CARDIOLOGY 2001; October 18-20, 2001; Hofburg, Vienna ... · T. Binder, G. Maurer, P. Probst Department of Cardiology, University of Vienna, Austria Background: Transcatheter atrial

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CARDIOLOGY 2001; October

18-20, 2001; Hofburg, Vienna

Austria

CARDIOLOGY 2001; October 18-20, 2001;

Hofburg, Vienna, Austria; Jointly organized

by: Division of Cardiovascular Diseases, Mayo

Clinic; Division of Cardiology, University of

Vienna

Journal für Kardiologie - Austrian Journal

of Cardiology 2001; 8 (Supplementum E)

Amyloidosein der

KardiologieAktuelle Fallberichte finden Sie unter diesem Link:

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3J KARDIOL SUPPL E/2001

CARDIOLOGY 2001ABSTRACTS

ENDOTHELIN-1 IS INVOLVED IN CORONARYNO-REFLOW

Ch. Adlbrecht, D. Bonderman,J. Jakowitsch, M. Gyöngyösi, W. Sperker,P. Probst, G. Maurer, H. D. Glogar,I. M. LangDepartment of Cardiology, University ofVienna, Austria

Background: No-reflow (NR) is a multi-factorial condition comprising an acutereduction in coronary flow (TIMI grade0–1) in the absence of epicardial vesselobstruction. Previous data have demon-strated that tissue factor that is shed fromthe atherosclerotic plaque, causes NR byinducing immediate and widespreadcoronary microvascular fibrin deposition.However, current concepts invoke vaso-constriction as an additional factor inNR. Therefore, we investigated the roleof endothelin (ET-1), a potent vasocon-strictor peptide that is present in athero-sclerotic lesions.

Methods and Results: Initial experimentsutilized homogenates from atherosclero-tic arteries and confirmed the presenceof ET-1 antigen at levels tenfold abovenormal plasma concentrations (0.4 ±0.07 fmol/ml). In the next step, right coro-nary arteries (RCAs) from 6 domestic pigswere selectively injected with 2 ml eachof homogenized atherosclerotic humanplaque material containing 6.9 ± 4 fmol/mlET-1 per g of tissue. In subsequent angio-grams, flow was compromised in 5 of 6animals. Fractional flow reserve droppedfrom 2.0 ± 1 to 0.8 ± 0.2 with a markeddecrease of baseline flow immediatelyafter the injection. To examine the role ofET-1 in human acute coronary NR, coro-nary blood was drawn from patients un-dergoing percutaneous interventions usingthe distal protection devices PercuSurgeGuardWire (n = 10), the Exciser CatheterSystem Thrombus Removal Device (n = 9)and Angioguard (n = 2). Fine particulatematerial that was recovered from each ofthose devices contained 0.13 ± 0.18 fmolET-1 antigen/40ml whole blood (PercuSurge), 0.11 ± 0.12 fmol ET-1 antigen/80mlwhole blood (Exciser), and 0.005 ± 0.02fmol ET-1 antigen/40000 ml (Angioguard).

Conclusions: The data suggest that ET-1is released into the coronary circulationfrom ruptured atherosclerotic plaque andcontributes to the no-reflow phenome-

non, possibly by inducing spasm in thedepending coronary microvasculature.

SYMPTOMATIC IMPROVEMENT AFTERTRANSCATHETER ATRIAL SEPTAL DEFECTCLOSURE IN ADULTS

H. Baumgartner, H. Gabriel, R. Rosenhek,T. Binder, G. Maurer, P. ProbstDepartment of Cardiology, University ofVienna, Austria

Background: Transcatheter atrial septaldefect (ASD) closure has been shown tobe feasible and safe. However, little isknown about the clinical outcome ofadult pts, particularly those of advancedage.

Methods: We performed transcatheterASD closure with the Amplatzer SeptalOccluder in 55 adults (mean age 47 ±17 years, 35 female) of whom 35 wereolder than 40 years (up to 82 yrs).Patients were followed for up to 2 years.

Results: ASD was successfully closed inall pts (device size 23 ± 6 mm, range10–34 mm). No major complicationsoccurred. Minor complications wereatrial fibrillation (2), transient AV-block(1) and transient ST-elevation (1). Atfollow-up, a mild residual left-to-rightshunt was found in 2 pts.

Prior to intervention, 24 pts were symp-tomatic of whom 19 were older than 40years. Most frequent symptoms werelimited exercise capacity and shortnessof breath (NYHA class 2–3 or 3 in 13 pts).At follow-up, all but one pt improved.This patient remained in NYHA class 3but had marked pulmonary hyperten-sion. All other patients were asymptoma-tic or had only mild shortness of breath.All of the 10 pts who were 65 yrs or olderand who were treated because of signifi-cant symptoms markedly improved.

Conclusion: Transcatheter atrial septaldefect closure can safely and success-fully be performed in adults. Sympto-matic improvement can generally be ex-pected even in patients of advanced age.

CAN TRANSOESOPHAGEAL ECHOCARDIO-GRAPHY ACCURATELY PREDICT THE IMPLANTSIZE FOR TRANSCATHETER ATRIAL SEPTALDEFECT CLOSURE?

H. Baumgartner, R. Rosenhek, H. Gabriel,T. Binder, G. Maurer, P. ProbstDepartment of Cardiology, University ofVienna, Austria

Background: Successful transcatheteratrial septal defect (ASD) closure requirescareful selection of the appropriatedevice size. Undersizing may result in aresidual shunt and even device emboli-zation. Balloon sizing is used to deter-mine the “stretched” defect diameter butit is time consuming. The purpose of thisstudy was to evaluate whether trans-oesophageal echo (TEE) can predict thestretched defect diameter and, therefore,the required device size.

Methods: Transcatheter ASD closure withthe Amplatzer ASD Occluder was per-formed in 55 adults (mean age 47 ± 17years, 35 female). The size of the devicewas determined by balloon sizing. Thestretched defect diameter was comparedwith the native diameter measured byTEE considering morphologic character-istics of the interatrial septum.

Results: The native defect diameter (TEE)was 15 ± 4 mm (6–22 mm). Thestretched diameter (balloon sizing) was23 ± 6 mm (10–34 mm). Thus, the sizeof the device exceeded the native defectdiameter by 65 ± 47 % (9 ± 5 mm) witha wide variation ranging from 6 to 200 %(1 to 16 mm). The relation between mor-phologic characteristics of the interatrialseptum (thickness, aneurysm, mobility,rim to the aorta) and the distensibility ofthe defect was studied. Although differen-ces between stretched and native diame-ters tended to be greater in pts with a thinand/or aneurysmatic interatrial septum,prediction of defect distensibility in indi-vidual pts was impossible. Even for thosepts in whom a high defect distensibilitywas expected from the morphologic ap-pearance of the interatrial septum, differen-ces between native and stretched diame-ters varied from 2 to 16 mm (10 to 200 %).

Conclusion: TEE is crucial for selectionof patients eligible for transcatheter ASDclosure and for the monitoring of the

CARDIOLOGY 2001,OCTOBER 18–20, VIENNA, AUSTRIA:ABSTRACTS

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procedure. However, the stretched defectdiameter and thus the size of the devicecannot be reliably predicted from theTEE determined native defect diametereven if the morphology of the residualinteratrial septum is considered.

INTRACORONARY THROMBECTOMY IN ACUTECORONARY SYNDROME WITH A NEWPERCUTANEOUS DEVICE:THE VIENNA X-SIZER STUDY

G. Beran1, I. M. Lang1, B. Syeda1,T. Stefenelli1, S. Denk1, A. Laggner2,H. D. Glogar1, P. Siostrzonek1

1Department of Cardiology, 2Departmentof Emergency Medicine, University ofVienna, Austria

Background: Thrombus formation follow-ing plaque rupture is responsible for acutevessel occlusion in acute myocardial in-farction (AMI) and contributes to compro-mised flow in unstable angina (UA). TheX-Sizer catheter is a new device for percu-taneous coronary thrombectomy. This pro-spective single-center controlled rando-mised study investigated the effects ofthe X-Sizer system with regard to epicar-dial flow and microcirculatory function inpts with acute coronary syndrome (ACS).

Methods: So far 44 patients (34 male;55.3 ± 9.6 yrs) with ACS (31 AMI, 13 UA)in native vessels were randomised totreatment with the X-Sizer followed byPTCA and/or stenting (n = 22) or to PTCAand/or stenting alone. Quantitative coro-nary angiographic (QCA) and Dopplerflow measurements, TIMI Frame Count,ST-segment score (= sum of ST-elevationin all 12 standard leads) and CK valueswere obtained. Major Adverse CardiacEvents (MACE) were determined after 30days.

Results: In all pts treated with X-Sizer thelesion could be successfully crossed. No

device related complications occurred.MACE after 30 days was observed in onept in the X-Sizer and in two pts in thecontrol group. Acute lumen gain, cor-rected TIMI Frame Count (cTFC), CKpeak and Coronary Flow Reserve (CFR)were not significantly different betweenthe two groups. However, ST-segmentscores immediately after, and 6 h postprocedure were significantly lower in theX-Sizer group (Table 1).

Conclusion: The initial results of thisongoing first randomised trial demon-strate safety and efficacy of the X-Sizercatheter for thrombus-removal in ACS. Asignificantly faster normalization of ST-segment elevation was observed in ptstreated with X-Sizer. This possiblyindicates improved myocardial salvageby additional use of the X-Sizer system.

EXPERIENCE WITH PROSTAGLANDIN E1BRIDGING TO HIGH DOSE BETA-BLOCKERTHERAPY IN ADVANCED HEART FAILUREPATIENTS – DIFFERENT OUTCOME INPATIENTS WITH AND WITHOUT CHRONICLOW DOSE BETA-BLOCKER PRETREATMENT

R. Berger, M. Hülsmann, A. Bojic,B. Stanek, R. PacherDepartment of Cardiology, Universityof Vienna, Austria

Background: PGE1 improves clinicalsymptoms, neurohumoral status andhaemodynamics and reduces the risk ofheart failure (HF) worsening. Thus it isused to initiate or increase �-blockertherapy in patients (pts) with HF worsen-ing. We compared the outcome of pts withand without chronic low dose �-blockerpretreatment before HF worsening.

Methods and Results: 66 HF pts in NYHAclass IV refractory to oral medical treat-ment received continuous iv PGE1. 34 pts

(LVEF 15 ± 5 %, RR mean 77 ± 14 mmHg,cardiac index 1.9 + 0.5 L/min/m2, plasmabig endothelin [ET] 7.4 ± 3.5 fmol/ml)were pretreated with 36 ± 30 % of themaximum �-blocker dose for 4 ± 3 months(group A), 32 pts (LVEF 16 ± 5 %, RR mean78 ± 14 mmHg, cardiac index 1.8 ±0.5 L/min/m2, plasma big ET 7.1 ±4.0 fmol/ml) were not (group B). After4.5 + 7.2 months �-blocker dose wasincreased to 80 ± 40 % of the maximumin group A (p = 0.0001), after 4.3 + 5.6months group B received 64 ± 39 % ofthe maximum �-blocker dose. Duringthis treatment period plasma big ET de-creased significantly compared to baseline(5.9 ± 4.2 fmol/ml in group A, p = 0.01vs baseline; 3.2 ± 2.1 fmol/ml in groupB, p = 0.0001 vs baseline; p = 0.003between groups), plasma big ET did notdecrease in group A, but decreased ingroup B below 4.3 fmol/ml (a cutpointrepeatedly shown to indicate very poorprognosis). In group A 7 pts (21 %) couldbe weaned from PGE1, 6 pts (18 %) receiveda left ventricular assist device, 16 pts (47 %)were transplanted and 5 pts (15 %) died.In group B 19 pts (59 %) could be weanedfrom PGE1 (p = 0.001 vs group A), 1 pt(3 %) received a left ventricular assistdevice, 12 pts (38 %) were transplantedand no pt died (p = 0.02 vs group A).

Conclusion: Despite similar baselinecharacteristics pts with chronic low dose�-blocker pretreatment before HF worsen-ing have a worse outcome compared to ptswithout �-blocker pretreatment before HFworsening when they are treated with PGE1as bridging to high dose �-blocker therapy.

PROGNOSTIC POWER OF NEUROHUMORALPARAMETERS IN CHRONIC HEART FAILUREDEPENDS ON THE CLINICAL STAGE AND ONTHE OBSERVATION PERIOD

R. Berger, K. Strecker, M. Hülsmann, B. Frey,A. Bojic, P. Moser, B. Stanek, R. PacherDepartment of Cardiology, University ofVienna, Ludwig Boltzmann Institute ofExperimental Endocrinology and LudwigBoltzmann Institute of CardiovascularResearch, Vienna, Austria

Background: Endothelin (ET) and natri-uretic peptides have prognostic signifi-cance in chronic heart failure (CHF). Asthe stimuli for formation of these neuro-

Table 1: G. Beran et al.Acute cTFC cTFC CFR ST-score ST-score ST-score

lumen gain pre post post pre (mm)* post 6 h post(mm)

X-Sizer 2.03 ± 0.9 77 ± 30 19 ± 11 1.54 ± 0.6 10.8 ± 15.6 2.5 ± 3.5** 1.6 ± 2.2**

Control 1.94 ± 0.6 73 ± 37 24 ± 14 11.55 ± 0.7 11.7 ± 7.1 5.5 ± 4.8** 4.0 ± 3.5*

Data are given as mean values ± SD, * in pts with AMI, ** p < 0. 05 (t-test)

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hormones are different, we investigatedwhether their prognostic power dependson the clinical stage and on the length ofthe observation period.

Methods and Results: Plasma levels ofbig ET, BNP, N-terminal BNP (N-BNP)and N-terminal ANP (N-ANP) in additionto 11 clinical and haemodynamic varia-bles were obtained from 453 patientswith LVEF � 35 %. According to theirNYHA class and LVEF, patients were strati-fied into group A – mild CHF (n = 114),group B – moderate CHF (n = 210) andgroup C – severe CHF (n = 128). For pre-diction of the combined endpoint deathor urgent HTX a multivariate analysis wasperformed after an observation period upto 1, 2 and 3 years in all patients and ineach subgroup. Best independent predic-tors were as follows:All patients: Up to 1 year – big ET (p =0.0001, x2 = 59), 2 and 3 years – N-ANP(p = 0.0001, x2 = 68; p = 0.0001, x2 = 89).Group A: Up to 2 and 3 years – N-ANP(p < 0.001, x2 = 12; p = 0.0001, x2 = 25).Group B: Up to 1 and 3 years – N-ANP(p = 0.0001, x2 = 16; p = 0.0001, x2 = 22),2 years – N-BNP (p = 0.0001, x2 = 19).Group C: Up to 1, 2 and 3 years – big ET(p = 0.0001, x2 = 23; p = 0.0001, x2 = 22;p = 0.0001, x2 = 20).

Conclusion: Big ET was the best indepen-dent marker for short-term prognosis andin severe CHF, natriuretic peptides (espe-cially N-ANP) were better markers forlong-term prognosis and in mild and mo-derate CHF.

ELEVATION OF SERUM BIG ENDOTHELIN ISASSOCIATED WITH IMPAIRMENT OFENDOTHELIUM MEDIATED VASODILATATIONIN PATIENTS WITH CHRONIC HEART FAILURE

R. Berger, K. Strecker, B. Stanek,M. Hülsmann, R. Pacher, Th. NeunteuflDepartment of Cardiology, University ofVienna, Ludwig Boltzmann Institute ofExperimental Endocrinology and LudwigBoltzmann Institute of CardiovascularResearch, Vienna, Austria

Background: We have previously repor-ted that ETA receptor blockade improvesimpaired endothelium-dependent flow-mediated vasodilatation (FMD) in CHFpatients. In the present study we investi-

gated the relationship between big ETplasma levels (by radioimmunoassay)and FMD (of the brachial artery by highresolution ultrasound).

Methods: 44 CHF patients (NYHA class I/II/III/IV–10/7/22/5 patients; LVEF < 30 %)and 13 age, sex and risk factor-matchedcontrols have been studied. Patients werestratified into group A, big ET below theupper normal range of 1.8 fmol/ml, group B,big ET between 1.8 and 4.3 fmol/ml (thelatter value being a cutpoint repeatedlyshown to indicate very poor prognosis)and group C, big ET above 4.3 fmol/ml.

Results: Big ET plasma levels were 3.5 ±2.2 fmol/ml in CHF patients and 2.1 ±0.6 fmol/ml in controls (p < 0.05). FMDwas 6.8 ± 5.2 % in CHF patients and10.6 ± 5.1 % in controls (p < 0.05).Comparing the control group and the CHFsubgroups (group A – n = 14, LVEF 19 ±4 %, group B – n = 16, LVEF 20 ± 5 %and group C – n = 14, LVEF 19 ± 6 %)with each other, FMD was similar betweencontrols and group A (10.5 ± 3.7 %), butdiffered significantly between controlsand group B (5.8 ± 6.1 %, p < 0.05), bet-ween controls and group C (4.2 ± 2.8 %,p < 0.01), between group A and group Bp < 0.05), and between group A and groupC (p < 0.01). The difference betweengroups B and C was not statistically signifi-cant. In a multivariate analysis includingage, gender, underlying heart disease,smoking, diabetes, hypercholesterolaemia,hypertension and big ET, big ET was thestrongest independent predictor of endo-thelial dysfunction (R = –0.53, p = 0.0002)with only diabetes mellitus providing ad-ditional information (R = 0.33, p = 0.002).

Conclusion: Patients with normal big ETplasma levels have a similar FMD com-pared to controls, whereas patients withelevated big ET plasma levels have an im-

paired FMD. Big ET is a strong indepen-dent predictor of endothelial dysfunction.

INCREASED PREVALENCE OF ELEVATEDPLASMA FACTOR VIII IN CHRONIC THROMBO-EMBOLIC PULMONARY HYPERTENSION

D. Bonderman, J. Jakowitsch, W. Klepetko,M. B. Lang, A. Weltermann, P. A. Kyrle,I. M. LangDepartment of Cardiology, University ofVienna, Austria

Background: Chronic thromboembolicpulmonary hypertension (CTEPH) is theresult of non-resolving pulmonary throm-boembolism, eventually leading to rightheart failure and death. In accordancewith the absence of deep vein thrombosis(DVT) in over 60 % of CTEPH patients,and a lack of risk factor sharing with DVT,there are no known abnormalities ofcoagulation and fibrinolysis that couldexplain the clinically progressive throm-bosis in the pulmonary vasculature ofthese patients.

Methods and Results: Because plasmafactor VIII above 150 IU/dl has beenshown to confer a 5-fold increased riskfor DVT, we measured plasma factor VIIIand levels in CTEPH patients (n = 87)and compared them with age and sexmatched healthy controls (n = 82). To ruleout dysfunctional endothelium of pulmo-nary hypertension as a source for elevatedplasma factor VIII, the data were also com-pared with matched samples from patientswith non-thromboembolic pulmonaryarterial hypertension (PAH, n = 68). InCTEPH patients factor VIII above 150 IU/dlwas more prevalent than in controls(85.7 % versus 18.2 %, p < 0.0001) andPAH patients (55.5 %, p = 0.002). More-

Table 2: D. Bonderman et al. Haemodynamic parameters and plasma factorVIII in 18 CTEPH patients before and after successful PTEParameter Baseline Postoperative P-valuemPAP (mmHg) 54 ± 14 32 ± 12 < 0.05CO (L/min) 4.4 ± 1.1 5.5 ± 1.1 < 0.05PVR (dynes x s x cm–5) 943 ± 435 317 ± 213 < 0.05MVS (%) 59 ± 11 67 ± 7 < 0.05Factor VIII (IU/dl) 224.4 ± 97.3 211.1 ± 97.2 0.71

mPAP = mean pulmonary arterial pressure, CO = cardiac output,PVR = pulmonary vascular resistance, MVS = mixed venous saturation

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over, CTEPH patients had higher levelsof factor VIII than controls (232.9 ±103.2 IU/dl versus 93.0 ± 23.3 IU/dl,p < 0.001) and PAH patients (168.2 ±81.2 IU/dl, p = 0.009). In addition, plasmavon Willebrand factor (vWF), a factorVIII-dependent risk factor for DVT, wassignificantly increased in CTEPH (267.9± 137.5 %) versus PAH (208.1 ± 112.7 %,p = 0.043). Haemodynamic improvementafter pulmonary thromboendarterectomy(PTE) did not normalize plasma factorVIII levels (224.4 ± 97.3 IU/dl versus211.1 ± 97.2 IU/dl, p = 0.71, n = 18) inCTEPH patients (Table 2).

Conclusions: The data support the con-cept of a thromboembolic origin of CTEPH.

SUBACUTE STENT THROMBOSIS ANDSEVERE GASTROINTESTINAL DISORDERS

D. Bonderman, P. Wexberg, P. Probst,H. D. Glogar, I. M. LangDepartment of Cardiology, University ofVienna, Austria

Background: Subacute thrombosis is apotentially lethal complication after co-ronary stent implantation. Initial attemptsto reduce its occurrence with heparinand/or warfarin were not satisfactory. Todate, a combination antiplatelet therapywith aspirin plus ADP inhibitors (ticlopi-dine, clopidogrel) has emerged as thestandard treatment for prevention of sub-acute stent thrombosis with a remainingincidence between 0.5 % and 0.8 %.

Methods: To examine whether incom-plete drug absorption due to severegastrointestinal (GI) disorders might ac-count for subacute stent thrombosis weretrospectively analysed the medicalhistories of all patients with angiographi-cally documented subacute stent throm-bosis (> 72 hours after stent implantation)at our centre between November 1995and July 2001. Patients receiving warfarinwere excluded from the analysis.

Results: Fourteen patients (0.5 %) hadexperienced subacute stent thrombosis.Of these patients 3 (21.4 %) had a shortbowel syndrome after gastrojejunostomydue to gastric ulcer, and one (7.1 %)suffered from diffuse erosive gastritis.Another 4 (28.6 %) patients had discon-tinued antiplatelet drug therapy.

Conclusions: Subacute stent thrombosisis associated with GI conditions where areduced surface area for drug absorptionmay lead to decreased plasma levels ofADP inhibitors. Pharmacokinetic studiesand, subsequently, different dosing regimesare required for patients with the shortbowel syndrome/erosive gastritis to pre-vent the occurrence of subacute stentthrombosis.

INHIBITION OF SMOOTH MUSCLE PRO-LIFERATION BY GPIIB-IIIA ANTAGONISTSIN-VITRO: EPTIFIBATIDE MORE EFFECTIVETHAN ABCIXIMAB OR TIROFIBAN

J. Fröhlich, J. Wojta, C. Kaun, K. Huber,G. ChristDepartment of Cardiology, University ofVienna, Austria

Background: Recent data suggest thatamong the platelet glycoprotein (GP) IIb-IIIa (�IIb�3) integrin antagonists not onlyabciximab (ReoPro®, a chimeric mono-clonal antibody), but also eptifibatide(Integrilin®, a cyclic heptapeptide) is ableto bind to integrin-receptors of the ��subunit family, whereas the affinity oftirofiban (Aggrastat®, a peptidomimetic)is restricted to �IIb�3. We were interestedwhether these differences in integrinspecificity might influence the effect onhuman smooth muscle cell (SMC) migra-tion and/or proliferation in-vitro.

Methods: A two-dimensional assaysystem for determination of SMC migra-tion/proliferation was used. Sterilizedsteel supports were inserted into gelatinecoated six well plates. Human umbilicalartery SMC were seeded into the middlehole of each support. At confluency,inserts were removed and after 24 hoursof serum deprivation, GP IIb-IIIa antago-nists were added in culture media with10 % calf serum. After 20 days cell-layerswere stained, digitally quantified (ScionImage) and in parallel cells counted.

Results: No GP IIb-IIIa antagonist influ-enced SMC area significantly at therapeu-tic plasma concentrations (abciximab:200 ng/ml; eptifibatide: 2 µg/ml, tirofiban:40 ng/ml). At 10� conc. eptifibatide re-duced SMC area significantly by 30 %(p = 0.01) and at 30� conc. by 41 %(p = 0.001), whereas abciximab and

tirofiban showed no significant influence.This effect was paralleled by a decreasein cell counts (30� conc.: 43 % reduction,p = 0.005), reflecting an inhibition ofcell proliferation.

Conclusions: Among the currentlyavailable GP IIb-IIIa antagonists, onlyeptifibatide showed a dose-dependentinhibition of SMC proliferation in ourin-vitro assay system. Abciximab andtirofiban exerted no significant effects. Asthese findings might be due to eptifibati-de’s broader range of integrin specificity(�IIb�3 and various a� subunits of integrin),compared to abciximab (�IIb�3 and ���3)or tirofiban (only �IIb�3), we hypothesizethat inhibition of SMC proliferation re-quires simultaneous blockade of severalintegrin receptors. The clinical relevanceof this phenomenon, with reduction of laterestenosis after percutaneous coronaryinterventions needs to be proven.

LONG-TERM OUTCOME OF PATIENTS WITHVENTRICULAR SEPTAL DEFECT CONSIDEREDNOT TO REQUIRE SURGICAL CLOSUREDURING CHILDHOOD

H. M. Gabriel1, M. Heger1, P. Innerhofer1,M. Zehetgruber1, G. Mundigler1,M. Wimmer2, G. Maurer1, H. Baumgartner1

1Department of Cardiology and2Department of Pediatric Cardiology,University of Vienna, Austria

Aim of the Study: The purpose of thestudy was to assess the long-term out-come of patients with small ventricularseptal defects (VSD) considered not torequire surgical closure during childhood.Although patients with small VSD havegenerally been considered not to requiresurgery, more recent data suggest that asignificant percentage of these patientsdevelop serious problems during adult life.

Methods: 229 consecutive pts (115 fe-males) with a VSD considered too smallto require surgery during childhood asdefined by normal pulmonary artery pres-sure (PAP), < 50 % shunt, pulmonary vas-cular resistance � 200 dynes � sec � cm–5,no VSD related aortic regurgitation, andno symptoms who had no additionalhaemodynamically relevant heart defectwere followed: Physical examination,ECG, and echocardiography were per-

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formed in all pts in 1 to 3 year intervals;exercise test and Holter monitoringcould be performed in 140 and 127 pts,respectively.

Results: Follow-up could be completed in222 pts (97 %). Mean age at last visit was30 ± 10 years. Spontaneous VSD closurewas observed in 14 pts (6 %). No pt died,4 pts (1.8 %) had an episode of endocar-ditis of whom 2 required aortic valve re-placement, one additional pt (0.4 %) hadsurgical closure for haemodynamic rea-sons. For 118 pts who entered the studybetween 1993–1996 and were prospec-tively followed for 7.4 ± 1.2 years, eventfree survival was 99.1 ± 0.8 % at 3 years,96.5 ± 1.7 % at 6 years, 95.5 ± 1.9 % at8 years. At last visit, 94.6 % of all ptsstudied were free of symptoms. LV sizeby echocardiography was normal in 198(89 %) patients, borderline in 23 patientsand definitely enlarged in only onepatient. None had systolic LV dysfunctionand PAP was normal in all except one.Mean exercise capacity was 92 ± 21 %of expected and 87 % of pts had no ar-rhythmias on Holter monitoring with therest showing benign rhythm disorders.

Conclusions: Outcome in well-selectedpts with a small VSD is good. Surgicalclosure does not appear to be requiredduring childhood as long as left-to-rightshunt is less than 50 % and signs of leftventricular volume overload are absent,when PAP is not elevated, and no VSDrelated aortic regurgitation or symptomsare present.

ANALYSIS AND STUDY OF SUDDENCARDIAC DEATHS IN CENTRAL GREECE(RETROSPECTIVE STUDY)

Th. Galeas, V. Galea, St. Mylonas,Ad. Bourdakis, K. RanellouB’Internal Medicine Clinic, GeneralHospital of Trikala, Greece

Purpose of study: The distribution ofsudden cardiac deaths by cause, gender,age, year and place of living has beenstudied all over the world. There are onlya few data analysis studies in Greece, sofar. The purpose of this study is to analyzeand study sudden cardiac deaths, whichoccurred in the county of Trikala duringthe period from 1990–2000.

Material and Methods: We wrote down268 cases of out-of-hospital suddencardiac deaths, which occurred in theadult population in the last 11 years.Necrotomy took place in the GeneralHospital of Trikala. Age and place ofliving were unknown in 12 and 14 cases,respectively. (Population of the county ofTrikala: 139,500, population of the cityof Trikala: 51,670). The sudden cardiacdeath is defined, in accordance to the in-ternational standards, as the natural,unexpected, cardiac death occurringwithin one hour of the onset of acutesymptoms. Chi2 and t-test were per-formed for statistical analysis.

Results: Sudden cardiac deaths: A: Byyear: 1990: 24, 1991: 31, 1992: 36, 1993:11, 1994: 26, 1995: 25, 1996: 21, 1997:16, 1998: 26, 1999: 26, 2000: 26. B: Bygender: 214 male (m) (80 %), mean age60.5 years old and 54 female (f) (20 %),mean age 67 years old. C: By age: 15–24: 1 (1 m, 0 f), 25–34: 9 (8 m, 1 f), 35–44:18 (17 m, 1 f), 45–54: 47 (43 m, 4 f), 55–64: 58 (46 m, 12 f), > 64: 123 (92 m, 31f). D: By place of living: city of Trikala:73, rest county: 157, other places: 24.E: By cause: acute myocardial infarction:242 (90.2 %), acute cardiac failure: 19(7 %), heart failure: 3 (1.2 %), acute car-diogenic pulmonary oedema: 1 (0.4 %),unexplained: 3 (1.2 %).

Conclusions: 1. The incidence of suddencardiac death has a significant prepon-derance in males compared with femalesand increases according to age. 2. Sud-den cardiac deaths occur more often outof the city of Trikala. 3. The major causeof sudden cardiac deaths is acute myo-cardial infarction.

PULMONARY TOXICITY OF AMIODARONE –CASE REPORT

S. Z. Geschev1, E. Wagner2, M. Mandl1,B. Grasl2, H. A. E. Schinko1

1Department of Pulmonology and2Department of Radiology, GeneralHospital, Linz, Austria

Introduction: Amiodarone is an anti-arrhythmic agent with significant benefitfor ventricular dysrhythmias in patientswho do not respond to most other anti-arrhythmic drugs. One of its side effectsis pulmonary toxicity.

Case Presentation: A 54 y.o. man wasadmitted to the hospital with fever,malaise, dyspnoea and non-productivecough. Three months before admissionthe patient underwent a coronary-arterybypass grafting because of three-vesselsdisease. Postoperatively, an episode ofsymptomatic atrial fibrillation was dia-gnosed and amiodarone was added at adose of 200 mg/d (without loading dose)to his basic medication. Four days beforeadmission a fever up to 39.2 °C anddyspnoea developed.

He appeared tachypnoeic the breathsounds were accentuated, but no crack-les were heard. The heart rate was 100,rhythmic. His blood gases revealed ahyperventilation with moderate hypo-xaemia. In chest x-ray bilateral inter-stitial infiltration was seen, a high reso-lution CT showed ground-glass opacitiesin both lungs with reticular abnormali-ties, septal thickening. Laboratory studiesdisclosed a mild leucocytosis, elevatedsedimentation rate and acute phase reac-tion. The thyroid hormones were withinnormal range. Pulmonary function testswere abnormal with severe decrease intotal lung capacity and carbon diffusingcapacity. In bronchoalveolar lavage therewas an increased number of neutrophils,lymphocytes and eosinophils, CD8+cells were also increased with a lowCD4/CD8 ratio. Foamy macrophageswere shown and the histology revealedwidened septa and mixed infiltrates. Thediagnosis of hypersensitivity pneumonitisdue to amiodarone was made and thepatient was started on corticosteroidsand oxygen. Amiodarone has been dis-continued. His condition stabilizedwithin 10 days and he was discharged.

Discussion: Pulmonary toxicity is thefeared side effect of amiodarone. In 20 %of the patients the pneumonitis developesacute, mimicking pneumonia. Differentialdiagnosis includes any type of interstitialpneumonia.

Conclusion: The diagnosis of amiodaronepneumonitis is one of exclusion. There isno threshold dose for developing pulmo-nary complications. In case of our patientit was a maintenance dose of 200 mg for2 months.

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ATORVASTATIN OR SIMVASTATIN CONCO-MITANT TO LDL-APHERESIS TREATMENT INPATIENTS WITH HOMOZYGOUS AND HETERO-ZYGOUS FAMILIAL HYPERCHOLESTEROLAEMIA:A PROSPECTIVE CROSSOVER STUDY

A. Goldammer1, G. Heinz2, M. Jansen1,W. H. Hörl1, K. Derfler1

1Department of Nephrology and Dialysis,2Department of Cardiology, University ofVienna, Austria

Background: To enable further reductionin LDL-cholesterol (LDL-C) in patientswith homozygous (n = 4) and severeheterozygous (n = 10) familial hyper-cholesterolaemia (FH) undergoing LDL-immunoapheresis we altered the con-comitant drug treatment from simvastatinto atorvastatin following a prospectivedesigned crossover study protocol.

Methods: While LDL-apheresis wasperformed at weekly intervals, lipoproteinvalues were compared under 40 mg ofsimvastatin followed by a wash-outperiod of 4 weeks and when patientsreceived atorvastatin therapy, startingwith a 10 mg dose and escalating every4 weeks up to 80 mg.

Results: Comparable levels of LDL-Cwere obtained when 10 mg of atorva-statin (206 ± 63 mg/dl) were adminis-tered as during treatment with 40 mgof simvastatin (212 ± 38 mg/dl). When4 weeks on 80 mg of atorvastatin a fur-ther 26 % reduction in LDL-C values(157 ± 34 mg/dl) was obtained, and ki-netic analysis demonstrated that LDL-Clevels increased from a post-treatmentvalue of 28.8 ± 14.2 mg/dl in a first or-der kinetic to 156.6 ± 25.5 mg/dl at day7. When these kinetic results were com-pared to those without concomitantlipid lowering drug treatment patientspresented LDL-C values below the rec-ommended target range for an extendedduration of almost 48 hours (until 72hours after LDL-apheresis). The levels ofHDL-cholesterol and plasma fibrinogenremained comparable during the entirestudy period. The change in lipid lower-ing drugs resulted in a 40 % reductionin LDL-apheresis treatments despite im-proved LDL-C levels prior to and follow-ing LDL-apheresis treatment.

Conclusion: Our results show that ag-gressive LDL-C reduction by atorvastatincombined with LDL-apheresis is a saveand efficient choice in lipoproteintherapy in patients with heterozygousand even homozygous FH.

RIGHT VENTRICULAR METASTATICCHORIOCARCINOMA OBSTRUCTINGIN- AND OUTFLOW TRACT

V. Gorjup1, B. Gersak1, T. Gulic2,N. Suligoj Cernic3

1Medical Center Ljubljana, 2GeneralHospital Maribor, 3General HospitalIzola, Slovenia

Objective: We wanted to demonstratethat fast diagnosis and immediate treat-ment of intracavitary myocardial neo-plasms as soon as they present them-selves with symptoms, is essential foraccurate treatment of these patients.

Methods: Surgical procedure was per-formed on a 34 year old man in whomECHO heart examination was revealinga metastatic tumour in the enlarged rightventricle (RV) obstructing the RV in-and outflow tract and extending fromthe tricuspid valve to the pulmonaryvalve, filling the entire ventricle andoutflow tract. The tumour was removedon arrested heart, the method enablingpreservation of the tricuspid valve andit’s supporting structures. The mass couldnot be removed from the RV free wall,since the tumour invaded it completelyand an attempt at removal would resultin complete absence of contractile forceof the RV. An additional chemotherapywas carried out with four cyclesaccording to the BEPO scheme.

Results: The results of histologic investi-gation of removed tissue revealed a meta-stasis of choriocarcinoma with compo-nents of immature teratoma, originatingfrom right testis.

Control CT of the thorax was performedafter six months, detecting no metastasesin the lung parenchyma. MRI of the heart,however, still showed a thickened RV freewall and apex, mass vascularity equalledthat of the myocardium – compared topostoperative heart US recordings, therewas no regression of the mass in the RV

wall. The patient is doing well one yearpostoperatively.

Conclusions: The diagnostic proceduresfor detecting the tumours should be non-invasive (ultrasound, CT, MRI) since inour opinion invasive methods, such asventriculography, do not give a betterinsight into the lesion, but may endangerthe patient with the risk of distal emboli-zation of the tumour. Immediate operationshould be practised for accurate treat-ment of these patients.

INTRAAORTIC BALLOON PUMP USE IN MEDICALINTENSIVE CARE UNIT IN MEDICAL CENTERLJUBLJANA. RESULTS OF 10 YEARS OF USE

V. Gorjup, A. Jazbec, M. HorvatMedical Intensive Care Unit, MedicalCenter Ljubljana, Slovenia

Aim of the study: Aim of our study wasto examine the use of an intraaorticballoon pump (IABP) in our ICU. Wewere interested in indications, com-plications and patients outcome.

Patients: From January 1, 1990 throughDecember 31, 2000 we inserted IABP to187 of our patients. We managed to re-trieve 164 of their medical records. Theaverage age of our patients was 64.1years (21–83 years), 106 were males.

Results: From 1990 through 1996 therewere 10 patients with IABP support peryear on average. With the introduction ofpercutaneous coronary interventions inacute coronary syndromes in 1997 thenumber of patients with IABP supportgradually rose up to 55 in 2000. Most ofthe patients required IABP support due tocardiogenic shock in the setting of acutemyocardial infarction (AMI). Other indi-cations were: unstable angina pectoris,mechanical complications and rhythmdisturbances during AMI, PTCA compli-cations and myocarditis. The average timeof IABP support was 4.1 days (few hoursto 15 days). Complications were rare (total8 %; 7 % vascular, 1 % infectious). Out-come was as follows: successful weaningand discharge from ICU – 45 patients, sur-gery – 66 patients, death – 58 patients.

Conclusions: Use of IABP in our unit isincreasing especially since introducing

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percutaneous intervention techniques inacute coronary syndromes. The increase isalso related to widening of indications forIABP support (bridging to surgery). Compli-cations and outcome are comparable withresults achieved in other centers.

IMPROVEMENT OF CARDIAC OUTPUT INSEVERE CHRONIC HEART FAILURE BYCOMBINING ACE-INHIBITORS AND EITHEREPROSARTAN OR TELMISARTAN

B. Gremmler, M. Kunert, H. Schleiting,L. J. UlbrichtDepartment of Cardiology,Marienhospital Bottrop, University ofWitten/Herdecke, Germany

Background: The importance of ACE-inhibitors in the therapy of chronic heartfailure is established. Angiotensin IIreceptor type 1 antagonists act accordingto a different pharmacological mecha-nism by additionally blocking the locallyand not ACE-generated angiotensin II inthe vessel wall and the myocardium.Furthermore, the AT-1-receptor antago-nists block the prejunctional AT-1-recep-tors and reduce the sympathetic outflow.We examined the hypothesis that an ad-ditional effect on cardioprotection can beachieved by the combination of commonACE- and bradykininase-inhibitor actionand the specific effects of sartans.

Methods: 51 patients (mean age 68.8 ±7.8 years) with severe chronic heartfailure receiving long-term medicationwith digitalis, diuretics, and ACE-inhibi-tors were randomised after clinical recom-pensation in a blind fashion to eitherEprosartan (n = 17; 508.8 ± 118.0 mg/d)or placebo (n = 17). Additionally aprospective study by using Telmisartan(n = 17; 66.1 ± 15.4 mg) was performed.Haemodynamic measurements weremade by impedance-cardiography atbaseline and after 9.9 ± 2.3 days.

Results: Additional treatment with sartansresulted in an improvement of cardiac out-put. There was an increase in cardiac out-put from 2.38 ± 0.58 to 3.19 ± 1.0 l/min

(p = 0.009) in the Eprosartan-group andfrom 2.24 ± 0.48 to 2.80 ± 0.75 l/min(p = 0.0013) in the Telmisartan-groupwhile there was no increase of cardiacoutput in the control group.

Conclusions: The additional treatment ofsevere heart failure patients who receiveddigitalis, diuretics, and ACE-inhibitorswith the AT 1-receptor antagonist Eprosar-tan or Telmisartan shows a beneficialeffect by increasing cardiac output. Thiseffect may be due to the sartans additio-nal property of blocking the autocrineinteraction of locally and not ACE-gene-rated angiotensin II with their respectivevascular and myocardial AT 1-receptorsas well as the influence on prejunctionalAT 1-receptors located on sympatheticnerve terminals.

DIFFERENT ORIGIN OF ELEVATED HEPATO-CYTE- AND VASCULAR ENDOTHELIALGROWTH FACTOR SERUM LEVELS INPATIENTS AFTER MYOCARDIAL INFARCTION.ROLE OF LEUKOCYTE ACTIVATION

A. Gutersohn1, A. H. Elmaagacli2,J. Buchholz3, O. Oldenburg1, J. Schaar1,D. Baumgart1, Th. Budde3, U. W. Schäfer2,R. Erbel1

1Department of Cardiology, 2Departmentof Bone Marrow Transplantation,University of Essen, 3Department ofCardiology, Alfried Krupp Hospital,Essen, Germany

Abstract withdrawn.

ASSOCIATION OF CORONARY CALCIUMWITH THE GNB3 POLYMORPHISM INEARLY CORONARY ARTERY DISEASE

A. Gutersohn1, A. Schmermund1, W. Siffert21Department of Cardiology, 2Departmentof Pharmacology University of Essen,Germany

Abstract withdrawn.

CHANGES IN MYOCARDIAL ELECTRICAL ANDMECHANICAL FUNCTION ASSESSED BYENDOCARDIAL MAPPING AFTER PER-CUTANEOUS TRANSLUMINAL CORONARYANGIOPLASTY

M. Gyöngyösi, A. Khorsand, S. Graf,H. Sochor, W. Sperker, H. D. GlogarDivision of Cardiology, University ofVienna, Austria

Background: Nonfluoroscopic electroana-tomical mapping displays simultaneouslythe myocardial viability and the regionalmechanical function of the heart, whichmight be improved after angioplasty ofthe narrowed coronary artery.

Purpose: We compared the pre-percuta-neous transluminal coronary angioplasty(PTCA) and follow-up (FUP) endocardialvoltage and local linear shortening (LLS)values in order to investigate the abilityof NOGA endocardial mapping fordetection of hibernating myocardium.

Methods: The left ventricular unipolarvoltage and LLS values were analysed inthe first 10 patients (8 male, 61 ± 12 yrs,all with stable angina pectoris, three-vesseldisease and previous myocardial infarction)before and 6 months after PTCA. TheNOGA segmental quantitative analysiswas performed after transformation of the3-dimensional endocardial map into po-lar map, containing 12 segments (anterior,lateral, posterior and septum, each of themwith apical, mid and basal subsegments).201-Thallium rest and late-rest images wereperformed in all patients, and the quanti-tative 201-Thallium uptake data wereanalysed by polar map analysis by divisioninto 12 comparable myocardial segments.

Results: On the basis of the PTCAlocalization, the myocardium wasdivided into “treated” and “untreated”regions. In the treated myocardial areas,the unipolar voltage values (from 7.71 ±3.37 to 9.74 ± 4.50 mV, p < 0.05; nor-mal value > 15 mV) and the LLS values(from 6.81 ± 5.70 % to 9.24 ± 6.12 %,p < 0.05, normal value > 11 %) increasedsignificantly. In contrast, in the untreated

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region, neither the unipolar voltage northe LLS values changed. A trend toincrease in 201-Thallium resting uptake(64.2 ± 14.8 % vs 69.3 ± 15.6 %, n.s.)and a significant improvement in 201-Thallium late resting uptake (index ofmyocardial viability) (55.4 ± 17.3 % vs68.3 ± 16.9 %, p < 0.05) could bedetected in the treated myocardialsegments. The 201-Thallium uptake didnot change in the non-treated areas.

Conclusion: Myocardial regions with par-allel decreased endocardial voltage andLLS values of NOGA endocardial mappingmight present hibernating myocardium, asa significant improvement of both thevoltage and LLS values have been detectedafter restoration of myocardial blood flow.

ACUTE STENT THROMBOSIS AFTER INTRA-CORONARY IMPLANTATION OF RG-13577COATED STENTS IN PIGS

M. Gyöngyösi1, W. Sperker1,U. Windberger2, H. D. Glogar1

1Department of Cardiology, 2Center forBiomedical Research, University ofVienna, Austria

Background: RG-13577 is a non-toxicsynthetic heparin-mimicking polyanioniccompound (polymer of 4-hydroxyphonoxyacetic acid) which has been shown toinhibit in-vitro vascular smooth musclecell proliferation induced by basicfibroblast growth factor and to block celldivision in the G1/S-phase transition. Theaim of the present study was to reduceneointimal hyperplasia using RG-13577-coated stents after intracoronary stentimplantation in pigs.

Methods: In general anaesthesia, the leftcoronary artery was cannulated in 14 do-mestic pigs. After administration of 200IU/kg heparin, 8 pigs received bare (non-coated native) Genius stents (EuroCorGmbH, Bonn, Germany) either in theleft anterior or left circumflex coronaryarteries. After 4 weeks follow-up (250 mgacetylic salicylic acid administered dailyper os to prevent stent thrombosis), repeatangiography and intravascular ultrasound(IVUS) using automatic pullback wereperformed. Six RG-13577-coated Geniusstents were implanted in 6 more pigs inone left coronary artery branch.

Results: Five of 6 pigs receiving RG-13577-coated Genius stents died within1 hour after stent implantation due toventricular fibrillation. In 2 pigs, acutestent occlusion was documented angio-graphically in-vivo, while post mortemangiography proved acute stent thrombo-sis in the hearts of 2 other pigs. In onepig, no visual documentation of stentocclusion was done. Coronary angiogra-phy revealed also acute stent thrombosisin the 6th (survived) pig with RG-13577-coated Genius stent, which experienceda small myocardial infarction. In theother group (bare stent group), no acuteor subacute complication occurred andall pigs survived the 4-week follow-up.Volume measurements by 3D-recon-struction of IVUS (EchoPlaque, IndecSystems, CA) revealed an intimal volumeof 20.31 ± 5.76 mm3 within the stents.IVUS showed a minimum lumen areaof 3.48 ± 0.68 mm2, a maximum vesselarea of 8.50 ± 0.79 mm2 and a maximalintimal area of 1.91 ± 0.53 mm2.

Conclusion: Even though RG-13577 hasheparin-like capabilities, intracoronaryimplantation of RG-13577 coated stentsleads to acute in-stent thromboses inpigs. Bare Genius stent implantationshows favourable results.

EXTERNAL ELECTRICAL CARDIOVERSION OFPERSISTENT ATRIAL FIBRILLATION (AF)

I. Hausleithner, H. Domanovits,M. Schillinger, F. Schadauer, G. Gamper,M. Röggla, A. N. LaggnerDepartment of Emergency Medicine,Vienna General Hospital, Austria

Background: Restoration of sinusrhythm (SR) is the primary goal inpatients with persistent AF. Direct-current electrical cardioversion (DCCV)can be performed primary or afterpharmacological failure.

Methods: Within 6 years DCCV wasapplied to 162 patients with 202

episodes of persi-stent AF. Responseto electrical therapywas assessed.

Results: SR wasrestored by DCCVin 185 episodes of

persistent AF (92 %). In 34 out of the202 episodes preceding pharmacologictherapy had failed. Non-responders toelectrical therapy had more often en-larged left atria. Choice of the initialenergy level was free. 200 Joule wereapplied for first shock in 165 cases andsucceeded in 75 % (124 episodes).Overall for successful termination amedian of 1.4 shocks was necessary. Noserious adverse events occurred duringobservation period prior to hospitaldischarge (Figure 1).

Conclusion: External electrical cardio-version is safe and effective for termi-nation of persistent AF. As initial shockenergy we recommend 200 J.

PREDICTION OF OUTCOME BY NEURO-HUMORAL ACTIVATION, SIX MINUTE WALKTEST AND THE MINNESOTA LIVING WITHHEART FAILURE QUESTIONNAIRE IN ANOUTPATIENT COHORT WITH CONGESTIVEHEART FAILURE

M. Hülsmann1, R. Berger1, B. Sturm1,A. Bojic2, B. Frey1, J. Bergler-Klein1,W. Woloszczuk3, R. Pacher1

1Department of Cardiology, 2LudwigBoltzmann Institute of CardiovascularResearch, and 3Ludwig BoltzmannInstitute of Experimental Endocrinology,University of Vienna, Austria

Introduction: Neurohumoral activation isa well-known phenomenon in congestiveheart failure. Due to the central mecha-nism it is a value tool as a prognosticmarker. Nevertheless no data existcomparing the most powerful markers asN-ANP, BNP, N-BNP and big-endothelin 1in one model in a widespread popula-tion of heart failure patients. The six-minute walk test is very controversialdiscussed in respect to its predictive powerand the Minnesota living with heart failurequestionnaire has never been evaluated,whether it is related to outcome.

Figure 1: I. Hausleitner et al.

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Aim of the study: To compare these para-meters in respect to short-term outcomein an ambulatory heart failure population.

Patients and methods: Ninety-six patients(57 ± 8 years, 82 % male, left ventricularejection fraction of 26 ± 10 %) whowere treated as out-patients in the heartfailure unit were included. Within oneday blood samples of N-ANP, N-BNP,BNP and big-endothelin 1 were obtainedas well as six-minute walk test and Min-nesota living with heart failure question-naire were measured. The predictivepower of these variables in respect toone-year event free survival was calcula-ted by a Cox regression analysis.

Results: All variables investigated had thepower to predict outcome in an univariateanalysis. Multivariate analysis revealedthat only N-ANP (x2 = 66, p < 0.0001)beside Minnesota living with heart failurequestionnaire (x2 = 11, p < 0.001) andBNP (x2 = 7, p < 0.01) are independentpredictors. Kaplan-Meier analysis revealeda significant difference in outcome afterthree months and one year at a cutpointof 5000 fmol/ml (p < 0.0001).

Conclusions: We conclude that in anopen clinical cohort of patients with bigdifferences in the progression of thedisease. N-ANP is the most reliable pre-dictor of worsening heart failure in short-term. Beside BNP, especially LHFQ is anexcellent substitute in case of lacking ofspecialized laboratories.

CIRCULATING LEVELS OF N-TERMINAL ATRIALNATRIURETIC PEPTIDES AND N-TERMINALBRAIN NATRIURETIC PEPTIDE IN ACUTE ANDCHRONIC CORONARY HEART DISEASE

Rudolf Jarai1, M. Gyöngyösi1,N. Jordanova1, Robert Jarai1,M. Gottsauner-Wolf1, J. Wojta1,W. Woloszczuk2, G. Geyer2, K. Huber1

1Department of Cardiology, 2Ludwig-Boltzmann Institute of ExperimentalEndocrinology, University of Vienna,Austria

Objectives: The peptides derived fromthe atrial natriuretic peptide (ANP)prohormone, proANP (1–30), proANP(31–67) and the N-terminal proANP (1–98)hormone have natriuretic, diuretic as

well as vasodilatatory effects and antago-nize the renin-angiotensin-aldosteronesystem. The N-terminal brain natriureticpeptide (Nt-proBNP) shares the same car-dioprotective properties. ProANP(1–98)and Nt-proBNP were found to be elevatedafter acute myocardial infarction. It is alsoknown that ischaemia and hypoxia mayenhance the secretion of the proANP (1–98) hormone by atrial cells. Up to dateno data are available about the plasmalevels of the different N-terminal ANPs inpatients with stable and unstable angina.

Methods: Plasma levels of proANP (1–30),proANP (31–67), proANP (1–98) andNt-proBNP hormones were determinedin 115 patients with different clinicalstages of coronary artery disease, ac-cording to the Canadian Cardiac Societyclassification (I–IV).

Results: ProANP (1–30) and proANP(31–67) levels were found to be higher inpatients with stable angina (CCS I, II) andeffort angina (CCS III) compared to patientswith angina at rest (CCS IV, p = 0.014,p = 0.02 and p = 0.003, respectively).The levels of proANP (1–98) hormonewere higher in the CCS III and IV groupscompared to chronic stable patients(CCS I–II, p = 0.006). In contrast, Nt-proBNP levels were significantly lower inCCS III–IV than in CCS I–II (p = 0.003).Patients, with “b” and “c” angiographiclesion type in the culprit lesion havesignificantly higher levels of bothproANP(1–98) and Nt-proBNP. This ten-dency was also found with mid-proBNP,but it did not reach statistical significance.

Conclusions: Acute ischaemia seems tohave inhibiting effects on the cleavage ofthe proANP (1–98) hormone leading todecreased levels of the potentially cardio-protective proANP (1–30) and (31–67).In contrast to other studies, our resultssuggest, that in patients with effort anginaand angina at rest, the Nt-proBNP andmid-proBNP levels are lower than inchronic stable patients.

The quality of the lesion type in thecoronary vessel seems to affect theplasma levels of proANP (1–98) and Nt-proBNP hormones.

PLASMA LEVELS OF CARDIAC TROPONIN T,TROPONIN I, CREATINKINASE MB FRACTION,C-REACTIVE PROTEIN AND FIBRINOGENCORRELATE WITH TIMI RISK SCORE ANDLONG-TERM FOLLOW-UP IN PATIENTS WITHANGINA PECTORIS

N. Jordanova, M. Gyöngyösi, M. Ploner,A. Anvari, Ch. Falkensamer, G. Zorn,K. HuberDepartment of Cardiology, Universityof Vienna, Austria

Background: The aim of the presentprospective study on 155 consecutivepatients (110 male, 63 ± 11 y) with typicalchest pain was to measure fibrinogen,C-reactive protein (CRP) and cardiac tro-ponin T (cTnT) at basal conditions, as wellas troponin I (cTnI), myoglobin, andcreatine phosphokinase myocardialfraction (CKMB) at baseline and after 6hours in order to prove the accuracy ofthese parameters as markers of differentrisk in accordance with the TIMI riskscore for subsequent major adversecardiac events (MACE).

Methods: The TIMI risk score was calcu-lated and the patients were classified intohigh (score 6–7, n = 27 patients, 17.4 %),medium (score 4–5, n = 64 patients,41.3 %) and low (score 0–3, 64 patients,41.3 %) risk groups.

Results: High risk patients experiencedsignificantly more frequently acute myo-cardial infarction (22.2 vs 6.3 and 3.1 %,p < 0.05), revascularization (37 vs 10.9and 10.9 %, p < 0.005), death (29.6 vs10.9 and 1.6 %, p < 0.05) and compositeMACE (63 vs 20.3 and 14.1 %, p < 0.001)than medium and low risk patients.Significantly elevated plasma levels werefound for TnI, CRP, CKMB, cTnT andfibrinogen in patients of the high risk groupas compared to patients with medium orlow risk (Table 3). Plasma levels of myo-globin did not identify the patients withmedium or high risk.

Receiver operator characteristic (ROC)analyses revealed the following cut-offpoints for high risk groups: for cTnI at base-line 0.3 U/l (predictive accuracy [p.a.] =0.837), for cTnI after 6 h 0.64 U/l (p.a. =0.908); for CRP at baseline 0.34 mg/dl(p.a. = 0.734), for CRP after 6 h 0.732 mg/dl

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(p.a. = 0.784), for CKMB at baseline2.25 U/l (p.a. = 0.761), for CKMB after6 h 2.9 (p.a. = 0.742) and for fibrinogenat baseline 367 mg/ml (p.a. = 0.737).

Conclusion: In our patients with typicalchest pain, the cut-off levels for determi-nation of a high-risk group according tothe TIMI risk score differ from those usedin general and are either lower (CRP andCKMB at baseline and CKMB after 6 h) orhigher (cTnI at baseline and after 6 h andCRP after 6 h) for the respective para-meters.

THE ON-X® HEART VALVE:ECHOCARDIOGRAPHIC CHARACTERISTICS

M. T. Kasimir, J. Bialy, G. Seebacher,N. Simon-Kupilik, R. Moidl, P. SimonDepartment of Cardiothoracic Surgery,University of Vienna, Austria

Background: The On-X® is a new mecha-nical heart valve with a special valve de-sign. An On-X® has a flared orifice inlet,an elongated orifice and thin leaflets thatare positioned parallel when the valve isopen. The position of the valve is supra-annulary.

Patients and Methods: 154 On-X® prothe-ses were implanted, 73 aortic and 81 mitralvalves. Mean age was 61.3 ± 10.3 a(range 30–79) for implantation in mitraland 59.2 ± 10.1 a (range 25–79) foraortic position. Echocardiograms wereperformed including complete Dopplerexamination at discharge, 3 to 6 monthsafter implantation and after one year.Appearance of the valve in echo-cardiography was observed.

Results: The On-X® showed a betterhaemodynamic as compared to Carbo-medics® and Carbomedics SAV® heartvalves. In both positions movements of

the leaflets could just poorly be seen. Incontrast to all other prostheses only avery minimal closing volume was found.Closing volumes were more often detec-ted in aortic positioned valves as inmitral positioned valves. The size of thisclosing volume did not correlate withvalve size (Table 4).

Conclusion: This new valve has superiorhaemodynamics and demonstratessignificant improvement in regard toclosing volumes. Due to design featuresthe leaflets can be seen poorly on echo.

PLATELET-MONOCYTE CROSS-TALK ANDTISSUE FACTOR EXPRESSION IN STABLEAND UNSTABLE ANGINA

C. W. Kopp, S. Steiner, D. Seidinger,N. Jordanova, M. Koreny, E. Minar, K. Huber2nd Department of Medicine, Universityof Vienna, Austria

Background: Tissue factor (TF) is themajor procoagulant in-vivo and usuallyabsent from blood cells. However,monocyte tissue factor (TF) expressionand platelet activation are both featuresof unstable angina.

Methods and Results: Monocyte-TF andprocoagulant activity (PCA), monocyte

platelet load (CD42+) and adherentplatelet activation were determined byflow cytometry and chromogenic assayfrom 57 coronary artery disease patientswith stable (SA, n = 42) and unstableangina (UA, n = 15). Monocyte TF levelsand PCA were significantly higher in UA(16.4 ± 3.3 MFI, 68.5 ± 38.2 units) com-pared with SA (14.1 ± 3.1 MFI, p = 0.03;47.9 ± 18.1 units; p = 0.04). Both plateletload (r = 0.69, p < 0.0001) and plateletactivation (r = 0.47; p = 0.002) as deter-mined by CD42 and CD62P expressionon CD14+ monocytes positively correlatedwith monocyte-TF expression. TF messen-ger RNA was expressed in 26 % of SAand in 37.5 % of UA.

Conclusions: We show elevated monocyte-TF expression and TF-dependent PCA inUA compared with SA patients. Monocyte-TF activity correlating with platelet loadand platelet activation may be triggeredby platelet leucocyte cross-talk in-vivo.

RELATIONSHIP BETWEEN BLOOD PRESSURE,LIPIDS AND THERAPY IN PATIENTS INSECONDARY PREVENTION OF IHD

J. Lietava1, V. Kosmálová1, R. Šidlo2

12nd Department of Internal Medicine,Comenius University and 2Department ofStatistics, Economic University1,Bratislava, Slovakia

Background: Hypertension is oftenassociated with hyperlipidaemiaincreasing the global atherosclerotic risk ina multiplicative way. The effect of thetherapy in secondary prevention has notbeen studied at Slovakia. This studyevaluates occurrence of hypertensionand effect of the hypotensive therapy inrelationship to lipid profile in high riskpatients with symptomatic IHD.

Table 4: M. T. Kasimir et al. Data of last timepoint of examinationOn-X® aortic valve On-X® mitral valveDiameter n Mean gradient Velocity Diameter n MVA19 mm 5 19.85 mmHg 2.4 m/s 23 mm 121 mm 22 11.5 mmHg 2.1 m/s 25 mm 24 2.9 cm²23 mm 22 11.1 mmHg 2.08 m/s 27 mm 41 2.6 cm²25 mm 17 9.8 mmHg 1.95 m/s 29 mm 227 mm 7 9.8 mmHg 2.0 m/s 31 mm 17 2.8 cm²

Table 3: N. Jordanova et al.High risk Medium risk Low risk p-value

n = 27 n = 64 n = 64cTnI baseline [U/l] 5.57 ± 8.27 0.32 ± 0.61 0.16 ± 0.31 < 0.001cTnI 6 h [U/l] 8.34 ± 9.32 0.78 ± 1.72 0.29 ± 0.63 < 0.001CRP baseline [mg/dl] 1.45 ± 1.91 0.49 ± 1.00 0.81 ± 1.59 0.019CRP 6 h [mg/dl] 1.95 ± 2.09 0.83 ± 1.34 0.62 ± 0.94 < 0.001Myoglobin baseline [U/l] 46.7 ± 46.9 28.9 ± 26.2 34.6 ± 33.6 0.055Myoglobin 6 h [U/l] 50.1 ± 42.5 40 ± 55.2 32.5 ± 27 0.127CKMB baseline [U/l] 14.9 ± 20.7 2.9 ± 4.9 2.6 ± 2.6 < 0.001CKMB 6 h [U/l] 9.8 ± 11.5 3.7 ± 5.4 4.5 ± 8.5 0.004CTnT baseline [U/l] 0.57 ± 1.1 0.03 ± 0.16 0.02 ± 0.09 < 0.001Fibrinogen [mg/ml] 385 ± 84 324 ± 63 322 ± 67 < 0.001

16 J KARDIOL SUPPL E/2001

CARDIOLOGY 2001ABSTRACTS

Patients and method: In a cross-sectionalmulticentre trial 5062 patients with sympto-matic IHD were examined and hyper-lipidaemia (total cholesterol > 5.2 mmol/l)screened for statin therapy (2237 M/2825 F).Both sexes were in middle age (56.6 ±10.37 vs 60.1 ± 9.51 yrs; p < 0.001),mildly obese (BMI 28.3 ± 3.96 vs 28.3 ±4.30 kg/m2; NS) with mild hypertension(SBP 139.7 ± 18.28 vs 144.6 ± 18.47 mmHg;p < 0.001) (DBP 85.5 ± 9.30 vs 86.1 ±9.36 mmHg; p < 0.001). Males sufferedmore MIs (36.0 % vs 10.5 %; p < 0.001)and were more often smokers (16.4 % vs4.9 %; 0.001). Diabetes mellitus wassimilarly distributed in both sexes (26.7 %vs 26.9 %; NS).

Results: Out of 5062 patients withsymptomatic IHD 2622 (51.8 %) weretreated hypertensives. Table 5 compilespercentages of hypertensives withcontrolled blood pressure during mono-and combined therapy.

Conclusion: Patients with symptomaticIHD and hyperlipidaemia exhibit 51.8 %occurrence of treated hypertension,which is controlled in 26.6 % of them.Paradoxically, with increasing complexityof the therapy decreases its effectiveness,probably conditioned by increasedseverity of hypertension.

DOPPLER GRADIENTS ACROSS SORINTILTING DISC VALVES ACCURATELY REFLECTCATHETER GRADIENTS IN-VITRO

J. Mascherbauer, H. Schima, G. Maurer,H. Baumgartner.Department of Cardiology, University ofVienna, Austria

Background: Significant discrepanciesbetween Doppler and catheter gradientshave been reported for bileaflet prosthetic

heart valves. They are caused by localizedgradients and pressure recovery. The oc-currence of this phenomenon appears tobe independent of the particular designof bileaflet valves. Tilting disc valves havebeen insufficiently studied so far. Whilegood agreement between Doppler andcatheter gradients was found for MedtronicHall valves, discrepancies have been re-ported for Björk-Shiley valves.

Methods: In a well-controlled pulsatileflow model we studied various sizes ofSorin tilting disc prostheses (19 to 25 mm)using continuous-wave and pulsed-waveDoppler as well as direct measurementsof pressure and flow rate. At each of 8different flow rates (cardiac output 2.0 to8.0 l/min) peak and mean Doppler andcatheter gradients were simultaneouslymeasured. Valve areas were calculatedusing the continuity equation and theGorlin formula.

Results: Excellent correlation and agree-ment between Doppler and catheter gra-dients were found (r = .95–.99 for peakgradients and r = .98–.99 for mean gradi-ents). For small valve sizes (19 and 21 mm)the mean difference between Doppler andcatheter gradients was 4.2 ± 3.3 mmHgfor peak and 0.5 ± 1.25 mmHg for meangradients, respectively. Orifice areas ascalculated by the Doppler continuityequation did not show flow dependentchanges. In contrast, orifice areas calcu-lated by the Gorlin formula increasedslightly by 10 to 15 % in small valves.

Conclusion: Peak and mean Dopplergradients across Sorin tilting disc valvesaccurately reflect the pressure drop asdetermined by catheter measurements.Prosthetic valve areas calculated withthe Gorlin formula increase with increas-ing flow in small valve sizes whereas noflow dependent changes were observedin continuity equation valve areas.

POLYMORPHIC MEMBRANE PROTEINS(PMPS) OF CHLAMYDIA PNEUMONIAEINDUCE THE CHEMOKINES INTERLEUKIN-8(IL-8) AND MACROPHAGE CHEMOTACTICPROTEIN-1 (MCP-1) AND THE PRO-INFLAMMATORY CYTOKINE INTERLEUKIN-6(IL-6) IN HUMAN UMBILICAL VEINENDOTHELIAL CELLS (HUVECS) IN-VITRO

A. Niessner1, C. Kaun1, G. Zorn1,G. Christiansen2, A. S. Pedersen2,S. Simon3, A. Georgopoulos3,W. Graninger3, G. Maurer1, K. Huber1,J. Wojta1

1Department of Internal Medicine II,University of Vienna, Austria, 2Depart-ment of Medical Microbiology,University Aarhus, Denmark, 3Depart-ment of Internal Medicine I, Universityof Vienna, Austria

Background: IL-6, IL-8 and MCP-1 arepresent in atherosclerotic lesions of thevessel wall. Based on clinical studies arole for C. pneumoniae in the develop-ment of atherosclerosis is currently dis-cussed. Recent in-vitro studies haveshown that C. pneumoniae can activatecultured endothelial cells thereby inducingamong other effects also IL-6, IL-8 andMCP-1 expression in these cells.

Aim: It was the aim of the present studyto investigate whether purified isolatedcomponents of C. pneumoniae, namelypolymorphic membrane proteins (PMPs)could affect production of IL-6, IL-8 andMCP-1 in human endothelial cells in-vitro.

Methods: HUVECs were incubated withpurified PMPs. In order to exclude pos-sible LPS-mediated effects aliquots of therespective PMPs were boiled for 5minutes prior to addition to HUVECs.Plasminogen activator inhibitor-1 (PAI-1),IL-6, IL-8 and MCP-1 were quantified byspecific ELISAs.

Results:1. Out of 15 PMPs tested PMP 20 andPMP 21 were the strongest inducers ofIL-6, IL-8 and MCP-1 production inHUVECs. The effects were dose and timedependent.

2. The effect of PMP 20 and PMP 21 onIL-6, IL-8 and MCP-1 was abolished byheat-treatment.

Table 5: J. Lietava et al.Mono Two Three � Four Together

drugs drugs drugs[%] [%] [%] [%] [%]

SBP > 139 mmHg 66.5 73.2 79.4 90.9 64.2DBP > 89 mmHg 44.9 53.4 54.4 63.6 35.8SBP + DBP normal 29.5 23.8 15.7 9.1 26.6

1556 895 159 12 2622

18 J KARDIOL SUPPL E/2001

CARDIOLOGY 2001ABSTRACTS

3. None of the PMPs tested had an effecton PAI-1 production in HUVECs.

Conclusions: We conclude from our datathat specific PMPs of C. pneumoniae in-duce the expression of pro-inflammatorycytokines in HUVECs in-vitro. If such amechanism is also operative in-vivo, C.pneumoniae could by specific interactionsof its PMPs with the endothelium con-tribute to the process of vascular injuryduring the development of an athero-sclerotic lesion.

SELDOM FIBROTIC BAND IN THE AORTICARCH AS A CAUSE OF AN INNOCENTMURMUR

J. Nothroff1, G. S. Suemenicht2, A. Wessel21Department of Thoracic andCardiovascular Surgery, 2Department ofPaediatric Cardiology, UniversityChildren’s Hospital Goettingen,Georg-August-University, Goettingen,Germany

Background: Children with innocentmurmurs are often referred to apaediatric cardiologist for diagnosis. Themost common murmurs of early child-hood are the so called Still’s murmursfollowed by pulmonary or aortic ejectionmurmur and venous hum. There alsoexists a high coincidence with falsetendinous structures within the leftventricle. We found another seldomreason for an innocent murmur.

Methods: We report 6 patients (age 5to 22 years) presented to our outpatientpediatric cardiology clinic for workupof heart murmur. None of them hadabnormalities on clinical exam, ECGor echocardiography. They presenteda similar murmur that in contrast toinnocent murmurs was also audible overthe back. The echocardiography wasdone on two different echo-machineswith cross-sectional and colour-Dopplerand the string was reproducible fromevery examiner.

Results: With closer examination ofthe aorta with cross-sectional echowe revealed an echogenic, tendinousstructure in all 6 patients crossing eitherthe lumen of the descending aorta oraortic arch as another cause for innocent

heart murmur. The characterization wasmade by auscultation, but localizationand proof was made by echocardio-graphy of existing intraaortic structures.

Conclusions: We suggest that if intra-ventricular echo is normal, and themurmur is not consistent with a Still’smurmur or aortic/pulmonic ejectionmurmur, that echo exam should includea thorough evaluation for seldom ten-dinous structures in the aortic arch. Moreinvasive diagnostic testing does notappear to be indicated, if the diagnosis ismade by an experienced cardiologist.

ELECTROPHYSIOLOGICALLY GUIDED RISKSTRATIFICATION AND ICD THERAPY INPATIENTS WITH UNEXPLAINED SYNCOPE,NO DOCUMENTED VENTRICULAR ARRHYTH-MIAS AND STRUCTURAL HEART DISEASE

T. Pezawas, G. Stix, M. Wolzt, J. Kastner,C. Mayer, D. Moertl, H. SchmidingerDepartment of Cardiology, University ofVienna, Austria

Aims: To evaluate electrophysiologicallyguided implantable cardioverter defibril-lator (ICD) therapy in patients with syn-cope, no documented ventricular tachy-cardia (VT) and structural heart disease.

Methods and Results: Programmed ven-tricular stimulation (PVS) was performedin 52 patients for risk stratification. Themean age was 62 ± 10 years; 40 patientshad ischaemic and 12 patients hadidiopathic cardiomyopathy. On PVSsustained VTs and ventricular fibrillationwere induced in 7 and 4 patients,respectively. Two non-inducible patientsspontaneously experienced symptomaticventricular tachyarrhythmias shortly afterPVS in hospital. These patients receivedan ICD (ICD group, n = 13). Theremaining non-inducible patients wereleft on best conventional therapy (nonICD group, n = 39). During a follow-upperiod of 4.6 ± 2.7 years, 5 ICD patientsreceived appropriate therapies. One and6 patients died in the ICD and non-ICDgroup, respectively, and all deaths werenon-sudden. Overall survival analysisrevealed no significant difference. Thepositive and negative predictive valuesof PVS for tachyarrhythmias or suddendeath were 36 % and 95 %, respectively.

Conclusions: In patients with structuralheart disease, unexplained syncope andno documented sustained ventricular ar-rhythmias PVS reliably identifies patientsat high risk for life-threatening tachyar-rhythmias. Patients with severely de-pressed left ventricular function and badclinical condition appear to benefit most.In this patient population primary ICD im-plantation appears the treatment of choice.

MILD AND MODERATE AORTIC STENOSIS:A SERIOUS DISEASE?

R. Rosenhek, T. Binder, M. Heger,C. Scholten, M. Zehetgruber, G. Maurer,H. BaumgartnerDepartment of Cardiology, Universityof Vienna

Background: Rapid progression frommild and moderate aortic stenosis tosevere disease has been observed. How-ever, the natural history of this diseaseremains insufficiently determined.

Methods: Therefore, we prospectivelyfollowed 176 consecutive patients (73female, age 58 ± 19 yrs) with mild tomoderate aortic stenosis (jet velocity2.5–4.0 m/s) from 1994 to 1999. Therate of progression of the peak aortic jetvelocity was calculated, and a survivalanalysis was performed.

Results: Mean follow-up was 3.9 ± 1.6 yrs.Kaplan-Meier event-free survival for theentire patient group, with endpointsdefined as death (n = 34) or aortic valvesurgery (n = 33), was 95 ± 2 % at 1 yr,75 ± 3 % at 3 yrs, and 60 ± 4 % at 5 yrs.Among 18 cardiac deaths, 6 were sudden,1 patient had endocarditis and 11 con-gestive heart failure. Mean rate of pro-gression of peak aortic jet velocity for theentire population was 0.24 ± 0.3 m/s/yr,but varied widely (–0.2 to 1.3 m/s/yr). Itwas significantly faster for patients withan endpoint (0.43 ± 0.04 m/s/yr), than forthose without event (0.14 ± 0.02 m/s/yr;p < 0.0001). Patients younger than 50years had a significantly better outcomewith event-free survival rates of 100 % at1 yr, 95 ± 3 % at 3 yrs, and 89 ± 5 % at5 yrs compared with 93 ± 2 %, 68 ± 4 %,and 49 ± 5 % for patients older than 50years (p < 0.0001). Peak aortic jet velocityat entry was also a significant predictorof outcome.

20 J KARDIOL SUPPL E/2001

CARDIOLOGY 2001ABSTRACTS

Of 129 patients with a follow-up echo-cardiographic exam, 59 (46 %) reacheda peak aortic jet velocity of 4 m/s orgreater during follow-up.

Conclusion: Rapid progression from mildor moderate to haemodynamicallysevere aortic stenosis is common. Inparticular, patients older than 50 yearsand patients in whom echocardiographicfollow-up reveals a rapid increase ofpeak aortic jet velocity have a poor out-come. Thus, moderate and even mildaortic stenosis cannot be considered abenign disease and rapid progression isfrequent.

THE ANGIOTENSIN-CONVERTING ENZYMEINHIBITOR LISINOPRIL LOWERS PLASMALEVELS OF C-REACTIVE PROTEIN AFTERMYOCARDIAL INFARCTION MORE EFFICIENTLYTHAN ANGIOTENSIN II TYPE 1 RECEPTORANTAGONISTS

W. S. Speidl, M. Nikfardjam,N. Jordanova, J. Wojta, K. HuberDepartment of Cardiology, University ofVienna, Austria

Background: Recent studies have shownthat atherosclerosis is prevented inanimal models and humans by blockageof the renin-angiotensin system via angio-tensin converting enzyme inhibitors (ACEI)or antagonists of the angiotensin II type 1receptor (AT1-antagonists), possibly by anantiinflammatory mechanism. Wecompared the antiinflammatory effects ofACEI and AT1-antagonists after acutemyocardial infarction (AMI) by measure-ment of high sensitivity C-reactive protein(CRP), a sensitive marker for ongoinginflammation and strong predictor ofcardiovascular risk.

Methods: 63 patients with their first AMIand after fibrinolytic therapy were includ-ed in our study and randomized in a 2:1ratio to receive either lisinopril 5 mg/d(n = 42) or an AT1-antagonist (losartan50 mg/d, n = 11; valsartan 80 mg/d,n = 10) starting 24 hours after the acuteevent. After 6 weeks of treatment theinitial dose of lisinopril was increasedduring two weeks in steps of 5 mg to40 mg/d whereas the initial dose of theAT1-antagonists was not changed. Blood

samplings were obtained after 10 days,6 weeks and 6 months of treatment.

Results: At 6 weeks, CRP-levels decreasedin both groups (lisinopril: p < 0.001, AT1-antagonists: p < 0.05). A further decreaseup to 6 months was only observed in thelisinopril group (p < 0.05) while nochange was seen in the AT1-antagonistgroup. After six months, median CRP-plasma levels in patients receiving lisino-pril were 67.6 % lower than in patientsreceiving AT1-antagonists (0.12 mg/dl vs0.37 mg/dl, p < 0.05).

Conclusion: The ACEI lisinopril loweredplasma levels of C-reactive protein moreefficiently than the AT1-antagonistslosartan and valsartan. ACE inhibitionand the stabilization of bradykinin andsubsequent increase in the production ofthe antioxidant nitric oxide (NO) may beresponsible for the stronger antiinflamma-tory effect of high dose lisinopril. Whetheran increase of dosage of AT1-antagonistsmight have similar antiinflammatoryeffects via other mechanisms, eg increasedNO production due to stronger stimulationof AT2 receptors remains to be proven.

INTRACORONARY ADMINISTRATION OF ACASPASE-1-INHIBITOR (AC-YVAD-CMK)REDUCES NEOINTIMAL HYPERPLASIA AFTERSTENTING OF PORCINE CORONARY ARTERIES

W. Sperker1, M. Gyöngyösi1,U. Windberger2, M. Gottsauner-Wolf1,P. Wexberg1, D. Bonderman1, I. M. Lang1,St. Marlovits3, H. D. Glogar1

1Department of Cardiology, 2Center forBiomedical Research, 3Department ofTrauma-Surgery, University of Vienna,Austria

Background: The irreversible caspase-1inhibitor Ac-YVAD-cmk inhibits apopto-sis and proinflammatory cytokine release.In contrast to apoptosis inhibition, thechloromethylketone chain of Ac-YVAD-cmk increases smooth muscle cell apo-ptosis through elastase inhibition. Theaim of the present study was to reduceneointimal proliferation after coronarystent implantation using Ac-YVAD-cmk.

Methods: After general anaesthesia,domestic pigs received intracoronaryinfusion of 50 mg Ac-YVAD-cmk

(dissolved in 1 ml dimethylsulfoxid[DMSO] and 59 ml phosphate buffer[PBS], infusion rate 6 ml/min) into theleft coronary artery (group 1, n =10),while 8 animals served as untreatedcontrols (group 2) and 6 further pigs asvehicle controls (DMSO + PBS) (group 3).One coronary stent was then implantedin the left anterior descending or circum-flex coronary artery. After 4 weeks,control angiography and intravascularultrasound (IVUS) were performed. IVUSparameters were measured using acomputer-assisted 3D analysis system.

Results: Ac-YVAD-cmk reduced in-stentneointimal volume (29.1 ± 12.5 vs 80.5± 24.9 and 67.4 ± 22.3 mm3, p < 0.005)and maximal area stenosis (38.6 ± 8.0 vs71.0 ± 6.4 and 67.0 ± 9.9 %, p < 0.001)assessed by IVUS in group 1 vs groups 2and 3, but did not influence vessel re-modeling (maximal vessel area 12.4 ± 3.3vs 13.5 ± 2.1 and 12.3 ± 2.7 mm3, non-significant). Smaller maximal neointimalthickness (0.38 ± 0.19 vs 0.94 ± 0.37and 0.97 ± 0.44 mm, p < 0.01) anddecreased maximal neointimal area(1.73 ± 1.53 vs 3.66 ± 1.54 and 4.03 ±0.86 mm2, p < 0.01) assessed by histology(computerized planimetry) were found inpigs in group 1 vs groups 2 and 3. IVUSresults (maximal neointimal area andneointimal thickness) correlated signifi-cantly with histological data (r = 0.774,p < 0.001 and r = 0.699, p < 0.001,respectively). Injury score did not differsignificantly between the groups.

Conclusion: Our data indicate that thecaspase-1 inhibitor Ac-YVAD-cmkreduces in-stent neointimal proliferation.IVUS allows a quantitative 3D analysisof experimental neointimal proliferationand vessel remodeling and is able toguide targeted histological analysis.

ARTERIAL COMPLIANCE: A PREDICTOR OFCARDIOVASCULAR DISEASES?

B. Syeda, M. Gottsauner-Wolf, S. Denk,P. Pichler, A. Khorsand, T. Schoenau,H. D. GlogarDepartment of Cardiology, University ofVienna, Austria

Background: Measures of the arterialcompliance can be derived non-invasivelyfrom pressure pulse contour analysis of

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