Key result
STE-ACS with normal coronaries linked to ~56% fewer MACE vs NSTE-ACS.
Why the study?
There are limited data regarding ACS in patients with normal coronary arteries, and clinical differences between STE-ACS and nSTE-ACS patients have not been sufficiently evaluated.
Does presentation with STE-ACS compared to nSTE-ACS affect midterm prognosis in patients with normal coronary arteries?
Cohort (n=190)
Does presentation with STE-ACS compared to nSTE-ACS affect midterm prognosis in patients with normal coronary arteries?
In patients with ACS and normal coronary arteries, nSTE-ACS is associated with more metabolic abnormalities and a higher rate of MACE compared to STE-ACS, which is more associated with inflammation.
May inform risk stratification in ACS with normal coronaries; leaves open whether STE-ACS versus nSTE-ACS differ in midterm prognosis.
OBJECTIVE: We sought to compare clinical profiles and midterm prognosis of patients with normal coronary arteries presenting with ST-elevation ACS (STE-ACS) versus non-ST-elevation ACS (nSTE-ACS). BACKGROUND: There are limited data regarding ACS in patients with normal coronary arteries, and especially clinical differences between ST-ACS and nSTE-ACS patients have not been evaluated sufficiently. METHODS: The study group comprised 190 patients (mean age: 53.2 years, 63.1% males, 63.6% STE-ACS) presenting with ACS and normal coronary angiograms. The participants were evaluated in terms of 42 clinical variables. MACE [cardiac death (CD) and hospitalization for angina (HA)] were the study end points. RESULTS: STE-ACS in comparison to nSTE-ACS patients were younger (P < 0.01), were more frequently males (P < 0.01), had more often infection prior to ACS (P < 0.01), higher hsCRP on admission (P < 0.01), and greater infarct size, measured by maximal troponin I (P < 0.01). By multivariate analysis in this subgroup, predictors of outcome were hsCRP (P = 0.03) and raised troponin I (P = 0.02). nSTE-ACS in comparison to STE-ACS patients were more obese (BMI, P < 0.01), had higher LDL cholesterol (P < 0.01), fasting glucose (P = 0.03). LDL cholesterol (P = 0.02) and fasting glucose (P = 0.03) emerged as independent predictors of outcome in these patients. Mean follow-up period was 25.4 months. STE-ACS patients had twice fewer MACE rate than nSTE-ACS patients [(1-CD, 12-HA; 11%) vs (1-CD, 16-HA; 25%), respectively, log rank P < 0.01]. CONCLUSIONS: STE-ACS and nSTE-ACS patients with normal coronary arteriography have different clinical profiles. In nSTE-ACS patients more pronounced metabolic abnormalities were identified, while in STE-ACS patients inflammatory background was more significant.
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Mazurkiewicz et al. (2009) conducted a cohort in Acute Coronary Syndrome (ACS) with normal coronary arteries (n=190). ST-elevation ACS (STE-ACS) vs. non-ST-elevation ACS (nSTE-ACS) was evaluated on MACE (cardiac death and hospitalization for angina) (p=<0.01). Patients with ST-elevation ACS and normal coronary arteries had a significantly lower rate of MACE compared to those with non-ST-elevation ACS (11% vs 25%, P<0.01).
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