Symptom burden, psychosocial distress and palliative care needs in heart failure - A cross-sectional explorative pilot study.

BACKGROUND: Beyond guideline-directed treatments aimed at improving cardiac function and prognosis in heart failure (HF), patient-reported outcomes have gained attention. PURPOSE: Using a cross-sectional approach, we assessed symptom burden, psychosocial distress, and potential palliative care (PC) needs in patients with advanced stages of HF. METHODS: At a large tertiary care center, we enrolled HF patients in an exploratory pilot study. Symptom burden and psychosocial distress were assessed using the MIDOS (Minimal Documentation System for Patients in PC) questionnaire and the Distress Thermometer (DT), respectively. The 4-item Patient Health Questionnaire (PHQ-4) was used to screen for anxiety and depression. To assess PC needs, physicians used the "Palliative Care Screening Tool for HF Patients". RESULTS: We included 259 patients, of whom 137 (53%) were enrolled at the Heart Failure Unit (HFU), and 122 (47%) at the outpatient clinic (OC). Mean age was 63 years, 72% were male. New York Heart Association class III or IV symptoms were present in 56%. With a mean 5-year survival 64% (HFU) vs. 69% (OC) calculated by the Seattle Heart Failure Model, estimated prognosis was comparatively good. Symptom burden (MIDOS score 8.0 vs. 5.4, max. 30 points, p < 0.001) and level of distress (DT score 6.0 vs. 4.8, max. 10 points, p < 0.001) were higher in hospitalised patients. Clinically relevant distress was detected in the majority of patients (HFU 76% vs. OC 57%, p = 0.001), and more than one third exhibited at least mild symptoms of depression or anxiety. Screening for PC needs revealed 82% of in- and 52% of outpatients fulfil criteria for specialized palliative support. CONCLUSION: Despite a good prognosis, we found multiple undetected and unaddressed needs in an advanced HF cohort. This study's tools and screening results may help to early explore these needs, to further improve integrated HF care.

Feature tracking cardiovascular magnetic resonance reveals recovery of atrial function after acute myocarditis.

Follow-up after acute myocarditis is important to detect persisting myocardial dysfunction. However, recovery of atrial function has not been evaluated after acute myocarditis so far. Thirty-five patients with strictly defined acute myocarditis underwent cardiovascular magnetic resonance (CMR, 1.5 T) in the acute stage at baseline (BL) and at 3 months follow-up (FU). The study population included 13 patients with biopsy-proven "cardiomyopathy-like" myocarditis (CLM) and 22 patients with "infarct-like" (ILM) clinical presentation. CMR feature tracking (FT) was performed on conventional cine SSFP sequences. Median LA-GLS increased from 33.2 (14.5; 39.2) at BL to 37.0% (25.2; 44.1, P = 0.0018) at FU in the entire study population. Median LA-GLS also increased from 36.7 (26.5; 42.3) at BL to 41.3% (34.5; 44.8, P = 0.0262) at FU in the ILM subgroup and from 11.3 (6.4; 21.1) at BL to 21.4% (14.2; 30.7, P = 0.0186) at FU in the CLM subgroup. Median RA-GLS significantly increased from BL with 30.8 (22.5; 37.0) to FU with 33.7% (26.8; 45.4, P = 0.0027) in the entire study population. Median RA-GLS also significantly increased from 32.7 (25.8; 41.0) at BL to 35.8% (27.7; 48.0, P = 0.0495) at FU in the ILM subgroup and from 22.8 (13.1; 33.9) at BL to 31.0% (26.0; 40.8, P = 0.0266) at FU in the CLM subgroup. Our findings demonstrate recovery of LA and RA function by CMR-FT strain analyses in patients after acute myocarditis independent from clinical presentation. Monitoring of atrial strain could be an important tool for an individual assessment of healing after acute myocarditis.

Early results of a real-world series with two transapical transcatheter mitral valve replacement devices.

AIMS: Transcatheter mitral valve replacement (TMVR) with dedicated devices promises to fill the treatment gap between open-heart surgery and edge-to-edge repair for patients with severe mitral regurgitation (MR). We herein present a single-centre experience of a TMVR series with two transapical devices. METHODS AND RESULTS: A total of 11 patients were treated with the Tendyne™ (N = 7) or the Tiara™ TMVR systems (N = 4) from 2016 to 2020 either as compassionate-use procedures or as commercial implants. Clinical and echocardiographic data were collected at baseline, discharge and follow-up and are presented in accordance with the Mitral Valve Academic Research Consortium (MVARC) definitions. The study cohort [age 77 years (73, 84); 27.3% male] presented with primary (N = 4), secondary (N = 5) or mixed (N = 2) MR etiology. Patients were symptomatic (all NYHA III/IV) and at high surgical risk [logEuroSCORE II 8.1% (4.0, 17.4)]. Rates of impaired RV function (72.7%), severe pulmonary hypertension (27.3%), moderate or severe tricuspid regurgitation (63.6%) and prior aortic valve replacement (63.6%) were high. Severe mitral annulus calcification was present in two patients. Technical success was achieved in all patients. In 90.9% (N = 10) MR was completely eliminated (i.e. no or trace MR). Procedural and 30-day mortality were 0.0%. At follow-up NYHA class was I/II in the majority of patients. Overall mortality after 3 and 6 months was 10.0% and 22.2%. CONCLUSIONS: TMVR was performed successfully in these selected patients with complete elimination of MR in the majority of patients. Short-term mortality was low and most patients experienced persisting functional improvement.

Predictive value of low testosterone concentrations regarding coronary heart disease and mortality in men and women - evidence from the FINRISK97 study.

INTRODUCTION: The relevance of low testosterone concentrations for incident coronary heart disease (CHD) and mortality has been discussed in various studies. Here, we evaluate the predictive value of low baseline testosterone levels in a large population-based cohort. METHODS: We measured the serum levels of testosterone in 7671 subjects (3710 male, 3961 female) of the population-based FINRISK97 study. RESULTS: The median follow-up (FU) was 13.8 years. During the FU, a total of 779 deaths from any cause, and 395 incident CHD events were recorded. The age-adjusted baseline testosterone levels were similar in subjects suffering incident events during FU and those without incident events during FU (men: 15.80 vs. 17.01 nmol L-1 ; P = 0.69, women: 1.14 vs. 1.15 nmol L-1 ; P = 0.92). Weak correlations of testosterone levels were found with smoking (R = 0.09; P < 0.001), HDL cholesterol levels (R = 0.22, P < 0.001), systolic blood pressure (R = -0.05; P = 0.011), BMI (R = -0.23; P < 0.001) and waist-hip-ratio (R = -0.21; P < 0.001) in men, and with eGFR (R = -0.05; P = 0.009) in women. Kaplan-Meier analyses did not reveal a positive association of testosterone levels with incident CHD or mortality. Accordingly, also in Cox regression analyses, testosterone levels were not predictive for incident CHD or mortality - neither in men (HR 1.02 [95%CI: 0.70-1.51]; P = 0.79 for lowest versus highest quarter regarding CHD and HR 1.06 [95%CI: 0.80-1.39]; P = 0.67 regarding mortality), nor in women (HR 1.13 [95%CI: 0.69-1.85]; P = 0.56 for lowest versus highest quarter regarding CHD and HR 0.99 [95%CI: 0.71-1.39]; P = 0.80 regarding mortality). CONCLUSIONS: Low levels of testosterone are not predictive regarding future CHD or mortality - neither in men, nor in women.

Dilated cardiomyopathy: from epidemiologic to genetic phenotypes: A translational review of current literature.

Dilated cardiomyopathy (DCM) is characterized by left ventricular dilatation and, consecutively, contractile dysfunction. The causes of DCM are heterogeneous. DCM often results from myocarditis, exposure to alcohol, drugs or other toxins and metabolic or endocrine disturbances. In about 35% of patients, genetic mutations can be identified that usually involve genes responsible for cytoskeletal, sarcomere and nuclear envelope proteins. Due to its heterogeneity, a detailed diagnostic work-up is necessary to identify the specific underlying cause and exclude other conditions with phenotype overlap. Patients with DCM show typical systolic heart failure symptoms, but, with progress of the disease, diastolic dysfunction is present as well. Depending on the underlying pathology, DCM patients also become apparent through arrhythmias, thromboembolic events or cardiogenic shock. Disease progression and prognosis are mostly driven by disease severity and reverse remodelling within the heart. The worst prognosis is seen in patients with lowest ejection fractions or severe diastolic dysfunction, leading to terminal heart failure with subsequent need for left ventricular assist device implantation or heart transplantation. Guideline-based heart failure medication and device therapy reduces the frequency of heart failure hospitalizations and improves survival.

[Troponins as biomarkers for myocardial injury and myocardial infarction]. / Troponine als Biomarker bei Myokardschaden und Myokardinfarkt.

Elevation of cardiac troponins above the 99th percentile of a healthy reference population is established as a marker for myocardial cell damage and is crucial for the diagnosis of myocardial infarction. In addition, corresponding clinical evidence of acute myocardial ischemia i.e. symptoms, changes in the electrocardiogram (ECG), wall motion abnormalities or suggestive angiographic findings are required for the diagnosis of myocardial infarction. Using modern highly sensitive assays myocardial infarction can be detected more frequently and earlier. On the other hand myocardial infarction can be ruled out with a higher diagnostic accuracy. Cardiac troponins are specific for myocardial cell damage but not for myocardial infarction and can be elevated in numerous other disease states. In these cases myocardial injury can be diagnosed independently of myocardial ischemia. Typical dynamics with rise and fall of troponin levels can distinguish acute myocardial injury (e. g. pericarditis/myocarditis and pulmonary embolism) from chronic myocardial injury (e. g. cardiomyopathy). Clinically, highly sensitive troponin assays are currently recommended in addition to the 0/3 h and 0/1 h algorithms for rapid inclusion or exclusion of myocardial infarction.

Analysis of Minimally Invasive Left Thoracotomy HVAD Implantation - A Single-Center Experience.

BACKGROUND: Minimally invasive left ventricular assist device (LVAD) implantation may reduce peri-/postoperative complications and risks associated with resternotomies. In this study, we describe our first results using a minimally invasive LVAD implantation technique (lateral thoracotomy [LT] group). These results were compared with LVAD implantations done via full median sternotomy (STX group). METHODS: HVAD (HeartWare, Framingham, Massachusetts, United States) implantations in 70 patients (LT group n = 22, 52 ± 15 years old; STX group n = 48, 59 ± 11 years old) were retrospectively analyzed. Minimally invasive access via left thoracotomy was feasible in 22 patients. Peri- and postoperative analyses of survival and adverse events were performed. RESULTS: No survival differences were observed between the LT and STX group (p = 0.43). LT patients without temporary right ventricular assist device (tRVAD) showed a significantly better survival rate compared to LT patients with concomitant tRVAD implantation (p = 0.02), which could not be demonstrated in the STX group (p = 0.11). Two LT and four STX patients were successfully bridged to heart transplantation and three STX patients were successfully weaned with subsequent LVAD explantations. LVAD-related infections (n = 4 LT group vs n = 20 STX group, p = 0.04) were less likely in the LT group. No wound dehiscence occurred in the LT group, whereas five were observed in the STX group (p = 0.17). The amount of perioperative blood transfusions (within the first 7 postoperative days) did not differ in both study groups (p = 0.48). CONCLUSION: The minimally invasive approach is a viable alternative with the possibility to reduce complications and should be particularly considered for bridge-to-transplant patients.

Acute and Long-Term Hemodynamic Effects of MitraClip Implantation on a Preexisting Secondary Right Heart Failure.

Positive results of MitraClip in terms of improvement in clinical and left ventricular parameters have been described in detail. However, long-term effects on secondary pulmonary hypertension were not investigated in a larger patient cohort to date. 70 patients with severe mitral regurgitation, additional pulmonary hypertension, and right heart failure as a result of left heart disease were treated in the heart centers Hamburg and Göttingen. Immediately after successful MitraClip implantation, a reduction of the RVOT diameter from 3.52 cm to 3.44 cm was observed reaching a statistically significant value of 3.39 cm after 12 months. In contrast, there was a significant reduction in the velocity of the tricuspid regurgitation (TR) from 4.17 m/s to 3.11 m/s, the gradient of the TR from 48.5 mmHg to 39.3 mmHg, and the systolic pulmonary artery pressure (PAPsyst) from 58.6 mmHg to 50.0 mmHg. This decline continued in the following months (Vmax TR 3.09 m/s, peak TR 38.6 mmHg, and PAPsyst 47.4 mmHg). The tricuspid annular plane systolic excursion (TAPSE) increased from 16.5 mm to 18.9 mm after 12 months. MitraClip implantation improves pulmonary artery pressure, tricuspid regurgitation, and TAPSE after 12 months. At the same time, there is a decrease in the RVOT diameter without significant changes in other right ventricular and right atrial dimensions.

Biomarkers for heart failure: small molecules with high clinical relevance.

Heart failure (HF) is a rising epidemic due to the ageing population and progress in all areas of medicine. Thus, research efforts are made to ensure a timely diagnosis, to improve prognosis and treatment of the disease and to facilitate risk prediction at the population level. Because of their noninvasive determination with mostly high sensitivity and accuracy, circulating blood biomarkers are becoming increasingly important for daily clinical practice. Natriuretic peptides, especially B-type natriuretic peptide (BNP), N-terminal pro-B-type natriuretic peptide (Nt-proBNP) and midregional pro-atrial natriuretic peptide (MR-proANP) and cardiac troponins are established blood biomarkers in HF diagnosis and prognosis of HF-related outcomes. Inflammatory molecules as C-reactive protein (CRP) may have added value in anti-inflammatory therapy guidance. Next-generation biomarkers including soluble source of tumorigenicity 2 (sST2), growth differentiation factor-15 (GDF-15), galectin-3 (Gal-3) and diverse microribonucleic acids (miRNAs) may have additional benefit in assessment of cardiac remodeling or differentiation of HF subtypes. Multimarker approaches containing different combinations of established and novel biomarkers might improve HF risk prediction at the population level once they are used on top of clinical variables.

Anticoagulation strategies in patients with atrial fibrillation after PCI or with ACS : The end of triple therapy?

Clinicians struggle daily with the optimal regimen for patients with an indication for antiplatelet therapy after stenting and in patients needing oral anticoagulation treatment for atrial fibrillation (AF). This is not only difficult in patients with acute coronary syndrome (ACS) but also in the large number of patients with AF undergoing elective percutaneous coronary intervention (PCI). The challenge is to strike a balance between the increasing risk of bleeding events and ischemic or thrombotic events. Until recently, guidelines were based on expert consensus and a few small, many of them retrospective, trials. A so-called triple therapy with a vitamin K antagonist (VKA) and dual antiplatelet therapy (DAPT) with aspirin and clopidogrel was recommended for patients with AF undergoing PCI in stable coronary artery disease or for those with ACS. However, severe bleeding complications remain a major issue during triple therapy, particularly in the growing aging population. In the past year, randomized controlled trials (RCT) with direct-acting oral anticoagulants (DOACs) have modified the standard use of care, now favoring dual therapy with DOACs. This review elucidates the current influential RCTs on the new antiplatelet and anticoagulation strategies for patients with AF undergoing PCI or with ACS, and discusses whether triple therapy is still required.

Plasma levels of hepatocyte growth factor and placental growth factor predict mortality in a general population: a prospective cohort study.

BACKGROUND: Circulating levels of growth factors involved in leucocyte production and angiogenesis could be indicative of underlying aberrations of tissue homeostasis and therefore be utilized as predictors of risk for all-cause cardiovascular disease (CVD) or cancer mortality. METHODS: Baseline plasma levels of a range of growth factors were measured in two cohorts of the population-based FINRISK study (1997 Discovery cohort, N = 8444, aged 25-74; 2002 Replication cohort, N = 2951, aged 51-74 years) using a multiplexed bead array methodology and ELISA. Participants were followed up by linking them to registry data. RESULTS: In the Discovery cohort (653 deaths; 216 CVD-related, 231 cancer-related), fully adjusted Cox proportional hazard regression models showed that increased plasma hepatocyte growth factor (HGF) and placental growth factor (PlGF) were associated with higher risk of 10-year mortality (HR, 1.29 [95% confidence interval (CI), 1.18-1.41] and HR, 1.23 [95% CI, 1.14-1.32], respectively). In the Replication cohort (259 deaths; 83 CVD-related, 90 cancer-related), baseline HGF levels also predicted all-cause mortality (HR, 1.2 [95% CI, 1.08-1.32]; PlGF data not available). By including HGF levels in a CVD mortality model, 9% of all CVD deaths were correctly reclassified in the Discovery cohort (categorical net reclassification improvement [NRI] for events, P = 4.0 × 10-4 ). Moreover, adding HGF to all-cause and CVD mortality models resulted in an overall clinical NRI of 0.10-0.18 in the Discovery cohort and meta-analyses (P < 0.05 for all tests). CONCLUSION: Blood levels of HGF and PlGF may serve as new biomarkers for predicting increased risk of death in the general population.

Tissue characterization by T1 and T2 mapping cardiovascular magnetic resonance imaging to monitor myocardial inflammation in healing myocarditis.

AIMS: Monitoring disease activity in myocarditis is important for tailored therapeutic strategies. This study evaluated the ability of T1 and T2 mapping cardiovascular magnetic resonance (CMR) to monitor the course of myocardial inflammation in healing myocarditis. METHODS AND RESULTS: Forty-eight patients with strictly defined acute myocarditis underwent CMR at 1.5 T in the acute stage, at 3-months (n = 39), and at 12-months follow-up (FU) (n = 21). Normal values were obtained in a control group of 27 healthy subjects. The CMR protocol included standard ('Lake-Louise') sequences as well as T1 (modified Look-Locker inversion recovery sequence, MOLLI) and T2 (gradient- and spin-echo sequence, GraSE) mapping. T1, T2, and extracellular volume (ECV) maps were generated using an OsiriX plug-in. Native myocardial T1, T2, and ECV values were increased in the acute stage, but declined with healing of myocarditis. The performances of global native T1 and T2 to differentiate acute from healed myocarditis stages were significantly better compared with all other global CMR parameters with AUCs of 0.85 (95% CI, 0.76-0.94) and 0.83 (95% CI, 0.73-0.93). Furthermore, regional native T1 and T2 in myocarditis lesions provided AUCs of 0.97 (95% CI, 0.93-1.02) and 0.93 (95% CI, 0.85-1.01), which were significantly superior to any other global or regional CMR parameter. CONCLUSION: Healing of myocarditis can be monitored by native myocardial T1 and T2 measurements without the need for contrast media. Both native myocardial T1 and T2 provide an excellent performance for assessing the stage of myocarditis by CMR.

Safety and efficacy of the percutaneous transaxillary access for transcatheter aortic valve implantation using various transcatheter heart valves in 100 consecutive patients.

OBJECTIVES: Transcatheter Aortic Valve Implantation (TAVI) can be performed via the transaxillary approach, but data about complications and procedural outcome is limited. INTRODUCTION: TAVI is an established treatment option for patients at high risk for conventional aortic valve replacement. Nowadays, the transfemoral approach is the most commonly used access for TAVI. Nevertheless, the transfemoral access is not suitable in many patients necessitating alternative approaches. METHODS: We analyzed the outcome of 100 consecutive cases receiving percutaneous transaxillary TAVI at two different hospitals. Data were retrospectively analyzed by means of procedural, hemodynamic and clinical outcome. In addition, 1st versus 2nd generation devices were analyzed. RESULTS: Mean age was 78.2±2.1years and the logEuroSCORE I was 24.6±13.9%. Transaxillary TAVI was performed in 85% via the left and in 15% via the right axillary artery. Device success was achieved in 95%. In general, there was a clear learning curve with this approach. No patient experienced a major and 11% a minor access site complication. There was one procedural death (annular rupture) and one peri-procedural TIA. 23% of the patients received a new pacemaker. At discharge, effective orifice area was 1.94±0.16cm2 and the mean aortic gradient was 6.8±2.1mmHg. Moderate aortic regurgitation/paravalvular leakage was documented in two patients. Mortality rates at 30days and one year were 6% and 14.8%. Last but not least, 2nd generation devices showed improved procedural outcomes. CONCLUSIONS: The percutaneous transaxillary access for TAVI is technically feasible and safe thereby yielding excellent clinical results. CONDENSED ABSTRACT: We investigated In 100 consecutive patients undergoing percutaneous transaxillary transcatheter aortic valve implantation thereby demonstrating that this approach is technically feasible and safe with acceptable numbers of minor vascular complications.

Homocysteine concentration in coronary artery disease: Influence of three common single nucleotide polymorphisms.

BACKGROUND AND AIMS: Whether single nucleotide polymorphisms (SNPs) of homocysteine metabolism enzymes influence the rate of cardiovascular (CV) events in coronary artery disease (CAD) patients remains controversial. METHODS AND RESULTS: In this analysis, 1126 subjects from the AtheroGene study with CAD and 332 control subjects without known CAD were included. The following SNPs were investigated: methylentetrahydrofolate reductase (MTHFR-C667T), methionin synthetase (MS-D919G), and cystathionin beta synthetase (CBS-I278T). The endpoint was the combination of cardiovascular death, stroke, and non-fatal myocardial infarction (N = 286). The median follow-up time was 6.4 years. Kaplan-Meier curve analysis showed an increasing event rate with rising homocysteine levels (p < 0.001) in CAD patients. Further, in Cox-Regression analysis homocysteine was a predictor of the endpoint with a hazard ratio (HR) of 6.5 (95% CI: 2.9-14.6, p < 0.001) in the adjusted model including cardiovascular risk factors. Of the three SNPs, homozygous MTHFR SNP increased homocysteine levels significantly in patients with CAD and individuals without CAD (both p < 0.001). The SNPs in MS and CBS were not related to relevant changes in homocysteine levels in CAD patients or controls. The different SNPs of MTHFR, MS, and CBS were not related to an increased event rate. CONCLUSION: Homocysteine level is a strong predictor of CV events. Subjects with and without CAD and SNPs in the enzyme MTHFR had increased homocysteine levels. This was not observed for MS and CBS SNPs. Although MTHFR SNPs alter homocysteine levels in patients and controls, these polymorphisms had no impact on prognosis in CAD patients.

Single nucleotide polymorphisms in an intergenic chromosome 2q region associated with tissue factor pathway inhibitor plasma levels and venous thromboembolism.

Essentials Tissue factor pathway inhibitor (TFPI) regulates the blood coagulation cascade. We replicated previously reported linkage of TFPI plasma levels to the chromosome 2q region. The putative causal locus, rs62187992, was associated with TFPI plasma levels and thrombosis. rs62187992 was marginally associated with TFPI expression in human aortic endothelial cells. Click to hear Ann Gil's presentation on new insights into thrombin activatable fibrinolysis inhibitor SUMMARY: Background Tissue factor pathway inhibitor (TFPI) regulates fibrin clot formation, and low TFPI plasma levels increase the risk of arterial thromboembolism and venous thromboembolism (VTE). TFPI plasma levels are also heritable, and a previous linkage scan implicated the chromosome 2q region, but no specific genes. Objectives To replicate the finding of the linkage region in an independent sample, and to identify the causal locus. Methods We first performed a linkage analysis of microsatellite markers and TFPI plasma levels in 251 individuals from the F5L Family Study, and replicated the finding of the linkage peak on chromosome 2q (LOD = 3.06). We next defined a follow-up region that included 112 603 single nucleotide polymorphisms (SNPs) under the linkage peak, and meta-analyzed associations between these SNPs and TFPI plasma levels across the F5L Family Study and the Marseille Thrombosis Association (MARTHA) Study, a study of 1033 unrelated VTE patients. SNPs with false discovery rate q-values of < 0.10 were tested for association with TFPI plasma levels in 892 patients with coronary artery disease in the AtheroGene Study. Results and Conclusions One SNP, rs62187992, was associated with TFPI plasma levels in all three samples (ß = + 0.14 and P = 4.23 × 10-6 combined; ß = + 0.16 and P = 0.02 in the F5L Family Study; ß = + 0.13 and P = 6.3 × 10-4 in the MARTHA Study; ß = + 0.17 and P = 0.03 in the AtheroGene Study), and contributed to the linkage peak in the F5L Family Study. rs62187992 was also associated with clinical VTE (odds ratio 0.90, P = 0.03) in the INVENT Consortium of > 7000 cases and their controls, and was marginally associated with TFPI expression (ß = + 0.19, P = 0.08) in human aortic endothelial cells, a primary site of TFPI synthesis. The biological mechanisms underlying these associations remain to be elucidated.

Current and cumulative night shift work and subclinical atherosclerosis: results of the Gutenberg Health Study.

PURPOSE: The study examines the association between exposure to current and cumulative night shift work and subclinical parameters of atherosclerosis. METHODS: Participants of a population-based cohort study (the Gutenberg Health Study, N = 15,010) aged 35-64 years were examined at baseline (2007-2012). Investigations included measurements of arterial stiffness, vascular function [reactive hyperaemia (RH) index], and intima media thickness (IMT). Also, a complete job history (including up to 15 periods), occupational exposures, a variety of lifestyle, and dispositional variables were enquired. RESULTS: Night shift work was performed by 1071 out of 8065 currently employed individuals. The strongest association after adjustment for age, sex, job complexity level, being a manager, overtime work, and noise appeared for more than 660 night shifts within the last 10 years and a significantly increased arterial stiffness of 0.33 m/s. This reflects a 4 % flow velocity increase for individuals with more than 660 night shifts compared to non-night workers. Regarding the entire professional life, night shift workers showed a significantly decreased vascular function by -0.054 RH index points by using the same adjustment. IMT values did not differ statistically from non-night workers. Lifestyle and dispositional factors showed an influence on all used subclinical atherosclerosis parameters. CONCLUSIONS: The cross-sectional results demonstrate an association between night work and detrimental changes in the atherosclerotic process. The association is more pronounced with more years in night shift and is partly explained by lifestyle and dispositional factors. Longitudinal analyses are necessary to confirm the results.

The predictive value of different equations for estimation of glomerular filtration rate in patients with coronary artery disease - Results from the AtheroGene study.

BACKGROUND: Impaired renal function leads to dramatically increased risk for the development and progression of coronary artery disease (CAD). Therefore we aimed to assess the predictive value of different equations for estimated glomerular filtration rate (eGFR) in CAD-patients. METHODS: From the AtheroGene study 2135 patients were included. eGFR was calculated using the 4-variable Modification of Diet in Renal Disease (4MDRD) equation for serum creatinine (sCr), the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation for sCr and cystatin C (CysC) each alone, and in combination (CysC/sCr). eGFR was assessed regarding the combined outcome of cardiovascular death and non-fatal myocardial infarction and regarding complex CAD represented by a SYNTAX score ≥23. Median follow-up was 4.3years. RESULTS: Only the CKD-EPI equation using CysC could differentiate between eGFR >90ml/min/1.73m(2) vs. eGFR 60-90ml/min/1.73m(2) according to the occurrence of an endpoint event (log-rank test p=0.009). In the Cox regression analysis only eGFR calculated by CKD-EPI equation for CysC (Hazard ratio per 1 standard deviation (HR) 1.27 (95% CI 1.07-1.50); p=0.007) and for CysC/sCr (HR 1.22 (95% CI 1.02-1.46); p=0.026) were predictive regarding the outcome after adjustment for cardiovascular risk factors and Nt-proBNP. Furthermore, only eGFR calculated by CKD-EPI equation for CysC (odds ratio (OR) 1.57 (95% CI 1.36-1.78); p<0.001) and for CysC/sCr (OR 1.32 (95% CI 1.13-1.53); p<0.001) were significantly associated with a SYNTAX score ≥23. CONCLUSION: In patients with CAD the CKD-EPI equation for CysC and for CysC/sCr provided the best predictive value regarding the prognosis and the severity of CAD.

PO-58 - Cardiovascular risk profile in survivors of adult cancer - results from the general population study.

INTRODUCTION: The advancements in cancer treatment and detection of early cancer have resulted in steady increase of adult cancer survivors over the years. However, due to the long term toxic effects of chemotherapy and radiotherapy, the incidence of cardiovascular diseases (CVD) is increasing in survivors. Identifying risk factors and interventions to reduce the excess burden of CVD in this vulnerable population is urgently needed. AIM: To investigate the cardiovascular risk factors (CVRFs), inflammation and coagulation profile in cancer survivors from a large population-based study. MATERIALS AND METHODS: Presence of CVRFs and laboratory markers have been compared in individuals with (n=1,359) and without (n=13,626) history of cancer. Standard laboratory profile, including blood glucose and lipid profile, has been evaluated in 15,010 individuals from the Gutenberg Health Study (GHS). Coagulation factors, D-dimer and von Willebrand factor (vWF) activity were available in N=4,993. RESULTS: The individuals with history of cancer were older compared to no history of cancer with mean age of 61,5years and 54.4years, respectively (p<0.001). Traditional CVRFs as diabetes (14% vs 8.8%), dyslipidemia (49.6% vs 43.7%) and hypertension (60.3 vs 48.7%) were more frequent whereas smoking was less frequent (14.5% vs 19.9%) in cancer survivors (p<0.001). The standard laboratory profile showed cancer survivors with lower erythrocyte, platelet and white blood cell counts and higher C-reactive protein (CRP), glucose, HbA1c and triglycerides levels (p<0.001). Multivariable logistic regression analysis adjusted for age, sex and CVRFs demonstrated an independent association with diabetes (odds ratio, OR: 1.24, 1.02-1.50; p=0.027) and higher CRP (OR: 1.01, 1.01-1.02; p=0.00071). Fibrinogen, FV, FVII, FVIII and FXI, D-dimer and vWF activity were higher in cancer survivors (p<0.001). Multivariable logistic regression confirmed an independent association with higher fibrinogen (OR: 1.002, 1.000-1.003) and vWF activity (OR: 1.005, 1.001-1.008). CONCLUSIONS: This is the first study investigating CVRFs, inflammation and coagulation profile in individuals with history of cancer from a well characterized population-representative adult sample. It gives evidence for higher prevalence of CVRFs, particularly diabetes in this vulnerable population. Markers of inflammation as CRP and fibrinogen and vWF activity were higher in cancer survivors independent of the cardiovascular risk profile. These results underline the increased risk of CVD and need for development of cardio-oncology programs offering cardiovascular prevention.

Association of Type D personality with cognitive functioning in individuals with and without cardiovascular disease - The Gutenberg Health Study.

OBJECTIVE: Distressed ('Type D') personality is associated with adverse health outcomes in patients with cardiovascular disease (CVD). While personality traits from the Five-Factor Model are related to cognitive functioning, neither Type D personality nor its underlying traits negative affectivity (NA) and social inhibition (SI) have been investigated regarding cognition. We therefore compared the predictive value of Type D classification and its subcomponents NA and SI on planning performance in individuals with and without CVD. METHODS: Type D personality traits (DS14) were determined in a population-based sample of 4026 participants (including 549 with CVD) aged 40-80years from the Gutenberg Health Study (GHS) and related to planning performance as assessed with the Tower of London task. Current depression and anxiety were controlled as state variables. RESULTS: Type D personality status was negatively associated with planning performance in the CVD patient group only (p<0.001) but had no impact in the non-CVD group (p=0.40). In the overall sample, NA was negatively and SI positively associated with planning performance. No differential effect on planning between groups was found for depression and anxiety. CONCLUSION: While the subcomponents NA and SI in the population-based sample confirm and extend previous research on personality traits and cognition, Type D personality classification in combination with CVD emerged as a risk factor for decreased cognitive functioning, independent of depression and anxiety. These findings implicate the need to early focus on individual differences in cognitive functioning in patients with CVD.