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Atherosclerotic plaques are the hallmark lesion of atherosclerosis

Coronary plaque composition and vulnerability1

Atherosclerotic plaques may remain asymptomatic, become an obstruction and cause angina, or become vulnerable to rupture that can cause acute thrombosis and CV events.

The key features of plaque that make it vulnerable to rupture1-5

  • Thin fibrous cap (< 65 μm)
  • Large lipid-rich or necrotic core (lipid arc > 90°)
  • Presence of inflammatory cells

The Science and Clinical Management of ASCVD

Download this overview that explains ASCVD and includes recent clinical guidelines for the treatment of patients with very high-risk ASCVD.

LDL-C lowering has been shown to decrease atherosclerotic burden6

Numerous clinical trials with statins using intravascular ultrasound (IVUS) imaging have demonstrated a direct relationship between LDL-C–lowering and a reduction in atheroma (plaque size) volume.

Correlation between LDL-C levels and percent atheroma volume (PAV)

* SATURN: effects of high-intensity statin vs high-intensity statin.

REVERSAL: effects of high-intensity statin vs moderate-intensity statin volume.7

ILLUSTRATE: effects of statin + CETP inhibitor vs statin + placebo.8

Serial intravascular ultrasound was used in the imaging trials to evaluate the various anti-atherosclerotic strategies.

LDL-C lowering has been shown to improve key features of vulnerable plaque9

Statin trials using optical coherence tomography (OCT), a catheter-based coronary artery visualization technique, demonstrate that achieving lower LDL-C levels with more intensive therapy is associated with increased fibrous cap thickness (FCT) and smaller lipid arc.4,9,10

Association between LDL-C levels and plaque features9

Patients in the study were stratified according to achieved LDL-C levels (< 50 [87 plaques], 50–70 [81 plaques], 70–100 [117 plaques], ≥ 100 mg/dL [130 plaques]). Data analyzed from the Cleveland Clinic FD-OCT Registry, which included 293 and 122 non-obstructive lipid and fibrous plaques in 280 stable statin-treated CAD patients evaluated by FD-OCT imaging in vessels requiring PCI.9

ASCVD = atherosclerotic cardiovascular disease; CETP, cholesteryl ester transfer protein; CAD, coronary artery disease; FD-OCT, frequency-domain optical coherence tomography; PCI, percutaneous coronary intervention.

  • References

    1. Bentzon JF, Otsuka F, Virmani R, Falk E. Mechanisms of plaque formation and rupture. Circ Res. 2014;114:1852-1866.
    2. Stefanadis C, Antoniou CK, Tsiachris D, Pietri P. Coronary Atherosclerotic Vulnerable Plaque: Current Perspectives. J Am Heart Assoc. 2017;6:e005543.
    3. Singh RB, Mengi SA, Xu YJ, Arneja AS, Dhalla NS. Pathogenesis of atherosclerosis: A multifactorial process. Exp Clin Cardiol. 2002;7:40-53.
    4. Mushenkova NV, Summerhill VI, Zhang D, Romanenko EB, Grechko AV, Orekhov AN. Current advances in the diagnostic imaging of atherosclerosis: insights into the pathophysiology of vulnerable plaque. Int J Mol Sci. 2020;21:2992.
    5. Atherosclerotic plaque vulnerability. ATHEROSCLEROTIC PLAQUE VULNERABILITY | LIPID LINK. www.lipidlink.com/atherosclerotic-plaque-vulnerability.html. Accessed August 12, 2024.
    6. Puri R, Nissen SE, Ballantyne CM, et al. Factors underlying regression of coronary atheroma with potent statin therapy. Eur Heart J. 2013;34:1818-1825.
    7. Nissen SE. Effect of intensive lipid lowering on progression of coronary atherosclerosis: evidence for an early benefit from the reversal of atherosclerosis with aggressive lipid lowering (REVERSAL) trial. Am J Cardiol. 2005;96:61F-68F.
    8. Nissen S, Tardif JC, Nicholls SJ, et al. Effect of torcetrapib on the progression of coronary atherosclerosis. N Engl J Med. 2007;356:1304-1316.
    9. Kataoka Y, Hammadah M, Puri R, et al. Plaque microstructures in patients with coronary artery disease who achieved very low low-density lipoprotein cholesterol levels. Atherosclerosis. 2015;242:490-495.
    10. Tardif JC, Lesage F, Harel F, Romeo P, Pressacco J. Imaging biomarkers in atherosclerosis trials. Circ Cardiovasc Imaging. 2011;4:319-333.