Key result
Higher platelet counts 12 hours post-pPCI linked to ~9% greater LVA risk per 10×10^9/L.
Why the study?
Does post-procedural platelet count predict the development of left ventricular aneurysm in patients with acute anterior STEMI following primary PCI?
Cohort (n=281)
Does post-procedural platelet count predict the development of left ventricular aneurysm in patients with acute anterior STEMI following primary PCI?
Odds Ratio: 1.092 (95% CI 1.015–1.188)
p-value: p=0.039
Higher platelet count 12 hours after primary PCI is independently associated with the development of left ventricular aneurysm at one year in patients with anterior STEMI.
Post-PCI platelet rise may aid LV aneurysm risk stratification; leaves open causal role and need for validation.
BACKGROUND: Left ventricular aneurysm (LVA) relates to worse prognosis in patients with myocardial infarction despite successful reperfusion treatment. There is no evidence that early detectable biomarkers can predict the risk for the future development of LVA. AIM: The aim of our study was to investigate the possible predictive value of periprocedural haematological parameters for LVA. METHODS: A total of 281 patients with acute anterior ST-segment elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (pPCI) were enrolled. Haematological parameters were measured on admission before pPCI and between 8 and 12 h after pPCI, separately. The development of LVA was evaluated at one-year follow-up. The patients were then divided into two groups: an LVA group and a non-LVA group. Univariate and multivariate logistic regression analyses were performed to find the predictors of LVA. RESULTS: A total of 34 (12.1%) patients developed LVA at one-year follow-up after pPCI. Multivariate analyses revealed that a 10 × 109/L increase in platelet count 12 h after pPCI (odds ratio [OR] 1.092, 95% confidence interval [CI] 1.015-1.188, p = 0.039), peak cardiac troponin I (OR 1.107, 95% CI 1.003-1.215, p = 0.000), and left ventricular ejection fraction (OR 0.853, 95% CI 0.772-0.943, p = 0.002) were independent risk factors for LVA. For the prediction of LVA, platelet count 12 h after pPCI at a cut-off value > 197 × 109/L yielded a receiver operating characteristic-area under the curve (ROC-AUC) of 0.635 (82.3% sensitivity, 44.1% specificity). CONCLUSIONS: Platelet count after pPCI was significantly associated with the development of LVA in anterior STEMI patients and may be available for early risk stratification of future LVA formation.
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Wang et al. (2018) conducted a cohort in acute anterior ST-segment elevation myocardial infarction (STEMI) (n=281). Post-procedural platelet count vs. Lower platelet count was evaluated on Development of left ventricular aneurysm (LVA) (OR 1.092, 95% CI 1.015-1.188, p=0.039). A 10 × 10^9/L increase in platelet count 12 hours after primary PCI was independently associated with the development of left ventricular aneurysm at one year (OR 1.092; 95% CI 1.015-1.188; p=0.039).
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