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ÖKG-Jahrestagung – Abstracts

J KARDIOL 2008; 15 (5–6)

185

Zur Publikation nachgereichte Abstracts

(Die Arbeiten wurden rechtzeitig eingereicht und positiv begutachtet,

wegen technischer Probleme aber zur Publikation nachgereicht)

Oncostatin M-enhanced Vascular Endothelial Growth

Factor Production by Human Vascular Smooth Mus-

cle Cells is Attenuated by Interferon-gamma 121

S. Demyanets, C. Kaun, G. Rega, K. Rychli, P. J. Hohensinner, S. Pfaffenberger,

T. Afonyushkin, V. N. Bochkov, G. Maurer, K. Huber, J. Wojta

Department of Internal Medicine II, Medical University of Vienna; 3

Med. Dept.,

Cardiology and Emergency Medicine, Wilhelminenhospital, Vienna

Background Vascular endothelial growth factor (VEGF) is present

in atherosclerotic lesions and involved in blood vessel growth and

in the regulation of the expression of prothrombotic and proinflam-

matory mediators in monocytes and endothelial cells at these sites.

Oncostatin M (OSM) is a member of the glycoprotein 130 (gp130)

receptor cytokine family. It is controversial whether interferon-γ

(IFN-γ), which is expressed at high levels in atherosclerotic lesions,

promotes or attenuates vascular remodelling in hyperproliferative

vascular disorders, such as neointima formation after balloon in-

jury.

Methods Human coronary artery smooth muscle cells (HCASMC)

and human aortic SMC (HASMC) were treated with the gp130

ligands OSM, cardiotrophin-1 (CT-1), cardiotrophin-like cytokine

(CLC), ciliary neurotrophic factor (CNTF), IL-6, IL-11 or leukemia

inhibitory factor (LIF). VEGF-A protein was determined by a spe-

cific ELISA and mRNA specific for VEGF-A, gp130, OSM receptor

(OSMR), IL-6 receptor (IL-6R) and LIF receptor (LIFR) was de-

tected by RT-PCR.

Results Only OSM increased VEGF production significantly in

both HCASMC and HASMC up to 7-fold in a dose- and time-

dependent manner. The effect of OSM on VEGF production was

reproducible in the preparation of HCASMC and HASMC derived

from different donors (n = 9 for HCASMC, n = 6 for HASMC).

OSM upregulated also mRNA specific for VEGF in these cells.

OSM induced Akt and p38 MAPK phosphorylations in HASMC.

PI3K inhibitors and p38 MAPK inhibitors reduced OSM-induced

Akt and p38 MAPK phosphorylation, and VEGF upregulation.

HCASMC and HASMC were shown to express gp130, OSMR, IL-

6R and LIFR. IFN-γ, but not IL-4 or IL-10, dose-dependently reduced

OSM-induced VEGF production on protein and mRNA levels in

both HCASMC and HASMC. We found a culture-condition-depend-

ent effect of OSM and IFN-γ on proliferation of these cells.

Conclusion We show here that OSM induces VEGF production

in vascular SMC. Since activated T-cells and macrophages have

been found in atherosclerotic lesions we hypothesize that OSM pro-

duced by these cells could induce VEGF production thereby con-

tributing to plaque angiogenesis and destabilization. IFN-γ attenu-

ates OSM-induced VEGF production by vascular SMC.

Immediate and Long-term Clinical Outcome After

Percutaneous Mitral Valvuloplasty (PMV) in Austria

118

J. Moser, T. Binder, H. Baumgartner, P. Probst, U. Klaar, G. Maurer, I. M. Lang

Division of Cardiology, Department of Internal Medicine II, Medical University of

Vienna

Introduction Since its introduction in 1984 by Inoue, the tech-

nique of percutaneous balloon mitral valvuloplasty (PMV) has been

confirmed as a safe and effective procedure, and is still first-line

therapy in patients with symptomatic mitral stenosis (MS) and suit-

able valve morphology.

Few long-term echocardiographic and clinical follow-up studies

of PMV are available in Europe, with a high percentage of elderly

patients and unfavorable valve morphologies.

Aims We evaluated immediate valvular changes (mitral valve area

and mean mitral valve gradient) after PMV performed between

1990 and 2005 at the General Hospital of Vienna, and long-term

clinical outcomes.

Methods and Results We report the immediate procedural

results of 141 patients (mean age 51.5 ± 16 years; range 17 to 82),

the long-term clinical outcomes in 90 patients over a mean observa-

tion period of 73.3 ± 56 months (range, 3 to 199 months). Echo-

cardiographic follow-ups were available in 89 patients after a mean

observation period of 62.7 ± 49 months (range, 1 to 194 months).

Kaplan-Meier analysis was performed to estimate event-free sur-

vival (death and mitral valve replacement).

There were 6 (4.3 %) unsuccessful PMV procedures, and one

(0.7 %) urgent mitral valve replacement. No procedure-related

deaths occurred. PMV resulted in an immediate increase in mitral

valve area from 1.04 ± 0.56 to 1.69 ± 0.38 cm² (p = 0.372), and

in a change of mean mitral valve gradient (mGrad) from 13.56 ±

11.08 mmHg to 5.59 ± 2.80 (p = 0.002). Mitral area loss was 1.44 ±

0.34 (p = 0.0001) at 62.7 ± 48 months after PMV, and mGrad had

increased to 7.62 ± 2.84 mmHg (p = 0.01). Mean NYHA functional

class was III prior to and II at 73.3 ± 56 months after PMV after

(p = 0.34). Atrial fibrillation was present in 50 patients (35.5 % of

117; 42.7 valid %) and in 59 patients (41,8 % of 76, 77.6 valid %)

after PMV (p = 0.0001). Survival free of mitral valve replacement

(MVR) was 75.4 %, 53.9 %, 44.3 % and 24.2 % at 1, 5, 10 and 15

years, respectively (n = 61, number of MVR: 36, Figure 9). Survivals

were 100 %, 89.4 %, 86.6 % and 70.7 % at 1, 5, 10 and 15 years,

with 7 reported deaths.

Conclusions Immediate and long-term clinical and echocardio-

graphic results of PMV in Austria, including many elderly patients

are good. PMV is an effective procedure to increase mitral valve

area, to decrease symptoms of MS (NYHA functional class) and to

Figure 9:

J. Moser et al.

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