Key result
Baseline circulating endothelial cells and acute vWF changes predict 14- and 30-day cardiac events in ACS.
Why the study?
TIMI risk score stratifies ACS patients by risk but the relationship between TIMI score and markers of endothelial damage, inflammation, and thrombogenesis was unclear.
Do plasma markers of endothelial damage, inflammation, and thrombogenesis correlate with TIMI risk score and predict short-term outcomes in patients with UAP/NSTEMI?
Cohort (n=88)
Do plasma markers of endothelial damage, inflammation, and thrombogenesis correlate with TIMI risk score and predict short-term outcomes in patients with UAP/NSTEMI?
In patients with UAP/NSTEMI, a high TIMI risk score is associated with greater vascular insult, inflammation, and thrombogenicity, with baseline circulating endothelial cells and changes in von Willebrand factor independently predicting short-term adverse cardiac events.
Answers are grounded in this paper and cite their sources.
May refine short-term ACS risk stratification beyond TIMI score; leaves open prospective validation before clinical adoption.
Risk stratification at presentation with acute coronary syndromes (ACS) on the basis of the TIMI risk score for unstable angina and non-ST-elevation myocardial infarction (UAP/NSTEMI) identifies patients at high risk of recurrent cardiac events and those who benefit from more aggressive treatment strategy. We hypothesised the following: (a) that a high TIMI risk score brings a greater degree of acute changes in endothelial damage/dysfunction (circulating endothelial cells [CECs], von Willebrand factor [vWf]), inflammation (interleukin-6, IL-6) and blood thrombogenicity (plasma tissue factor, TF); and (b) that these indices are higher in those with high TIMI risk score who experienced recurrent cardiac event at day 14 and day 30. TIMI risk scores were determined at admission and 48 hours later in 88 ACS patients (60 male, age 67+/-12 yrs) with UAP or NSTEMI. CECs, IL-6 and TF levels were measured at both time points and the acute change (delta) calculated. Patients were split into high (score > or =4) or low (<4) TIMI score groups. The composite end point of death, myocardial infarction, and refractory angina requiring revascularisation following 14 and 30 days' follow-up was ascertained. Fifty-eight patients with high TIMI risk score (mean 4.7) had significantly higher baseline and 48 h CEC, vWf, IL-6,TF and deltaTF levels, compared to low TIMI risk score (mean 2.4) patients (all p<0.05). Multivariate Cox regression analysis adjusted for clinical variables and TIMI risk score expressed as either continuous or categorical variable identified baseline CECs and deltavWf levels (both p< or =0.01) as independent predictors of subsequent cardiac events at both 14 days and 30 days. TIMI risk score for UA/NSTEMI identifies those patients with more profound vascular insult, inflammation and thrombogenicity that, in the 'high risk' patient group, predicts short-term outcomes, although vascular damage was the more sensitive predictor. These indices may further refine global risk stratification for short-term adverse cardiac events in these patients.
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Lee et al. (2005) conducted a cohort in Acute coronary syndromes (UAP/NSTEMI) (n=88). High TIMI risk score (≥4) and elevated biomarkers vs. Low TIMI risk score (<4) was evaluated on Composite of death, myocardial infarction, and refractory angina requiring revascularisation at 14 and 30 days (p=≤0.01). In patients with acute coronary syndromes, baseline circulating endothelial cells and acute changes in von Willebrand factor independently predicted 14- and 30-day cardiac events (P≤0.01).
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