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Biomedical subjects

Christoph Bode

Publications and source records attributed to Christoph Bode.

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

START Trial: a pilot study on STimulation of ARTeriogenesis using subcutaneous application of granulocyte-macrophage colony-stimulating factor as a new treatment for peripheral vascular disease.

BACKGROUND: Granulocyte-macrophage colony-stimulating factor (GM-CSF) was recently shown to increase collateral flow index in patients with coronary artery disease. Experimental models showed beneficial effects of GM-CSF on collateral artery growth in the peripheral circulation. Thus, in the present study, we evaluated the effects of GM-CSF in patients with peripheral artery disease. METHODS AND RESULTS: A double-blinded, randomized, placebo-controlled study was performed in 40 patients with moderate or severe intermittent claudication. Patients were treated with placebo or subcutaneously applied GM-CSF (10 microg/kg) for a period of 14 days (total of 7 injections). GM-CSF treatment led to a strong increase in total white blood cell count and C-reactive protein. Monocyte fraction initially increased but thereafter decreased significantly as compared with baseline. Both the placebo group and the treatment group showed a significant increase in walking distance at day 14 (placebo: 127+/-67 versus 184+/-87 meters, P=0.03, GM-CSF: 126+/-66 versus 189+/-141 meters, P=0.04) and at day 90. Change in walking time, the primary end point of the study, was not different between groups. No change in ankle-brachial index was found on GM-CSF treatment at day 14 or at day 90. Laser Doppler flowmetry measurements showed a significant decrease in microcirculatory flow reserve in the control group (P=0.03) and no change in the GM-CSF group. CONCLUSIONS: The present study does not support the use of GM-CSF for treatment of patients with moderate or severe intermittent claudication. Issues that need to be addressed are dosing, the selection of patients, and potential differences between GM-CSF effects in the coronary and the peripheral circulation.

Angioplasty, Balloon↗
PubMed2005

Anti-tumor necrosis factor-{alpha} therapies attenuate adaptive arteriogenesis in the rabbit.

The specific antagonists of tumor necrosis factor-alpha (TNF-alpha), infliximab and etanercept, are established therapeutic agents for inflammatory diseases such as rheumatoid arthritis and Crohn's disease. Although the importance of TNF-alpha in chronic inflammatory diseases is well established, little is known about its implications in the cardiovascular system. Because proliferation of arteriolar connections toward functional collateral arteries (arteriogenesis) is an inflammatory-like process, we tested in vivo the hypothesis that infliximab and etanercept have antiarteriogenic actions. Sixty-three New Zealand White rabbits underwent femoral artery occlusion and received infliximab, etanercept, or vehicle according to clinical dosage regimes. After 1 wk, collateral conductance, assessed with fluorescent microspheres, revealed significant inhibition of arteriogenesis (collateral conductance): 52.4 (SD 8.1), 35.2 (SD 7.7), and 33.3 (SD 10.1) ml x min(-1) x 100 mmHg(-1) with PBS, infliximab, and etanercept, respectively (P < 0.001). High-resolution angiography showed no significant differences in number of collateral arteries, but immunohistochemical analysis demonstrated a decrease in mean collateral diameter, proliferation of vascular smooth muscle cells, and reduction of leukocyte accumulation around collateral arteries in treated groups. Infliximab and etanercept bound to infiltrating leukocytes, which are important mediators of arteriogenesis. Infliximab induced monocyte apoptosis, and neither substance affected monocyte expression of the adhesion molecule Mac-1. We demonstrated that TNF-alpha serves as a pivotal modulator of arteriogenesis, which is attenuated by treatment with TNF-alpha inhibitors. Reduction of collateral conductance is most likely due to inhibition of perivascular leukocyte infiltration and subsequent lower vascular smooth muscle cell proliferation. This is the first report showing a negative influence of TNF-alpha inhibitors on collateral artery growth.

Angiography↗
PubMed2005

Maintenance of long-term clinical benefit with sirolimus-eluting coronary stents: three-year results of the RAVEL trial.

BACKGROUND: The use of sirolimus-eluting coronary stents has been associated with a nearly complete elimination of restenosis at 6 months and with a very low 1-year incidence of major adverse cardiac events (MACE). This analysis examined whether these beneficial effects persist over the longer term. METHODS AND RESULTS: This multicenter trial randomly assigned 238 patients to revascularization of single, de novo, native coronary artery lesions with sirolimus-eluting versus conventional bare-metal stents. Survival free from target lesion revascularization (TLR), target vessel failure (TVF), and MACE up to 3 years of follow-up was compared between the 2 treatment groups. Complete data sets were available in 94.2% of patients treated with sirolimus-eluting stents and in 94.1% of patients randomized to the control group. The cumulative 1-, 2-, and 3-year event-free survival rates were 99.2%, 96.5%, and 93.7% for TLR and 95.8%, 92.3%, and 87.9% for TVF, respectively, in the sirolimus-eluting stent group, versus 75.9%, 75.9%, and 75.0% for TLR and 71.2%, 69.4%, and 67.3% for TVF in the control group (P<0.001 for both comparisons at 3 years). Rates of MACE at 3 years were 15.8% in patients randomly assigned to sirolimus-eluting stents versus 33.1% in patients assigned to bare-metal stents (P=0.002). One patient treated with a sirolimus-eluting stent died of a cardiac cause between 12 and 36 months. CONCLUSIONS: Treatment of de novo coronary stenosis with sirolimus-eluting stents was associated with a sustained clinical benefit and very low rates of TLR and of other MACE up to 3 years after device implantation.

Coronary Restenosis↗
PubMed2005

[Direct inhibition of thrombin. A new strategy for the treatment of atrial fibrillation and acute coronary syndrome?].

Direct inhibition of thrombin is a promising new strategy for the treatment of cardiovascular disease and thrombosis. Three intravenous (lepirudin, bivalirudin and argatroban) and one oral direct thrombin inhibitor (ximelagatran) are currently available and approved for some clinical indications in the treatment of cardiovascular disease and venous thrombosis. Further indications are under investigation in large clinical trials. The bivalent direct thrombin inhibitor (DTI) lepirudin is used for anticoagulation of patients with heparin-induced thrombocytopenia (HIT) as is the monovalent DTI argatroban. The bivalent DTI bivalirudin has been studied extensively in the REPLACE 1 and 2 trials. Results from these studies demonstrate that bivalirudin is as effective as heparin for patients undergoing percutaneous coronary intervention (PCI) and leads to less bleeding complications. Efficacy and safety of anticoagulation with bivalirudin in patients with unstable angina or non-ST elevation myocardial infarction (NSTEMI) are currently under investigation in the ACUITY trial. A fixed dose of 36 mg twice daily ximelagatran, an oral prodrug of melagatran, has been shown to be safe and as effective as warfarin for the treatment of patients with nonvalvular atrial fibrillation in the SPORTIF III and V trials. This review focuses on the pharmacology of the DTIs and discusses the results of major clinical trials with DTIs in nonvalvular atrial fibrillation and acute coronary syndromes.

Acute Coronary Syndrome↗
PubMed2005

[Future developments in the therapy of acute ST segment elevation myocardial infarction].

The treatment and therapy of acute myocardial infarction has substantially improved during the past decades. After thrombotic coronary occlusion had been identified as the underlying cause of myocardial infarction, thrombolysis emerged as the standard therapy. The development of more and more effective thrombolytic therapies and optimization of adjunctive antithrombotic therapies resulted in improved clinical outcomes and decreased mortality rates of acute myocardial infarction patients. Optimization of percutaneous coronary intervention (PCI) techniques including implantation of coronary stents shifted the therapeutic approach from thrombolysis toward acute mechanical reperfusion. The safety and efficacy profile of PCI has been made possible by the development of potent antiplatelet agents such as clopidogrel and glycoprotein (GP) IIb/IIIa antagonists. For the future therapy of acute myocardial infarction the following goals will be important to consider: (1) are there ways to increase the percentage of patients reaching out for medical support when suffering from acute myocardial infarction?, (2) what strategies will be useful to shorten coronary reperfusion time?, (3) are there means to protect affected myocardium from ischemic damage?, and (4) can necrotic myocardium be reconstituted functionally? Potential approaches such as improved public information, combination of thrombolytic and interventional therapy to accelerate coronary reperfusion, pharmacological protection of myocardium by modulation of myocardial metabolism or protection from reperfusion damage as well as progenitor cell therapy are discussed in this overview.

Angioplasty, Balloon, Coronary↗
PubMed2005

Leukocyte subpopulations and arteriogenesis: specific role of monocytes, lymphocytes and granulocytes.

OBJECTIVE: Circulating leukocytes play a crucial role during arteriogenesis. However, known pro-arteriogenic compounds (MCP-1, GM-CSF) acting via monocytic pathways also exert positive effects on granulocytes and lymphocytes. The role of these two cell types in arteriogenesis remains yet to be clarified, which was the aim of the current study. METHODS: Ninety New Zealand White Rabbits received either phosphate buffered saline (PBS), monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), neutrophil activating protein-2 (NAP-2) or lymphotactin (Ltn) via osmotic minipumps after unilateral femoral artery ligation. In vitro stimulation and in vivo assessment of chemoattraction confirmed cell-specific action of the compounds in rabbits. Arteriogenesis was evaluated by angiography and collateral conductance measurements using fluorescent microspheres. Quantitative immunohistology was used to quantify transmigrated leukocyte subtypes after infusion of the factors. RESULTS: MCP-1 infusion attracts monocytes and granulocytes, whereas IL-8 attracts all three cell types albeit monocytes to a significantly lower degree than MCP-1. NAP-2 and lymphotactin selectively attract granulocytes, respectively, lymphocytes. Of the tested cytokines, only MCP-1 stimulates arteriogenesis, as assessed by collateral conductance measurements ((ml/(min 100 mmHg)): PBS, 50.70+/-5.15; MCP-1, 216.30+/-12.30; IL-8, 58.91+/-5.56; NAP-2, 66.83+/-8.72; Ltn, 52.80+/-5.37) and angiographic findings. CONCLUSION: This study for the first time provides evidence that not granulocytes or T-lymphocytes but monocytes are the key mediators of arteriogenesis.

Animals↗
PubMed2005

Left atrial appendage flow velocity as a quantitative surrogate parameter for thromboembolic risk: determinants and relationship to spontaneous echocontrast and thrombus formation--a transesophageal echocardiographic study in 500 patients with cerebral ischemia.

BACKGROUND: Hemostasis in the left atrial (LA) appendage (LAA) is an important cause in the formation of thrombi. Determination of the LAA flow velocity (LAAV) could be a quantitative parameter for estimating thromboembolic risk. The objective of this study was to: (1) determine the relationship between LAAV and qualitative parameters with elevated thromboembolic risk (thrombus/spontaneous echocontrast [SEC]); and (2) define factors that influence LAAV. METHODS: In all, 500 patients with stroke were examined consecutively by transesophageal echocardiography. In addition to measurement of the LAAV, the atrial appendage was examined for the presence of thrombi or SEC. RESULTS: LAAV differed significantly among patients with sinus rhythm (71 +/- 16 cm/s), paroxysmal atrial fibrillation (AF) and in sinus rhythm during transesophageal echocardiography (46 +/- 13 cm/s), paroxysmal AF and AF during transesophageal echocardiography (32 +/- 12 cm/s), and chronic AF (27 +/- 9 cm/s, P < .001). Independent of the rhythm, the risk of thrombus/SEC increased significantly at an LAAV less than 55 cm/s. At an LAAV 55 cm/s or more there is only a minimal risk of thrombus/SEC (negative predictive value 100% and 99%, respectively). Multivariate analysis showed that LAAV is the strongest predictor for the occurrence of thrombus/SEC (P < .0001). Further multivariate analysis showed that left ventricular ejection fraction, LA size, (paroxysmal) AF, age, and sex are independent parameters influencing LAAV. CONCLUSION: Independent of the basic rhythm, there is a close relationship between LAAV and qualitative parameters of elevated thromboembolic risk. LAAV could, therefore, be a quantitative surrogate parameter for risk stratification. It is influenced by both cardiac and extracardiac factors.

Adult↗
PubMed2005

Delayed adaptation of ventricular repolarization after sudden changes in heart rate due to conversion of atrial fibrillation. A potential risk factor for proarrhythmia?

AIMS: Onset and termination of atrial fibrillation are often associated with abrupt changes in heart rate. Presence and time-course of delayed adaptation of the QT/QTc interval are unknown, but a temporary "mismatch" between rate and the QT interval may enhance the risk of proarrhythmia. METHODS: In a prospective two-part study, time-course of adaptation of ventricular repolarization after abrupt changes in heart rate was assessed during termination of Holter ECG-documented atrial fibrillation episodes (Group 1, 32 patients) and subsequently in 20 patients with sick sinus syndrome and cardiac pacing initiating abrupt bi-directional changes in paced heart rate (Group 2). RESULTS: Conversion of atrial fibrillation showed a 32+/-21 bpm fall in heart rate (P<0.05). Restoration of the QTc interval afterwards was delayed by < or =1 min in 27%, by 1-2 min in 21%, by 2-5 min in 11% and by >5 min in 41% of the cases. Atrial pacing simulating a 30 bpm fall/increase in atrial rate demonstrated that a subsequent transient rate-QT mismatch is a physiological phenomenon (fall of 100 to 70 bpm: initially 90% of the proper QTc interval, compared with 94% after conversion of atrial fibrillation). The restoration curve of QTc adaptation showed an initially fast and subsequently slower time component, with interindividual variation. Clinical parameters, baseline heart rate or the direction of rate changes were not predictive. CONCLUSION: Delayed adaptation of ventricular repolarization following atrial fibrillation onset and termination is common, requiring minutes for restoring the QT/QTc steady state. Clinical parameters fail to predict patients with a long-lasting rate-QT mismatch. It may carry a significant arrhythmogenic risk particularly in patients on QT altering medication.

Adaptation, Physiological↗
PubMed2004

Differential effects of MCP-1 and leptin on collateral flow and arteriogenesis.

OBJECTIVE: Strategies to therapeutically stimulate collateral artery growth in experimental models have been studied intensively in the last decades. However, the experimental methods to detect collateral artery growth are discussed controversially and vary significantly. We compared different methods in a model of arteriogenesis in the rabbit hind limb and determined the effects on collateral flow of a known pro-arteriogenic factor, monocyte chemoattractant protein-1 (MCP-1), and a cytokine not previously evaluated for its arteriogenic efficacy, the adipocytokine leptin. METHODS AND RESULTS: Forty-two New Zealand White rabbits received either MCP-1, leptin or PBS after ligation of the right femoral artery. The pro-arteriogenic effect of MCP-1 was confirmed by flow measurements during reactive hyperemia, as demonstrated by increased flow ratio (PBS 0.56+/-0.07 vs. MCP-1 0.77+/-0.06, no unit, p<0.0001), ankle-brachial index and microsphere-based conductance measurements (PBS 50.8+/-2.1 vs. MCP-1 225.8+/-8.8 ml/min/100 mm Hg, p<0.001). Biological activity of leptin on rabbit monocytes was shown by a dose dependent increase in Mac-1 expression. In-vivo administration of leptin also led to an increase in hyperemic flow and flow ratio (leptin 0.69+/-0.03, p<0.05 vs. PBS), but not to an increase in collateral conductance (leptin 54.7+/-4.1 ml/min/100 mm Hg, p=ns vs. PBS) or proliferation of vascular smooth muscle cells (Ki-67 staining: PBS 24.7+/-3.9%, leptin 22.7%+/-0.8% (p=ns), MCP-1 32.0+/-1.9% (p<0.01)). Ki-67 mRNA measured by real-time polymerase chain reaction increased (8.8+/-3.1-fold, p<0.01) during natural arteriogenesis, and was further enhanced (25.5+/-8.1-fold, p<0.005) after stimulation with MCP-1. CONCLUSION: MCP-1 and leptin increase collateral flow in the rabbit hind limb model. In contrast to MCP-1, leptin does not enhance direct markers of vascular proliferation such as collateral conductance under maximal vasodilation and proliferation indices. The observed increase in hyperemic collateral flow thus most probably can be attributed to the well-documented vasodilatory effects of leptin. These data stress the necessity of the use of proliferation markers and microsphere-based conductance measurements under maximal vasodilation in order to separate effects of substances on vascular proliferation from effects on vasodilation.

Animals↗
PubMed2004

LE-PAS, a novel Arnt-dependent HLH-PAS protein, is expressed in limbic tissues and transactivates the CNS midline enhancer element.

A growing family of helix-loop-helix PAS (HLH-PAS) transcription factors has emerged recently. These proteins form heterodimers and are involved in adaptation to environmental or physiologic stresses as well as in embryonic development. We describe the cloning and characterization of a novel HLH-PAS protein termed LE-PAS (limbic-enriched PAS) in mouse. LE-PAS consists of 802 amino acids and has a predicted molecular mass of 87.4 kDa. In adult mice, it is expressed exclusively in brain. Northern blot and in situ hybridization analysis indicate that LE-PAS is expressed in the limbic system and olfactory bulb. By in vitro overexpression in COS-7, cells we found that LE-PAS is a nuclear protein. Reporter gene analysis indicated that LE-PAS transactivates the CNS midline enhancer (CME) motif but not the xenobiotic response element in an Arnt-dependent fashion and without prior activation of LE-PAS protein. Our observation suggests that LE-PAS shares a similar mode of function with HLH-PAS proteins such as single minded or trachealess indicating that LE-PAS also has constitutive or developmental functions which may be critical for regulating the transcriptional control of limbic patterning and function.

Amino Acid Sequence↗
PubMed2004

Single-chain antibodies for the conformation-specific blockade of activated platelet integrin alphaIIbbeta3 designed by subtractive selection from naive human phage libraries.

Binding of fibrinogen to platelet integrin alphaIIbbeta3 mediates platelet aggregation, and thus inhibition of alphaIIbbeta3 represents a powerful therapeutic strategy in cardiovascular medicine. However, the currently used inhibitors of alphaIIbbeta3 demonstrate several adverse effects like thrombocytopenia and bleeding, which are associated with their property to bind to non-activated alphaIIbbeta3. To circumvent these problems, we designed blocking single-chain antibody-fragments (scFv) that bind to alphaIIbbeta3 exclusively in its activated conformation. Two naive phage libraries were created: a natural phage library, based on human lymphocyte cDNA, and a synthetic library, with randomized VHCDR3. We performed serial rounds of subtractive panning with depletion on non-activated and selection on activated alphaIIbbeta3, which were provided on resting and ADP-stimulated platelets and CHO cells, expressing wild-type or mutated and thereby activated alphaIIbbeta3. In contrast to isolated, immobilized targets, as generally used for phage display, this unique cell-based approach for panning allowed the preservation of functional integrin conformation. Thereby, we obtained several scFv-clones that demonstrated exclusive binding to activated platelets and complete inhibition of fibrinogen binding and platelet aggregation. Interestingly, all activation-specific clones contained an RXD pattern in the HCDR3. Binding studies on transiently expressed point mutants and mouse-human domain-switch mutants of alphaIIbbeta3 indicate a binding site similar to fibrinogen. In conclusion, we generated human activation-specific scFvs against alphaIIbbeta3, which bind selectively to activated alphaIIbbeta3 and thereby potently inhibit fibrinogen binding to alphaIIbbeta3 and platelet aggregation.

Animals↗
PubMed2004

Human hibernating myocardium is jeopardized by apoptotic and autophagic cell death.

OBJECTIVES: The aim of the present study was to objectify the loss of myocytes and the mechanism by which myocytes die in human hibernating myocardium (HHM). BACKGROUND: Intracellular degeneration, reduced cellular protein synthesis, and the replacement fibrosis contribute to structural disintegration of HHM. METHODS: In 14 patients, HHM was diagnosed by dobutamine echocardiography, radionuclide ventriculography, and thallium-201 scintigraphy. Functional recovery was documented by repeating the preoperative clinical investigations three months after successful coronary artery bypass graft surgery (CABG). During CABG, transmural biopsies were taken from the center of HHM regions and studied by electron microscopy, immunohistochemistry, the terminal deoxynucleotidyl transferase-mediated nick end-labeling (TUNEL) method, reverse transcription-polymerase chain reaction, and Western blotting. Control samples were taken from nondiseased human myocardium. RESULTS: All patients showed significant improvement or normalization of the regional function of HHM. Ubiquitin-related autophagic cell death was evident ultrastructurally by the occurrence of autophagic vacuoles, cellular degeneration, and nuclear disassembly. Ubiquitin-protein complexes were found in 0.03 +/- 0.008% (control: 0%, p < 0.005) of all myocytes. The proteasome 20S subunit/total myocytes were reduced from 63.3 +/- 9.6% in control myocardium to 36.9 +/- 8.4% in HHM. Complement-9, indicating oncosis, was found in only one of 14 biopsies. TUNEL-positive myocytes were 0.002 +/- 0.0003%. Electron microscopy showed apoptotic cells in 3 of 14 samples. However, the bcl-2/bax ratio was significantly reduced. Moreover, caspase-3 messenger ribonucleic acid was 8.5 times upregulated, and caspase-3 was activated. Cell death was absent in controls. CONCLUSIONS: In HHM, ubiquitin-related autophagic cell death and apoptosis cause a loss of myocytes. This plays an important role in progressive tissue damage and causes a reduction of the extent of functional recovery of HHM.

Aged↗
PubMed2004

Reoxygenation of hypoxic coronary smooth muscle cells amplifies growth-retarding effects of ionizing irradiation.

BACKGROUND: Hypoxic human coronary smooth muscle cells (HCSMCs) are possible targets for brachytherapy to prevent restenosis after percutaneous transluminal coronary angiography. It is unclear whether growth kinetics and gene expression of these cells undergoing gamma-irradiation are changed by reoxygenation. METHODS AND RESULTS: Hypoxic (H) and hypoxia-reoxygenated (H-R) HCSMCs were irradiated with gamma-radiation at single doses of 4, 8, and 16 Gy using a 60Co-source. Vascular endothelial growth factor gene expression of HCSMCs was dramatically suppressed in H-R versus H cells independent of the radiation dose (15+/-7% versus 2183+/-2023%, P<0.01, H-R versus H cells). An oxygen enhancement ratio of 1.8 was calculated after irradiation from the retarded growth of H-R versus hypoxic HCSMCs. Production of reactive oxygen species by HCSMCs after irradiation increased by 15+/-2% in H-R cells versus 7+/-1% in H cells (P<0.05). CONCLUSIONS: Reoxygenation of hypoxic HCSMCs markedly amplifies growth-retarding effects of ionizing irradiation. On the basis of these findings, oxygenating radiosensitizers should be analyzed with regard to suitability for coronary brachytherapy to prevent restenosis.

Brachytherapy↗
PubMed2004

Drug-eluting stents for in-stent restenosis and acute myocardial infarction: present data from nonrandomized studies.

In-stent restenosis (ISR) remains the "Achilles' heel" of percutaneous stent angioplasty treatment of patients with atherosclerotic disease of the coronary arteries. Recently, drug-eluting stents (DES) have ushered in a revolution in the treatment of these patients, yet, to date, their efficacy and safety have been demonstrated primarily for native de novo coronary lesions. For ISR, intracoronary brachytherapy using beta- or gamma-radiation is considered the standard of care. Nevertheless, DES are used for ISR lesions in clinical practice. This review outlines the few results currently available from small observational studies and larger registries. The designs of two ongoing randomized trials evaluating the sirolimus-eluting and the paclitaxel-eluting stent versus brachytherapy in patients with ISR lesions are also presented. Patients with acute myocardial infarction (AMI) have mostly been investigated in the context of small, uncontrolled studies and registries. The incomplete evidence to date is that implantation of sirolimus-eluting stents in patients with AMI is safe and effective.

Administration, Topical↗
PubMed2004

Long-term survival after pacemaker implantation. Prognostic importance of gender and baseline patient characteristics.

Permanent cardiac pacing is the treatment of choice in severe and symptomatic bradycardia. To determine factors associated with longer survival we analysed the survival times and baseline characteristics of 6505 patients after pacemaker implantation. This longitudinal study with 30 years of follow-up was performed in a single centre university hospital with all-cause mortality as the end-point. In 6505 patients we analysed a total of 30948 years of patient follow-up, median survival was 101.9 months ( approximately 8.5 years), with 44.8% of patients alive after 10 years and 21.4% alive after 20 years. In all subgroups women had a significantly longer survival than men (118 vs 91.7 months, P<0.0001), despite a markedly higher age at implantation (73.2 years vs 71 years, P<0.0001). Survival of patients with sick-sinus-syndrome was significantly better than in patients with high degree AV-block, which in turn, was better than survival of patients with atrial fibrillation (132.9 months vs 94.2 months vs 85.1 months, P<0.0001). Multivariate analysis revealed several independent factors: age, gender, decade of implantation, type of pacemaker, index arrhythmia and initial symptoms. Interestingly, if only the patients of the last decade were analysed multivariately, neither pacing mode nor index arrhythmia were independently associated with survival. In conclusion, survival of patients with pacemakers is independently influenced by several baseline characteristics which can identify patients with very long survival.

Aged↗