Prognosis and Management of Atrial Fibrillation in Different Clinical Settings: Acute Myocardial Infarction
G. ZUIN, M. CELESTRE, F. DIPEDE
Introduction
Atrial fibrillation (AF) is a common arrhythmia in patients with acute myocardial infarction (AMI) found in around 10–20% of all such patients.
AF is caused by ischemic myocardium (atrial and ventricular), pericarditis, and left ventricular dysfunction. In a large, community study [1] conducted in the pre-fibrinolytic era over the 10-year period from 1975 to 1986, the incidence of AF was 16.6%. Mortality was higher in the AF group than in the non-AF group both in-hospital (27.6% vs 16.6%) and after a 5-year follow-up period. Congestive heart failure, cardiogenic shock, and other signs of left ventricular dysfunction were frequently found in patients with AF. However, a multivariate analysis showed that both in-hospital and long-term progno- sis were not affected by AF (OR 1.18, 95% CI 0.90–1.52), suggesting that the prognostic impact of AF may be mediated by left ventricular dysfunction.
In a large study conducted in the fibrinolytic era (GUSTO-I trial) [2], AF was present on admission in 2.5 % of patients and developed during hospi- talisation in an additional 7.9% of cases. Patients with AF were more often affected by three-vessels disease and in-hospital stroke , and the adjusted 30- day mortality rate was significantly higher (OR 1.3, 95% CI 1.3–1.5).
Data derived from the GISSI-3 trial [3], which included 17.944 patients receiving fibrinolytic therapy, within the first 24 h after AMI, showed an inci- dence of in-hospital AF of 7.8%. AF correlated with advanced age, female sex, higher Killip class, previous myocardial infarction, hypertension, dia- betes, and heart failure. After adjustment for other prognostic factors, AF remained an independent predictor of increased in-hospital (RR 1.98, 95%
Division of Cardiology, Cardiovascular Department, Umberto I Hospital, Mestre- Venice, Italy
CI 1.67 to 2.34) and long-term (RR 1.78, 95% CI 1.60 to 1.99) mortality.
Similar results were found in other studies [4–6]. In the GRACE registry [4], 5.0% of the patients with AMI had previous AF and 7.7% had a new onset of AF. Patients with AF were older, more likely to be women, with previous MI, stroke, or congestive heart failure, and previous revascularisation, and had an in-hospital complicated course. However, only new-onset AF was an inde- pendent predictor of all adverse in-hospital outcomes.
In the GUSTO 3 trial [7] 3906 patients (6.5%) out of 13 858 with AMI treated with fibrinolytic therapy who were in sinus rhythm at the time of enrolment developed AF. Worsening heart failure, hypotension, third-degree heart block, and ventricular fibrillation were independent predictors of new- onset AF. Patients with AF had an increased 30-day and 1-year mortality rate even after adjustment for baseline factors and pre-AF complications. These data suggest that AF is often a consequence of post-AMI complications, but is itself an independent predictor of a worse outcome.
The effects of fibrinolysis on AF were analysed by the authors of the SPRINT registry [8], who compared the incidence of AF in patients with AMI treated in the prefibrinolytic era vs those treated in the fibrinolytic era. They reported an overall incidence of AF of 9.9% and 8.9%, respectively, and a similar 30-day (27.6% vs 25.1%) and 1-year (42.5 % vs 38.4%) mortality.
However, AF in the fibrinolytic era occurred in older and sicker patients.
Therefore, the mortality rate, after adjustment for confounding factors dur- ing these two periods was significantly reduced (more than 30%) in mortali- ty treated with fibrinolysis.
The effects of primary percutaneous coronary intervention (PCI) on AF have been rarely evaluated. In patients treated with primary PCI [9], 4.3%
had AF on admission and 7.7% developed AF during hospitalisation. AF cor- related with age, Killip class, previous infarction and stroke, shock, multives- sel disease, and poor reperfusion of the infarct-related artery. AF was not an independent predictor of in-hospital mortality but was an independent pre- dictor of 1-year mortality (OR 1.64, 95% CI 1.05–2.55).
Pharmacological treatment with drugs aimed to reduce the size of the infarct and ventricular remodelling has also been beneficial in reducing the incidence of AF. In the GISSI-3 [3], patients treated with nitrates and ACE inhibitors showed a trend towards a reduced incidence of AF, suggesting that haemodynamic impairment was the most likely mechanism underline this arrhythmia. In the TRACE study [5], patients with AMI between day 2 and day 6 after the onset of symptoms were included and randomised to ACE- inhibitor treatment or placebo. The risk of new, in-hospital AF was reduced by 45% with trandolapril treatment. Beta-blockers such as carvedilol seem to reduce atrial arrhythmias. In the CAPRICORN study [10], patients with left ventricular dysfunction were treated with carvedilol added to an ACE
128 G. Zuin et al.
inhibitor 3–21 days after AMI. The incidence of AF was 5.4% in the placebo group and 2.3 % in the carvedilol group, with a carvedilol/placebo hazard ratio (HR) of 0.41 (95% CI 0.25–0.68 , P = 0.0003).
The occurrence of AF increases the risk of ischaemic stroke. Data obtained from patients enrolled in the GRACE registry [11] showed a 1.3%
incidence of in-hospital stroke in patients with AMI. AF was one of the strongest risk factors for in-hospital non-haemorrhagic stroke, together with in-hospital CABG, previous stroke, and advanced age. These data are consis- tent with the findings of the GUSTO-I study [2].
Management
The management of AF includes antiarrhythmic therapy or electrical car- dioversion. Recent ACC/AHA practice guidelines [12] for the management of patients with ST-elevation myocardial infarction, give the following sugges- tions:
1. Patients with a sustained AF and haemodynamic compromise should be treated with direct cardioversion, preceded by brief general anaesthesia.
For episodes of AF that do not respond to electrical cardioversion or recur after a brief period of sinus rhythm, antiarrhythmic drugs are rec- ommended, with the aim of slowing the ventricular response. The agents that we use are: i.v. amiodarone or i.v. digoxin.
2. Patients with sustained AF and ongoing ischaemia but without haemody- namic compromise should be treated with one or more of the following : beta-blocker and/or i.v. diltiazem or verapamil and/or direct cardiover- sion.
3. In patients with sustained AF without haemodynamic compromise or ischaemia, rate control is indicated.
In addition, patients with sustained AF should be treated with anticoagu- lants.
Conclusions
Atrial fibrillation in AMI is often secondary to other post-AMI complica- tions, but is itself an independent predictor of a worse outcome. AF can be prevented by optimising the treatment of AMI with reperfusion therapy, beta-blockers, and ACE inhibitors. When AF occurs, it should be treated with DC shock as soon as possible and/or drugs with little haemodynamic impact according to the clinical status.
129 Prognosis and Management of Atrial Fibrillation in Different Clinical Settings
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