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Biomedical subjects

Christiaan J Vrints

Publications and source records attributed to Christiaan J Vrints.

At least 19 recordsLinked to original sources

B-type natriuretic peptide and assessment of jeopardised myocardium in acute myocardial infarction.

BACKGROUND: B-type natriuretic peptide (BNP) is used as prognostic marker in acute coronary syndromes. It is unknown whether BNP reflects the amount of jeopardised myocardium in the initial phase of acute ST-elevation myocardial infarction (STEMI). METHODS: Patients admitted for percutaneous coronary intervention in the acute phase of STEMI were studied. Samples for BNP were taken at the time of coronary intervention and were correlated with the amount of jeopardised myocardium. This was defined on coronary angiography as the vascular region distal to the infarct-related lesion and was expressed by a vascular score. The extend of epicardial injury on ECG was evaluated by: summation of ST-segment elevation in the infarct-related leads, number of leads with > or = 1 mm ST-segment elevation and number of leads with > or = 1 mm ST-segment depression/elevation. RESULTS: A total of 113 patients (median age (25th, 75th percentile) 61 (54, 69)) were studied. Median BNP was 27 pg/ml (12, 62) and was assessed 225 min (150, 315) after onset of pain. There was no significant relation between BNP and vascular score (r=0.026, p=0.8). The only independent variable of BNP was time delay between onset of pain and sample collection. Stepwise regression identified the extent of ST-segment elevation as independent predictor of the vascular score. CONCLUSION: At initial presentation of STEMI, BNP measurement does not allow a correct prediction of jeopardised myocardium. In contrast, ST-segment analysis, in particularly the extent of ST-segment elevation, provides useful information about the extent of jeopardised myocardium.

Aged↗

Relation of B-type natriuretic peptide early after acute myocardial infarction to left ventricular diastolic function and extent of myocardial damage determined by magnetic resonance imaging.

Early after acute myocardial infarction, the relation between plasma B-type natriuretic peptide (BNP) and extent of myocardial scar formation and diastolic dysfunction remains unclear. In 32 consecutive patients early (5 +/- 3 days) after a first acute myocardial infarction, delayed contrast-enhanced magnetic resonance (MR) imaging was performed to define myocardial scar. Diastolic function was assessed using phase-contrast MR measurements of mitral flow and septal tissue velocities (tissue MR imaging) to estimate left ventricular (LV) filling pressures. MR study was immediately followed by BNP measurement. BNP related to LV ejection fraction (r = -0.52, p = 0.002), extent of myocardial scar (percent delayed hyperenhancement of LV mass, r = 0.49, p = 0.005; transmural index, r = 0.58, p <0.001), and estimated LV filling pressures (ratio of early diastolic mitral flow velocity to early diastolic mitral annular velocity, r = 0.51, p = 0.003). In multivariate analysis, transmural index and early diastolic mitral flow velocity/early diastolic mitral annular velocity were independent predictors of BNP levels (p <0.05, power of 0.99 at alpha = 0.05). In conclusion, among patients with recent myocardial infarction, high BNP levels are independently associated with extent of myocardial scar tissue and estimated LV filling pressures.

Blood Flow Velocity↗

Usefulness of type D personality in predicting five-year cardiac events above and beyond concurrent symptoms of stress in patients with coronary heart disease.

Psychological stress and type D personality have been associated with adverse cardiac prognosis, but little is known about their relative effect on the pathogenesis of coronary heart disease (CHD). "Type D" refers to the tendency to experience negative emotions and to inhibit the expression of these emotions in social interactions. We investigated the relative effect of stress and type D personality on prognosis at 5-year follow-up. At baseline, 337 patients with CHD who participated in cardiac rehabilitation filled in the General Health Questionnaire (psychological stress) and the Type D personality scale. Patients were followed for 5 years. The end point was major adverse cardiac events, which were defined as a composite of cardiac death, myocardial infarction, and cardiac revascularization (coronary artery bypass grafting/percutaneous coronary intervention). There were 46 major adverse cardiac events at follow-up, including 4 deaths and 8 myocardial infarctions. Type D patients had an increased risk of death/infarction (odds ratio 4.84, 95% confidence interval 1.42 to 16.52, p = 0.01) compared with non-type D patients, independent of disease severity. Stress (p = 0.011) and type D (p = 0.001) were related to an increased risk of developing a major adverse cardiac event after adjusting for gender, age, and biomedical risk factors. Multivariate analysis yielded left ventricular ejection fraction < or =40%, no treatment with coronary artery bypass grafting, and type D personality (odds ratio 2.90, 95% confidence interval 1.42 to 5.92, p = 0.003) as independent predictors of major adverse cardiac events, whereas psychological stress was marginally significant (odds ratio 2.01, 95% confidence interval 0.99 to 4.11, p = 0.054). In conclusion, type D personality is a psychological factor that may optimize risk stratification in patients with CHD. Type D reflects more than temporary changes in general stress level because it predicted cardiac events after controlling for concurrent symptoms of stress.

Adult↗

Decreased number of circulating plasmacytoid dendritic cells in patients with atherosclerotic coronary artery disease.

BACKGROUND: Dendritic cells are potent antigen-presenting and immune modulating cells that have been implicated in the development of atherosclerosis. In human blood, two distinct lineages are distinguished: plasmacytoid dendritic cells and myeloid dendritic cells. Although dendritic cells have been described in atherosclerotic plaques, no information exists concerning circulating blood dendritic cells in atherosclerosis. This study aims to evaluate the number of circulating dendritic cells in patients with coronary artery disease. The relation with the extent of coronary artery disease, the clinical syndrome and with a marker of inflammation will be documented. METHODS: Patients with angiographically proven coronary artery disease (n=18) and age and sex-matched controls (n=18) were included. Myeloid dendritic cells and plasmacytoid dendritic cells were detected with the specific blood dendritic cell antigens, blood dendritic cell antigen-1 and blood dendritic cell antigen-2, respectively. RESULTS: Absolute and relative numbers of circulating plasmacytoid dendritic cells were significantly lower in patients with coronary artery disease (5722+/-601/ml and 0.08+/-0.01%) than in controls (12,640+/-1289/ml and 0.21+/-0.02%). Plasmacytoid dendritic cells were more decreased in patients with troponin-positive unstable coronary syndromes than in patients with low troponin values, and tended to be lower in more extensive coronary artery disease. Absolute myeloid dendritic cells numbers tended to be reduced in patients, whereas relative numbers were significantly decreased: 11,857+/-1895/ml versus 15,226+/-928/ml and 0.17+/-0.03% versus 0.26+/-0.01% in controls. CONCLUSIONS: The present study shows a significant decrease of circulating blood dendritic cell antigen-2 positive plasmacytoid dendritic cells in patients with coronary artery disease. The decrease tended to be more pronounced in unstable coronary syndromes and extensive coronary artery disease, suggesting a possible role of dendritic cells in plaque progression and rupture.

Adult↗

Type D personality is associated with increased levels of tumour necrosis factor (TNF)-alpha and TNF-alpha receptors in chronic heart failure.

BACKGROUND: Pro-inflammatory cytokines and their circulating receptors are powerful predictors of poor outcome in patients with chronic heart failure (CHF). We hypothesized that Type D personality, known to independently predict long-term mortality in patients with coronary heart disease, would relate to immune activation in CHF. METHODS: 91 stable CHF patients (79% males, mean age 57+/-13 yrs, 58% ischemic heart disease) with left ventricular ejection fraction <or=35% completed a psychological questionnaire to assess Type D personality (i.e., the tendency to experience negative emotions and to inhibit their expression). Plasma levels of tumour necrosis factor (TNF)-alpha, soluble TNF-alpha receptor 1 and 2 (sTNFR1 and sTNFR2) and interleukin-6 (IL-6) were measured by ELISA. RESULTS: Type D patients (n=30) had higher levels of TNF-alpha (5.1+/-2.9 versus 3.9+/-2.6 pg/ml, p=0.066), sTNFR1 (1656+/-1057 versus 1098+/-424 pg/ml, p=0.009) and sTNFR2 (2869+/-1510 versus 2011+/-794 pg/ml, p=0.006) as compared to non-Type D patients (n=61), whereas IL-6 was not different. After controlling for sex, age, ischemic etiology and disease severity, multivariate analysis yielded Type D as the strongest predictor of increased TNF-alpha (OR=2.9, p=0.048) and sTNFR2 levels (OR=3.9, p=0.018). For sTNFR1, the effect of Type D was no longer significant in this analysis (OR=2.7, p=0.112). CONCLUSIONS: Type D personality was independently associated with increased circulating levels of TNF-alpha and sTNFR2 in patients with CHF. This study provides the strongest evidence to date that chronic emotional distress may be associated with immune activation in heart failure.

Aged↗

Feasibility of tissue magnetic resonance imaging: a pilot study in comparison with tissue Doppler imaging and invasive measurement.

OBJECTIVES: This research was intended to determine the feasibility of tissue magnetic resonance (MR) imaging in comparison with tissue Doppler imaging and its potential implications for the estimation of filling pressure, in comparison with invasive measurement. BACKGROUND: Evaluation of diastolic function using MR imaging is commonly confined to the study of transmitral flow. However, transmitral flow is unreliable for the estimation of left ventricular (LV) filling pressures in hypertrophy and normal systolic function. Normalizing early mitral velocity (E) for the influence of myocardial relaxation by combining E with early diastolic mitral septal tissue velocity (Ea) provides better Doppler estimates of filling pressures. METHODS: Eighteen patients with hypertensive heart disease (LV mass index: 114 +/- 21 g/m(2)), absence of valvular regurgitation, and with normal or mildly reduced systolic function (LV ejection fraction: 57.6 +/- 6.5%) referred for cardiac catheterization, underwent consecutive measurement of mitral flow and septal tissue velocities with phase-contrast MR and Doppler. These data were compared with mean pulmonary capillary wedge pressure (PCWP). RESULTS: There was a strong relation between MR (11.6 +/- 4.3) and Doppler-assessed (12.1 +/- 3.5) E/Ea (95% confidence interval of -1.5 to 0.5) (r = 0.89, p < 0.0001). In addition, E/Ea related strongly to invasively measured PCWP (MR: r = 0.80, p < 0.0001 and Doppler: r = 0.85, p < 0.0001). CONCLUSIONS: Tissue MR imaging is a feasible method to assess Ea. Combining E and Ea allowed similar estimation of filling pressure by MR and Doppler, in good agreement with invasive measurement. The potential confounding effect of valvular regurgitation needs further study.

Blood Flow Velocity↗

Intracellular monocyte cytokine production and CD 14 expression are up-regulated in severe vs mild chronic heart failure.

BACKGROUND: The role of circulating monocytes in the process of low-grade inflammation, characteristic of chronic heart failure (CHF), has recently been questioned. Lipopolysaccharide (LPS) desensitization has been proposed to mediate reduced monocyte cytokine elaboration in patients with severe CHF. METHODS: Intracellular monocyte production of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and tumor necrosis factor (TNF)-alpha, and monocyte CD 14 expression were measured flow-cytometrically without and after 8-hour LPS stimulation in 46 patients with CHF and in a healthy control group. RESULTS: Basal cytokine concentrations were similar for the control and the mild CHF groups (New York Heart Association [NYHA] Class I or II). After LPS stimulation, IL-6 (p=0.002) and TNF-alpha levels (p=0.001) were lower in the latter group, whereas IL-1 beta production was comparable. For the moderate-severe CHF patients, unstimulated IL-1 beta (p=0.04) was higher, whereas IL-6 (p=0.2) and TNF-alpha (p=0.1) levels were not different from the controls. Measurement of LPS-stimulated cytokine production showed no differences between the control group and patients with moderate-severe CHF (all p= 0.5). Upon comparing mild vs moderate-severe CHF patients, higher levels of unstimulated cytokine production (IL-1 beta, p=0.002; IL-6, p=0.01; TNF-alpha, p=0.003), stimulated IL-1 beta (p=0.002) and IL-6 (p=0.008) were found in the latter patients. CD 14 expression in the moderate-severe CHF group was higher than in the mild-CHF group (p = 0.03) and was strongly related to stimulated IL-1 beta (r=0.62, p<0.0001), IL-6 (r=0.56, p=0.0002) and TNF-alpha (r=0.41, p=0.006) production. CONCLUSIONS: CD 14 expression and monocyte cytokine production, both unstimulated and after LPS stimulation, are increased in moderate-severe CHF when compared with mild CHF. These data suggest that circulating monocytes, possibly via increased CD 14 expression, may play a significant role in the immunologic dysbalance observed in advanced CHF.

Cytokines↗

Effect of short-term treatment with pravastatin on cytokines and cytokine receptors in patients with chronic heart failure due to ischemic and nonischemic disease.

The antiinflammatory effect of lipoproteins through neutralization of circulating endotoxin has questioned the safety of lipid-lowering drugs in chronic heart failure (CHF). We measured serum levels of interleukin-6, tumor necrosis factor (TNF)-alpha, and soluble TNF-alpha receptors 1 and 2 before and after 1-month treatment with pravastatin 40 mg in 58 patients with CHF. Short-term treatment with pravastatin attenuated the immune response in patients with CHF due to ischemic or nonischemic etiology.

Aged↗

Flow-mediated vasodilation: a diagnostic instrument, or an experimental tool?

Brachial arterial flow-mediated dilation (FMD), assessed by high-resolution ultrasonography, reflects endothelium-dependent vasodilator function. FMD is diminished in patients with atherosclerosis and with coronary risk factors, and improves with risk-reduction therapy. Therefore, the measurement of FMD can be a good prognostic instrument in preventive cardiology, is useful to predict short-term postoperative cardiovascular events in a high-risk population and to assess long-term cardiovascular risk in a lower risk population, and is an excellent experimental tool to detect changes in endothelial function after new therapeutic interventions. In this review article, the pathophysiology of FMD, based on reactive hyperemia, is extensively discussed. Furthermore, an overview is given of the actual clinical indications of FMD measurement.

Arterial Occlusive Diseases↗

Quantitative coronary arteriography on digital flat-panel system.

On images acquired with a digital flat-panel (DFP) detector, known for its better image quality, the performance of a validated quantitative coronary arteriography (QCA) software, CAASII (Cardiovascular Angiography Analysis System or CAAS), and a DFP-dedicated QCA algorithm (flat-panel analysis software or FPAS) was compared in a phantom and a patient study. On phantom, FPAS performed with higher accuracy the quantification of the smallest tubes and the calibration of an empty catheter. The overall accuracy and precision for the quantification procedure was better for FPAS (0.07 +/- 0.04 mm) than for the CAAS (0.19 +/- 0.06 mm; P = 0.03 and P < 0.01, respectively). In the patient study, the main difference between the two algorithms was found in the small diameters: CAAS almost always gave higher values than FPAS for the minimal luminal diameter (P < 0.001) and could only give values up to 70% for diameter stenosis. In conclusion, the FPAS can be considered more appropriate for assessing severe stenoses on digital flat-panel images.

Algorithms↗

Influence of zero flow pressure on fractional flow reserve.

Fractional flow reserve (FFR) is a commonly used index to assess the functional severity of a coronary artery stenosis. It is conventionally calculated as the ratio of the pressure distal (Pd) and proximal (Pa) to the stenosis (FFR= Pd/Pa). We hypothesize that the presence of a zero flow pressure (Pzf), requires a modification of this equation. Using a dynamic hydraulic bench model of the coronary circulation, which allows one to incorporate an adjustable Pzf, we studied the relation between pressure-derived FFR = Pdo/Pa, flow-derived true FFRQ = Qs/QN (= ratio of flow through a stenosed vessel to flow through a normal vessel), and the corrected pressure-derived FFRc = (Pd-Pzf)/(Pa-Pzf) under physiological aortic pressures (70 mmHg, 90 mmHg, and 110 mmHg). Imposed Pzf values varied between 0 mmHg and 30 mmHg. FFRc was in good agreement with FFRQ, whereas FFR consistently overestimated FFRQ. This overestimation increased when Pzf increased, or when Pa decreased, and could be as high as 56% (Pzf=30 mmHg and Pa =70 mmHg). According to our experimental study, calculating the corrected FFRC instead of FFR, if Pzf is known, provides a physiologically more accurate evaluation of the functional severity of a coronary artery stenosis.

Blood Pressure↗

Combined endurance/resistance training reduces NT-proBNP levels in patients with chronic heart failure.

AIMS: This study was designed to evaluate the effects of combined endurance/resistance training on NT-proBNP levels in patients with chronic heart failure (CHF). The safety of resistive weight training for patients with CHF is questioned. Possible detrimental effects include an increase in ventricular diastolic pressure and secondary unfavourable remodelling. Circulating levels of the N-terminal fragment of brain natriuretic peptide (NT-proBNP) reflect left ventricular diastolic wall stress and are strongly related to mortality and treatment success in CHF. METHODS AND RESULTS: In this study, 27 consecutive patients with stable CHF and left ventricular ejection fraction (LVEF) <35% were enrolled in a 4 months non-randomized combined endurance/resistance training programme. Blood sampling for measurement of NT-proBNP, functional assessment, cardiopulmonary exercise testing, echocardiography and radionuclide angiography were performed at entry and after 4 months. After 4 months, exercise training caused a significant reduction in circulating concentrations of NT-proBNP (2124+/-397 pg/ml before, 1635+/-304 pg/ml after training, p=0.046, interaction), whereas no changes were observed in an untrained heart failure control group. NYHA functional class (p=0.02, interaction), maximal (peak VO2: p=0.035, interaction; maximal workload: p<0.00001, interaction) and submaximal (workload at anaerobic threshold: p=0.001, interaction; rate-pressure product at anaerobic threshold: p=0.001, interaction) exercise parameters as well as work efficiency (Wattmax/VO2peak: p=0.0001, interaction) were significantly improved. In addition, a decrease in left ventricular end-systolic diameter was observed in the trained heart failure group (p=0.016). CONCLUSION: Four months of combined endurance/resistance training significantly reduced circulating levels of NT-proBNP in patients with CHF, without evidence of adverse remodelling. Exercise training might offer additional non-pharmacological modulation of the activated neurohormonal pathways in the setting of CHF.

Bicycling↗

Selective intestinal decontamination in advanced chronic heart failure: a pilot trial.

BACKGROUND AND AIMS: Endotoxin, derived from intestinal aerobic Gram-negative bacilli (AGNB), could be an important monocyte activator in chronic heart failure (CHF). The effect of selective decontamination of the digestive tract (SDD) on intracellular monocyte cytokine production, monocyte CD14 expression, circulating endotoxin and cytokines, and flow-mediated dilation (FMD) was studied in patients with severe CHF. METHODS AND RESULTS: Ten patients with CHF (NYHA class III-IV) were enrolled in a non-placebo controlled pilot trial involving the administration of SDD (polymyxin B, tobramycin) for 8 weeks. One patient was later excluded due to cardiac transplantation. Before treatment, after 4 and 8 weeks therapy, and 6 weeks post-treatment, monocyte CD14 expression, intracellular monocyte production of interleukin-1beta [IL-1beta], interleukin-6 [IL-6], tumour necrosis factor (TNF)-alpha with and without lipopolysaccharide (LPS) stimulation were measured. Concentrations of endotoxin and cytokines (IL-1beta, IL-6, TNF-alpha) were also determined. AGNB in faeces, intestinal endotoxin and FMD were assessed at baseline, after 4 weeks of treatment and 6 weeks post-treatment. SDD eradicated intestinal AGNB (P<0.00001) and decreased faecal endotoxin concentrations (P<0.00001). There was a significant decline in monocyte CD14 expression (P=0.03) and in IL-1beta (P=0.0001), IL-6 (P=0.02) and TNF-alpha (P=0.0002) production after 4 and 8 weeks of treatment in the basal state and for IL-1beta (P=0.008) and IL-6 (P=0.005) after LPS stimulation. FMD significantly improved at 4 weeks and returned to baseline after treatment discontinuation (P=0.002). Circulating concentrations of endotoxin and cytokines remained unchanged. CONCLUSION: Reduction of the intestinal endotoxin pool led to a decrease in monocyte CD14 expression and intracellular cytokine production in patients with severe CHF. The improvement of peripheral endothelial function could be a marker of the anti-inflammatory effect of SDD.

Adult↗

Immunohistostaining assays for detection of Chlamydia pneumoniae in atherosclerotic arteries indicate cross-reactions with nonchlamydial plaque constituents.

Detection of Chlamydia pneumoniae antigens in PCR-negative atheromata by immunohistochemistry assays has given rise to controversies regarding a link between the bacterium and atherosclerosis. One hundred ninety-seven human arterial segments removed surgically were examined for C. pneumoniae DNA by conventional PCR with three different primer pairs and by real-time PCR in two different laboratories. No C. pneumoniae DNA was detected. Eighty atherosclerotic lesions were studied by immunohistochemistry assays. Immunoreactivity for C. pneumoniae was frequently present but was not related to the extent of atherosclerosis. Mammary arteries showed immunoreactivity. Serial sections of 17 atheromata were analyzed by Western blotting, histological staining, and UV fluorescence microscopy. Chlamydial proteins were not detected. The sites with positive results by C. pneumoniae immunohistostaining assays precisely matched the sites with autofluorescent ceroid deposits. Immunoblotting and antigenic staining for C. pneumoniae were negative in tests with fetal aortas. The absence of C. pneumoniae DNA in human atherosclerotic lesions, together with negative results for C. pneumoniae proteins by Western blotting analysis, and the perfect matching of C. pneumoniae immunoreactive sites with sites with autofluorescent ceroid deposits suggest a nonspecific reactivity of antichlamydial antibodies with plaque constituents. On the basis of the results of the present study, there are no arguments for an etiologic role of C. pneumoniae in atherosclerosis.

Antigens, Bacterial↗

Multivessel variant angina unresponsive to urapidil.

We present a case of variant angina complicated by recurrent sudden cardiac death. During coronary angiography a diffuse 3-vessel vasoconstriction was observed progressing to a more severe vasoconstriction in the mid LAD. Intracoronary administration of urapidil did not reverse the vasoconstriction of the LAD; instead an occlusive vasospasm occurred accompanied by marked ischaemia.

Aged↗

Association of lipoproteins with cytokines and cytokine receptors in heart failure patients. Differences between ischaemic versus idiopathic cardiomyopathy.

AIMS: The observation that low total cholesterol predicted poor survival in patients with chronic heart failure, has questioned the beneficial effect of lipid-lowering in this population. This study investigated the relation between lipoprotein concentrations and the levels of interleukin (IL)-6, tumour necrosis factor (TNF)-alpha and the soluble TNF-alpha receptors in patients with chronic heart failure due to coronary artery disease (CAD) or idiopathic dilated cardiomyopathy (IDCM). METHODS AND RESULTS: Seventy-one patients with chronic heart failure due to CAD (n=36) or IDCM (n=35) were enrolled. Plasma concentrations of lipoproteins, IL-6, TNF-alpha, soluble TNF-alpha receptor 1 (sTNFR1) and 2 (sTNFR2) were measured. Total cholesterol/HDL-cholesterol (CHOL/HDL) correlated with levels of TNF-alpha (r=0.24, P=0.035), sTNFR1 (r=0.32, P=0.008) and sTNFR2 (r=0.37, P=0.002). In the CAD group, CHOL/HDL and triglycerides (TG) correlated with sTNFR2 (r=0.48, P=0.005 for CHOL/HDL, r=0.40, P=0.015 for TG). No relation was found between lipoproteins and cytokines or sTNF-alpha receptors for IDCM patients (P>0.1). CONCLUSIONS: An atherogenic lipid profile favoured the inflammatory process in patients with heart failure due to CAD. No relation between lipoproteins and cytokines was detected in case of IDCM.

Adult↗

Cytokines and immune activation in systolic heart failure: the role of Type D personality.

The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and its soluble receptors 1 (sTNFR1) and 2 (sTNFR2) are predictors of mortality in chronic heart failure (CHF) but the determinants of these increased levels of disease-promoting cytokines are largely unknown. Type D personality refers to the combination of the tendency to experience negative emotions (negative affectivity) and the tendency to inhibit the expression of emotions in social interaction (social inhibition). Type D is an independent predictor of cardiac events in coronary patients who are at risk for CHF. The present study examined the effect of Type D personality on TNF-alpha, sTNFR1, and sTNFR2 in 42 men with CHF (meanage=57.9+/-10.5 years). There was a significant multivariate effect of Type D on TNF-alpha measures (p=.006); i.e., circulating levels of TNF-alpha (4.8+/-0.9 versus 2.5+/-0.2 pg/ml, p=.003), sTNFR1 (1814+/-314 versus 1134+/-78 pg/ml, p=.014), and sTNFR2 (2465+/-243 versus 1874+/-118 pg/ml, p=.019) were significantly higher in Type D patients as compared to non-Type D patients. The effect size (ES) of Type D personality ranged from rather large (sTNFR1, ES=0.77; sTNFR2, ES= 0.73) to large (TNF-alpha, ES=0.90). After controlling for ischemic etiology and severity of heart failure, Type D personality emerged as an independent predictor of increased circulating levels of both TNF-alpha (OR=9.5, 95% CI 2.1-43.8, p=.004) and TNF-alpha receptors (OR= 6.1, 95% CI 1.4-25.8, p=.014). These findings are consistent with the prognostic power of Type D personality regarding long-term morbidity and mortality in patients with established coronary heart disease. This study suggests that individual differences in personality contribute to the psychoneuroimmunological aspects of heart failure.

Affect↗

Regular use of margarine-containing stanol/sterol esters reduces total and low-density lipoprotein (LDL) cholesterol and allows reduction of statin therapy after cardiac transplantation: preliminary observations.

Seventeen stable cardiac transplant recipients, of whom 16 were on statin therapy, used margarine with stanol/sterol esters. Total cholesterol in the treatment group was lowered from 211 mg/dl (range 168 to 244) to 177 mg/dl (136 to 241) (17% reduction, p = 0.003) and low-density lipoprotein (LDL) cholesterol was reduced from 125 mg/dl (73 to 161) to 98 mg/dl (57 to 146) (22% reduction, p = 0.0006). LDL cholesterol reached the pre-defined cut-off level of 115 mg/dl in 12 of 17 patients and statin dosages were reduced. In 8 of 12 patients, LDL cholesterol remained at <115 mg/dl 6 weeks after statin reduction.

Adult↗