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Fig. 11. This 44-yr-old male presented with prolonged chest pain. In this AIVR, there is no retrograde conduction; rather, there are occasional sinus capture beats which conduct with first-degree AV block and inferior ST elevation.

Fig. 11. This 44-yr-old male presented with prolonged chest pain. In this AIVR, there is no retrograde conduction; rather, there are occasional sinus capture beats which conduct with first-degree AV block and inferior ST elevation.

of AIVR may actually increase with successful reperfusion therapy, which generally connotes a better prognosis. Thus, AIVR that is well-tolerated hemodynamically is typically not treated.

Ventricular Premature Beats

Ventricular premature beats (VPBs) are extremely common in both the AMI and non-AMI settings. As described above, VPBs and so-called "warning arrhythmias" have not been reliably linked with malignant ventricular arrhythmias. In fact, in the post-MI setting, suppression of asymptomatic VPBs with various antiarrhythmic drugs has been associated with a higher mortality (see CAST Trial). Thus, specific antiarrhythmic therapy for VPBs other than beta-blockade and aggressive electrolyte repletion is not recommended.

Reperfusion Arrhythmias

As alluded to previously, efforts to identify clinically significant dysrhythmias following reperfusion therapy have been largely unrewarding. In animal models of infarction using coronary ligation, reperfusion is accompanied by a high incidence of VT and VF. Some thrombolytic trials such as ISAM (87) and ASSET (88) have documented a high incidence of low-grade ventricular ectopic activity (VEA), but no significant difference in the likelihood of life-threatening arrhythmias compared with conventional therapy. Several hypotheses for the discrepancy between the animal models and human clinical experience have been offered. One potential explanation is that coronary occlusion in animal models typically lasts less than 1 h, unlike in typical AMI, when treatment may not occur for 6-12 h after the onset of symptoms. The recent EMIP study (65), in which thrombolytic therapy was delivered extremely early, documented a relatively

Ami Atrial Fibrillation
Fig. 12. This 64-yr-old female presented with acute antolateral MI, CHF, and marked sinus tachycardia. Despite aggressive treatment, sinus tachycardia persisted and the patient succumbed to cardiogenic shock and recurrent ventricular arrhythmias.

high incidence of VF. However, there was a high incidence of cardiogenic shock in the group receiving prehospital thrombolytic therapy, suggesting that much of this VF was secondary rather than primary (89). A second potential explanation for the lower incidence of VF in humans compared with experimental models is that more rapid reperfusion in animals without residual stenoses may predispose to malignant arrhythmias (90). Although some clinical studies have suggested that AIVR and low-grade ventricular ectopy are indicative of reperfusion (91), in the TAMI trial (92), these arrhythmias were not unreliable markers of successful reperfusion.

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