ORIGINAL ARTICLES

Acute coronary syndromes

Predictors of slow flow during primary percutaneous coronary intervention: an intravascular ultrasound-virtual histology study

J H Bae¹, T-G Kwon¹, D-W Hyun¹, C S Rihal² and A Lerman²

¹ Division of Cardiology, Konyang University Hospital, Daejeon, South Korea
² Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA

Correspondence to:
Dr Jang-Ho Bae, Division of Cardiology, College of Medicine, Konyang University Hospital, 685 Gasoowon-dong, Seo-gu, Daejeon, South Korea; janghobae{at}yahoo.co.kr

Objectives: Slow flow phenomenon is a serious complication of percutaneous coronary intervention (PCI) and is associated with a poor prognosis. We sought to evaluate the characteristics of lesions predisposing to the slow/no-reflow phenomenon during primary PCI in patients with acute myocardial infarction.

Methods: The study subjects consisted of 57 consecutive patients (mean age 58.5 (SD 14.5) years, 45 males) who underwent primary PCI for acute myocardial infarction and intravascular ultrasound-virtual histology (IVUS-VH) examination. Slow flow was defined as thrombolysis in myocardial infarction grade 2 after PCI.

Results: Slow flow developed in 12 patients (eight males). Patients with slow flow were likely to be older (67.5 (13.8) years vs 56.2 (13.9) years, p = 0.015), had more cardiogenic shock (16.7% vs 2.2%, p = 0.046), larger fibrofatty volume over the entire lesion length (36.7 (25.5) mm³ vs 18.0 (18.6) mm³, p = 0.006), higher remodelling index (1.10 (0.17) vs 0.99 (0.16), p = 0.043), larger plaque area (16.2 (5.4) mm² vs 12.5 (4.9) mm², p = 0.025), fibrous area (8.0 (3.3) mm² vs 5.4 (3.0) mm², p = 0.014) and fibrofatty area (2.7 (2.2) mm² vs 1.3 (1.6) mm², p = 0.016) at the minimal lumen site than those without slow flow (37 males). Multivariate analysis revealed that the fibrofatty volume over the entire lesion length was the only independent factor (β = 0.359, 95% confidence interval 0.002 to 0.012, p = 0.006) for slow flow during primary PCI.

Conclusions: This study suggests that slow flow may be dependent on the tissue characterisation (fibrofatty volume) of the underlying lesion at the time of the primary PCI for acute myocardial infarction.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

• Mitani, Y., Ohashi, H., Sawada, H., Ikeyama, Y., Hayakawa, H., Takabayashi, S., Maruyama, K., Shimpo, H., Komada, Y. (2009). In Vivo Plaque Composition and Morphology in Coronary Artery Lesions in Adolescents and Young Adults Long After Kawasaki Disease: A Virtual Histology-Intravascular Ultrasound Study. Circulation 119: 2829-2836 [Abstract] [Full Text]  
• Raichlin, E., Bae, J.-H., Kushwaha, S. S., Lennon, R. J., Prasad, A., Rihal, C. S., Lerman, A. (2009). Inflammatory burden of cardiac allograft coronary atherosclerotic plaque is associated with early recurrent cellular rejection and predicts a higher risk of vasculopathy progression.. J Am Coll Cardiol 53: 1279-1286 [Abstract] [Full Text]  
• Hong, Y. J., Jeong, M. H., Choi, Y. H., Ko, J. S., Lee, M. G., Kang, W. Y., Lee, S. E., Kim, S. H., Park, K. H., Sim, D. S., Yoon, N. S., Youn, H. J., Kim, K. H., Park, H. W., Kim, J. H., Ahn, Y., Cho, J. G., Park, J. C., Kang, J. C. (2009). Impact of plaque components on no-reflow phenomenon after stent deployment in patients with acute coronary syndrome: a virtual histology-intravascular ultrasound analysis. Eur Heart J 0: ehp034v1-8 [Abstract] [Full Text]