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Biomedical subjects

P Erne

Publications and source records attributed to P Erne.

At least 19 recordsLinked to original sources
PubMed2006

[Modern echocardiography: possibilities and limitations].

Echocardiography has revolutionized the cardiac evaluation in non-invasive cardiology. Two-dimensional and colour Doppler echocardiography have the potential to provide quantitative insighths into the hearts anatomy, valve and ventricular function in a excellent time and spacial resolution. In addition integration of Doppler allows the quantification of stenotic lesions and hemodynamics. Stressechocardiography has gained wide acceptance for the evaluation of ischemia. Reduced echoquality can be overcome by latest probe technology (harmonic imaging and postprocessing), transesophageal echocardiography and echocontrast studies. However echocontrast will be used for myocardial perfusion imaging also. Three dimensional echocardiography is ready for clinical application. Good formation and continuous training in echocardiography according to international guidelines will help to reduce interobserver and intraobserver variability.

Contrast Media↗
PubMed2006

[Temporal trends in treatment of ST segment elevation myocardial infarction in Switzerland from 1997 to 2005].

From 1997 to 2005, 19461 patients admitted for acute coronary syndrome in 68 hospitals in Switzerland were included in the AMIS Plus registry, of whom 11 543 showed ST segment elevation or left bundle branch block on the ECG at admission. During this period, there was an important increase in the proportion of patients treated by primary percutaneous coronary intervention (8% to 74%), and a marked reduction in the use of thrombolysis (47% to 6%) and also in the proportion of patients who did not receive any reperfusion treatment (45% to 20%). Furthermore, there was a decrease in hospital mortality (12% to 7%). Main predictors of hospital mortality were withholding PCI and thrombolysis, advanced age and the presence of cardiogenic shock. Moreover, primary PCI was associated with lower hospital mortality when compared to thrombolysis.

Angioplasty, Balloon, Coronary↗
PubMed2005

LDL induces intracellular signalling and cell migration via atypical LDL-binding protein T-cadherin.

Cadherins are a superfamily of adhesion molecules that mediate Ca(2+)-dependent cell-cell adhesion. T-cadherin (T-cad), a unique glycosylphosphatidylinositol-anchored member of the cadherin superfamily, was initially identified by immunoblotting of vascular cell membranes as an atypical low affinity low density lipoprotein (LDL)-binding protein. It is not known whether this heterophilic interaction is physiologically relevant. Expression of T-cadherin is upregulated in vascular cells during atherosclerosis, restenosis and tumour angiogenesis, conditions characterized by enhanced cell migration and growth. Elevated levels of serum low density lipoproteins (LDL), which result in cholesterol accumulation in vascular wall, is a widely accepted risk factor in atherosclerosis development. Additionally to its metabolic effects, LDL can produce hormone-like effects in a number of cell types. This study has utilized HEK293 cells and L929 cells stably transfected with T-cadherin cDNA to investigate T-cad-dependent responses to LDL. Stable expression of T-cad in both HEK293 and L929 cells results in significantly (p < 0.05) elevated specific surface binding of [I125]-LDL. Compared with mock-transfectants, cells expressing T-cad exhibit significantly (p < 0.01) enhanced LDL-induced mobilization of intracellular Ca(2+)-stores and a significantly (p < 0.01) increased migration toward an LDL gradient (0.1% BSA + 60 microg/ml LDL) in Boyden chamber migration assay. Thus LDL-binding to T-cad is capable of activating physiologically relevant intracellular signaling and functional responses.

Animals↗
PubMed2005

Trends in reperfusion therapy of ST segment elevation myocardial infarction in Switzerland: six year results from a nationwide registry.

OBJECTIVE: To document the trends in reperfusion therapy for ST segment elevation myocardial infarction (STEMI) in Switzerland. DESIGN: National prospective multicentre registry, AMIS Plus (acute myocardial infarction and unstable angina in Switzerland), of patients admitted with acute coronary syndromes. SETTING: 54 hospitals of varying size and capability in Switzerland. PATIENTS: 7098 of 11 845 AMIS Plus patients who presented with ST segment elevation or left bundle branch block on the ECG at admission. MAIN OUTCOME MEASURES: In-hospital mortality and its predictors at admission by multivariate analysis. RESULTS: The proportion of patients treated by primary percutaneous coronary intervention (PCI) progressively increased from 1997 to 2002, while the proportion with thrombolysis or no reperfusion decreased (from 8.0% to 43.1%, from 47.2% to 25.6%, and from 44.8% to 31.4%, respectively). Overall in-hospital mortality decreased over the study period from 12.2% to 6.7% (p < 0.001). Main in-hospital mortality predictors by multivariate analysis were primary PCI (odds ratio (OR) 0.52, 95% confidence interval (CI) 0.33 to 0.81), thrombolysis (OR 0.63, 95% CI 0.47 to 0.83), and Killip class III (OR 3.61, 95% CI 2.49 to 5.24) and class IV (OR 5.97, 95% CI 3.51 to 10.17) at admission. When adjusted for the year, multivariate analysis did not show PCI to be significantly superior to thrombolysis for in-hospital mortality (OR 1.2 for PCI better, 95% CI 0.8 to 1.9, p = 0.42). CONCLUSION: Primary PCI has become the preferred mode of reperfusion for STEMI since 2002 in Switzerland, whereas use of intravenous thrombolysis has decreased from 1997 to 2002. Furthermore, there was a major reduction of in-hospital mortality over the same period.

Aged↗
PubMed2004

[Pharmacological basis of antihypertensive drug therapy].

In order to lower arterial blood pressure, antihypertensive drugs decrease cardiac output, total peripheral resistance or both. Diuretics, beta-blockers, and central adrenergic inhibitors decrease cardiac output. ACE inhibitors, angiotensin II antagonists, calcium antagonists, alpha-blockers, central adrenergic inhibitors, and after a delay also diuretics and beta-blockers decrease peripheral resistance. Diuretics are first line therapy for treating low renin hypertension. Beta blockers are used for treating high renin hypertension and patients suffering additional coronary artery disease. ACE inihibitors can be given for treating high renin hypertension particularly in conjunction with diabetes, heart failure or left ventricular hypertrophy. Combining ACE inhibitors with diuretics potentiates the antihypertensive effect. Angiotensin II antagonists exert fewer side effects and better renal protection than ACE inhibitors. The main indication for calcium antagonists is low renin hypertension, their advantages being strong blood pressure reduction as well as in preventing stroke. Central alpha2 receptor agonists and other vasodilators are chosen only in selected cases and mostly in combination with other antihypertensive drugs.

Adrenergic beta-Antagonists↗
PubMed2003

[Tachyarrhythmias--when rapid pace is pathological].

Tachycardias are classified as supraventricular and ventricular tachycardias. Supraventricular and ventricular tachycardias may occur as a complication of almost any underlying cardiac disease and many extracardiac causes. In addition, patients without any detectable structural heart disease may present with these arrhythmias. In this overview, we discuss the clinical presentations, the pathophysiological mechanisms and the therapeutical strategies in patients with tachyarrhythmias.

Anti-Arrhythmia Agents↗
PubMed2003

Successful brachytherapy of coronary vasospasm.

Brachytherapy is a proposed treatment for in-stent restenosis and is the subject of several clinical trials and debates. The standard treatment of patients with variant angina is to eliminate vasoconstrictive factors and to administer vasodilating drugs. This is the first description of successful brachytherapy for coronary spasm.

Brachytherapy↗
PubMed2001

Expression of cell adhesion molecule T-cadherin in the human vasculature.

Alterations in expression of surface adhesion molecules on resident vascular and blood-derived cells play a fundamental role in the pathogenesis of cardiovascular disease. Smooth muscle cells (SMCs) have been shown to express T-cadherin (T-cad), an unusual GPI-anchored member of the cadherin family of adhesion molecules. Particular relevance for T-cad in cardiovascular tissues is indicated by our present screen (immunoblotting) of human tissues and organs whereby highest expression of T-cad was found in aorta, carotid, iliac and renal arteries and heart. To explore the (patho)physiological role for T-cad in the vasculature we performed an immunohistochemical analysis of T-cad expression in normal human aorta and atherosclerotic lesions of varying severity. T-cad was present both in the intima and media and was expressed in endothelial cells (ECs), SMCs and pericytes, but not in monocytes/macrophages, foam cells and lymphocytes. In the adventitia T-cad was present in the wall of vasa vasorum and was expressed in ECs, SMCs and pericytes. T-cad was differentially expressed in SMCs from distinct vascular layers of normal aorta (for example, high in the subendothelial (proteoglycan) layer of the intima, low in the musculoelastic intimal layer and in the media), as well as at different stages of lesion progression. In SMCs there was an apparent inverse relationship between the intensities of T-cad and smooth muscle alpha-actin expression, this being most prominent in lesions. The findings suggest a phenotype-associated expression of T-cad which may be relevant to control of the normal vascular architecture and its remodelling during atherogenesis.

Aorta↗
PubMed2001

Monocyte integrin expression and monocyte-platelet complex formation in humans with coronary restenosis.

1. In the present study, we sought to determine whether patients with restenosis after coronary stenting possess increased monocyte reactivity, as manifested by a higher level of adhesion molecule expression and an enhanced propensity to form monocyte-platelet aggregates after activation in vitro. 2. Anti-coagulated peripheral venous blood from 24 patients, 10 with and 14 without angiographically verified restenosis, was obtained. Leucocyte antigen expression and the number of leucocyte-platelet complexes were measured by flow cytometry after activation in whole blood. 3. Surface integrin Mac-1 (CD11b/CD18) and VLA-4 (CD49d/ CD29) expression on monocytes and the relative number of monocyte-platelet complexes after in vitro activation were significantly elevated in patients with restenosis compared with patients without restenosis (fluorescence intensities of 1425 +/- 76 vs 1195 +/- 71, 87 +/- 7 vs 65 +/- 6 and 47 +/- 4 vs 29 +/- 3% for for Mac-1, VLA-4 and monocyte-platelet complexes, respectively; P < 0.05 for each parameter). 4. The results suggest that restenosis is associated with increased monocyte VLA-4 and Mac-1 integrin expression and monocyte-platelet complex formation, which can be revealed after activation in vitro.

Blood Platelets↗
PubMed2000

The glycosyl phosphatidylinositol anchor of human T-cadherin binds lipoproteins.

T-cadherin (T-cad) is a Ca(2+)-dependent cell adhesion glycoprotein bound to the plasma membrane via a glycosylphosphatidylinositol (GPI) anchor. T-cad expressed on vascular smooth muscle cells (SMC) binds lipoproteins on blot. To analyze the molecular basis for the interaction of T-cad with lipoproteins we expressed recombinant human T-cad in HEK293 cells. Whereas membrane-bound T-cad from SMC and T-cad transfected HEK293 cells bind lipoproteins, T-cadherin proteins cleaved from the cell surface by phosphatidylinositol-specific phospholipase C (PI-PLC) do not. The lipoprotein-binding function is also lacking both for a recombinant human T-cad expressed in HEK293 cells without the GPI signal sequence, and for a human T-cad form expressed in Escherichia coli that contains the signal sequence for GPI attachment but is not modified with a GPI. We conclude that the GPI moiety of T-cadherin is necessary and sufficient to mediate lipoprotein binding.

Amino Acid Sequence↗
PubMed2000

Urokinase plasminogen activator enhances neointima growth and reduces lumen size in injured carotid arteries.

OBJECTIVES: Increases in urokinase plasminogen activator (uPA) have been reported in tissues undergoing remodelling, but its effects on the vessel intima formation are not known. We investigated its effects on carotid artery intima, media and lumen size, as well as smooth muscle cell (SMC) proliferation and migration in vivo. DESIGN AND METHODS: Carotid arteries of rats were distended with an inflated balloon catheter and uPA, or uPA-neutralizing antibodies were applied perivascularly in pluronic gel; control rats received vehicle. Carotid artery structure, cell migration and proliferation were assessed after 4 days by quantitative morphometry and immunohistochemistry. RESULTS: Four days after increasing vessel uPA, the intima/media ratio was double compared to that in control rats (both P < 0.05). The size of the lumen reduced by 75%, compared to the vehicle-treated vessels (P < 0.05). The elevation in uPA also increased SMC numbers in the intima and media, compared to the vehicle-treated vessels (both P < 0.05). Antibody neutralizing endogenous uPA attenuated the growth responses in the distended arteries, reduced neointimal SMC numbers by approximately 50% and prevented much of the reduction in lumen size. CONCLUSIONS: Thus, local increases in uPA in distended, injured arteries augment SMC migratory and proliferative responses, leading to increases in the thickness of the carotid artery intima and media and a reduction in lumen size; effects at least partially attributable to its proteolytic properties.

Animals↗
PubMed1999

LDL binds to surface-expressed human T-cadherin in transfected HEK293 cells and influences homophilic adhesive interactions.

T-cadherin (T-cad) is an unusual glycosylphosphatidylinositol-anchored member of the cadherin family of cell adhesion molecules. Binding of low density lipoproteins (LDLs) to T-cad can be demonstrated on Western blots of smooth muscle cell lysates, membranes and purified proteins. Using HEK293 cells transfected with human T-cad cDNA (T-cad+), we have investigated the adhesion properties of expressed mature and precursor proteins and examined the postulate that LDL represents a physiologically relevant ligand for T-cad. T-cad+ exhibits an increased Ca(2+)-dependent aggregation (vs. control) that was reduced by selective proteolytic cleavage of precursor T-cad and abolished after either proteolytic or phosphatidylinositol-specific phospholipase C (PI-PLC) cleavage of both mature and precursor proteins, indicating that both proteins function in intercellular adhesion. T-cad+ exhibited a significantly increased specific cell surface-binding of [(125)I]-LDL that was sensitive to PI-PLC pre-treatment of cells. Ca(2+)-dependent intercellular adhesion of T-cad+ was significantly inhibited by LDL. Our results support the suggestion that LDL is a physiologically relevant ligand for T-cad.

Cadherins↗