Usefulness of coronary atheroma burden to predict cardiovascular events in patients presenting with acute coronary syndromes (from the PROSPECT study)
Selected in The American Journal of Cardiology by D. Milasinovic
Shan P, Mintz GS, McPherson JA, De Bruyne B, Farhat NZ, Marso SP, Serruys PW, Stone GW, Maehara A
Am J Cardiol. 2015 Dec 1;116(11):1672-7
LinkRead the abstract
Latest contributionsClinical outcomes and cost-effectiveness of fractional flow reserve-guided percutaneous coronary intervention in patients with stable coronary arte... Efficacy and safety of Ticagrelor over time in patients with prior MI in PEGASUS-TIMI 54 2017 ESC Focused update on Dual Antiplatelet Therapy (DAPT)
What is known
Coronary atheroma burden, as measured by the intravascular ultrasound (IVUS)-derived percent atheroma volume (PAV), was shown to be predictive of major cardiovascular adverse events (MACE). However, most of the previously studied patients had stable angina and the occurrence of MACE was not related to the imaged coronary tree segment.
A prospective natural-history study of coronary atherosclerosis (PROSPECT trial) that included a three-vessel IVUS after successful percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS), showed that the occurrence of MACE during 3-year follow-up was equally related to both initially treated and untreated lesions (12.9% vs. 11.6%, respectively).
This secondary, patient-level analysis of the PROSPECT trial investigated the impact of total baseline PAV on the rate of 3-year nonculprit lesion-related MACE.
- 660 ACS patients were included (30% STEMI, 66.2% NSTEMI, 3.8% unstable angina), with 3229 IVUS-defined nonculprit lesions that were untreated based on angiographic findings.
- Nonculprit lesion was IVUS-defined as plaque burden (PB) ≥40% on ≥3 consecutive frames.
- External elastic membrane (EEM) and lumen areas were determined at ≈0.4mm intervals.
- Overall atheroma burden was calculated by summing all nonculprit lesions on a patient level: PAV = (∑ (EEM area – lumen area) / ∑ (EEM area) x 100.
- MACE was defined as cardiac death, cardiac arrest, myocardial infarction (MI) and/or rehospitalization for unstable/progressive angina, unrelated to the initially treated lesions.
- Cumulative 3-year nonculprit lesion-related MACE was significantly less frequent in the lowest patient tertile (PAV <47.7%) compared to both intermediate (47.7%≤ PAV <50.9%) and high (PAV ≥50.9%) tertiles (6.3% vs. 14.7% vs. 15.1%, respectively; p=0.009).
- This difference in MACE was driven mainly by a higher rate of progressive angina in patients in high (12.2%) and intermediate (10.7%) versus low (3.1%) baseline PAV tertiles (p=0.003).
- Multivariable regression found insulin-dependent diabetes mellitus, presence of ≥1 thin-cap fibroatheroma by virtual histology (VH-TCFA) and PAV to be independent MACE predictors.
- The combined presence of at least two of the three high-risk plaque characteristics (minimal lumen area (MLA) ≤4 mm2, VH-TCFA and/or PB ≥70%) was more frequent in patients in intermediate and high, compared to low PAV tertile (p<0.001 for every combination).
- By multivariable linear regression, male gender, age and prior cardiac intervention were independently associated with an increase in baseline PAV.
This study reaffirmed the association between baseline atheroma burden and MACE, with the added value of specifically relating MACE to angiographically mild, previously untreated coronary lesions. Higher degree of baseline atheroma burden was associated mainly with more rehospitalizations due to progressive angina and subsequent revascularizations. Although the low overall rates of hard clinical endpoints, such as death or MI, in this and also previous studies, preclude a definitive conclusion regarding the clinical relevance of total baseline atheroma burden as expressed by PAV, the following two discussion points seem warranted:
- In ACS patients, the discrepancy between angiographic findings of mild nonculprit stenoses and IVUS-measured high degree of total atheroma burden may be associated with incomplete revascularization and consequently worse outcomes;
- The mechanisms behind the observed association of PAV and MACE need to be further elucidated and may include high total baseline PAV being a marker of disease progression and/or related to the presence of high-risk plaque characteristics.