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 therapy short (1 week-1 month).
β-Blockers are used for rate control, but are not appropriate in patients with acute HF. In ill patients with acute HF, some degree of tachycardia may be tolerated to prevent a shock state (heart rate of 100–110 bpm). Anti-congestive measures and afterload reduction improve the AF rate; if needed, digoxin and IV amiodarone may be added for rate control.
H. Accelerated junctional rhythm (also called non-paroxysmal junctional tachycardia)
The accelerated junctional rhythm is an automatic rhythm originating from the AV node at a rate of 70–130 bpm, often ~80 bpm. The junctional rhythm is faster than the sinus rhythm, which leads to AV dissociation. Sometimes, the junctional and sinus rhythms compete at close rates, leading to isorhythmic AV dissociation, i.e., some beats may be sinus beats preceded by sinus P waves, while the other beats may be junctional beats dissociated from P waves and showing up at any deceleration of the sinus P rate (see Chapter 13, Figure 13.9). The QRS is narrow, except in patients with a baseline bundle branch block. This rhythm may occur with inferior MI, is benign and transient, and does not generally require any specific therapy unless the patient is in shock. In shock, atrial pacing at a rate faster than the junctional rhythm may be performed to promote AV synchrony and a more appropriate rate for shock.
Persistent sinus tachycardia is a strong negative prognostic marker; it often signifies pump failure from a large MI. Do not necessarily attempt to slow it down, and avoid β-blockers in the first 24 hours if the heart rate exceeds 110 bpm. One may attempt to slow it down in young patients with hyperdynamic circulation and limited-size MI. Sinus tachycardia may improve with anticongestive measures and afterload reduction.
V. Bradyarrhythmias, bundle branch blocks, fascicular blocks
A. Inferior MI
The sinus nodal artery originates from the proximal RCA (60%) or the LCx (40%). The AV nodal artery originates from the AV groove con- tinuation of a dominant RCA (90%) or a dominant LCx (10%).
In inferior MI, sinus bradycardia and AV blocks may develop in the first 24 hours, at which time they are usually brief and result from the increased vagal tone that accompanies inferior MI. Beyond 24 hours, the AV block is due to ischemia and edema of the AV node and is more persistent, but eventually resolves within a few days (<1 week). The AV node is resistant to ischemia, and therefore it almost never infarcts. When AV block is seen along with a fast P-wave rate, the block is due to nodal ischemia or edema, rather than a high vagal tone.
The AV block being at the nodal level, it may manifest as first-degree AV block, second-degree type I AV block, or complete AV block with a junctional rhythm (rate 40–100). Those blocks are usually well tolerated,
