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Biomedical subjects

S Genth-Zotz

Publications and source records attributed to S Genth-Zotz.

12 recordsLinked to original sources
PubMed2004

[Acute coronary syndrome (without ST-elevation)].

Antithrombotic therapy in acute coronary syndrome without ST-segment elevation should be initiated with aspirin 100 mg/day (loading dose 250-500 mg) and Clopidogrel 75 mg/day (loading dose 300 mg). In addition, anticoagulation with unfractionated heparin or low molecular weight heparin should be started. A GP IIb/IIIa receptor blocker can be given either upfront (Eptifibatide/Tirofiban) or directly in the cathlab preceding PCI (Abciximab). Aspirin should be given in the chronic phase lifelong, Clopidogrel for at least nine months. An invasive strategy is recommended in high-risk patients within 48 hours.

Acute Disease↗
PubMed2004

[Genetic variation of the cholesterol ester transfer protein gene and the prevalence of coronary artery disease. The AtheroGene case control study].

BACKGROUND: Various functional polymorphisms of the cholesteryl ester transfer protein ( CETP) gene influence CETP activity and the concentration of high-density lipoprotein (HDL) cholesterol. Beside other functional variants mainly the promoter polymorphism CETP/C-629A is currently discussed as a risk factor of coronary artery disease (CAD). We evaluated in a large case-control study the impact of various CETP genotypes and haplotypes on HDL concentration and the prevalence of CAD. METHODS AND RESULTS: In 1214 patients with documented CAD as well as 754 population controls we determined the CETP/C-629A, TaqIB, I405V, R451Q, and A373P polymorphisms. All genotypes have an impact on the HDL concentration; univariate genotype and haplotype analyses demonstrate a significant effect of A-allel carriers on the elevation of HDL concentration. In addition, among all genotypes determined, the C-629A polymorphism is associated with the prevalence of CAD in a codominant fashion. Homozygous A-allel carriers reveal a relative risk of 0.6 (95% CI 0.44-0.82; P = 0.005) compared to the wild type. Adjustment for classical risk factors did not alter this association significantly, whereas after controlling for HDL concentration no independent significance between CETP/C-629A genotype and prevalence of CAD was observed anymore. CONCLUSION: CETP genotypes have an significant but moderate impact on systemic HDL-cholesterol concentration. The A-allel of the CETP/C-629A polymorphism is associated with a reduced CAD risk. This risk reduction is probably mediated by elevated HDL-concentration. Whether genotyping of the CETP/C-629A polymorphism provides information over and above that obtained by HDL-cholesterol measurement has to be further investigated in various prospective studies.

Carrier Proteins↗
PubMed2004

[Immunactivation in chronic heart failure. Inflammatory mediators].

Inflammatory cytokines are thought to contribute to the development and progression of chronic heart failure (CHF). It has been shown that especially tumor necrosis factor-alpha (TNF) is activated in patients with CHF and exerts detrimental effects on the myocardium. Recent studies have demonstrated that circulating levels of TNF, soluble TNF receptors 1 and 2 and interleukin-6 are strong prognostic markers. The results of two randomized studies directly antagonizing TNF in CHF patients were rather disappointing. Nevertheless, TNF antagonism remains a therapeutic option and should be focussed on patients with systemic immune activation, particularly at times of exacerbation.

Adjuvants, Immunologic↗
PubMed2002

Cachexia: a therapeutic approach beyond cytokine antagonism.

Cachexia is seen in a number of chronic diseases, and it is always associated with a poor prognosis. Irrespective of etiology, the development of cachexia appears to share a common pathophysiological pathway. This includes induction of proteasome-dependent myofibril-degradation, which is thought to be secondary to stimulation by enhanced levels of pro-inflammatory cytokines. Elevation of tumor necrosis factor-alpha (TNFalpha) and other plasma cytokines has been demonstrated in many conditions associated with cachexia. Despite improved pathophysiological understanding, a specific treatment for cachexia has not yet been established. Whilst direct TNFalpha antagonism has therapeutic appeal, this review will focus on manipulation of downstream pathways and the potential benefits. For example, nuclear factor-kappaB (NF-kappaB) is one of the most important signal transducers of TNFalpha, and drugs targeting this signalling cascade might be useful in the treatment of cachexia. Although the use of some of these substances, for example glucocorticoids, remains controversial, others may prove beneficial in the treatment of this syndrome. The role of other approaches such as proteasome-inhibitors remains to be elucidated. Alternatively, interleukin-10 and other immunosuppressive cytokines may also be able to counterbalance certain features of cachexia.

Cachexia↗
PubMed2001

[Tumor necrosis factor alpha in chronic heart failure. Clinical manifestation and therapeutic possibilities].

BACKGROUND: Chronic heart failure (CHF) may be seen as a multi-system disorder with its origin in the heart but including many extracardiac manifestations. Immunological abnormalities are recognized in this context, in particular, changes in the expression of mediators of the innate immune response. IMPORTANCE OF TNF: Higher levels of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF) are found in the circulation and in the myocardium of patients with chronic heart failure than in controls. TNF has been implicated in a number of pathophysiological processes that are thought to be important to the progression of chronic heart failure. Therapies directed against this cytokine might therefore represent a novel approach to heart failure management.

Animals↗
PubMed2001

Spontaneous echo contrast caused by platelet and leukocyte aggregates?

BACKGROUND AND PURPOSE: Spontaneous echocardiographic contrast (SEC) is correlated to clinical thromboembolic events. We sought to determine the origin of SEC by utilizing direct analysis of left atrial blood. METHODS: We examined the blood of 13 patients with and 19 without SEC. Blood samples were taken from the femoral vein and artery and from the right and left atria after transseptal puncture. Samples were incubated with fluorescence-labeled antibodies directed against the platelet (CD41a-PE, CD42b-PE, and CD62p-FITC) and leukocyte membrane epitopes (CD45-APC and CD14-FITC). The expressed epitopes were analyzed by dual laser flow cytometry immediately after blood withdrawal. RESULTS: In the peripheral blood of both groups, more activation and aggregation were found in the venous blood than in the arterial blood (CD41a, P=0.007; CD14neutro, P=0.017; and leukocyte-platelet aggregates [LTAg], P=0.002). In patients without SEC, the degree of activation and aggregation of the cardiac samples closely resembled the results of the peripheral samples. The degree of activation and aggregation was significantly higher in the right atrium than in the left atrium (LTAg, P<0.01; leukocyte activation, P<0.01; CD41a, P<0.01; CD62p, P<0.02). In contrast, in patients with SEC the parameters of platelet and leukocyte activation as well as LTAg was significantly higher in the left atrium than in the right atrium of the same patient (all P<0.01). A correlation between the amount of SEC and platelet-monocyte aggregates could be found (r=0.92, P<0.0001). CONCLUSIONS: The hypothesis that platelet aggregates are involved in the pathogenesis of SEC is supported by the fact that platelets in the left atrium of patients with SEC showed more activation.

Adult↗
PubMed2000

MIC trial: metoprolol in patients with mild to moderate heart failure: effects on ventricular function and cardiopulmonary exercise testing.

UNLABELLED: Beta-blocker therapy results in a functional benefit in patients with heart failure (CHF) due to idiopathic dilated cardiomyopathy (DCM). This study assessed if similar effects were observed in patients with ischemic heart disease (CAD), NYHA II-III after 6 months of therapy with metoprolol. METHODS AND RESULTS: Fifty-two patients with CHF secondary to DCM (26 patients) and CAD (26 patients) and a left ventricular ejection fraction (EF)<40% were enrolled in the placebo-controlled study. The study medication was titrated over 6 weeks, the mean final dosage was 135 mg/day. Three patients died due to cardiogenic shock, two received placebo and one metoprolol. Eight patients did not complete the study due to non-compliance. Metoprolol significantly reduced heart rate at rest and after submaximal and maximal exercise. Vo(2)-max and Vo(2)-AT as well as the 6-min walk test improved significantly after metoprolol treatment. There was a significant increase in EF at rest (27.3-35. 2%), submaximal (28.5-37.7%) and maximal exercise (28.7-40.9%) in the metoprolol-treated patients. No differences were found between patients with CAD and DCM. We also observed reduced left ventricular volumes. CONCLUSION: The additional therapy with metoprolol improved cardiac function and the cardiopulmonary exercise capacity in patients with CHF.

Adrenergic beta-Antagonists↗
PubMed1999

[Determination of left ventricular mass by transthoracic three-dimensional echocardiography in patients with dilated cardiomyopathy].

Conventional echocardiographic methods of measuring left ventricular mass (LVM) are limited by assumptions of ventricular geometry and image plane positioning. Three-dimensional (3D) echocardiography offers a promising new approach for more accurate determination of LVM. This study was performed to compare LVM measurement by one- (1D), two- (2D), and 3D echocardiography with magnetic resonance imaging (MRI) in patients (pts) with dilated cardiomyopathy (DCM). 36 pts (age 18-74) with DCM underwent imaging by conventional 1D and 2D echocardiography as well as transthoracic 3D echocardiographic data acquisition. Also, pts were imaged with cardiac MRI. Due to echocardiographic and MRI quality and because of exclusion criteria's for MRI, it was not possible to accomplish each LVM determination method for each patient. LVM was determined by Devereux and area-length algorithm for the conventional echocardiography. 3D echocardiographic data was calculated after manual delineation of endo- and epicardial boundaries--slice by slice (5 mm)--in 3 perpendicular cut planes. LVM was determined by multiplying the myocardial volume by the specific density of the myocardium. To determine LVM in MRI, the even summation of slices method for myocardial volume measurement was used defined by the endo- and epicardium in short axis images. There was no significant correlation (r = 0.42) for measuring LVM between 1D echocardiography and MRI in pts with DCM. A significant correlation was obtained between 2D (r = 0.64, p < 0.01) echocardiography and MRI as well between 3D (r = 0.78, p < 0.01) and MRI in determination of LVM. Compared with 1D and 2D echocardiography, the 3D analysis achieved a significantly higher agreement with the results of the MRI (1D: 399.2 g, 2D: 285.9 g, 3D: 172.6 g versus MRI: 199.1 g). Interobserver variability was 5.1% for measuring LVM by 3D echocardiography (1D: 11.2%, 2D: 9.1%). In conclusion, in pts with DCM the determination of LVM was incompletely characterized by 1D and 2D echocardiography compared with results of MRI. The best correlation and high agreement for determination of LVM was obtained with 3D echocardiography compared with MRI.

Adolescent↗
PubMed1998

Changes of neurohumoral parameters and endothelin-1 in response to exercise in patients with mild to moderate congestive heart failure.

UNLABELLED: Plasma endothelin levels are increased in patients with moderate and severe CHF. Conflicting data exist about the endothelin-1 (ET) level in patients with mild to moderate CHF and the effect of maximal exercise on plasma ET levels. METHODS AND RESULTS: We determined the plasma levels of ET and various neurohumoral parameters in 93 patients with CHF in functional class II and III of the NYHA classification at rest and after maximal bicycle exercise. Baseline ET level was increased compared to an age-matched healthy volunteer group (6.95+/-0.31 vs 3.29+/-0.17 pg/ml, mean+/-S.E.M., P<0.05), without significant differences between NYHA class II and III patients. Maximal exercise did not increase the ET level. In contrast, the neurohumoral parameters were significantly increased with maximal exercise. In conclusion, plasma levels of ET are increased in patients with mild to moderate CHF. However, no further increase in response to exercise was observed. Thus, it is highly unlikely that exercise capacity may be limited by ET-mediated peripheral vasoconstriction.

Aged↗
PubMed1998

High- versus low-dose ACE inhibition in chronic heart failure: a double-blind, placebo-controlled study of imidapril.

OBJECTIVES: To determine dose-related clinical and neurohumoral effects of angiotensin-converting enzyme (ACE) inhibitors in patients with chronic heart failure (CHF), we conducted a double-blind, placebo-controlled, randomized study of three doses (2.5 mg, 5 mg and 10 mg) of the long-acting ACE inhibitor imidapril. BACKGROUND: The ACE inhibitors have become a cornerstone in the treatment of CHF, but whether high doses are more effective than low doses has not been fully elucidated, nor have the mechanisms involved in such a dose-related effect. METHODS: In a parallel group comparison, the effects of three doses of imidapril were examined. We studied 244 patients with mild to moderate CHF (New York Heart Association class II-III: +/-80%/20%), who were stable on digoxin and diuretics. Patients were treated for 12 weeks, and the main end points were exercise capacity and plasma neurohormones. RESULTS: At baseline, the four treatment groups were well-matched for demographic variables. Of the 244 patients, 25 dropped out: 3 patients died, and 9 developed progressive CHF (3/182 patients on imidapril vs. 6/62 patients on placebo, p < 0.05). Exercise time increased 45 s in the 10-mg group (p = 0.02 vs. placebo), but it did not significantly change in the 5-mg (+16 s), and 2.5-mg (+11 s) imidapril group, compared to placebo (+3 s). Physical working capacity also increased in a dose-related manner. Plasma brain and atrial natriuretic peptide decreased (p < 0.05 for linear trend), while (nor)epinephrine, aldosterone and endothelin were not significantly affected. Renin increased in a dose-related manner, but plasma ACE activity was suppressed similarly (+/-60%) on all three doses. CONCLUSIONS: Already within 3 months after treatment initiation, high-dose ACE inhibition (with imidapril) is superior to low-dose. This is reflected by a more pronounced effect on exercise capacity and some of the neurohormones, but it does not appear to be related to the extent of suppression of plasma ACE.

Adult↗
PubMedDate not supplied

Recombinant growth hormone therapy in patients with ischemic cardiomyopathy : effects on hemodynamics, left ventricular function, and cardiopulmonary exercise capacity.

BACKGROUND: We studied the effects of recombinant growth hormone (rhGH) on exercise capacity and cardiac function in patients with ischemic cardiomyopathy. METHODS AND RESULTS: Seven patients (aged 55+/-9 years) with mild to moderate congestive heart failure (ejection fraction 31+/-4%) who were on standard therapy were included. The patients were studied at baseline, after 3 months of rhGH treatment, and 3 months after rhGH discontinuation. Cardiac function was assessed by exercise capacity, right heart catheterization at rest and after submaximal exercise, MRI, echocardiography, and Holter monitoring. When administered at a dose of 2 IU/d, rhGH doubled the serum concentration of insulin-like growth factor-I. rhGH improved clinical symptoms and exercise capacity significantly (New York Heart Association class 2.4+/-0.5 initially versus 1.4+/-0.5 at 3 months [mean+/-SD], P<0.05; VO2max 13.6+/-3.8 versus 17.4+/-5.4 mL. kg-1. min-1, P<0.05). Additionally, pulmonary capillary wedge pressures at rest and after submaximal exercise were reduced significantly. Cardiac output increased, particularly at rest (5.0+/-1.1 versus 5.8+/-1.3 L/min; P<0.05). Posterior wall thickness was increased (1.08+/-0.1 versus 1. 24+/-0.3 cm; P<0.05), and the end-diastolic and end-systolic volume indexes decreased significantly after rhGH treatment. There was no significant increase in left ventricular ejection fraction. The improvements were partially reversed 3 months after rhGH discontinuation. CONCLUSIONS: The administration of rhGH for 3 months in patients with ischemic cardiomyopathy results in significant improvement in hemodynamics and clinical function. The attenuation of left ventricular remodeling persisted 3 months after discontinuation of treatment.

Combined Modality Therapy↗