may be used in case of hypotension.
III. Recurrent infarction and ischemia
Within 30 days, recurrent infarction or ischemia occurs in ~10–15% of patients treated with fibrinolytic therapy, vs. <4% of patients treated with PCI (less so with stenting, ~2%).26,44,45 Recurrent infarction is usually due to reocclusion and is also called “infarct extension,” which is different from “infarct expansion” (LV remodeling).
It is diagnosed based on clinical grounds, ECG, and a reincrease of a downtrending troponin by >20%.
Treatment – Escalate β-blockers, NTG, and readminister anticoagulants. Emergent PCI is indicated in STEMI or hemodynamic instability. Otherwise, a non-urgent coronary angiogram is usually performed. For recurrent ST elevation, the fibrin-specific fibrinolytics may be (re-)administered if PCI cannot be performed in a timely fashion.
IV. Tachyarrhythmias
A. Ventricular tachyarrhythmias: VF and sudden death
Improvements in reperfusion therapy have reduced the 30-day mortality of a STEMI patient presenting to the hospital from 15% to 5–6%. Yet, out-of-hospital mortality remains very high, and is responsible for most MI fatalities, mainly in the first hour after MI onset. In fact, the risk of out-of-hospital cardiac arrest in STEMI is ~30%,132,133 mainly in the first hour after STEMI onset, when over half of all VF episodes occur;134 and between hours 1 and 4, where most of the remaining VF events occur.
Conversely, for patients who make it to the hospital without cardiac arrest, the risk of primary VF within 48 hours is ~4%, mostly in the first 4 hours after symptom onset, and the risk of VT and/or VF is ~10%.135
B. Ventricular tachyarrhythmias: VF
In the reperfusion era, sustained VF occurs in 4% of patients hospitalized with acute STEMI. There are three types of VF, mostly character- ized in fibrinolytic trials:
Primary VF is defined as VF occurring in the first 48 hours after MI without an associated shock or severe HF. It occurs because of rapid potassium fluxes with increased automaticity and dispersion of repolarization, or increased sympathetic or vagal tone. It mostly occurs in the first 4 hours. Primary VF, whether in the first 4 hours or at 4–48 hours, is associated with a 2–4 times increased in-hospital mortality, from the VF episode itself, VF recurrence, or the larger ischemic burden. However, VF does not affect long-term mortality in survivors, even on unadjusted analyses.135–137 In fact, primary VF correlates with the extent of initial ischemia and is much more commonly seen in STEMI than NSTEMI, but does not correlate with the eventual infarct size and is at least as frequently seen in inferior as in anterior MI (GISSI-2, Apex-AMI analyses). Sinus bradycardia or pauses may precipitate VF in patients with inferior MI.Even after primary PCI, a small but significant proportion of patients have VT/VF at 24–48 hours (~1.5% of patients).138,139 This post-PCI VT/VF carries an increase in short-term,139 but not long-term, mortality.
Post-PCI VF may reflect stent thrombosis and warrants thorough clinical and ECG investigation.
Secondary VF is defined as VF occurring in association with HF or shock (<48 h or >48 h) and portends a poor early and long-term survival, mainly from a downhill HF course.136,137
Late VF is defined as VF occurring after 48 hours without an associated HF or shock. It is secondary to the myocardial scar and correlates with pump failure, extensive myocardial damage, and increased long-term mortality.135
C. Ventricular tachyarrhythmias: sustained VT
There are two types of VT:
Polymorphic VT is usually an ischemic rhythm that occurs in the first 48 hours of MI or during ischemic recurrences.140 In contrast to torsades de pointes, this polymorphic VT is usually associated with a normal or a minimally prolonged QT interval. Similar to primary VF, it is associated with increased short-term but not long-term mortality.141
Monomorphic VT, whether occurring early (in the first 48 hours) or late (>48 hours), is a sign of extensive myocardial damage and por- tends a strikingly increased in-hospital but also long-term mortality, even when it is not accompanied by HF or shock (GUSTO-1 data).135,142,143 It is rarely seen, in ~2% of MI.
Polymorphic VT usually corresponds to active ischemia, many times without underlying anatomic substrate/scar or with less underlying anatomic substrate and higher EF than monomorphic VT.144 Monomorphic VT, on the other hand, usually reflects the presence of an often large scar and originates in the border zone between viable and infarcted tissue.135
D. Ventricular tachyarrhythmias: non-sustained VT (NSVT)
Early NSVT (<48 hours) is not associated with any impairment of short- or long-term survival.141 Late NSVT (≥4 beats) is associated with impaired long-term survival.145 NSVT does not require any specific therapy; provide general MI therapy and, more specifically, a β-blocker if possible.
E.Accelerated idioventricular rhythm = slow VT = slow wide ventricular rhythm at a rate of 60–100 (120) bpm. Its incidence is 20% in the first 48 hours, mostly after successful reperfusion. Its occurrence immediately after fibrinolytic therapy may signal reperfusion; however, since it frequently occurs without reperfusion, it cannot be used as a standalone reperfusion marker. In any case, it is benign and resolves spontaneously; no specific treatment is required.
F. Acute therapy of sustained VT/VF
DC cardioversion and IV amiodarone (first choice), procainamide, or lidocaine for 6–24 hours. Use procainamide cautiously in HF, as it has a negative inotropic effect.
Revascularization
β-Blockers if possible
Keep K levels >4.0–4.5 mEq/l and Mg >2 mg/dl
Consider repeating the coronary angiogram in case of recurrent VT or VF despite earlier reperfusion therapy
Primary VT prophylaxis with antiarrhythmic drugs (e.g., lidocaine) is not indicated and does not improve outcomes
G. Atrial fibrillation, atrial flutter
In the reperfusion era, the incidence of new AF or atrial flutter in acute MI, usually paroxysmal AF/atrial flutter, is ~10%. This incidence is increased in patients with HF, large MI (including RV MI), pericarditis, or older age. AF is associated with an increased in-hospital as well as long-term mortality, which is partly related to the associated pump failure and the late VT/VF.146 Post-MI AF has been associated with a striking increase in the risk of in-hospital but also long-term stroke across multiple studies, even when AF is only transient.146 In the GUSTO-1 trial, the in-hospital stroke risk was 3.1% with AF vs. 1.3 % without AF.147 Another study addressed patients with inferior MI and preserved EF who had transient AF, i.e., AF that spontaneously reverted to sinus rhythm before hospital discharge; these patients had a much higher risk of AF at 1 year than patients without transient AF (22% vs. 1.3%) and a high risk of stroke under aspirin therapy (~10% vs. 2%), despite a normal EF. This suggests that AF occurring during MI is not a transient phenomenon, but rather a chronic process with a high stroke risk.148
This high risk of stroke supports anticoagulation for peri-MI AF and is further supported by another registry analysis.149 However, in the era of PCI and routine dual antiplatelet therapy, the role of anticoagulation for transient, peri-MI AF is unclear. The in-hospital use of unfractionated heparin is encouraged to reduce the in-hospital stroke risk, and chronic NOAC therapy is considered along with clopidogrel in patients with a low bleeding risk, while keeping aspirin