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The association of lipoprotein-associated phospholipase A2 with inflammation and SYNTAX score in ACS
Session:
Posters 2 - Écran 9 - Doença Coronária
Speaker:
Cátia Santos Ferreira
Congress:
CPC 2019
Topic:
E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
Theme:
13. Acute Coronary Syndromes
Subtheme:
13.1 Acute Coronary Syndromes – Pathophysiology and Mechanisms
Session Type:
Posters
FP Number:
---
Authors:
Cátia Santos Ferreira; Rui Baptista; Luís Candal Leite; Manuel Oliveira Santos; João André Ferreira; Ana Vera Marinho; Patrícia M. Alves; Anália Carmo; João Pego; Lino Gonçalves
Abstract
<p>BACKGROUND:The occurrence of an acute coronary syndrome (ACS) reflects several pathophysiological mechanisms, including the anatomical severity of pre-existing coronary artery disease (CAD) and the inflammatory component of atherosclerosis. Reflecting the latter, lipoprotein-associated phospholipase A2 (Lp-PLA2) levels are an independent risk factor for plaque rupture. We aimed to assess the association between Lp-PLA2 levels and the type of ACS, the thrombotic burden and the severity of CAD.</p> <p>METHODS: We conducted a prospective, observational cohort study, including 97 consecutive patients with ACS admitted to a Cardiac Care Unit. Two groups were created: group 1 (G1) with Lp-PLA2 <200 ng/ml (n=80) and group 2 (G2) with Lp-PLA2 ≥200 ng/ml (n=17). This cut-off was predefined, considering Lp-PLA2 ≥200 ng/ml portend a moderate- to high- risk of cardiovascular disease. Coronary angiograms were blindly reviewed to assess blood flow pre- and post-percutaneous coronary intervention (PCI) (thrombolysis in myocardial infarction (TIMI) flow grade (TFG)); the thrombus burden (thrombus burden score, TBS) and the myocardial perfusion after PCI (TIMI myocardial perfusion grade, TMPG).</p> <p>RESULTS: Demographic data was similar between the groups except for age (G1: 68±13 vs G2:59±12years, p=0.01), LDL cholesterol (G1: 111±34 vs G2:163±42 mg/dL, p<0.001), smoking habits (20% vs 47%, p=0.03) and history of CAD (23% vs 0%, p=0.04). Regarding the thrombotic burden, we found a non-significant higher TBS in G2 (3.3±2.1 vs. 2.1±2.1, p=0.06), in line with a higher probability of G2 patients presenting with a ST-segment elevation myocardial infarction (STEMI) vs. non-STEMI (70.6% vs 40%, p=0.02). Even though a higher TBS could also be manifest by with a lower post-PCI TFG or TMPG, we found no interaction between Lp-PLA2 levels and TFG (r<sup>2</sup>=0.09, p=0.46) or TMPG (r<sup>2</sup>=0.005, p=0.97). Additionally, we found that patients with higher levels of Lp-PLA2 (G2) had a lower number of diseased vessels (1.2±0.5 vs 1.8±1.1, p=0.001) and a lower SYNTAX score (9.6±7.0 vs 14.6±12.2, p=0.03), globally reflecting less severe CAD. No differences in in-hospital mortality were found.</p> <p>CONCLUSION: We found that higher Lp-PLA2 levels were associated with a higher probability of a STEMI and a numerically higher thrombotic burden; conversely, there was an association with a lower SYNTAX score, supporting its role as a marker of the inflammatory component of an ACS, but not its anatomical severity.</p>
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