Kardio 365 - úvodní stránka
nepřihlášen  
Change language:    

IMPACT OF ATHEROSCLEROTIC DISEASE PROGRESSION FOR REPEAT REVASCULARIZATION IN DIABETIC PATIENTS IN THE DRUG-ELUTING STENT ERA

P. Toušek, J. Oreglia, B. Farah, J. Fajadet (Prague, Toulouse, France)
Tématický okruh: Intervenční kardiologie
Typ: Poster - lékařský, XVI. výroční sjezd ČKS

Background : 
Impact of restenosis or atherosclerosis progression on revascularization in drug-eluting stent era is not well known.

Aim : 
To determinate if repeat revascularization in the diabetic patients treated with prior DES, is the result of DES restenosis or due to native progression of atherosclerotic disease in the coronary vasculature.

Methods and Results:
We followed 364 consecutive diabetic patients (264 men, age 68 + 8.8 years)  treated between April 2005 and September 2006 with at least one DES. Out of these 292 patients (80%) had multivessel coronary disease, 148 patients (41%) had previous coronary revascularization and 109 patients (30%) had insulin-dependent DM.  During the follow-up (range 12-28 months, mean 18 + 8 months) there were 39 repeat revascularizations (38 PCI, 1 CABG). In 20 patients repeat revascularization was performed for restenosis (18 after DES implantation, 1 after BMS implantation and 1 after balloon angioplasty), out of which in 3 patients treatment was also required for disease progression. In 19 patients PCI was performed for symptomatic atherosclerotic disease progression without restenosis. Thus disease progression contributed to 52% of repeat revascularization procedures. Furthermore, in 5 of 6 patients (83%) admitted for myocardial infarction, culprit lesion was caused by atherosclerotic disease progression.

Conclusion
Atherosclerotic disease progression was more than 50% the cause of revascularization in diabetics patients treated previously with DES and was the main cause of readmission for myocardial infarction. Major  adverse clinical events in trials with long term follow-up in diabetic patients can thus be influenced by native disease progression and not by DES failure and therefore should be interpreted with caution.