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Biomedical subjects

Stephan B Felix

Publications and source records attributed to Stephan B Felix.

At least 19 recordsLinked to original sources
PubMed2026

Impact of renal dysfunction on immediate versus staged revascularization of non-culprit lesions in patients with ST segment elevation myocardial infarction: a pre-specified subgroup analysis of the randomized MULTISTARS AMI trial.

BACKGROUND: Renal dysfunction might affect outcomes in patients with ST-segment elevation myocardial infarction (STEMI) and multivessel coronary artery disease (MVD) undergoing percutaneous coronary intervention (PCI). METHODS: In MULTISTARS AMI, patients with STEMI and MVD were randomized to immediate or staged PCI of non-culprit lesions. In this pre-specified analysis, patients were stratified according to the presence of renal dysfunction at baseline, defined at an estimated glomerular filtration rate (eGFR) of 60&#xa0;ml/min/1.73 m2. Patients with an eGFR&#x2009;<&#x2009;30&#xa0;ml/min/1.73 m2 were excluded from the trial. The primary endpoint was a composite of death, non-fatal myocardial infarction, stroke, unplanned revascularization, or hospitalization for heart failure at 1&#xa0;year. RESULTS: In MULTISTARS AMI, 108 (13%) of 832 patients had renal dysfunction. The primary endpoint occurred more frequently in patients with renal dysfunction (19.4% vs. 11.2%, unadjusted HR 1.82, 95% CI 1.13-2.94), primarily driven by higher rates of death. Among patients with renal dysfunction, the rates of the primary end point were 14.5% and 24.5% in the immediate and staged PCI groups (unadjusted HR 0.55, 95% CI 0.23-1.33). There was no interaction between renal dysfunction and the randomized treatment assignment with respect to the primary end point (adjusted HR 1.30, 95% CI 0.8-2.20, pint 0.82). The occurrence of acute renal insufficiency was statistically similar in patients with renal dysfunction who underwent immediate and staged PCI (10.9% vs. 18.9%, unadjusted HR 0.61, 95% CI 0.22-1.72, pint 0.09). Renal dysfunction at baseline emerged as a strong risk factor for the development of acute renal insufficiency (adjusted HR 5.0, 95% CI 2.30-10.70, p&#x2009;<&#x2009;0.01). CONCLUSIONS: Outcomes with immediate compared to staged multivessel PCI did not appear significantly altered by the presence of renal dysfunction&#xa0;at baseline. (Supported by Boston Scientific; MULTISTARS AMI ClinicalTrials.gov number, NCT03135275).

Humans↗
PubMed2025

Genome-wide association study meta-analysis provides insights into the etiology of heart failure and its subtypes.

Heart failure (HF) is a major contributor to global morbidity and mortality. While distinct clinical subtypes, defined by etiology and left ventricular ejection fraction, are well recognized, their genetic determinants remain inadequately understood. In this study, we report a genome-wide association study of HF and its subtypes in a sample of 1.9 million individuals. A total of 153,174 individuals had HF, of whom 44,012 had a nonischemic etiology (ni-HF). A subset of patients with ni-HF were stratified based on left ventricular systolic function, where data were available, identifying 5,406 individuals with reduced ejection fraction and 3,841 with preserved ejection fraction. We identify 66 genetic loci associated with HF and its subtypes, 37 of which have not previously been reported. Using functionally informed gene prioritization methods, we predict effector genes for each identified locus, and map these to etiologic disease clusters through phenome-wide association analysis, network analysis and colocalization. Through heritability enrichment analysis, we highlight the role of extracardiac tissues in disease etiology. We then examine the differential associations of upstream risk factors with HF subtypes using Mendelian randomization. These findings extend our understanding of the mechanisms underlying HF etiology and may inform future approaches to prevention and treatment.

Humans↗
PubMed2004

Potential role of humoral immunity in cardiac dysfunction of patients suffering from dilated cardiomyopathy.

OBJECTIVES: This research was conducted to evaluate the role played by the humoral immune system in cardiac dysfunction among dilated cardiomyopathy (DCM) patients, as enabled by immunoadsorption therapy (IA) that effectively removes functionally active cardiac autoantibodies from plasma. BACKGROUND: Various circulating autoantibodies have been detected among patients suffering from DCM. METHODS: Before IA, antibodies were purified from plasma of 45 DCM patients (left ventricular ejection fraction [LVEF] <30%). We analyzed the functional effects of antibodies (300 mg/l) on calcium transients and on systolic cell shortening in adult rat cardiomyocytes. After this in vitro analysis, IA was performed in four courses at one-month intervals until month 3. RESULTS: Antibodies from 29 patients induced a reduction (>10%) in calcium transients (mean reduction: -16.5 +/- 1.9%) and a simultaneous reduction (>10%) of cell shortening (mean reduction: -21.2 +/- 1.8%) on cardiomyocytes (p < 0.001) (cardiodepressant group). Antibodies from 16 patients did not significantly influence calcium transients and cell shortening (<10%) (non-cardiodepressant group). During the first IA course, the cardiodepressant group demonstrated an acute increase in cardiac index (CI) from 2.2 +/- 0.1 l/min/m(2) to 2.9 +/- 0.1 l/min/m(2) (p < 0.001). In the non-cardiodepressant group, hemodynamics did not significantly change throughout three months. After three months before the final IA course (prolonged effects), the CI was 2.1 +/- 0.1 l/min/m(2) in the non-cardiodepressant group and 2.9 +/- 0.1 l/min/m(2) in the cardiodepressant group (p < 0.001). After three months LVEF increased only in the cardiodepressant group: from 20.8 +/- 1% to 30.5 +/- 1% (p < 0.01). CONCLUSIONS: In the majority of DCM patients, disturbances of humoral immunity with production of cardiodepressant antibodies may play a functional role in cardiac dysfunction. Evidence of cardiodepressant antibodies predicts hemodynamic benefits during IA.

Animals↗
PubMed2004

Association between high serum ferritin levels and carotid atherosclerosis in the study of health in Pomerania (SHIP).

BACKGROUND AND PURPOSE: Several studies have provided evidence for a relationship between body iron load and cardiovascular disease. We analyzed the association of serum ferritin levels with carotid atherosclerosis. METHODS: We assessed intima-media thickness and plaque prevalence in the carotid arteries by high-resolution ultrasound among 2443 participants (1200 women; age, 45 to 79 years) in the Study of Health in Pomerania (SHIP), a population-based study in northeast Germany. RESULTS: In multivariate analysis, serum ferritin levels were not independently associated with carotid intima-media thickness among women or men. In contrast, the relationship between serum ferritin levels and carotid plaque prevalence was significant among men (odds ratio per 1-SD increase of serum ferritin levels, 1.33; 95% confidence interval, 1.08 to 1.44) yet not among women (odds ratio, 1.29; 95% confidence interval, 0.98 to 1.75). However, both men and women showed a dose-response relation between serum ferritin levels and carotid atherosclerosis in which higher serum ferritin levels were associated with greater odds ratios for carotid plaque prevalence. Additionally, there was an interaction of serum ferritin levels with low-density lipoprotein (LDL) cholesterol (P=0.039) among men in which the association of serum ferritin levels with carotid plaque prevalence became stronger with increasing LDL cholesterol levels. CONCLUSIONS: Our study identified a relationship between serum ferritin levels and carotid atherosclerosis that was potentiated by LDL cholesterol. This relationship adds support to the hypothesis of a link between iron and cardiovascular disease.

Aged↗
PubMed2004

Hepatitis B and C virus infection and the risk of atherosclerosis in a general population.

BACKGROUND: The development of atherosclerosis has an inflammatory component. Currently it is not clear, whether hepatitis B and C virus infections are associated with the risk of atherosclerosis. The aim of the present analysis was to investigate those relationships in a population sample. METHODS AND RESULTS: The study of health in Pomerania (SHIP) is a cross-sectional study of the adult population in the northeast of Germany. HBs antigen (HBsAg) and IgG antibodies against hepatitis B and C virus (anti-HBs and anti-HCV) were determined by enzyme linked immunosorbent assays. Fifteen subjects (0.4%) were positive for HBsAg, and 21 subjects (0.5%) were positive for anti-HCV. Among the persons who had no history of anti-hepatitis B vaccination, 213 individuals (5.0%) were found to be as positive for anti-HBs. These individuals and those with prevalent anti-HCV antibodies were regarded as cases (n = 233). The control group comprised of 4033 individuals. Multivariable analyses revealed that there was no independent association between anti-HBs and anti-HCV antibody seropositivity and atherosclerotic end-points such as prevalent myocardial infarction, stroke, carotid intima-media thickness (IMT), carotid plaques and stenoses. CONCLUSION: There is no association between serological markers for hepatitis B and C virus infection and the risk of atherosclerosis in this population sample.

Adult↗
PubMed2004

Plasma fibrinogen levels are associated with a strong family history of myocardial infarction.

Family history of myocardial infarction (MI) is a known risk factor for coronary artery disease (CAD). The aim of the present study was to investigate whether there is a specific risk factor profile for CAD in individuals with a strong family history of MI occurring at any age. The Study of Health in Pomerania is a cross-sectional, population-based study in the north-east of Germany. A random sample was drawn from the population aged 20-79 years. From 3793 subjects with siblings, 34 (0.9%) reported a history of MI in at least one parent and one sibling. We matched these cases with 136 controls (1 : 4 matching for age, sex and presence of sibling). We then compared cases and controls with respect to known risk factors for MI. Subjects with a dual parental and sibling history of MI had higher plasma fibrinogen levels (3.5 versus 3.0 g/l, respectively), and also more often angina pectoris than the matched controls (P < 0.05). Multivariable analysis revealed an independent association between dual parental and sibling history of MI and plasma fibrinogen levels. We conclude that plasma fibrinogen levels may indicate an inheritable risk for CAD in subjects with a strong family history of MI.

Adult↗
PubMed2004

Thyroid function and carotid wall thickness.

Decreased serum TSH levels predict vascular mortality in older people. There is a need to investigate mechanisms that could explain this association. This study was designed to investigate the relationship between thyroid function and the carotid intima-media thickness (IMT). The Study of Health in Pomerania is a population-based survey in Germany. Data from 2086 individuals at least 45 yr old with carotid ultrasound and without known thyroid disorders were analyzed. Twenty-nine participants (1.4%) had elevated serum TSH levels, 300 (14.4%) had decreased serum TSH levels, and 12 (0.6%) participants were hyperthyroid. A linear relationship between thyroid function and IMT was found. The highest IMT values were observed in participants with hyperthyroidism, the lowest in subjects with elevated serum TSH levels (P < 0.01). A multivariable regression analysis identified thyroid function as an independent risk factor for increased IMT. Other risk factors for increased IMT included male gender, advanced age, diabetes mellitus, current smoking, and the use of antihypertensive medication; increased pulse pressure, serum low-density cholesterol, and total cholesterol/high-density lipoprotein ratio; as well as a decreased heart rate and a positive history of myocardial infarction. We conclude that there is an independent association between thyroid function and the IMT of the carotid artery.

Carotid Arteries↗
PubMed2003

Beta1-adrenoceptor antibodies induce apoptosis in adult isolated cardiomyocytes.

beta(1)-Adrenoceptor autoantibodies are present in about 30% of patients suffering from dilated cardiomyopathy. The apoptotic effects mediated by beta(1)-adrenoceptor antibodies remain to be studied. Monoclonal antibodies were raised against a synthetic peptide corresponding to the second extracellular loop of the human beta(1)-adrenoceptor in balb/C mouse, and were characterized by enzyme immunoassay. Purified immunoglobulin G from nonimmunized animals (controls) did not influence the rate of apoptosis. beta(1)-Adrenoceptor antibodies caused a dose-related increase in apoptotic cells: annexin test (dilution 1:2: 21+/-1.1% apoptotic cells vs. 4+/-0.4% apoptotic cells in controls; p<0.01); TdT-mediated dUTP nick end labeling (TUNEL) test (dilution 1:2: 26+/-2% apoptotic cells vs. 10+/-2% apoptotic cells in controls; p<0.01). The effect of the beta(1)-adrenoceptor antibodies was blocked by the antigenic peptide and by the antagonist metoprolol (10 micromol/l). The apoptotic effect induced by isoproterenol was attenuated by the beta(1)-adrenoceptor antibody. After pre-incubation of cardiomyocytes with the protein kinase A inhibitor Rp-Adenosine-3',5'-cyclic monophosphothioate triethylamine (RpcAMPS), beta(1)-adrenoceptor antibody was not capable of inducing an increase of the rate of apoptosis. beta(1)-Adrenoceptor antibodies induced apoptosis in adult rat cardiomyocytes via the protein kinase A cascade.

Adrenergic beta-Agonists↗
PubMed2003

Interaction of CA repeat polymorphism of the endothelial nitric oxide synthase and hyperhomocysteinemia in acute coronary syndromes: evidence of gender-specific differences.

We have recently shown that high CA repeat copy numbers (> or = 34 repeats) in intron 13 of the endothelial nitric oxide (eNOS) gene are associated with excess risk of coronary artery disease. Hyperhomocysteinemia interacts by several mechanisms with the NO system, thereby favoring endothelial dysfunction. Since hyperhomocysteinemia evidently promotes prothrombotic activation, we investigated a possible interaction among hyperhomocysteinemia, the eNOS CA repeat polymorphism, and acute coronary syndromes. The median value of homocysteine in our study population was 9.4 micromol/l. We accordingly determined the relative risk of acute coronary syndromes for homocysteine values higher than 9.4 micromol/l and 9.4 micromol/l or lower in the entire coronary artery disease group, and at different CA repeat cutoff values (34, 35, 36, 37, 38 CA repeats). For the entire coronary artery disease group ( n=1000), homocysteine levels higher than 9.4 micromol/l were not significantly associated with acute coronary syndromes. Although the CA repeat copy numbers were not associated with acute coronary syndromes in the overall group, the relative risk among women with homocysteine higher than 9.4 micromol/l for developing acute coronary syndromes increased nonsignificantly from 0.98 at cutoff 34 CA repeats to 1.68 at 35 CA repeats and significantly to 4.89 at 36 CA repeats, 11.20 at 37 CA repeats, and 18.32 at 38 CA repeats. This effect modification was not observed in men. These data suggest gender-specific gene-environment interaction between the CA repeat eNOS polymorphism and homocysteine in acute coronary syndromes.

Acute Disease↗
PubMed2003

Activation of Akt is essential for acetylcholine to trigger generation of oxygen free radicals.

OBJECTIVES: Acetylcholine (ACh) receptor activation in the heart causes mitochondrial production of reactive oxygen species (ROS) that is dependent on mitochondrial K(ATP) channel opening. Recent data show that Akt (also known as protein kinase B) is phosphorylated at its activation site following exposure to ACh. However, since no reliable Akt inhibitor is available, it has not been possible to determine whether Akt activation is an actual step in the protective pathway. METHODS: Cultured rat vascular smooth muscle cells (A7r5) were transiently transfected with a dominant negative Akt (Akt-AAA), thus inhibiting the ability of ACh in these cells to phosphorylate Akt. Transfected cells were identified by co-transfection of enhanced green fluorescent protein (EGFP). ROS production was determined by incubating the cells for 15 min with 1 mM reduced MitoTracker Red which becomes fluorescent only after reacting with ROS. Cells were then triple-washed to remove any voltage-dependent pool of dye and single cell fluorescence was measured. RESULTS: ACh exposure (2 mM) led to a 1.64+/-0.15-fold increase in the average fluorescence over that seen in untreated cells (P=0.002). A similar increase in ROS production occurred after treatment with either the K(ATP) channel opener diazoxide (DIAZ) or the potassium ionophore valinomycin (VAL). Akt-AAA transfection abolished ACh-induced ROS production, but not increased ROS production after treatment with either DIAZ or VAL. CONCLUSION: Thus, at least in the smooth muscle cell model, Akt phosphorylation is an important step in the signal transduction pathway leading from ACh receptor activation to the generation of ROS. The experiments reveal that Akt is positioned between the receptor and the K(ATP) channel in this model.

Acetylcholine↗
PubMed2003

Hemodynamic improvement and removal of autoantibodies against beta1-adrenergic receptor by immunoadsorption therapy in dilated cardiomyopathy.

The removal of beta(1)-adrenergic receptor (beta(1)AR) autoantibodies by immunoadsorption (IA) has been proposed as a potential mechanism for the improvement of the left ventricular function in dilated cardiomyopathy (DCM). In the present study, the possible association between removal of the autoantibodies against the human beta(1)AR with the hemodynamic improvement induced by IA was investigated.IA was performed in 22 DCM patients (n=22; NYHA III-IV, EF<30%, stable medication). The beta(1)AR autoantibodies from column eluents (CE) were detected by enzyme-linked immunosorbent assay (ELISA) and BIAcore methods. CE of 32% (7/22) of the patients was found to be antibody-positive with ELISA or BIAcore. In addition, a bioassay system was also used for the detection of this autoantibody. Seventy-three percent (16/22) of the patients were found to be antibody-positive by this method. However, independent of the beta(1)AR antibody detection method, both antibody-positive and antibody-negative groups showed similar acute and prolonged hemodynamic improvements during IA therapy. Furthermore, antibody-positive and -negative groups received a comparable improvement of left ventricular ejection fraction. These results suggest that different mechanisms are involved in the hemodynamic improvement induced by IA. The beneficial hemodynamic effects induced by IA are not directly associated with the removal of beta(1)AR autoantibodies.

Autoantibodies↗
PubMed2003

Identification and characterization of KAT, a novel gene preferentially expressed in several human cancer cell lines.

We describe the molecular characterization of a novel human gene on chromosome 1q23.3, termed KAT, which is highly conserved among mammals. The KAT gene spans a genomic region of approximately 1.6 kilobases and consists of 4 exons encoding a 115 amino acid protein with a molecular mass of about 12.5 kDa. The gene is expressed in several human tissues, including kidney, liver, skeletal muscle, heart, colon, thymus, spleen, placenta and lung. We identified an alternatively spliced form, lacking exon 2, in human and mouse tissues. In silico analysis of expressed sequence tags, derived from different types of human tumors, revealed another splice variant. This transcript is characterized by retention of the third intron, leading to a truncated translation product. The KAT protein is localized around the nuclear membranes. It was found to be expressed in several breast, colon and lung carcinoma cell lines, but not in normal breast epithelial cell lines. In addition, KAT protein was detected in invasive ductal carcinoma, but not in adjacent tissues. This suggests a role of this gene in tumorigenesis.

Alternative Splicing↗
PubMed2002

Potential role of autoantibodies belonging to the immunoglobulin G-3 subclass in cardiac dysfunction among patients with dilated cardiomyopathy.

BACKGROUND: Immunoadsorption capable of removing circulating autoantibodies represents an additional therapeutic approach in dilated cardiomyopathy (DCM). The role played by autoantibodies belonging to the immunoglobulin (Ig) subclass G-3 in cardiac dysfunction remains to be elucidated. METHODS AND RESULTS: Patients with DCM (left ventricular ejection fraction <30%) participated in this case-control study. Nine patients underwent immunoadsorption with protein A (low affinity to IgG-3), and 9 patients were treated with anti-IgG, which removes all IgG subclasses. Immunoadsorption was performed in 4 courses at 1-month intervals until month 3. In the 2 groups, immunoadsorption induced comparable reduction of total IgG (>80%). IgG-3 was effectively eliminated only by anti-IgG adsorption (eg, during the first immunoadsorption course; protein A, -37+/-4%; anti-IgG, -89+/-3%; P<0.001 versus protein A). The beta1-receptor autoantibody was effectively reduced only by anti-IgG (P<0.01 versus protein A). Hemodynamics did not change in the protein A group. In the anti-IgG group during the first immunoadsorption course, cardiac index increased from 2.3+/-0.1 to 3.0+/-0.1 L x min(-1) x m(-2) (P<0.01 versus protein A). After 3 months, before the last immunoadsorption course, cardiac index was 2.2+/-0.1 L x min(-1) x m(-2) in the protein A group and 3.0+/-0.2 L x min(-1) x m(-2) in the anti-IgG group (P<0.01 versus protein A). Left ventricular ejection fraction increased only in the anti-IgG group (P<0.05 versus protein A). CONCLUSIONS: Autoantibodies belonging to IgG-3 may play an important role in cardiac dysfunction of DCM. The removal of antibodies of the IgG-3 subclass may represent an essential mechanism of immunoadsorption in DCM.

Adrenergic beta-Antagonists↗
PubMed2002

Removal of cardiodepressant antibodies in dilated cardiomyopathy by immunoadsorption.

OBJECTIVES: The objective of this study was to investigate whether immunoadsorption (IA) removes cardiodepressant antibodies from the plasma of patients with dilated cardiomyopathy (DCM), as well as to describe their effects on isolated rat cardiomyocytes. BACKGROUND: Immunoadsorption induces early hemodynamic improvement in patients with DCM. The mechanisms for this improvement remain to be elucidated. METHODS: Patients with DCM (n = 11; left ventricular ejection fraction < 30%, cardiac index [CI] < 2.5 l/min per m(2)) were treated with IA on three consecutive days, with one IA session daily, by application of specific antibody columns directed against human immunoglobulin (Ig). Immunoadsorption was also conducted on 500 ml of blood taken from nine healthy donors (control subjects). After passage of plasma, the IA columns were regenerated. Column eluent (CE) was collected and dialyzed (100 kD). Confocal laser scanning microscopy was used to analyze the effects of CE on cell contraction and on Ca(2+)-dependent fluorescence in isolated, field-stimulated adult rat cardiomyocytes loaded with cell-permeable Fluo-3. Immunoprecipitation with different preparations of myocardial protein fractions was used for characterization of cardiotropic antibodies. RESULTS: During IA, the IgG plasma level decreased from 10.7 +/- 0.6 to 2.4 +/- 0.1 g/l (mean +/- SEM), and the CI increased from 2.2 +/- 0.1 to 2.7 +/- 0.2 l/min per m(2) (p < 0.01). The CE obtained from control subjects did not influence Ca(2+) transients or cell shortening of cardiomyocytes. In contrast, in patients with DCM, the CE collected during the first regeneration cycle of the first IA session caused an immediate and dose-related decrease of Ca(2+) transients (dilution 1:5; -22.7 +/- 5.5%; p < 0.01) and cell shortening (dilution 1:5; -29.9 +/- 6.0%, p < 0.01). Early hemodynamic improvement among the patients correlated with the cardiodepressant effect of CE on the isolated cardiomyocytes. Purification of CE by protein A adsorption indicated that the cardiodepressant substances are antibodies. Immunoprecipitation revealed that the eliminated antibodies are capable of binding to various myocardial proteins. CONCLUSIONS: Cardiac autoantibodies play a functional role in DCM, and their removal may induce early hemodynamic improvement.

Animals↗
PubMed2002

Laser-facilitated thrombectomy: a new therapeutic option for treatment of thrombus-laden coronary lesions.

To overcome the adverse complications of balloon angioplasty in thrombus burden lesions (i.e., distal embolization, platelet activation, no-reflow phenomenon with persistent myocardial hypoxemia), mechanical removal of the thrombus or distal embolization protection devices is required. Pulsed ultraviolet excimer laser light at 308 nm can vaporize thrombus and suppress platelet aggregation. Clinical experience has already shown its efficacy in acute ischemic-thrombotic acute coronary syndromes. Unlike other thrombectomy devices, a 308 nm excimer laser can ablate thrombi as well as the underlying plaque, speed up thrombus clearing, and enhance thrombolytic and GP IIb/IIIa activity. It can also be employed in patients with contraindications for systemic thrombolytic agents or GP IIb/IIIa antagonists. Our report covers clinical data and technical aspects concerning three patients with acute myocardial infarction who presented with a large thrombus burden. After successful laser-transmitted vaporization of the thrombus mass in these patients, the remaining thrombus burden was evacuated, and normal antegrade coronary flow was successfully restored. This approach can be useful for selective patients with acute coronary syndromes.

Aged↗
PubMed2002

A randomized trial of 5 vs. 6 French transradial percutaneous coronary interventions.

Transradial coronary interventions (TCI) are occasionally limited by radial spasms and postprocedural radial occlusions, which are related to the radial diameter and which possibly may be reduced by the use of smaller guiding catheter. However, 5 Fr, 0.058" lumen diameter guiding catheter affords less strength, visibility, and backup. In a randomized study, we investigated procedural and clinical success and vascular access complications of 5 Fr in comparison to 6 Fr guiding catheter. One hundred seventy-one patients with coronary lesions suitable for at least 5 Fr transradial approach (i.e., normal Allen test, only balloon angioplasty and stent) were randomly assigned for 5 or 6 Fr TCI. The primary combined endpoint was procedural and clinical success, and secondary endpoints were vascular access complications and the occurrence of postprocedural radial occlusions at 1-month follow-up. Procedural success was achieved in 95.4% of 5 Fr and 92.9% of 6 Fr patients. Selective cannulation of the coronary ostium failed in 1.1% of 5 Fr and 4.8% of 6 Fr patients (P = 0.08). Minor hematomas without need for surgical repair or blood transfusions occurred in 1.1% (5 Fr) and 4.8% (6 Fr; P = 0.07); 1.1% of 5 Fr and 5.9% of 6 Fr patients (P = 0.05) suffered loss of radial pulse due to radial occlusion. Selected noncomplex coronary lesions can successfully and safely be treated either with 5 or 6 Fr guiding catheters. A tendency of higher procedural success rates and lower vascular access complications was documented after 5 Fr in comparison to 6 Fr TCI. This was particularly the case among patients with small radial diameters.

Aged↗
PubMed2002

Area ablation: a new lasing concept provides significantly enhanced acute and long-term results for treatment of in-stent restenosis.

BACKGROUND AND OBJECTIVES: Debulking is still a technique of choice for in-stent restenosis (ISR). Excimer laser debulking has enabled high procedural success with very low complication rates, but has demonstrated markedly heterogeneous results owing to differences in lasing and laser technology, and selected patient populations. Since new area-ablation technique enables ablation of larger areas than its own device size, we have evaluated their effectiveness and safety in an uncontrolled study. STUDY DESIGN/MATERIALS AND METHODS: Fifty-three patients with diffuse ISR were treated by laser area ablation, followed by adjunctive balloon angioplasty. Primary endpoint was percent of binary stenosis at 6-month follow-up; secondary endpoints were procedural success; target lesion revascularization (TLR); major adverse cardiac events (MACE); diameter stenosis (DS); and minimal lumen diameter (MLD) before and after laser debulking, and at 6-month follow-up. RESULTS: Laser debulking was feasible (as defined as < or =30% residual stenosis) in 98.1% of patients. At 6-month follow-up, binary stenosis was 26.4%; angiographic TLR, 20.7%; and MACE, 3.7%. DS decreased from 87+/-17% to 20 +/- 9% after laser debulking, and to 9+/-7% after PTCA; it was 29+/-14% at follow-up (P-values in comparison to baseline: 0.0047; 0.0036; 0.0064). MLD increased from 0.6+/-0.3 to 2.4+/-0.5 mm after laser debulking, to 2.8+/- 0.6 mm after adjunctive PTCA, and to 1.9 +/- 0.4 mm at follow-up (P-values in comparison to baseline: 0.0059; 0.0031; 0.0088). CONCLUSIONS: Owing to a significantly greater MLD, area ablation facilitates significantly enhanced immediate and follow-up results for diffuse ISR, including a simpler and more effective laser-debulking procedure than former lasing techniques.

Aged↗