Characteristics of culprit atheromatous plaques obtained in vivo by intravascular ultrasound radiofrequency analysis: Results from the CULPLAC study

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• 作者：José ; D. Cascó ; n-Pé ; rez ; MD ; PhD^a ; ^{josedomingocascon@gmail.com} ; José ; M. de la Torre-Herná ; ndez ; MD ; PhD ; FESC^b ; Marí ; a C. Ruiz-Abelló ; n ; MD ; PhD^a ; ^c ; Miryam Martí ; nez-Pascual ; MD^a ; Rosario Má ; rmol-Lozano ; MD^a ; José ; Ló ; pez-Candel ; MD ; PhD^a ; Pedro Cano ; MD^a ; Concepció ; n Ferná ; ndez ; MD^a ; José ; L. Ramos ; MD^a ; Manuel Villegas ; MD ; PhD^a ; Francisco Picó ; -Aracil ; MD ; PhD^a
• 刊名：American Heart Journal
• 出版年：2013
• 出版时间：March, 2013
• 年：2013
• 卷：165
• 期：3
• 页码：400-407
• 全文大小：493 K

文摘

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Objectives

We used virtual histology-intravascular ultrasound (VH-IVUS) to investigate the characteristics of culprit lesions in acute coronary syndromes (ACS).

Background

Autopsy studies of patients who died of ACS have shown that culprit atheromatous plaques almost always contain a large lipid-necrotic core covered by a ruptured thin fibrous cap. There are no studies of sufficient size that have assessed the in vivo characterization of plaques responsible for ACS.

Methods

Patients undergoing angiography for stable ischemic heart disease and ACS (with and without ST-segment elevation) were enrolled in a prospective study. Lesions in patients with stable angina were classified as stable and those in patients with ACS as culprit or nonculprit.

Results

The study included 189 patients: VH-IVUS was used to assess 253 lesions (73 stable, 82 nonculprit, and 98 culprit lesions).

The thin-cap fibroatheroma phenotype (VH-TCFA) was more frequent among lesions in patients with ACS (55.1 % in culprit lesions, 36.6 % in nonculprit lesions and 14.4 % in stable lesions; P = .007). The arc of the VH-TCFA exposed to the vessel lumen was significantly greater in culprit lesions than in nonculprit lesions (122.28¡ã ¡À 58 vs 89.46¡ã ¡À 52; respectively; P = .007).

Multivariate analysis showed that VH-TCFA (OR 2.1; P = .033), calcified nodules (OR 2.1; P = .046), positive remodeling (OR 3.5; P < .001) and necrotic core volume (OR 1.02;P = .009) were independently associated with a clinically identified culprit lesion.

Conclusions

Plaque phenotype, rather than the proportion of each tissue, appears to be associated with plaque instability. VH-TCFA, particularly subtype IV, is associated with lesions responsible for ACS.