Fig. 7. This 80-yr-old woman suffered an anterior MI, presenting with sinus tachycardia, an incomplete RBBB, and left anterior fascicular block (A). Note the precordial ST elevation. Minutes later, this relatively narrow wide-complex tachycardia (B) was recorded. Note the incomplete RBBB and right axis deviation, consistent with a fascicular tachycardia originating from the left anterior fascicle. The mechanism is likely abnormal automaticity caused by ischemia/injury to the anterior fascicle. Note the retrograde P waves. This tachycardia terminated spontaneously, and did not recur.

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Fig. 8. This patient presented with an anterior MI and had recurrent episodes of nonsustained polymorphic VT. Primary angioplasty and stenting of a subtotally occluded LAD was performed, and no further VT occurred.

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Fig. 8. This patient presented with an anterior MI and had recurrent episodes of nonsustained polymorphic VT. Primary angioplasty and stenting of a subtotally occluded LAD was performed, and no further VT occurred.

Prognosis and Incidence

Using the standard, broad definition of VT, the SPRINT investigators found the incidence of primary VT to be 3.7% (80). Seventeen percent of these patients, or 0.6% of the entire cohort, had sustained primary VT; 50% of these episodes were polymorphic. Patients with sustained VT had a substantially higher in-hospital cardiac mortality than patients with NSVT or no VT, but there was no difference in survival at 1 yr among patients who survived until hospital discharge. Mont and colleagues (81) reviewed 1120 consecutive AMI patients; 1.9% had early (<48 h) sustained monomorphic VT (SMVT). These patients had larger infarcts, and were more likely to have antecedent BBB than patients who did not have VT. Patients with early SMVT had a much higher mortality in-hospital (43% vs 11%) and after discharge than patients without VT. Patients with VT had larger infarcts, worse Killip class, and a higher risk of recurrent ventricular arrhythmias than patients who had VF.

As with VF, so-called "warning arrhythmias" do not accurately predict VT (82). One study conducted in the pre-thrombolytic era suggested a connection between accelerated idioventricular rhythm (AIVR) and VT (83). In a recent meta-analysis (16), thrombolytic therapy was associated with an increased incidence of VT compared with conventional therapy, but "VT" was broadly defined, including clinically insignificant short salvos as well as sustained VT. As with VT, hypokalemia predisposes to VT (see Fig. 4) (50,51).

Extremely rapid monomorphic VT may be seen in acutely ischemic or infarcted ventricles and has been labeled ventricular flutter. Polymorphic VT (PVT) (see Fig. 8) rarely occurs in the setting of an acute MI, but is often preceded by symptoms or electrocardiographic signs of ischemia (79). These episodes are usually not consistently related to a long QT interval, sinus pauses, or electrolyte abnormalities, as in other forms of PVT, and connote a high mortality. Lidocaine may be used initially; if ineffective, iv amiodarone may suppress the arrhythmia. Intraortic balloon counterpulsation may be of benefit, but revascularization seems to provide the most definitive therapy for this arrhythmia (79).

Few data are available regarding nonsustained VT (NSVT) in the setting of AMI (see Fig. 9). In one series, patients with NSVT had a higher incidence of VF than control patients, but overall did not have a higher in-hospital mortality. The timing of the NSVT may be important. Patients with NSVT within the first few hours of presentation with AMI did not have an increased mortality. Patients with NSVT occurring more

Fig. 9. This patient presented with recurrent nonsustained VT early in the setting of an acute anterior MI. The patient was treated with primary angioplasty, beta-blocker, and an ACE inhibitor, and VT did not recur after 36 h from symptom onset.

than 12 h after presentation, however, did have a substantially higher mortality than control patients (84).


Management of VT depends on the degree of hemodynamic compromise associated with the arrhythmia. For purposes of management, pulseless VT and sustained PVT should be considered like VF and treated with an unsynchronized discharge of 200 J as quickly as possible. Monomorphic VT is often highly sensitive to electrical energy; some cases can be reverted to sinus rhythm with a discharge of 25 J or less. This sensitivity explains the occasional reversion to sinus rhythm following a "chest thump" (that delivers approx 0.5-1.0 J). Although a chest thump can occasionally convert VT (or rarely VF), a thump can also cause VT to deteriorate to VF. Thus, "thump-version" should be attempted with caution. After successful resuscitation from sustained VT, patients should receive iv lidocaine, amiodarone, or procainamide (see Table 2).

If a pulse is present, but VT is accompanied by hypotension, ischemia, or significant heart failure, immediate cardioversion should be considered. If the tachycardia is hemo-dynamically tolerated, a synchronized cardioversion (50-200 J) should be performed following administration of sedation/anesthesia. Frequently, several different leads must be checked in order to find one in which synchronization is possible. If a rapid rate or the particular QRS morphology during VT makes synchronization impossible, an unsynchronized discharge should be delivered.

VT that is tolerated hemodynamically may be treated initially with iv antiarrhythmic drugs. Lidocaine, amiodarone, or procainamide may be administered intravenously as previously mentioned (see Table 2). Following acute management of the VT, a continuous infusion of the effective agent may be continued for 6-24 h. If pharmacologic

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