the analysis. Linear regression was used to identify proinsulin-associated genetic variants. Results We identified a proinsulin locus on chromosome 15 (rs8029765) and replicated it in data from 20,003 additional individuals. An 11-SNP score, including the previously identified and the chromosome 15 proinsulin-associated loci, was significantly and negatively associated with baseline IMT mean and IMT max (the primary cIMT phenotypes) but not with progression measures. However, MR-Eggers refuted any significant effect of the proinsulin-associated 11-SNP score, and a non-pleiotropic SNP score of three variants (including rs8029765) demonstrated no effect on baseline or progression cIMT measures. Conclusions We identified a novel proinsulin-associated locus and demonstrated that whilst proinsulin levels are associated with cIMT measures, proinsulin per se is unlikely to have a causative effect on cIMT. [ABSTRACT FROM AUTHOR]

Introduction: Hepatitis C is a major health problem: approximately 170 million people are infected with the hepatitis C virus worldwide. It is unclear whether chronic hepatitis C affects atherosclerosis and whether it can cause endothelial and/or autonomic nervous system (ANS) dysfunction. Materials and methods: From April 2008 through April 2009, we studied 76 patients with biopsyconfirmed chronic hepatitis C and no evidence of cirrhosis, ascites, portal hypertension, encephalopathy, or hepatocellular carcinoma. The age-, sex-, BMI- and cardiovascular risk factor- matched control group comprised 76 healthy, HCV-negative individuals with no evidence of liver, autoimmune, or immunoproliferative diseases and no history of cardiovascular events. Twenty five of the hepatitis C patients were treatment-naive; the other 51 had been treated with interferon (but only 25 had persistent virological responses). Color Doppler sonography was used to measure the intima-media-thickness (IMT) of the common and internal carotid arteries. Endothelial function was assessed in the brachial artery with the flow-mediated-dilatation (FMD) test. The ANS was assessed with the tilt, laying to standing, Valsalva, hand grip, deep breath, and stroop tests. Results: The case group (mean age 52 + 13 years) had a significantly higher internal carotid IMT (0.86 + 0.3 vs 0.67 + 0.1 mmfor controls; p = 0.002). Chronic hepatitis C was also associated with an odds ratio for carotid plaque formation (reflected by an IMT > 1.3 mm) of 2.15. Cases also had significantly reduced FMD in the brachial artery (0.46 + 0.9 vs 0.76 + 0.7 for controls; p = 0.005) and significantly altered sympathetic and parasympathetic function (p = 0.001 vs controls in the Valsalva, hand grip, deep breath, and stroop tests). Within the case group, all alterations were more severe in patients with significant viremia. Discussion: Our findings suggest that chronic hepatitis C may be a nonclassic cardiovascular risk factor since it seems to influence the onset of pre-atherosclerotic lesions and to promote atherosclerotic plaque formation in patients with pre-existing increases in carotid IMT. It also seems to cause dysfunctions of the vascular endothelium and ANS. Conclusions: Chronic hepatitis C may increase cardiovascular risk and promote ANS dysfunctions, particularly when patients have experienced treatment failure and have persistent viremia. These patients may require cardiovascular and neurologic follow-up.

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Background and purpose Polymorphic paraoxonase ( PON1) variants can variably prevent low- and high-density lipoprotein oxidation, but their role in provoking atherosclerosis remained unclear. We addressed this issue by profiling PON1 polymorphisms and enzymatic activities, and assessing atherosclerosis and cerebral arteriosclerosis severity in post-stroke patients. Methods Carotid artery intima-media-thickness ( IMT), cerebral white matter lesions ( WML), serum PON1 -108 C/ T, Q192 R and L55 M polymorphisms, and PON and acetylcholinesterase (AChE) enzyme activities were determined in 237 patients. Results Genetic variation at the PON1 locus showed a strong influence on PON1 activity in ischaemic stroke patients, but lacked direct influence on IMT. Stroke patients with PON1 QQ192 or MM55 genotypes demonstrated lower PON and arylesterase activities at both Day 1 and 12 months post-stroke than patients with either RQ/ RR192 or LM/ LL55 genotypes ( P < 0.001). Furthermore, patients with carotid atherosclerosis and/or cerebral arteriosclerosis expressed as IMT, carotid plaques and WML had lower 12 months PON1 activity than patients without ( P = 0.02, P = 0.027 and P = 0.001, respectively), and PON and AChE hydrolysis rates were more tightly correlated in patients carrying the PON1 192 R compared with the 192 QQ allele, in a gene dose-dependent manner ( P < 0.001). Conclusion Our findings show inverse PON1 activity-carotid atherosclerosis and -cerebral arteriosclerosis association in stroke patients: the lower the PON1 activity the more progressed is the atherosclerotic process and the weaker is the association with AChE activity. Extending previous PON1 genetic studies in stroke populations, our study emphasizes the PON1 activity as a potential anti-atherogenic element and proposes involvement of cholinesterase activities in its effects. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Chronic low-grade inflammation is associated with atherosclerosis. Ultrasound imaging allows measurement of intima-media thickness (IMT) and plaque. We investigated the association between inflammatory markers and carotid and femoral atherosclerosis. Methods: We studied 554 subjects with primary dyslipidemia (57% men, median age 49 years) and 246 age- and sex-matched normolipidemic subjects. Carotid and femoral arteries were imaged bilaterally with a standardized protocol. Mean and maximum common carotid IMT (CC-IMT and MaxCC-IMT) and common femoral IMT (F-IMT and MaxF-IMT), and carotid and femoral plaque were assessed. Carotid atherosclerosis was defined by CC-IMT and/or plaque height >75th percentile of a reference population. White blood cell count (WBCC) was measured in all subjects. High-sensitivity C-reactive protein (CRP) was measured in 330 dyslipidemic subjects. Results: The age- and sex-adjusted probability of carotid atherosclerosis and femoral plaque increased by 20% (odds ratio [OR] 1.20; 95% CI, 1.10–1.31) and 25% (1.25; 1.13–1.38), respectively, for each 1000/mm3 WBCC increment. WBCC was associated with age- and sex-adjusted CC-IMT and MaxCC-IMT (p <0.05, both), and F-IMT and MaxF-IMT (p <0.001, both). Adjustment for cardiovascular risk factors did not influence these associations. CRP was associated with CC-IMT and MaxCC-IMT (p <0.05, both), but the associations disappeared after adjustment for body mass index. CRP was unrelated to carotid plaque or measures of femoral atherosclerosis. Conclusions: WBCC, but not CRP, related to early and advanced measures of atherosclerosis independently of risk factors. Our findings support using the heretofore undervalued WBCC as an easy-to-measure, low-cost diagnostic marker of atherosclerosis. [Copyright &y& Elsevier]

Summary: Introduction: Hepatitis C is a major health problem: approximately 170 million people are infected with the hepatitis C virus worldwide. It is unclear whether chronic hepatitis C affects atherosclerosis and whether it can cause endothelial and/or autonomic nervous system (ANS) dysfunction. Materials and methods: From April 2008 through April 2009, we studied 76 patients with biopsy-confirmed chronic hepatitis C and no evidence of cirrhosis, ascites, portal hypertension, encephalopathy, or hepatocellular carcinoma. The age-, sex-, BMI- and cardiovascular risk factor-matched control group comprised 76 healthy, HCV-negative individuals with no evidence of liver, autoimmune, or immunoproliferative diseases and no history of cardiovascular events. Twenty five of the hepatitis C patients were treatment-naive; the other 51 had been treated with interferon (but only 25 had persistent virological responses). Color Doppler sonography was used to measure the intima-media-thickness (IMT) of the common and internal carotid arteries. Endothelial function was assessed in the brachial artery with the flow-mediated-dilatation (FMD) test. The ANS was assessed with the tilt, laying to standing, Valsalva, hand grip, deep breath, and stroop tests. Results: The case group (mean age 52±13 years) had a significantly higher internal carotid IMT (0.86±0.3 vs 0.67±0.1mm for controls; p=0.002). Chronic hepatitis C was also associated with an odds ratio for carotid plaque formation (reflected by an IMT ≥ 1.3mm) of 2.15. Cases also had significantly reduced FMD in the brachial artery (0.46±0.9 vs 0.76±0.7 for controls; p=0.005) and significantly altered sympathetic and parasympathetic function (p=0.001 vs controls in the Valsalva, hand grip, deep breath, and stroop tests). Within the case group, all alterations were more severe in patients with significant viremia. Discussion: Our findings suggest that chronic hepatitis C may be a nonclassic cardiovascular risk factor since it seems to influence the onset of pre-atherosclerotic lesions and to promote atherosclerotic plaque formation in patients with pre-existing increases in carotid IMT. It also seems to cause dysfunctions of the vascular endothelium and ANS. Conclusions: Chronic hepatitis C may increase cardiovascular risk and promote ANS dysfunctions, particularly when patients have experienced treatment failure and have persistent viremia. These patients may require cardiovascular and neurologic follow-up. [Copyright &y& Elsevier]

Children after heart transplantation are considered as at-risk patients for extracardiac atherosclerotic complications. Noninvasive ultrasound measurement of the common carotid artery (IMT) provides valid information about the endothelial structure of the vascular system. Twenty-two patients (17 male, mean age 12.4 ± 4.5 yr) after heart and (5.7 ± 4.5 yr) heart–lung transplantation were enrolled. The mean IMT was measured and compared with a control group (18 children, 10 male, mean age 11.8 ± 1.8 yr) and to normative data. Transplanted children had a higher IMT than controls (0.453 ± 0.003 vs. 0.424 ± 0.002 mm, p < 0.001). IMT-SDS was increased as well (1.6 ± 0.1 vs. 0.8 ± 0, p < 0.001). Transplanted children had a higher LDL/HDL-ratio (2.2 ± 0.2 vs. 1.2 ± 0.1, p < 0.001). Time after transplantation, age at the time of transplantation, or medical therapy did not influence the findings. We found evidence for subclinical atherosclerosis in children after heart and heart–lung transplantation. Even if single atherosclerotic risk factors could not be identified, transplanted children seem to be at risk for atherosclerosis. Our findings support the recently published statement of the AHA-Expert panel: after heart transplantation atherosclerotic complications may occur with increased incidence. We propose the IMT-measurement in these patients as an easy method to assess the vascular status and to guide preventive measures. [ABSTRACT FROM AUTHOR]

Background First-degree offspring (OFF) of type 2 diabetic (T2DM) patients bear a ~40% lifetime risk of developing T2DM. They are insulin resistant and carry a risk of premature atherosclerosis, the extent of which can be estimated by intima media thickness (IMT) of the carotid artery (CA). Thus, this study examines parameters of glucose and lipid metabolism, insulin sensitivity, beta cell function (BCF) and IMT with their interrelationships in middle-aged OFF. Materials and methods T2DM-OFF ( n = 18, 14f/4m, 45·6 ± 2·1 years, BMI: 26 ± 1 kg m−2) were compared with 18 matching humans without a family history of diabetes (CON; 14f/4m, 44·5 ± 2·1 years, BMI: 24 ± 1 kg m−2; each P > 0·30), all with normal glucose tolerance as tested by three-hour (75 g) oral glucose tolerance tests (OGTT). Two-hour hyperinsulinaemic (40 mU min−1·m−2)isoglycaemic clamp tests were performed with simultaneous measurement of endogenous glucose (D-[6,6-2H2]glucose) production (EGP). IMT [internal (ICA), common CA, and bulb] were measured sonographically. BCF was assessed by Adaptation Index (AI). Results Before and during OGTT, both groups were similar in plasma glucose, insulin, C-peptide and free fatty acids (FFA), whereas OFF showed ~30% lower ( P < 0·03) fasting plasma triglycerides before OGTT. During hyperinsulinaemic clamps, insulin sensitivity was ~38% lower ( P < 0·03) in OFF who showed higher plasma FFA (44 ± 9 µmol L−1) than CON (26 ± 3 µmol L−1, P < 0·05) after 90 min. EGP was similar in both groups. OFF had 38% ( P < 0·007) reduced AI. ICA-IMT was ~18% higher in OFF ( P < 0·002), but did not correlate with insulin sensitivity. Conclusion The data obtained show middle-aged T2DM-OFF with normal glucose tolerance displaying reduced total insulin sensitivity and impaired beta cell function, which relates to impaired insulin-dependent suppression of plasma FFA and increased ICA-IMT. [ABSTRACT FROM AUTHOR]

Background In contrast to the well-accepted benefits of moderate exercise, recent research has suggested potential deleterious effects of repeated marathon running on the cardiovascular system. We thus performed a comprehensive analysis of markers of subclinical vascular damage in a cohort of runners having finished multiple marathon races successfully. Design This was a prospective, observational study. Methods A total of 97 healthy male Munich marathon participants (mean age 44 ± 10 years) underwent detailed training history, cardiopulmonary exercise testing for assessment of peak oxygen uptake, ultrasound for assessment of intima-media-thickness as well as non-invasive assessments of ankle-brachial index, augmentation index, pulse wave velocity and reactive hyperaemia index. Results Runners had previously completed a median of eight (range 1-500) half marathons, six (1-100) full marathons and three (1-40) ultramarathons; mean weekly and annual training volumes were 59 ± 23 and 1639 ± 979 km. Mean peak oxygen uptake was 50 ± 8 ml/min/kg, and the Munich marathon was finished in 3:45 ± 0:32 h. Runners showed normal mean values for intima-media-thickness (0.60 ± 0.14 mm), ankle-brachial index (1.2 ± 0.1), augmentation index (17 ± 13%), pulse wave velocity (8.7 ± 1.4 cm/s) and reactive hyperaemia index (1.96 ± 0.50). Age was significantly and independently associated with intima-media-thickness ( r = 0.531; p < 0.001), augmentation index ( r = 0.593; p < 0.001) and pulse wave velocity ( r = 0.357; p < 0.001). However, no independent associations of peak oxygen uptake, marathon finishing time, number of completed races or weekly and annual training km with any of the vascular parameters were observed. Conclusions In this cohort of healthy male runners, running multiple marathon races did not pose an additional risk factor for premature subclinical vascular impairment beyond age.