Günter Christ

Medical University of Vienna, Wien, Vienna, Austria

Are you Günter Christ?

Claim your profile

Publications (87)394.76 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Systems of care to treat acute ST-elevation myocardial infarction (STEMI) have been developed world wide in the past decade. Their effectiveness can only be proven by including and analyzing outcome data of consecutive patients in registries, which is not the case in the majority of STEMI networks. This study investigates 1-year mortality in STEMI patients in Vienna included over a 14 months time interval. The Vienna STEMI network is organized by a specific rotational system and offers both, primary percutaneous intervention (PPCI) and thrombolytic therapy (TT) as reperfusion strategies according to the recent guidelines. At the time of investigation, the Vienna STEMI network consisted of the Viennese Ambulance Systems and five high-volume interventional cardiology departments. This network has been organized in order to increase the number of STEMI patients admitted for PPCI and to offer the fastest available reperfusion strategy, in the majority PPCI but in selected patients also TT (STEMI of short duration, mainly anterior wall MI and mainly patients younger than 75 years), followed by rescue PCI in non-responders and elective angiography with/without PCI in responders to TT during the index hospital stay. One-year all-cause mortality rates in the Vienna STEMI network by use of the fastest available reperfusion strategy were 13.4 % in patients who received reperfusion therapy after 2 h of symptom onset and 7.4 % in patients treated within 2 h; (p = 0.017). Whereas PPCI and TT demonstrated a nonsignificant difference in 1-year mortality rates when initiated within 2 h of symptom onset (10.0 % vs 5.7 %; p = 0.59), PPCI was more effective in acute STEMI of > 2 h duration as compared to TT but this difference did not reach statistical significance (12.1 % vs 18.2 %; p = 0.07). The reassuring long-term results of the Viennese STEMI network are another example of a specific regional system of care to offer timely diagnosis, transfer and reperfusion in patients with STEMI. In contrast to other metropolitan areas where TT has almost completely abandoned, we still use pharmacological reperfusion as a backup in case of expected and unacceptable time delays for PPCI in order to reduce myocardial damage especially in patients with larger infarctions of short duration with a low risk of bleeding complications.
    No preview · Article · Jul 2015 · Wiener klinische Wochenschrift

  • No preview · Article · May 2015 · Wiener klinische Wochenschrift

  • No preview · Article · May 2015 · Wiener klinische Wochenschrift

  • No preview · Article · May 2015 · Wiener klinische Wochenschrift
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective To evaluate the clinical utility of individualising dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) in an all-comers population, including ST-elevation myocardial infarction (STEMI) patients. Setting Tertiary care single centre registry. Participants 1008 consecutive PCI patients with stent implantation, without exclusion criteria. Intervention Peri-interventional individualisation of DAPT, guided by multiple electrode aggregometry (MEA), to overcome high on-treatment platelet reactivity (HPR) to ADP-induced (≥50 U) and arachidonic acid (AA)-induced aggregation (>35 U). Outcome measures The primary efficacy end point was definite stent thrombosis (ST) at 30 days. The primary safety end point was thrombolysis in myocardial infarction (TIMI) major and minor bleeding. Secondary end points were probable ST, myocardial infarction, cardiovascular death and the combined end point: major cardiac adverse event (MACE). Results 53% of patients presented with acute coronary syndrome (9% STEMI, 44% non-ST-elevation). HPR to ADP after 600 mg clopidogrel loading occurred in 30% of patients (73±19 U vs 28±11 U; p<0.001) and was treated by prasugrel or ticagrelor (73%), or clopidogrel (27%) reloading (22±12 U; p<0.001). HPR to ADP after prasugrel loading occurred in 2% of patients (82±26 U vs 19±10 U; p<0.001) and was treated with ticagrelor (34±15 U; p=0.02). HPR to AA occurred in 9% of patients with a significant higher proportion in patients with HPR to ADP (22% vs 4%, p<0.001) and was treated with aspirin reloading. Definite ST occurred in 0.09% of patients (n=1); probable ST, myocardial infarction, cardiovascular death and MACE occurred in 0.19% (n=2), 0.09% (n=1) and 1.8% (n=18) of patients. TIMI major and minor bleeding did not differ between patients without HPR and individualised patients (2.6% for both). Conclusions Individualisation of DAPT with MEA minimises early thrombotic events in an all-comers PCI population to an unreported degree without increasing bleeding. A randomised multicentre trial utilising MEA seems warranted. Trial registration number http://www.clinicaltrials.gov; NCT01515345.
    Full-text · Article · Oct 2014 · BMJ Open
  • [Show abstract] [Hide abstract]
    ABSTRACT: This was a prospective study comparing two groups: personalized and non-personalized treatment with P2Y12 receptor blockers during a 12-month follow-up. We aimed to investigate whether personalized antiplatelet treatment in patients with high on treatment platelet reactivity (HTPR) improves clinical outcome. Platelet reactivity was assessed by adenosine diphosphate induced aggregation using a multiple electrode aggregometry (MEA) in 798 patients with coronary artery disease undergoing percutaneous coronary intervention (PCI). Patients with HTPR received up to four repeated loading doses of clopidogrel or prasugrel in the personalized treatment group (n=403), while no change in the treatment strategy was undertaken in patients with HTPR in the non-personalized treatment group (n=395). There were fewer major adverse cardiac events (MACE) in the personalized treatment group than in the non- personalized treatment group (7.4% vs. 15.3%; respectively; p<0.001). The multivariate Cox regression analysis showed that the relative risk to develop MACE was 51% lower in the personalized treatment group as compared to the non-personalized treatment group (HR=0.49; 95%CI: 0.31-0.77; p<0.001). Similarly, there was a clear net benefit of the personalized antiplatelet treatment over the non-personalized treatment (ischemic and bleedings events: 8.2% vs. 18.7%; respectively; HR=0.46; 95%CI: 0.29-0.70; p<0.001). Further analysis indicated that patients with aggregation values within the therapeutic window (21-49U) experienced the lowest event rates (stent thrombosis and major bleeding: 2.5%) as compared to poor responders (>50U: 5.4%) or ultra-responders (0-20U: 5.2%). In conclusion, personalized antiplatelet treatment improved patients outcome without increasing bleeding complications compared to the non-personalized treatment during a 12-month follow-up.
    No preview · Article · Aug 2014 · Clinical Science

  • No preview · Article · Feb 2014 · JACC Cardiovascular Interventions
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Drug-eluting stents (DES) reduce late lumen loss compared to bare metal stents but were not able to eradicate in-stent restenosis (ISR) fully. Vascular endothelial growth factor (VEGF) may inhibit late lumen loss through accelerated reendothelialisation, but may also promote neointima formation by proinflammatory effects. The aim of this study was to evaluate whether endogenous plasma levels of VEGF are associated with development of ISR after implantation of DES. Methods and results: We studied 85 patients who were treated with 159 DES. VEGF plasma levels were determined before and 24 hours after PCI. During the eight-month follow-up period, two patients (2.4%) died of cardiovascular causes and 12 patients (14.5% of patients, 7.6% of stents) developed angiographic ISR. Basal VEGF plasma levels were not different in patients with and without ISR at follow-up. In contrast to patients without ISR, VEGF increased significantly upon PCI in patients with ISR (p<0.005). Patients with a decrease of VEGF after PCI had a restenosis rate of 2.4% compared to a restenosis rate of 26.2% in patients with an increase of VEGF after the procedure (p<0.05). This was independent from clinical and angiographic risk factors. Conclusions: Basal plasma levels of VEGF are not associated with the development of ISR. However, an increase of VEGF after PCI is associated with a dramatically increased ISR rate after implantation of DES.
    Full-text · Article · Oct 2013 · EuroIntervention: journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Current guidelines still recommend the bolus and infusion administration of glycoprotein IIbIIIa inhibitors in patients with high-risk acute coronary syndrome undergoing percutaneous coronary intervention. We sought to evaluate the extent of platelet inhibition by a blocking and bridging strategy with intracoronary abciximab bolus-only administration and oral loading of adenosine diphosphate receptor antagonists. Fifty-six consecutive high-risk acute coronary syndrome patients with bolus-only abciximab administration (0.25mg/kg i.c.) and loading with 600mg clopidogrel (55%) or 60mg prasugrel (45%) were included in this study. Platelet aggregation induced by thrombin receptor-activating peptide and adenosine diphosphate was measured by multiple electrode aggregometry up to 7days. Thrombin receptor-activating peptide induced platelet aggregation was significantly suppressed for a minimum of 48h (45±17U) and returned to a normal range (>84U) after 6days (90±26U; p<0.001). Co-medication with prasugrel significantly reduced adenosine diphosphate-induced (p=0.002) and thrombin receptor-activating peptide-induced (p=0.02) platelet aggregation compared with clopidogrel throughout the observation period. No stent thrombosis or repeat myocardial infarction occurred at 30-day follow-up. Immediate blocking of platelet aggregation in high-risk acute coronary syndrome patients by intracoronary abciximab bolus-only administration and bridging to prolonged inhibition via oral blockade of ADP receptors effectively inhibited overall platelet reactivity for at least 48h, questioning the value of continuous abciximab infusion. Co-medication with prasugrel vs. clopidogrel synergistically augmented platelet inhibition.
    Full-text · Article · Jun 2013 · Thrombosis Research
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We present the case of a 51-year-old male patient who received adjuvant chemotherapy consisting of oxaliplatin, bolus and continuous 5-fluorouracil (5-FU) and leucovorin after anterior resection because of locally advanced rectal cancer. Preoperative chemotherapy with capecitabine (an oral 5-FU prodrug) had been well tolerated. Two days after initiation of the first course of chemotherapy, the patient reported typical chest pain. The ECG showed ST elevations and prominent T waves in almost all leads. Due to suspicion of a high-risk acute coronary syndrome, an urgent cardiac catheterization was performed. It showed a generally reduced coronary flow with multiple significant stenoses (including the ostia of the left and right coronary artery), as well as a highly reduced left ventricular function with diffuse hypokinesia. Due to the meanwhile completely stable situation of the patient after medical acute coronary syndrome treatment, no ad hoc intervention was performed to allow further discussion of the optimal management. Thereafter, the patient remained clinically asymptomatic, without any rise in cardiac necrosis parameters; only NT-pro-BNP was significantly elevated. A control cardiac catheterization 2 days later revealed a restored normal coronary artery flow with only coronary calcifications without significant stenoses, as well as a normal left ventricular ejection fraction. Cardiovascular symptoms occurred on the second day of continuous 5-FU treatment. As cardiotoxic effects seem to appear more frequently under continuous application of 5-FU, compared to the earlier established 5-FU bolus regimens, treating medical oncologists should pay special attention to occurring cardiac symptoms and immediately interrupt 5-FU chemotherapy and start a cardiologic work-up.
    Full-text · Article · Jun 2012 · Case Reports in Oncology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background and objectives: Clopidogrel non-responsiveness is associated with adverse clinical outcome. We aimed to investigate whether individualized antiplatelet treatment in clopidogrel non-responders is an effective and safe strategy. Methods: This was a prospective non-randomized non-blinded study comparing two cohorts (guided and non-guided treatment) with a follow-up of 1-month. Responsiveness to clopidogrel was assessed by multiple electrode aggregometry (MEA) in 798 patients with coronary artery disease undergoing percutaneous coronary intervention (PCI). In the guided group (n=403) clopidogrel non-responders received repeated loading doses of clopidogrel or prasugrel, in the non-guided group (n=395) clopidogrel non-responders did not undergo any change in treatment. Results: Stent thrombosis occurred significantly less often in the guided group than in the non-guided group (0.2% vs. 1.9%; p=0.027). The multivariate Cox regression analysis showed that patients in the non-guided group were at a 7.9-fold higher risk to develop stent thrombosis compared to the guided group (OR: 7.9; 95% CI: 1.08-69.2; p=0.048). In line with this, acute coronary syndrome occurred significantly less often in the guided group than in the non-guided group (0% vs. 2.5%; p=0.001) whereas there was no difference in the event rates of cardiac death (2% vs. 1.3%; p=0.422) or major bleedings (1% vs. 0.3%; p=0.186). Conclusion: Personalized antiplatelet treatment according to the platelet function testing with MEA resulted in an improved efficacy with an equal safety compared to the standard treatment.
    Full-text · Article · May 2012 · International journal of cardiology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND: High platelet reactivity (HPR) under treatment with clopidogrel or aspirin is associated with adverse outcome. We aimed to investigate whether high platelet reactivity (HPR) to both aspirin and clopidogrel is a stronger predictor of adverse events compared to isolated HPR to clopidogrel or aspirin. METHODS: In this prospective cohort study platelet reactivity to adenosine diphosphate (ADP) and arachidonic acid (AA) was assessed by Multiple Electrode Aggregometry (MEA) in 403 patients undergoing percutaneous coronary intervention. The rates of the composite of cardiac adverse events (acute coronary syndrome, stent thrombosis, stroke, death and revascularization) were recorded during 12-month follow-up. RESULTS: The composite endpoint of cardiovascular adverse events occurred more often in patients with high platelet reactivity (HPR) to both agonists ADP and AA (37.5%) than in those with isolated HPR to ADP (33.3%), AA (25.6%) or without any HPR (18.6%; p=0.003). Classification tree analysis indicated that any HPR emerged as an independent predictor influencing outcome, which was associated with a 1.75 higher risk of cardiac adverse events (OR=1.75: 95%CI=1.1-2.9). Interestingly, the predictive value of HPR tended to be greater among patients with diabetes mellitus (OR=2.18; 95%CI=1.20-3.95). C-reactive protein and diabetes mellitus were independent predictors of high platelet reactivity to both agonists. CONCLUSIONS: Dual low responsiveness to clopidogrel and aspirin is a strong predictor of cardiac adverse events, especially in patients with diabetes mellitus, which underlines the need for personalized antiplatelet treatment.
    Full-text · Article · Feb 2012 · International journal of cardiology
  • [Show abstract] [Hide abstract]
    ABSTRACT: The objective of this study was to evaluate improvement opportunities in the emergency department for timely ST-segment elevation myocardial infarction management and evaluated the new process flow. In a prospective study, we compared time from door to cath laboratory before and after implementation of a new ST-segment elevation myocardial infarction (STEMI) protocol. The new protocol included a blend of strategies to reduce door to cath laboratory time. We included 55 patients. After implementing a new STEMI protocol, we included 54 patients. Time to cath laboratory was 21 (interquartile range, 9-40) minutes before and 10 (interquartile range 5-25) minutes after initiation of the new protocol (P = .02). A door to cath laboratory time less than 15 minutes was reached in 36% of our patients in phase 1 and in 61% in phase 2 (odds ratio; 0.36, 95% confidence interval, 0.16-0.81; P = .01). Simple changes in organizational strategies resulted in a significantly faster care for patients with acute uncomplicated STEMI.
    No preview · Article · Jul 2011 · The American journal of emergency medicine

  • No preview · Article · Apr 2011 · Journal of the American College of Cardiology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Enhanced platelet inhibition by clopidogrel decreases the risk of ischemic events but carries a risk for a concomitant increase in bleeding. To compare the efficacy and safety of two clopidogrel loading regimens (300mg vs. 600mg) in patients undergoing percutaneous coronary intervention (PCI) at one month after start of therapy. A systematic literature search of MEDLINE, EMBASE, CENTRAL, and Web of Science databases using predefined search terms for relevant articles in any language. Randomised controlled trials and non-randomised studies reporting adjusted effect estimates were included. Summary estimates of the risks ratios (RRs) with therapy were calculated using a random-effect model. Outcomes evaluated were combined major adverse cardiovascular events (MACE) and major bleedings. Results Seven studies met the inclusion criteria and included 25,383 patients. A 600mg clopidogrel loading was associated with a 34% relative risk reduction of MACE (RR=0.66; 95% confidence intervals CI=0.52-0.84; p<0.001). Sub-analysis revealed a 47% risk reduction of MACE in randomised trials (RR=0.53; 95%CI=0.32-0.88; p=0.01) and a 31% relative risk reduction in non-randomised trials (RR=0.69; 95%CI=0.54-0.90; p=0.005) in patients receiving 600mg loading with clopidogrel. In patients suffering from acute coronary syndrome, 600mg clopidogrel loading was associated with a 24% relative risk reduction in MACE (RR=0.76; 95%CI=0.60-0.95; p=0.02). Importantly, the 600mg clopidogrel loading dose was not associated with an increased risk of major bleedings (RR=0.91; 95%CI=0.73-1.15; p=0.44). This meta-analysis demonstrates that intensified clopidogrel loading with 600mg reduces the rate of major cardiovascular events without increase in major bleeding compared to 300mg in patients undergoing PCI during one month follow-up.
    Full-text · Article · Jan 2011 · Heart (British Cardiac Society)
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: ST-elevation myocardial infarction (STEMI) results from acute thrombotic obstruction of a coronary artery. Percutaneous coronary intervention (PCI) is the treatment of choice to restore blood flow. The incidence of guidewire-induced reopening of the infarct-related coronary artery (IRA) and its association with post-procedural TIMI flow and long-term mortality were assessed. Angiograms of consecutive STEMI patients admitted to the catheter laboratory of the Medical University of Vienna between January 2003 and December 2005 were analysed. TIMI flow was graded prior to and after guidewire insertion into the distality of the IRA, and at the end of the procedure. Initial TIMI 0 flow was present in 476 (47.0%) of 1,012 cases. Target vessel reopening after guidewire insertion defined as any flow >TIMI 0 flow occurred in 150 patients (37.2%), and was associated with improved survival after a median of 914 (609-1,238) days (p=0.017). Reflow after guidewire insertion was an independent predictor of post-procedural TIMI flow (odds ratio=3.10, 95% confidence interval [CI]=1.64 - 5.86], p<0.001) and mortality (hazard ratio=0.51, CI=0.28 - 0.94], p=0.029). Target vessel reopening by guidewire insertion is a new predictor of prognosis. Target vessel flow after guidewire insertion should be assessed in a standardised fashion during PCI.
    Full-text · Article · Jan 2011 · Thrombosis and Haemostasis
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To investigate whether proton pump inhibitors (PPIs) negatively affect clinical outcome in patients treated with clopidogrel. Systematic review and meta-analysis. Outcomes evaluated were combined major adverse cardiac events (MACE), myocardial infarction (MI), stent thrombosis, death and gastrointestinal bleeding. Studies included were randomized trials or post-hoc analyzes of randomized trials and observational studies reporting adjusted effect estimates. Twenty five studies met the selection criteria and included 159 138 patients. Administration of PPIs together with clopidogrel corresponded to a 29% increased risk of combined major cardiovascular events [risk ratio (RR) = 1.29, 95% confidence intervals (CI) = 1.15-1.45] and a 31% increased risk of MI (RR = 1.31, 95%CI = 1.12-1.53). In contrast, PPI use did not negatively influence the mortality (RR = 1.04, 95%CI = 0.93-1.16), whereas the risk of developing a gastrointestinal bleed under PPI treatment decreased by 50% (RR = 0.50, 95% CI = 0.37-0.69). The presence of significant heterogeneity might indicate that the evidence is biased, confounded or inconsistent. The sensitivity analysis, however, yielded that the direction of the effect remained unchanged irrespective of the publication type, study quality, study size or risk of developing an event. Two studies indicate that PPIs have a negative effect irrespective of clopidogrel exposure. In conclusion, concomitant PPI use might be associated with an increased risk of cardiovascular events but does not influence the risk of death. Prospective randomized trials are required to investigate whether a cause-and-effect relationship truly exists and to explore whether different PPIs worsen clinical outcome in clopidogrel treated patients as the PPI-clopidogrel drug-drug interaction does not seem to be a class effect.
    Full-text · Article · Dec 2010 · Journal of Thrombosis and Haemostasis
  • Source

    Preview · Article · Mar 2010 · Journal of the American College of Cardiology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Our aim was to test whether serum levels of matrix metalloproteinase (MMP)-2 and -9 are associated with the development of in-stent restenosis (ISR) after implantation of drug-eluting stents (DES). With the introduction of DES coronary ISR could be reduced dramatically. However, it still plays a significant role, particularly after treatment of multiple, complex lesions. We studied 85 patients who were treated with 159 DES. Blood samples for measurement of MMP-2 and -9 antigen and activity were taken directly before and 24 h after percutaneous coronary intervention (PCI). Restenosis was evaluated at 6 to 8 months by coronary angiography. During the follow-up period, 2 patients (2.4%) died of cardiovascular causes, and 12 patients developed angiographic ISR. Patients with ISR showed significantly higher serum activity of MMP-9 at baseline (p = 0.017) and of MMP-2 (p < 0.0001) and MMP-9 (p < 0.0001) after the procedure. The PCI increased serum activity of MMP-2 (p = 0.005) and MMP-9 (p = 0.008) only in patients with ISR. The restenosis rates of patients in the highest quartile of MMP-2 after and MMP-9 before and after PCI were 40.0%, 38.9%, and 42.9% compared with 6.3%, 7.7%, and 4.0% in the lower quartiles, respectively. This was independent of clinical and procedural characteristics. Elevated serum activities of MMP-2 and -9 are associated with dramatically increased restenosis rates after PCI with implantation of DES. Determination of MMP levels might be useful for identification of patients who are at high risk for ISR despite implantation of DES.
    Full-text · Article · Jan 2010 · JACC. Cardiovascular Interventions
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The prognostic value of the vasodilator-stimulated phosphoprotein (VASP) phosphorylation assay and multiple electrode aggregometry (MEA) for thrombotic adverse events has been shown in independent studies. As no direct comparison between the two methods has been made so far, we investigated which laboratory approach has a better predictive value for stent thrombosis. The VASP phosphorylation assay and MEA were performed in 416 patients with coronary artery disease undergoing percutaneous coronary intervention. The rate of stent thrombosis was recorded during a 6-month follow-up. Definite stent thrombosis occurred in three patients (0.7%) and probable stent thrombosis in four (1%). Receiver operating characteristic (ROC) analysis demonstrated that MEA distinguishes between patients with or without subsequent stent thrombosis better than the VASP phosphorylation assay: the area under the ROC curve was higher for MEA (0.92; P=0.012) than for the VASP phosphorylation assay (0.60; P=0.55). At equal levels of sensitivity (100%), the specificity was greater for MEA than for the VASP phosphorylation assay (86% vs. 37%). Stent thrombosis occurred in 9% of patients with platelet hyperreactivity in MEA, who were simultaneously clopidogrel non-responders in the VASP phosphorylation assay. Interestingly, clopidogrel non-responders in the VASP phosphorylation assay without platelet hyperreactivity in MEA did not suffer from stent thrombosis. Platelet hyperreactivity in MEA might be a better risk predictor for stent thrombosis than the assessment of the specific clopidogrel effect with the VASP phosphorylation assay.
    Full-text · Article · Nov 2009 · Journal of Thrombosis and Haemostasis

Publication Stats

3k Citations
394.76 Total Impact Points

Institutions

  • 2003-2011
    • Medical University of Vienna
      • • Department of Emergency Medicine
      • • Department of Vascular Biology and Thrombosis Research
      • • Department of Clinical Pharmacology
      Wien, Vienna, Austria
  • 1987-2003
    • University of Vienna
      • • Department of Internal Medicine III
      • • Laboratory for Clinical Experimental Physiology
      Wien, Vienna, Austria
  • 2001
    • Vienna General Hospital
      Wien, Vienna, Austria