Chest
Volume 126, Issue 3, September 2004, Pages 702-708
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Clinical Investigations
CARDIOLOGY
Intracoronary Verapamil Rapidly Terminates Reperfusion Tachyarrhythmias in Acute Myocardial Infarction

https://doi.org/10.1378/chest.126.3.702Get rights and content

Background:

The restoration of coronary flow after transient ischemia immediately induces life-threatening ventricular tachyarrhythmias. Although most of these arrhythmias disappear spontaneously, some of them induce serious hemodynamic changes. This retrospective study investigates the efficacy of therapy with intracoronary verapamil to terminate reperfusion-induced ventricular tachyarrhythmias in patients with acute myocardial infarction (AMI).

Methods and results:

Between February 1992 and February 2003, 390 patients with a diagnosis of AMI were enrolled into the study. All patients received mechanical revascularization therapy within 6 h of onset of symptoms, and 109 patients experienced reperfusion-induced tachyarrhythmias. A subset of these patients was treated with intracoronary verapamil (0.25 to 1.0 mg) to terminate the reperfusion-induced tachyarrhythmia. They were evaluated for immediate termination of the tachyarrhythmias, hemodynamic changes, resumption rates, and major complications. Thirty-one patients (28%) were treated with intracoronary verapamil for the immediate termination of reperfusion-induced ventricular tachyarrhythmias. These tachyarrhythmias included 6 premature ventricular contractions, 19 accelerated idioventricular rhythms, 3 ventricular tachycardias, 2 ventricular fibrillations (VFs), and 1 torsades de pointes. Intracoronary verapamil was effective in rapidly terminating all reperfusion-induced arrhythmias except for VFs. The side effects of treatment included temporary hypotension (two patients) and bradycardia (one patient), although all patients recovered spontaneously. No major complications were induced by the intracoronary use of verapamil, and no resumptions of arrhythmias were documented.

Conclusion:

Intracoronary administration of verapamil can safely terminate reperfusion-induced ventricular tachyarrhythmias in a rapid manner. However, this effect was not seen for reperfusion-induced VF.

Section snippets

Study Population

The study population consisted of 390 consecutive patients admitted to Hiroshima City Asa Hospital from 1992 to 2003 with the following conditions: (1) diagnosis of AMI; and (2) percutaneous coronary intervention (PCI) therapy within 6 h of the onset of symptoms for Thrombolysis in Myocardial Infarction (TIMI)11 grade 0/1 coronary flow. The study admission criteria included prolonged chest pain (ie, of > 30 min duration), typical ECG changes, successful reperfusion therapy within 6 h of the

Patient Population

Over an 11-year period, 390 patients were admitted to our hospital with a diagnosis of AMI and received mechanical revascularization therapy for TIMI grade 0/1 coronary flow within 6 h of symptom onset. Among these, 109 patients in the acute phase and with an occurrence of reperfusion arrhythmias were enrolled into the study. Thirty-one patients were treated by the intracoronary use of verapamil, 22 patients were treated by other antiarrhythmic drugs (lidocaine, 16 patients; disopyramide, 6

Discussion

Our results confirm that the intracoronary use of verapamil can safely terminate reperfusion-induced ventricular tachyarrhythmias. Furthermore, we saw no evidence for the resumption of arrhythmias after treatment. It is important to rapidly terminate reperfusion ventricular arrhythmias, because hemodynamics have the potential to quickly deteriorate, especially during reperfusion-induced VT or VF.1213 AIVR also may induce hypotension in patients with depressed cardiac function.14 To our

Conclusions

In conclusion, our study demonstrates that the intracoronary administration of verapamil can rapidly and safely terminate reperfusion-induced ventricular tachyarrhythmias. These effects were demonstrated for patients with reperfusion-induced AIVR, TdP, and VT, but intracoronary administration of verapamil could not effectively terminate reperfusion-induced VF in vivo.

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