Vol 68, No 10 (2010)
Original articles
Published online: 2010-10-22

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Virtual histology intravascular ultrasound evaluation of the left anterior descending coronary artery in patients with transient left ventricular ballooning syndrome

Tomasz Pawłowski, Gary S. Mintz, Tomasz Kulawik, Robert J. Gil
DOI: 10.33963/v.kp.79929
Kardiol Pol 2010;68(10):1093-1098.

Abstract


Background: Transient left ventricular ballooning syndrome (TLVBS) has been recently recognised as an acute disease mimicking myocardial infarction.
Aim: We used greyscale and virtual histology (VH) intravascular ultrasound (IVUS) to study the presence and characteristics of atherosclerotic plaque in the left anterior descending (LAD) artery in patients with TLVBS.
Methods: The study population consisted of 14 consecutive patients with a TLVBS diagnosis based on typical symptoms and balloon-like left ventricle abnormalities. The IVUS imaging and analysis included at least the mid and proximal segments of each LAD. Virtual histology (VH)-IVUS analysis colour-coded plaque as calcific, fibrotic, fibrofatty, and necrotic core; VH-IVUS-derived thin-cap fibroatheroma (TCFA) and high-risk plaques were identified.
Results: The total length of the IVUS-analysed LAD averaged 55 ± 14 mm. Greyscale analysis revealed a mean plaque burden of 28.9 ± 11%. There were 7 ruptured plaques; these were present in mid-segments of the LAD in 3 patients, and in the proximal segment in 4 patients. The VH-TCFAs were found in 8 patients, while the remaining 6 patients had a necrotic core > 25%. The average number of VH-TCFAs was 4.8 ± 2.9 per patient. Combining greyscale and VH-IVUS data, 8 patients had either a ruptured plaque or a VH-TCFA, while the other 6 patients had a necrotic core > 25%. The distance from the coronary ostium to the cross-sections with a VH-TFCA was 20 ± 2.8 mm.
Conclusions: Vulnerable plaques are observed in patients with TLVBS. Our findings support the hypothesis that TLVBS may be related to the natural course of atherosclerotic plaque development. Further study into the relations between vulnerable plaque surface, platelet activity and subsequent thrombus formation is needed in this population.
Kardiol Pol 2010; 68, 10: 1093-1098

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