In vivo detection of vulnerable plaques can help predict future acute cardiac events

In vivo detection of high-risk coronary plaques by radiofrequency intravascular ultrasound and cardiovascular outcome: results of the ATHEROREMO-IVUS study

Literature - Cheng JM Eur Heart J. 2014 - Eur Heart J. 2014 Mar;35(10):639-47

Cheng JM, Garcia-Garcia HM, de Boer SP, et al.
Eur Heart J. 2014 Mar;35(10):639-47


Post-mortem studies have revealed that acute coronary syndromes (ACS) are most often caused by thin-cap fibroatheroma (TCFA) lesions [1-3]. Being able to detect coronary lesions that are prone to rupture may have important prognostic value and help choose the best treatment. It is, however, hard to detect these high-risk lesions on coronary angiography [4].
Intravascular ultrasound (IVUS) radiofrequency analyses, or IVUS virtual histology, allow for differentiation of various plaque phenotypes, and could thus be appropriate for detection of plaques at high risk of rupture [5-7].
This study aimed to investigate the prognostic value of in vivo detection of high-risk plaques by IVUS, in patients undergoing coronary angiography for ACS (n=318) or stable angina (n=263).
Data of 581 patients enrolled in the European Collaborative Project on Inflammation and VascularWall Remodeling in Atherosclerosis – Intravascular Ultrasound (ATHEROREMO-IVUS) study were used to this end. The primary endpoint was major adverse cardiac events (MACE), encompassing mortality, ACS and unplanned coronary revascularisation. Culprit lesion-related events were not counted.

Main results

  • The presence of TCFA lesions (present: 10.8% vs. absent: 5.6%; adjusted HR: 1.98, 95% CI: 1.09–3.60; P= 0.026) and lesions with a plaque burden of at least 70% (16.2% vs. 5.5%; adjusted HR: 2.90, 95% CI: 1.60–5.25; P< 0.001) were independently associated with a higher occurrence of MACE. Lesions with a minimal luminal area of 4.0 mm2 or less was not associated with more MACE.
  • Presence of TCFA lesions was significantly associated with the composite of death or ACS (7.5% vs. no TCFA lesions 3.0%; adjusted HR: 2.51, 95% CI: 1.15–5.49; P=0.021).
  • Larger TCFA lesions further increased the risk of occurrence of MACE (if minimal luminal area of 4.0 mm2 or less, or a plaque burden > 70%, or both).
  • TCFA lesions with a plaque burden of >70% were associated with a higher MACE rate at any time during follow-up, while smaller TCFA lesions were only associated with a higher MACE rate after 6 months.


These data show that the presence of a TCFA lesion as assessed by IVUS in a non-culprit coronary artery is of predictive value for the occurrence of MACE that is not related to the index procedure. Larger TCFA lesions yielded higher event rates, while smaller TCFA lesions were only predictive of clinical events on the longer term.
Thus, virtual histology appears to be a useful tool for visualisation of such vulnerable coronary lesions in vivo, as the presence of such lesions predicted the occurrence of acute cardiac events, in particular death and ACS, both in patients who underwent coronary angiography for ACS and stable angina.

Find this article on Pubmed


1. Virmani R, Burke AP, Farb A, Kolodgie FD. Pathology of the vulnerable plaque. J Am Coll Cardiol 2006;47:C13–C18.
2. Naghavi M, Libby P, Falk E, et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: part I. Circulation 2003;108:1664–1672.
3. Naghavi M, Libby P, Falk E, et al. From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: part II. Circulation 2003;108: 1772–1778.
4. Glaser R, Selzer F, Faxon DP, et al. Clinical progression of incidental, asymptomatic lesions discovered during culprit vessel coronary intervention. Circulation 2005;111:143–149.
5. Nair A, Margolis MP, Kuban BD, Vince DG. Automated coronary plaque characterisation with intravascular ultrasound backscatter: ex vivo validation. Euro Intervention 2007;3:113–120.
6. Garcia-Garcia HM, Mintz GS, Lerman A, et al. Tissue characterization using intravascular radiofrequency data analysis: recommendations for acquisition, analysis, interpretation and reporting. EuroIntervention 2009;5:177–189.
7. Rodriguez-Granillo GA, Garcia-Garcia HM, Mc Fadden EP, et al. In vivo intravascular ultrasound-derived thin-cap fibroatheroma detection using ultrasound radiofrequency data analysis. J Am Coll Cardiol 2005;46:2038–2042.
8. De Boer SPM, Cheng JM, Garcia-Garcia HM, et al. Relation of genetic profile and novel circulating biomarkers with coronary plaque phenotype as determined by intravascular ultrasound: rationale and design of the ATHEROREMO-IVUS study. EuroIntervention 2013; published online ahead of print doi:pii:20130113-01.

Facebook Comments


We’re glad to see you’re enjoying PACE-CME…
but how about a more personalized experience?

Register for free