DISCLOSURES Steven E Nissen MD I have no
- Slides: 20
DISCLOSURES Steven E. Nissen, MD I have no real or apparent conflicts of interest to report.
The Vulnerable Plaque “Hype”othesis
Plaque Rupture: Sudden Cardiac Death
Vulnerable Plaque: Hype vs. Reality • A Pub. Med search for “vulnerable plaque” or “high-risk” plaque yields >2, 000 references over the past 20 years. • Many techniques to “detect” vulnerable plaques have come and gone with initially promising “findings” followed by a sobering reality check. – Thermography, spectroscopy, palpography, virtual histology, OCT, and many more. • A large number of startup companies with “breakthrough” approaches have come and gone, leaving investors with empty pockets, but no progress.
What Went Wrong? • The exact characteristics of “vulnerable” plaque remain uncertain. The evidence for the importance of “thin cap fibroatheromas” is flimsy at best. • Vulnerability is diffuse and global, not local. • Even if we knew what to look for, we would have to scan every branch of every vessel, a virtual impossibility. • Evidence suggests that atheromatous lesions are everywhere and ruptured plaques ubiquitous. • Even if we could identify such lesions, current treatment modalities increase, not decrease adverse outcomes.
ACS: The Tip of the Atherothrombotic “Iceberg” Acute Plaque Rupture (UA/ NSTEMI/TIA/stroke) Clinical Subclinical Presence of Multiple Coronary Plaques Persistent Hyperreactive Platelets Bhatt DL. Journal of Invasive Cardiology. 2003; Vol. 15: Suppl B, 3 B-10 B. Vascular Inflammation
The “Vulnerable” Patient • The entire concept of “vulnerable plaque” is an overly simplistic characterization of an exceedingly complicated phenomenon. • In patients with acute plaque rupture, there is widespread inflammation, white blood cell activation, increased thrombogenicity, and oxidative stress. • These increase biomarkers demonstrate that systemic factors are more important than local anatomy in determining who will have a acute event.
Long-term Outcome in Stented ACS Patients Baseline CRP Predicts 5 Year Survival 1. 0 Survival (months) CRP < 3 mg/l (n = 412) 0. 9 CRP 3 - 10 mg/l (n = 362) 0. 8 CRP > 10 mg/l (n = 268) p < 0. 0001 by log rank [OR adj. = 4. 1] 0. 7 0 10 20 30 Survival (months) Mueller et al. , Circ 105: 1412– 15, 2002 40 50 60
Multiple Ruptured Plaques in ACS Patients (%) 80% of Patients with 1 plaque Number of ruptured plaques in addition to culprit lesion Rioufol G et al. Circulation. 2002; 106: 804 -808.
CRP and Multiple Plaques in ACS Patients with Multiple Plaques ≥ 2 (p < 0. 001) Percent of Patients M. N. Zairis et al. Atherosclerosis. 2002; 164. 355 -359. CRP Tertile (mg/L)
CD 40 L in ACS: 6 Month Risk of Death/MI Variable HR (95% CI) p Age > 65 yr 1. 36 (0. 91 -1. 82) 0. 34 Diabetes mellitus 1. 22 (0. 83 -1. 49) 0. 61 ST-segment 1. 04 (0. 76 -1. 54) 0. 74 Troponin T >0. 1 µg/l 2. 94 (1. 75 -7. 26) <0. 001 C-reactive protein >10. 0 mg/l 2. 03 (1. 11 -3. 59) 0. 02 Soluble CD 40 ligand >5. 0 µg/l 2. 71 (1. 51 -5. 35) 0. 001 Heeschen, et al, NEJM, 348: 1104 -11, 2003
AMI Trial: IVUS in Segment Proximal to Stent
Prevalence: Ulceration Proximal to Culprit Lesion 20% 19% MI All Angina Unstable Angina Stable Angina 15% 10% 7% p=0. 014 5% 4% 0% 0% MI All Angina Unstable Angina Stable Angina
Prognostic Value of MPO in Chest Pain Adverse Cardiac Events in Troponin Negative Patients 6 months (n=462) 30 days (n=462) 1. 00 Unadjusted Adjusted 0. 75 Sensitivity Q 2 Myeloperoxidase Q 3 0. 50 CRP 0. 25 Q 4 0 Troponin T CK-MB 2 4 6 8 10 0. 00 0. 25 Odds Ratio Brennan et al. , NEJM 349: 1595 -604, 2003 0. 50 0. 75 1 -Specificity 1. 00
Plaque “Sealing” aka Prophylactic Stenting Intervention has many acute and late risks that exceed any projected benefit from treating asymptomatic lesions.
Syntax: Repeat Revascularization Unacceptably high recurrence rates in the first year
Restenosis is Not An Entirely Benign Entity STEMI (2. 2%) NSTEMI (7. 3%) Exertional angina (64. 1%) UA requiring hospitalization (26. 4%) M. Chen and colleagues, AHJ 151: 1260, 2006
Summary • Atherosclerosis is a systemic disease with widespread inflammation and multiple ruptured plaques, not one or two. • Platelets, white cells and other systemic factors play an critical role in determining “patient vulnerability. ” • No imaging technique has shown the ability to reliably predict behavior of individual plaques. • Imaging to guide local treatment would require interrogation of all three major epicardial vessels, a practical impossibility. • No studies have demonstrated improved outcomes following stenting of “vulnerable plaques. ”
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