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Diabetes and pre-infarct angina. Time to rethink comorbidities in the reperfusion-injury phenomenon?
Session:
Painel 6-Doença Coronária 1
Speaker:
Marta Fontes Oliveira
Congress:
CPC 2020
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:
Marta Fontes Oliveira; Susete Vieira; Mariana Santos; Ricardo Costa; André Dias De Frias; Andreia Campinas; Sofia Cabral; André Luz; Severo Torres
Abstract
<p><strong>Background</strong>: Pre-infarct angina (PIA) reduces infarct by limiting the reperfusion-injury and represents the most efficient endogenous form of myocardial conditioning yet discovered. Diabetes is thought to be a major obstacle to conditioning. We aimed to study if the effect of PIA is influenced by diabetes and to appreciate its long-term effect on major adverse cardio-cerebrovascular events (MACCE).</p> <p><strong>Methods</strong>: We retrospectively evaluated consecutive patients with left anterior descendent (LAD)-related STEMIs admitted in a tertiary centre from January 2008 to August 2018 who underwent primary angioplasty (PCI). PIA was defined as at least one episode of chest, arm or jaw pain during the preceding 48h before STEMI diagnosis. Peak creatine kinase and peak Troponin T were used as a surrogate of infarct size. We evaluated the association between PIA, diabetes and infarct size using Kruskal-Wallis rank. Interaction between PIA and DM was analysed using multiple linear regression (logarithmic-transformed CK and TnT). Associations between the studied variables and clinical outcomes after reperfusion were assessed using Cox models.</p> <p><strong>Results</strong>: From 1143 STEMI-patients, 484 were LAD-STEMI. A quarter had diabetes (25%, n=119), 32.8% (n=158) had PIA. The proportion of PIA was not different between diabetics and non-diabetics (approximately 25%). PIA globally reduced infarct size independent of age and sex, diabetes, ischemic time and glomerular filtration rate (β=-0.29, p=0.003 for CK peak and β=-0.33, p=0.002 for TnT peak). In subgroup analysis, the global protective effect of PIA was confirmed for non-diabetic patients (CK 1732 [959 - 3574] vs 2365 [1366 - 4282] U/L, p=0.0061, TnT 3.78 [2.20 – 8.77] vs 5.66 [3.00 - 9.96] ng/mL, p=0.0259). In diabetic patients, PIA was associated with reduced but not significantly different infarct size (peak CK 1540 [741 - 3853] vs 2260 [1169 - 4752] U/L, p=0.0724, peak TnT 4.72 [2.00 – 9.80] vs 8.14 [3.22 - 13.19] ng/mL, p=0.0532). However, no significant interaction was found between PIA and diabetes for TnT or CK peaks (p for interaction 0.571 and 0.532, respectively). During a median follow-up period of 17.8 [12.2 - 25.4] months, 103 (21.4%) MACCE events occurred. PIA was associated with a significant reduction in the incidence of MACCE (HR 0.53 (95% CI 0.31 - 0.89)) driven by a significative reduction of mortality (HR 0.35 (95% CI 0.16 - 0.74)). No interaction was found between diabetes and PIA on its effect on MACCE events.</p> <p><strong>Conclusion</strong>: Our study confirmed PIA as a potent stimulus to reduce infarct size and improve prognosis in patients with anterior wall myocardial infarction. Contrary to previously presumed, this study does not confirm that diabetes blunts the protective effect of PIA on infarct size.</p>
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