Evaluation of culprit saphenous vein graft lesions with optical coherence tomography in patients with acute coronary syndromes

Periklis Davlouros, Anastasia Damelou, Vasileios Karantalis, Ioanna Xanthopoulou, Eleni Mavronasiou, Grigorios Tsigkas, George Hahalis, Dimitrios Alexopoulos
JACC. Cardiovascular Interventions 2011, 4 (6): 683-93

OBJECTIVES: This study sought to assess, with optical coherence tomography (OCT), presumably culprit atherosclerotic lesions of saphenous vein grafts (SVGs) in patients with acute coronary syndromes (ACS).

BACKGROUND: Atherosclerotic lesions of SVGs have been studied in vivo with angioscopy and intravascular ultrasound. However, imaging with OCT, which has a higher resolution than intravascular ultrasound and better penetration than angioscopy, has not been conducted systematically.

METHODS: Using a nonocclusive OCT technique, we performed angiography and OCT of culprit SVG lesions in patients with unstable angina (UA), ST-segment elevation myocardial infarction (STEMI), and non-STEMI. Fibrous and fatty tissue, calcification, thrombus, and plaque rupture were defined according to OCT objective criteria.

RESULTS: Twenty-eight SVGs (average age 14.6 years) in 26 patients were imaged. Lesions on angiography were complex (96.4%), with ulceration in 32.1% and thrombus in 21.4%. OCT disclosed a fibrofatty composition in all lesions, calcification in 32.1%, plaque rupture in 60.7%, and thrombus in 46.4%. Thrombus was progressively more frequent across groups (UA to STEMI, p = 0.003; UA vs. myocardial infarction, p = 0.006). A thin fibrous cap was marginally more frequent in myocardial infarction patients (UA vs. myocardial infarction, p = 0.06; STEMI 100% vs. non-STEMI 53.3% vs. UA 20%, p = 0.03). OCT features of friability were present in 67.9% of SVGs not correlating with clinical presentation.

CONCLUSIONS: OCT of culprit lesions of old SVGs in patients with ACS demonstrates fibrofatty composition, relatively thin fibrous cap, plaque rupture, and thrombus, which correlate with the clinical spectrum of ACS. This suggests that similar mechanisms with native vessels' atherosclerosis may be involved in SVG-related ACS.

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