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IVUS Guidance

Abstract

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In vivo intravascular ultrasound-derived thin-cap fibroatheroma detection using ultrasound radiofrequency data analysis Impact of plaque components on no-reflow phenomenon after stent deployment in patients with acute coronary syndrome: a virtual histology-intravascular ultrasound analysis Differential prognostic effect of intravascular ultrasound use according to implanted stent length Intravascular ultrasound assessment of the effects of rotational atherectomy in calcified coronary artery lesions Is intravascular ultrasound beneficial for percutaneous coronary intervention of bifurcation lesions? Evidence from a 4,314-patient registry Intravascular ultrasound predictors for edge restenosis after newer generation drug-eluting stent implantation Comprehensive intravascular ultrasound assessment of stent area and its impact on restenosis and adverse cardiac events in 403 patients with unprotected left main disease Histopathologic validation of the intravascular ultrasound diagnosis of calcified coronary artery nodules

Original Research2008 Mar 1;101(5):568-72.

JOURNAL:Am J Cardiol. Article Link

A three-vessel virtual histology intravascular ultrasound analysis of frequency and distribution of thin-cap fibroatheromas in patients with acute coronary syndrome or stable angina pectoris

Hong MK, Mintz GS, Lee CW et al. Keywords: Three-Vessel Virtual Histology; intravascular ultrasound analysis; frequency; distribution; thin-cap fibroatheromas; acute coronary syndrome; stable angina pectoris

ABSTRACT


The frequency and distribution of thin-cap fibroatheromas (TCFA) have important clinical implications. We evaluated the frequency and distribution of TCFA identified by virtual histology intravascular ultrasound (VH-IVUS) in acute coronary syndrome (ACS) and stable angina pectoris (SAP). Preintervention 3-vessel VH-IVUS was performed in 105 patients with ACS and 107 with SAP. The length of left anterior descending artery imaged was 72 +/- 16 mm-54 +/- 12 mm in the left circumflex and 92 +/- 19 mm in the right coronary. VH-IVUS-derived TCFA (VH-TCFA) had a necrotic core > or =10% of plaque area without overlying fibrous tissue in a plaque burden > or =40%. There were 76 ruptured plaques (55 in ACS and 21 in SAP) and 439 VH-TCFA (262 in ACS and 177 in SAP, 2.5 +/- 1.5 vs 1.7 +/- 1.1 TCFA per patient with ACS and with SAP, respectively; p <0.001). Twelve patients with ACS and 1 with SAP had multiple ruptured plaques (p <0.001); 76 patients with ACS and 58 with SAP had multiple VH-TCFA (p = 0.009). Presentation of ACS was the only independent predictor for multiple ruptured plaques (p = 0.013) or multiple VH-TCFA (p = 0.011). Eighty-three percent of VH-TCFA were located within 40 mm of the coronary: 111 < or =10 (25%), 110 from 11 to 20 (25%), 83 from 21 to 30 (19%), and 61 from 31 to 40 mm (14%). The axial distribution of VH-TCFA was similar in patients with ACS and those with SAP and was similar to the axial distribution of ruptured plaques. In conclusion, 3-vessel VH-IVUS imaging showed a higher frequency of VH-TCFA in primary and secondary lesions in patients with ACS compared with those with SAP, but showed a similar clustering of VH-TCFA in the proximal 40 mm of each coronary artery.