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Biomedical subjects

Werner G Daniel

Publications and source records attributed to Werner G Daniel.

At least 37 records · Page 2Linked to original sources
PubMed2005

Analysis of coronary calcifications versus Framingham and PROCAM risk assessment in patients with a first myocardial infarction.

UNLABELLED: We compared the extent of coronary calcifications as quantified by electron beam tomography (EBT) to the predicted 10-year cardiovascular event risk based on Framingham and PROCAM algorithms in patients with a first myocardial infarction (MI). METHODS: In 156 patients (56.7 +/- 22 years), EBT was performed <4 weeks after MI. Coronary calcifications were quantified using the "Agatston Score" and age-related calcium percentiles were determined. The predicted 10-year event risk was determined using Framingham and PROCAM algorithms. RESULTS: Coronary calcifications were present in 148 patients with a mean "Agatston Score" of 589.2 +/- 976. The "Agatston Score" was >400 in 44% and >90th percentile in 42% of the patients. Framingham risk was >20% in 32% and PROCAM risk was >20% in 28%. CONCLUSION: Coronary calcifications were detected in the vast majority of patients with a first MI, independent from the patient's age. The determination of age-related percentiles was superior to the Framingham or PROCAM algorithm.

Adult↗
PubMed2005

Visualization of coronary artery anomalies by contrast-enhanced multi-detector row spiral computed tomography.

BACKGROUND: We investigated the potential of 16-slice multi-detector row spiral CT (MDCT) with retrospective ECG-gating for evaluation of coronary artery anomalies. METHODS: A total of 35 patients (23 men, 12 women, 19-81 years) in whom anomalous coronary arteries had been detected by invasive coronary angiography underwent MDCT (Sensation 16, Siemens, Germany). During one breathhold, a contrast-enhanced (90 ml, 5 ml/s) volume data set of the heart was acquired (16x0.75mm collimation, gantry rotation 375 ms). Images were reconstructed with a slice thickness of 1.0 mm in 0.5-mm intervals using retrospective ECG-gated reconstruction. The 35 data sets and 80 data sets of patients with angiographically normal coronary anatomy were analysed in random order concerning the origin and course of the coronary arteries. The results were compared to invasive coronary angiography. RESULTS: All patients with coronary artery anomalies and all controls with normal coronary anatomy were identified by MDCT. In addition, the origins and course concerning their anatomical relationship to adjacent cardiac structures were visualized in all patients, including right-sided origin of the left main (n=10), left anterior descending coronary artery (n=4) or left circumflex coronary artery (n=10); left-sided origin of the right coronary artery (n=6); four coronary fistula to the pulmonary artery (two from the left anterior descending, one from the right coronary artery, one from the left main), and one fistula from the circumflex coronary artery to the left atrium CONCLUSIONS: The study demonstrates that MDCT is a reliable noninvasive technique to identify and define anomalous coronary arteries and their course.

Adult↗
PubMed2005

ACE inhibition lowers angiotensin-II-induced monocyte adhesion to HUVEC by reduction of p65 translocation and AT 1 expression.

Angiotensin-converting enzyme (ACE) inhibitors interfere with several key events of vascular inflammation resulting in impressive reductions in coronary vascular events. However, in human arteries ACE inhibitors block the production of angiotensin II (AngII) incompletely because of the involvement of alternative pathways in local AngII formation. Therefore, our study concentrated on the presumed modulation by ACE inhibition of local AngII-mediated inflammatory actions by a mechanism independent of blockage of AngII formation. We analyzed the effect of the ACE inhibitor ramiprilat on AngII-dependent cell adhesion molecule (CAM) expression and adhesion of monocytic THP-1 cells to endothelial cells. AngII induced upregulation of P-selectin, VCAM-1 and ICAM-1 on endothelial cells via activation of AT 1, which was correlated with enhanced THP-1 adhesion in flow chamber assays. Both enhanced adhesion and adhesion molecule expression were significantly reduced by pretreatment with ramiprilat. Ramiprilat reduced AT 1 expression on endothelial cells and decreased the AngII-induced p65 translocation into the nucleus. Diminished AT 1 expression and adhesion molecule expression in response to ramiprilat treatment were partially reversed after incubation with a bradykinin 2 receptor antagonist, suggesting that elevated bradykinin levels under ACE inhibition may be involved in the beneficial effect of ACE inhibitors. Thus, modulation of the local AngII system by ramiprilat may at least in part contribute to the benefits of ACE inhibition in the treatment of atherosclerotic diseases.

Adrenergic beta-Antagonists↗
PubMed2005

Detection of coronary artery stenoses using multi-detector CT with 16 x 0.75 collimation and 375 ms rotation.

AIMS: Insufficient spatial and temporal resolutions have limited image quality and accuracy of multi-detector CT (MDCT) for coronary artery visualization and detection of stenoses. We assessed the accuracy of a new 16-slice scanner with 370 ms rotation and 0.75 mm collimation for detection of coronary stenoses using an analysis approach based on coronary artery segments. METHODS AND RESULTS: Fifty consecutive patients scheduled for diagnostic coronary angiography in stable clinical condition and sinus rhythm were enrolled. All patients with a heart rate > 60 b.p.m. received 100 mg atenolol p.o. and up to four doses of 5 mg metoprolol i.v. before the scan. MDCT was performed using 16 x 0.75 mm collimation, 120 kV, and ECG-gated tube current modulation. Ninety millilitres of contrast agent was injected intravenously. MDCT images were visually analysed using the 16-segment coronary artery model of the American Heart Association and compared with invasive, quantitative coronary angiography in a blinded fashion. A significant stenosis was assumed if the diameter reduction was > or = 50%. Mean heart rate was 58 b.p.m. during MDCT. After exclusion of two patients with not fully evaluable data sets, MDCT correctly identified at least one coronary stenosis in all 25 patients with significant coronary lesions in angiography and correctly demonstrated the absence of stenoses in 19/23 patients (sensitivity 100%, specificity 83%). Sensitivity and specificity for all 50 patients were 93 and 83%, respectively. On a per-segment basis, nine coronary segments distal of total occlusions and 128 coronary segments with a reference diameter < 1.5 mm were excluded from the analysis. Twenty-eight of the included 663 segments (4%) were unevaluable due to calcification or motion artefact. In the remaining 635 segments, 50/53 stenoses were detected by MDCT (sensitivity 94%, specificity 96%, negative predictive value 99%, positive predictive value 69%). CONCLUSION: Increasing temporal and spatial resolutions of MDCT lead to improved evaluation and diagnostic accuracy for detection of coronary stenoses.

Adult↗
PubMed2005

Enhanced external counterpulsation: a new technique to augment renal function in liver cirrhosis.

BACKGROUND: Advanced liver cirrhosis is characterized by cardiovascular changes, such as low arterial blood pressure, peripheral vasodilation and renal vasoconstriction. As a consequence, renal hypoperfusion, impaired diuresis and natriuresis and eventual hepatorenal syndrome may ensue. Previous studies using head-out water immersion to increase central blood volume have demonstrated the functional nature of the renal abnormalities. Enhanced external counterpulsation (EECP) is a new non-invasive cardiac assist device to augment diastolic blood pressure by electrocardiogram-triggered diastolic inflation and deflation of cuffs wrapped around the lower extremities. We investigated whether EECP would improve renal dysfunction of liver cirrhosis. METHODS: Twelve healthy controls and 19 patients with liver cirrhosis were observed during 2 h of baseline followed by 2 h of EECP. The following parameters of renal and cardiovascular function were measured: renal plasma flow by para-aminohippurate clearance, glomerular filtration rate (GFR) by inulin clearance, urine flow rate, urinary excretion rates of sodium and chloride, mean arterial blood pressure (MAP), renal vascular resistance (RVR) and plasma concentrations of renin, atrial natriuretic peptide (ANP), endothelin-1, antidiuretic hormone, epinephrine and N-epinephrine. RESULTS: EECP was well tolerated by healthy controls and cirrhotic patients alike. EECP increased MAP (cirrhotic patients: from 74+/-18 to 88+/-20 mmHg, P<0.01; controls: from 89+/-8 to 94+/-5 mmHg, P = NS) and ANP (cirrhotic patients: from 23+/-18 to 30+/-20 ng/l, P<0.05; controls: from 11+/-4 to 16+/-5 ng/l, P<0.01). The plasma renin concentration decreased (cirrhotic patients: from 98+/-98 to 58+/-57 ng/l, P<0.01; controls: from 4.6+/-1.6 to 3.4+/-1.1 ng/l, P<0.01). This was associated with improvement of the urinary flow rate (cirrhotic patients: from 3.6+/-1.8 to 4.6+/-0.7 ml/min, P<0.05; controls: from 1.8+/-1.5 to 2.8+/-1.9 ml/min, P<0.05), as well as of the sodium and chloride excretion rates in both groups. However, in contrast to healthy controls, GFR and renal plasma flow in cirrhotic patients failed to rise significantly. Renal vascular resistance fell numerically in healthy controls (68+/-5 vs 55+/-4 mmHg . min/l; P = NS). In contrast, RVR showed a significant increase by approximately 20% in cirrhosis (67+/-4 vs 80+/-8 mmHg . min/l; P<0.05). Endothelin-1 levels fell in controls (0.38+/-0.42 vs 0.31+/-0.35; P<0.05), whereas they remained statistically unchanged in cirrhotic patients. Epinephrine, N-epinephrine and vasopressin were not altered by EECP in either group. CONCLUSIONS: EECP is an effective procedure to augment renal excretory function in healthy volunteers as well as in patients with cirrhosis. In healthy volunteers, GFR and renal plasma flow increased during EECP. In contrast, these parameters remained unchanged in the patients and their renal vascular resistance increased during EECP. Therefore, EECP improves diuresis, but does not influence the vasoconstrictive dysregulation of the kidneys in liver cirrhosis.

Adult↗
PubMed2005

Connective tissue growth factor is overexpressed in complicated atherosclerotic plaques and induces mononuclear cell chemotaxis in vitro.

OBJECTIVE: Atherosclerotic blood vessels overexpress connective tissue growth factor (CTGF) mRNA, but the role of CTGF in atherosclerosis remains controversial. To assess the hypothesis that CTGF is involved in atherosclerotic plaque progression, we investigated CTGF protein expression and distribution in the different types of plaque morphology. METHODS AND RESULTS: Serial cross-sections of 45 human carotid plaques were immunohistochemically analyzed for the presence of CTGF protein, neovascularization (von Willebrand factor), macrophages (CD68), and T cells (CD3). The lesions were categorized according to American Heart Association (AHA) classification as fibrous (type IV and V) or complicated plaques (type VI). The levels of CTGF were significantly higher in complicated compared with fibrous plaques (P=0.002). CTGF accumulated particularly in the rupture-prone plaque shoulder and in the areas of neovascularization or infiltration with inflammatory cells. Macrophage-like cells stained positive for CTGF protein in plaques. Subsequent in vitro studies showed that although monocyte-derived macrophages do not produce CTGF on stimulation with transforming growth factor-beta, lipopolysaccharide, or thrombin, they take it up from culture medium. Furthermore, CTGF induces mononuclear cell chemotaxis in a dose-dependent manner. CONCLUSIONS: CTGF protein is significantly increased in complicated compared with fibrous plaques and may enhance monocyte migration into atherosclerotic lesions, thus contributing to atherogenesis.

Aged↗
PubMed2005

Transradial stenting of the iliac artery: a case report.

In this case report, stenting of the common iliac artery via the radial access route with 6 Fr equipment, including an extra long multipurpose catheter, is presented. Radial access avoids bleeding and ischemia that may complicate retrograde or crossover access to the iliac artery.

Angioplasty, Balloon↗
PubMed2005

The expression of macrophage migration inhibitory factor 1alpha (MIF 1alpha) in human atherosclerotic plaques is induced by different proatherogenic stimuli and associated with plaque instability.

OBJECTIVES: Macrophage migration inhibitory factor 1alpha (MIF), a cytokine with immunoregulatory functions has been suggested to be involved in atherosclerotic plaque development. However, little is known about MIF-inducing conditions in the atherosclerotic process and the association of MIF with plaque instability. METHODS AND RESULTS: Forty-two carotid endatherectomy samples from 36 patients and 4 aortic samples from young accident victims (as healthy controls) were analyzed for MIF staining. MIF expressing tissues in the atherosclerotic plaques are mainly mononuclear cells (MNCs), but also endothelial cells of intimal microvessels (MVECs). The magnitude and the intensity of their MIF expression was associated with the progression of plaques from early lesions (Stary I-III) to complicated plaque stages (Stary IV-VIII). In highly inflammatory and neovascularized regions of the plaques the colocalization of MIF expressing MNCs with CD40-L+ and angiotensin II (Ang II)-producing MNCs could be established. This finding supports the notion that CD40-L fusion protein and Ang II are able to induce MIF production in the monocytic cell line THP-1. Furthermore hypoxia (< or =1% O2) as a further proinflammatory and especially proangiogenetic factor was able to stimulate MIF secretion by THP-1, human monocytes and HUVECs. Hyperglycemia and insulin remained without effect. CONCLUSION: MIF is expressed in advanced atherosclerotic lesions in close correlation with signs of instability, such as mononuclear cell inflammation and neointimal microvessel formation. Furthermore, the colocalization of MIF with Ang II-producing MNCs and CD40-L+ cells in these plaques and the finding that proathero- and -angiogenic mediators such as CD40-L, Ang II and hypoxia are able to stimulate MIF expression in vitro suggest an important role of MIF in the modulation of atherosclerotic plaque stability.

Aged↗
PubMed2005

Influence of ultrasound operating parameters on ultrasound-induced thrombolysis in vitro.

The effect of operating parameters on the thrombolytic potency of ultrasound (US) is important for potential therapeutic applications, but is not fully understood. Fresh human whole-blood thrombi were exposed in vitro to focused US from a diagnostic transducer driven by an impulse generator via an amplifier to vary duration (10 to 60 min), intensity (7 to 90 W/cm(2)), frequency (2 to 4.5 MHz), pulsed wave duty cycle (1:5 to 1:100 and continuous wave mode) and pulse length (100 to 400 micros). Segments of thrombi (498 +/- 73 mg) were submersed and insonated in saline solution. Thrombolytic efficiency was expressed as percentage loss of mass compared with controls (noninsonified thrombi). Ultrasound exposure achieved a significantly higher thrombolysis than no US, 56 +/- 16 % vs. 29 +/- 11 % (n = 232, p < 10(-6)). There was an exponential saturation-type correlation with duration of insonation (r(2) = 0.64) and intensity (r(2) = 0.97), an inverse correlation with US frequency at matched intensities (r(2) = 0.76, p < 10(-5)), a logarithmic relationship with duty cycle in pulsed mode (r(2) = 0.86) and a modest direct effect of pulse length (r(2) = 0.57, p < 10(-5)). Thus, thrombolytic efficiency of US depends directly on duration, intensity, duty cycle and pulse length and inversely, on frequency.

Case-Control Studies↗
PubMed2005

Enhanced levels of platelet P-selectin and circulating cytokines in young patients with mild arterial hypertension.

BACKGROUND: Emerging evidence links inflammation to atherosclerosis (AS). Although some studies have addressed the role of inflammation in patients with arterial hypertension (AH), its overall contribution in AH is far from being understood. Therefore, the present pilot study was designed to examine the role of platelet P-selectin and various inflammatory mediators in young patients with moderate AH without signs of target organ damage. METHODS AND RESULTS: Fifteen patients with mild AH [33.8 +/- 7.3 years, mean arterial pressure (MAP) 106.6 +/- 10.4 mmHg] and 15 healthy normotensive controls (31.7 +/- 10.6 years) were examined. Platelet P-selectin was analysed by flow cytometry. Plasma levels of monocyte-chemoattractant-protein-1 (MCP-1), high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-6, tumour necrosis factor alpha (TNFalpha), and IL-10 levels were measured by enzyme immunoassay (EIA). Patients with mild AH showed significantly enhanced expression of platelet P-selectin [17.2 +/- 5.4 versus 10.6 +/- 4.2 mean fluorescence intensity (MFI), P < 0.001]. P-selectin expression positively correlated with MAP (r = 0.43, P < 0.05). Furthermore, patients with mild AH had significantly enhanced plasma levels of hsCRP (2.7 +/- 3.8 versus 0.6 +/- 0.9 mg/l, P < 0.01), IL-6 (1.4 +/- 0.7 versus 0.6 +/- 0.3 pg/ml, P < 0.001), TNFalpha (2.8 +/- 0.7 versus 2.4 +/- 0.4 pg/ml, P < 0.05), and MCP-1 (291.3 +/- 100.7 versus 214.3 +/- 8.3 pg/ml, P < 0.05). IL-6 levels positively correlated with hsCRP levels (r = 0.47, P < 0.05) and mean arterial pressure (MAP) (r = 0.44, P < 0.05). CONCLUSIONS: This pilot study demonstrates that in an early stage of AH, inflammatory pathways are already activated. Besides pro-inflammatory cytokines, platelets seem to play a significant role in mediating inflammation in AH, which could lead to target organ injury. Further investigations have to clarify the role of early anti-inflammatory therapy, in patients with mild to moderate AH, in alleviating hypertensive target organ damage.

Adult↗
PubMed2004

ACE inhibition lowers angiotensin II-induced chemokine expression by reduction of NF-kappaB activity and AT1 receptor expression.

OBJECTIVE: Angiotensin converting enzyme (ACE) inhibitors significantly improve survival in patients with atherosclerosis. Although ACE inhibitors reduce local angiotensin II (AngII) formation, serine proteases form AngII to an enormous amount independently from ACE. Therefore, our study concentrates on the effect of the ACE-inhibitor ramiprilat on chemokine release, AngII receptor (ATR) expression, and NF-kappaB activity in monocytes stimulated with AngII. METHODS AND RESULTS: AngII-induced upregulation of IL-8 and MCP-1 protein and RNA in monocytes was inhibited by the AT1R-blocker losartan, but not by the AT2R-blocker PD 123.319. Ramiprilat dose-dependently suppressed AngII-induced upregulation of IL-8 and MCP-1. The suppressive effect of ramiprilat on AngII-induced chemokine production and release was in part caused by downregulation of NF-kappaB, but more by a selective and highly significant reduced expression of AT1 receptors as shown in monocytes and endothelial cells. CONCLUSION: In our study we demonstrated for the first time that ramiprilat reduced expression of AT1R in monocytes and endothelial cells. In addition, ramiprilat downregulated NF-kappaB activity and thereby reduced the AngII-induced release of IL-8 and MCP-1 in monocytes. This antiinflammatory effect, at least in part, may contribute to the clinical benefit of the ACE inhibitor in the treatment of coronary artery disease.

Angiotensin II↗
PubMed2004

Comparison of measurement of cross-sectional coronary atherosclerotic plaque and vessel areas by 16-slice multidetector computed tomography versus intravascular ultrasound.

In 26 patients, 16-slice multidetector computed tomography (MDCT) with 0.75-mm collimation and intravascular ultrasound (IVUS) of 1 coronary artery were performed. At 100 sites within the coronary arteries, the measurement of cross-sectional luminal area and, if detectable, the cross-sectional area of atherosclerotic plaque was performed independently with IVUS and MDCT. The mean luminal area (r = 0.92), measured at 100 sites, and plaque area (r = 0.55), measured at 65 sites, were significantly correlated (p <0.001) between MDCT and IVUS. The mean luminal area and mean plaque area were slightly but significantly overestimated with MDCT. MDCT permits the noninvasive measurement of coronary cross-sectional luminal and plaque areas with moderate accuracy.

Coronary Angiography↗
PubMed2004

Atorvastatin induces tissue transglutaminase in human endothelial cells.

Tissue transglutaminase (tTgase) contributes to the organisation of the basement membrane and is therefore thought to be important for the integrity and stability of the vessel wall. In the present study, we hypothesised that the HMG-CoA reductase inhibitor atorvastatin may up-regulate the tTgase expression in endothelial cells and thereby exert beneficial effects on endothelial function. Treatment of human umbilical vein endothelial cells (HUVEC) with atorvastatin (1-10 microM) caused a clear increased expression of tTgase in both permeabilised and non-permeabilised HUVEC. In contrast, stimulation of HUVEC with TNFalpha had no substantial effect on tTgase expression or localisation but inhibited the atorvastatin-induced up-regulation and externalisation of tTgase. Propidium iodide staining revealed that statin-induced apoptosis is not responsible for the enhanced expression. By inducing the expression of tTgase, statins may promote tTgase-mediated stabilisation of the basement membrane. This effect of atorvastatin may contribute to the beneficial role of statins on endothelial function.

Apoptosis↗