Hintergrund und Fragestellung: Die
Progression der koronaren Herzkrankheit (KHK) wird nur unvollständig
verstanden. Dies gilt für native Stenosen wie für
In-Stent-Restenosen (ISR) als Extremform akzelerierter Arteriosklerose.
Fragestellung der vorliegenden angiographischen Studie war, ob Restenosierung
nach Stentim-plantation mit der Progression unbehandelter Läsionen
assoziiert ist.
Patienten und Methodik: Insgesamt 179
höhergradige native Koronarstenosen (mittlerer Stenosegrad
68±16 %) von 131 Patienten wurden mittels
Stentimplantation behandelt; zusätzliche 101 mäßig-
bis mittelgradige Läsionen (Stenosegrad > 30 %)
wurden so belassen. 6±2 Monate später erfolgte
eine quantitative koronarangiographische Evaluierung der Koronarien
hinsichtlich ISR (Stenosegrad > 50 %),
koronarer Progression (Zunahme des Stenosegrades um > 20 %)
bzw. Regression (Abnahme um > 20 %).
Angiographische, prozedurale und klinische Charakteristika wurden
auf eine Assoziation zu ISR, Progression und/oder Regression
untersucht.
Ergebnisse: In 70 der 179 (39 %)
behandelten Zielstenosen wurde eine ISR nachgewiesen. Prädiktiv
für ISR waren Diabetes mellitus (p = 0,04)
sowie die kumulative Dauer der Inflationen (p = 0,01)
als prozeduraler Parameter. Signifikante Progression wurde in zehn der
101 (10 %) primär unbehandelten Läsionen
nachgewiesen. Progression bei vormalig angiographisch normalem Segment
oder Regression waren nicht zu beobachten. Die Progression nativer Plaques
war in neun Fällen mit Auftreten einer ISR und nur in einem
Fall mit deren Fehlen assoziiert (p = 0,01).
Prädiktiv für Plaqueprogression waren Nikotinabusus
(p = 0,02), nicht jedoch Medikation und
prozedurale bzw. angiographische Parameter.
Folgerungen: Die Befunde der vorliegenden
Pilotstudie zeigen die Restenosierung nach Stentimplantation der
Zielstenose mit der Progression anderer primärer unbehandelter
Läsionen assoziiert und legen damit gemeinsame systemische
Pathomechanismen für beide Arterioskleroseformen nahe.
Bei Nachweis einer ISR sollte grundsätzlich auch die Darstellung
vormals unbehandelter Koronarien erfolgen, insbesondere wenn vorbestehende
Plaques bekannt sind.
Background and objectives: Progression
of coronaryartery di-sease is only incompletely understood regarding
de-novo stenoses as well as in-stent restenoses (ISR) indicative
of acce-lerated atherosclerosis. The objective of the present angiographic
study was to prove an association between target lesion ISR and
progression of primarily untreated coronary lesions.
Patients and methods: A total of 179
high-grade native coronary stenoses (mean diameter stenosis 68±16 %)
of 131 patients were treated by stent implantation. Additional 101
lesions remained untreated because of their moderate to intermediate
diameter stenoses (>30 %). Quantitative
coronary angiographic analysis was performed 6±2 months
later to evaluate ISR (diameter stenosis > 50 %),
coronary progression (>20 % increase
in diameter stenosis) and regression (>20 % decrease),
respectively. Angiographic, procedural and clinical characteristics
were assessed for a possible association with ISR and/or
coronary progression and regression, respectively.
Results: ISR was seen in 70 of 179 (39 %)
stented target lesions. Presence of diabetes mellitus (p = 0.04)
and cumulative duration of inflations (p = 0.01)
as procedural determinant were predictive for ISR. Significant progression
was found in ten of 101 (10 %) primarily untreated
lesions. Progression of previously normal segments or regression
were not seen. Progression of native plaques was associated with
ISR presence in nine cases and with ISR absence in only one case
(p = 0.01). Of note, smoking (p = 0.02)
turned out to be predictive for plaque progression, whereas medication
and procedural/angiographic parameters were not.
Conclusions: The findings of the present
pilot study demonstrate target lesion ISR associated with progression
of other primarily untreated lesions and thereby suggest that both
atherosclerosis types share common systemic pathogenetic mechanisms.
With presence of ISR, coronary angiography should also include primarily
untreated arteries, especially in case of preexisting plaques.
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Prof. Dr. med. Gerhard Bauriedel
Medizinische Klinik und Poliklinik II, Universitätsklinikum
Bonn
Sigmund-Freud-Straße 25
53105
Bonn
Phone: 0228/2876670
Fax: 0228/2874983
Email: Gerhard.Bauriedel@ukb.uni-bonn.de