Antonios Kilias

Early but not late stent thrombosis is influenced by residual platelet aggregation in patients undergoing coronary interventions

AIMS Recent studies suggest a relevant association of post-interventional residual platelet aggregation (RPA) under therapy with oral platelet inhibitors and the occurrence of atherothrombotic events. The influence of post-interventional RPA on the incidence of stent thrombosis (ST) has not been sufficiently evaluated in consecutive unselected cohorts of percutaneous coronary intervention (PCI) patients. The aim of this observational study was to investigate the impact of RPA on the incidence of ST within 3 months in patients treated with dual antiplatelet therapy. METHODS AND RESULTS The study population included a consecutive cohort of 1019 patients treated with PCI [n = 741 bare-metal stent (BMS) and n = 278 drug-eluting stent (DES)] due to symptomatic coronary artery disease. Residual platelet activity was assessed by adenosine disphosphate (20 micromol/L)-induced PA after 600 mg clopidogrel loading dose. Maximum RPA was measured as peak of aggregation, final RPA was measured 5 min after addition of agonist. The primary endpoint was the occurrence of ST within 3 months defined according to academic research consortium (ARC) criteria. Final and maximum RPA were independent predictors of ST after 3 months. In secondary analysis, the observed effects were independently associated with early ST (HR 1.05, 95% CI 1.01-1.08 and HR 1.05, 95% CI 1.01-1.09, P < 0.01, respectively). However, incidence of 3-month late stent thrombosis (LAT) was not influenced by post-interventional RPA in multivariable analysis. CONCLUSION Post-interventional RPA is associated with the occurrence of early ST in patients treated with either BMS or DES; however, there is no predictive value of RPA for the incidence of 3-month LAT, suggesting the involvement of other possible mechanisms like discontinuation of antiplatelet therapy.

Plasma levels of stromal cell-derived factor-1 in patients with coronary artery disease: Effect of clinical presentation and cardiovascular risk factors

OBJECTIVE To investigate the possible association of plasma levels of stromal cell-derived factor-1 (SDF-1; CXCL12) with clinical presentation of symptomatic coronary artery disease (CAD) and with cardiovascular risk factors. METHODS A cath lab cohort of 492 consecutive patients with symptomatic CAD were recruited. Blood for plasma-SDF-1 determination was taken at the time of heart catheterization before percutaneous coronary intervention. RESULTS Plasma-SDF-1 was significantly decreased in ST-elevation myocardial infarction (STEMI) compared to stable angina pectoris (SAP) or to non-ST-elevation myocardial infarction (NSTEMI) (SAP vs. NSTEMI vs. STEMI: [pg/ml]: mean ± SD: 2110 ± 562 vs. 2127 ± 467 vs. 1834 ± 377; P < 0.001) independent of cardiovascular therapy. A weak correlation was observed between cholesterol levels and plasma SDF-1 in the whole study population. Left ventricular function and diabetes mellitus associated with plasma SDF-1 levels in patients with NSTEMI, while among STEMI patients, those with hyperlipidemia presented with even further decreased SDF-1 levels. CONCLUSION Plasma SDF-1 is significantly decreased in patients with STEMI, a fact which may reflect the importance of SDF-1 regulation in patients with acute myocardial infarction.

Expression of platelet‐bound stromal cell‐derived factor‐1 in patients with non‐valvular atrial fibrillation and ischemic heart disease

Summary.  Aims: Blood cell infiltration and inflammation are involved in atrial remodelling during atrial fibrillation (AF) although the exact mechanisms of inflammatory cell recruitment remain poorly understood. Platelet‐bound stromal cell‐derived factor‐1 (SDF‐1) is increased in cases of ischemic myocardium and regulates recruitment of CXCR4+ cells on the vascular wall. Whether platelet‐bound SDF‐1 expression is differentially influenced by non‐valvular paroxysmal or permanent atrial fibrillation (AF) in patients with stable angina pectoris (SAP) or acute coronary syndrome (ACS) has not been reported so far. Methods and results: A total of 1291 consecutive patients with coronary artery disease (CAD) undergoing coronary angiography were recruited. Among the patients with SAP, platelet‐bound‐SDF‐1 is increased in patients with paroxysmal AF compared with SR or to persistent/permanent AF (P < 0.05 for both). Platelet‐bound SDF‐1 correlated with plasma SDF‐1 (r = 0.488, P = 0.013) in patients with AF and ACS, which was more pronounced among patients with persistent AF (r = 0.842, P = 0.009). Plasma SDF‐1 was increased in persistent/permanent AF compared with SR. Patients with ACS presented with enhanced platelet‐bound‐SDF‐1 compared with SAP. Interestingly, among patients with ACS, patients with paroxysmal or persistent/permanent AF presented with an impaired platelet‐bound SDF‐1 expression compared with patients with SR. Conclusions: Differential expression of platelet‐bound and plasma SDF‐1 was observed in patients with AF compared with SR which may be involved in progenitor cell mobilization and inflammatory cell recruitment in patients with AF and ischemic heart disease. Further in vivo studies are required to elucidate the role of SDF‐1 in atrial remodeling and the atrial fibrillation course.

A patient with a rare cause of elevated troponin I.

A 46-year-old male patient was admitted to our emergency room due to instable angina pectoris and progressive dyspnea. Relevant stenosis of coronary arteries was excluded by coronary angiography. MRI revealed septal linear late enhancement. Interestingly, the incidental finding of an abnormal ‘‘black’’ liver on cardiac MRI indicated an iron overload. Myocardial biopsy confirmed a significant myocardial iron deposition. Elevated serum transferrinsaturation index confirmed the diagnosis of an iron overload. Finally, genetic testing confirmed a homozygous C282Y mutation. Acute decompensated heart failure with troponin elevation is a rare first clinical presentation of hereditary hemochromatosis (HH). With the use of advanced diagnostic modalities (MRI, biopsy) and genetic testing, we confirmed our diagnosis. A 46-year-old male patient was admitted to our emergency room due to instable angina pectoris and progressive dyspnea (NYHA III). The patient was completely healthy until a week earlier, when he had an upper respiratory tract infection. The patient had no cardiovascular risk factors or other diseases up to unclear arthralgias. There was no family history of cardiac or hematological disease. The physical examination on admission revealed diminished breath sounds, expiratory crackles at both lung bases, and slight peripheral edema. A 12-lead electrocardiogram (ECG) showed T wave inversion in leads I, aVL, II, III, aVF and V3–V6 (Fig. 1a, b). Chest X-ray and additional computed tomography (CT) revealed a cardiomegaly, minimal pleural effusions, and pneumonia on both sides superimposed on pulmonary edema (Fig. 1c). A pulmonary artery embolism was excluded. Results of laboratory tests indicated elevated serum troponin I levels (0.05 lg/dl) and transaminases (GOT: 63 U/l, GPT: 61 U/l). Creatinine clearance and creatine kinase levels were within the normal range. Echocardiographic examination revealed a marginal dilatation of the left ventricle with a systolic dysfunction (ejection fraction about 40 % with global hypokinesia). A relevant valvular heart disease could be excluded. Due to elevated troponin levels, pathological ECG and systolic dysfunction, a coronary angiography, was performed [1–3]. Coronary angiography excluded the presence of relevant stenoses in the coronary arteries. Laevocardiography confirmed moderate global hypokinesia without significant mitral regurgitation. In order to clarify the cause of the underlying cardiomyopathy, a cardiac magnetic resonance imaging (MRI) was performed. Cardiac MRI revealed a septal linear late enhancement consistent with potential myocarditis or dilatative cardiomyopathy. Interestingly, the incidental finding of an abnormal ‘‘black’’ liver on MRI indicated a possible iron or copper overload (Fig. 1d, e). To finally clarify the underlying myocardial disease, a right ventricular endomyocardial biopsy was performed at the interventricular septum. Whereas no signs of myocarditis or dilatative cardiomyopathy could be detected, Prussian Blue staining of & Peter Seizer Peter.Seizer@med.uni-tuebingen.de

TCT-454 Does metallic stent design influence acute and longterm clinical outcome in second generation Everolimus-Eluting stents? Results of a single-center, 2-phase all-comer stent registry

TCT-454 Does metallic stent design influence acute and longterm clinical outcome in second generation Everolimus-Eluting stents? Results of a single-center, 2-phase all-comer stent registry Suzanne Fateh-Moghadam, Tobias Schlegel, martin Steeg, antonios Kilias, Wolfgang Bocksch University Tuebingen/Cardiology, Tuebingen, Germany; Medizinische Klinik III, Universtaet Tuebingen; Cardiovascular Disease and Medical Intensive Care Unit, Karl-Olga-Krankenhaus, Affiliated Hospital University of Ulm; Medizinische Klinik III/ Kardiologie und Kreislauferkrankungen, Universitätsklinikum Tübingen; Tubingen University Hospital, Stuttgart, Germany