SPC365

What is the prognosis for patients who develop new-onset atrial fibrillation in the first 48 hours after an acute coronary syndrome?

Session: Posters - E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
Speaker: Isabel Campos

Congress: CPC 2021
Topic: E. Coronary Artery Disease, Acute Coronary Syndromes, Acute Cardiac Care
Theme: 13. Acute Coronary Syndromes
Subtheme: 13.2 Acute Coronary Syndromes – Epidemiology, Prognosis, Outcome
Session Type: Posters
FP Number: ---
Authors: Isabel Durães Campos; Cátia Oliveira; Paulo Medeiros; Carla Rodrigues; Rui Flores; Fernando Mané; Rodrigo Silva; Carlos Galvão Braga; Catarina Vieira; Jorge Marques

<p style="text-align:justify"><span style="font-size:14pt"><span style="font-family:&quot;Courier New&quot;"><span style="color:#000000"><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Atrial fibrillation (AF) is a common complication in acute coronary syndrome (ACS). However, treating patients (pts) with new-onset AF (NOAF) after an ACS remains a challenge. Although it seems intuitive that pts who develop AF within the first 48h have increased morbidity and mortality, your prognosis is unclear because there are no robust studies in the literature to confirm this association. </span></span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:14pt"><span style="font-family:&quot;Courier New&quot;"><span style="color:#000000"><strong><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Aim:</span></span></strong><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"> To characterize the population of pts who developed NOAF in the first 48 hours after an ACS and to compare the prognosis between these pts and pts who didn&rsquo;t develop AF.</span></span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:14pt"><span style="font-family:&quot;Courier New&quot;"><span style="color:#000000"><strong><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Methods:</span></span></strong><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"> 2916 ACS pts admitted consecutively in our coronary care unit during 6years were analyzed retrospectively.Of these pts, 343 (11.7%) had AF within the first 48h, of which 99 (3.4%) had pre-existing AF and 243 (8.3%) presented NOAF. Pts were divided into two groups: group 1 -ACS pts who developed NOAF in the first 48h (n=243; 8.8%); group 2 &ndash; ACS pts who did not develop AF (n=2517; 91.2%). Pts with pre-existing AF were excluded (n=156; 5.4%). Primary endpoint were the occurrence of death at 6 months; follow-up was completed in 95.8% of pts.</span></span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:14pt"><span style="font-family:&quot;Courier New&quot;"><span style="color:#000000"><strong><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Results:</span></span></strong><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"> Group 1 pts were older (72&plusmn;12 vs 62&plusmn;13, p&lt;0.001), with higher proportion of women (30,9% vs 20,9%, p&lt;0.001), hypertensive (78,5% vs 60,7%, p&lt;0.001), smokers (17,4% vs 32,6%, p&lt;0.001), previous CABG (7,9% vs 3,8%, p=0.06) and stroke (10,7% vs 6,8%, p=0.035). Group 1 had a higher proportion of STEMI pts (58,5% vs 46,5%, p &lt;0.001) and, during hospitalization, had more often respiratory infection (p&lt;0.001), malignant arrhythmias (p&lt;0.001), heart failure (p&lt;0.001), stroke (p=0.001), higher values of NT-proBNP (p &lt;0.001) increased C-reactive protein levels (p&lt;0.001), leukocytes (p=0.020), peak of TropI (p=0.029) and creatinine (p&lt;0.001).&nbsp; On echocardiography, group1 had greater LA diameter (45&plusmn;6 VS 41&plusmn;5mm, p&lt;0.001), more frequent significant mitral regurgitation (13,9% vs 2,9%, p&lt;0.001), worst LVEF(41&plusmn;10% vs 46&plusmn;10%, p&lt;0,001) and a higher value of pulmonary artery pressure (39&plusmn;12 vs 24&plusmn;10, p&lt;0,001). Group 1 were less likely to have undergone coronary revascularization (84% vs 74%, p=0.005). In multivariate analysis, age&ge;75 (OR 1.05,p&lt;0.001), LVEF&le;40% (OR 2.50, p&lt;0.001), LA diameter (OR 1.59,p=0.027), more significant mitral regurgitation (OR 2.49, p=0.001) and Killip class &gt; 1 (OR 1.51,p=0.015) remained independent predictors of NOAF. In multivariate analysis and after adjusting for different baseline characteristics, pts with NOAF have the same risk of 6-months mortality compared to those who didn&rsquo;t develop AF [OR 1.03,p=0.91].</span></span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:14pt"><span style="font-family:&quot;Courier New&quot;"><span style="color:#000000"><strong><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Conclusion:</span></span></strong><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"> The incidence of NOAF was 8.8% in our population, which is similar to the literature. Age, LVEF, LA diameter, a significant mitral regurgitation and Killip class &gt; 1 were independent predictors of NOAF after ACS. Pts with NOAF in the first 48h after an ACS had worse clinical manifestations during hospitalization but no higher 6-months mortality risk.</span></span></span></span></span></p>