TY - JOUR
T1 - Low doses of intracoronary enalaprilat suppress reperfusion-associated ventricular arrhythmias after primary percutaneous coronary interventions for acute myocardial infarction
AU - Bonnemeier, Hendrik
AU - Schäfer, Ulrich
AU - Ortak, Jasmin
AU - Kurz, Thomas
AU - Katus, Hugo A.
AU - Richardt, Gert
AU - Schunkert, Heribert
PY - 2007/1
Y1 - 2007/1
N2 - Background: In the era of early reperfusion therapy, life-threatening ventricular arrhythmias (VA) remain common after recanalization of an occluded coronary artery. Experimental studies reported that angiotensin-converting (ACE) inhibitors suppress reperfusion-induced VA. However, whether ACE inhibitors lower the incidence of reperfusion clinical VA is unknown. We examined the effects of low doses of intracoronary (i.c.) enalaprilat (EN) as an adjunct to direct percutaneous coronary interventions (PCI) on reperfusion VA in the acute phase of myocardial infarction (MI). Methods: We randomly assigned 22 patients with a first acute MI, who underwent successful direct PCI, to EN, 50 μg, i.c., or placebo (PL), administered immediately after reperfusion. VA were manually edited and counted from 24-hour Holter recordings begun upon hospital admission. Results: There were no significant between-groups differences in clinical characteristics. Mean RR interval before and after PCI, and the incidence of VA before PCI were similar in both groups. After PCI the incidence of reperfusion-induced VA was significantly lower in the EN-treated group (VPB/h: PL 29.9 ± 12 vs EN 43.2 ± 42, P < 0.05; couplets/h: EN 0.9 ± 0.7 vs PL 4.1 ± 5.0, P < 0.01; triplets/h: EN 0.3 ± 0.2 vs PL 1.2 ± 1.5, P < 0.05; ventricular tachycardia/h: EN 0.3 ± 0.1 vs PL 0.8 ± 0.5, P < 0.01). Conclusions: Compared with PL, i.c. EN significantly lowered the incidence of reperfusion-associated VA. This previously unrecognized antiarrhythmic effect might be an important therapeutic benefit conferred by ACE inhibitors, beyond limitation of infarct size.
AB - Background: In the era of early reperfusion therapy, life-threatening ventricular arrhythmias (VA) remain common after recanalization of an occluded coronary artery. Experimental studies reported that angiotensin-converting (ACE) inhibitors suppress reperfusion-induced VA. However, whether ACE inhibitors lower the incidence of reperfusion clinical VA is unknown. We examined the effects of low doses of intracoronary (i.c.) enalaprilat (EN) as an adjunct to direct percutaneous coronary interventions (PCI) on reperfusion VA in the acute phase of myocardial infarction (MI). Methods: We randomly assigned 22 patients with a first acute MI, who underwent successful direct PCI, to EN, 50 μg, i.c., or placebo (PL), administered immediately after reperfusion. VA were manually edited and counted from 24-hour Holter recordings begun upon hospital admission. Results: There were no significant between-groups differences in clinical characteristics. Mean RR interval before and after PCI, and the incidence of VA before PCI were similar in both groups. After PCI the incidence of reperfusion-induced VA was significantly lower in the EN-treated group (VPB/h: PL 29.9 ± 12 vs EN 43.2 ± 42, P < 0.05; couplets/h: EN 0.9 ± 0.7 vs PL 4.1 ± 5.0, P < 0.01; triplets/h: EN 0.3 ± 0.2 vs PL 1.2 ± 1.5, P < 0.05; ventricular tachycardia/h: EN 0.3 ± 0.1 vs PL 0.8 ± 0.5, P < 0.01). Conclusions: Compared with PL, i.c. EN significantly lowered the incidence of reperfusion-associated VA. This previously unrecognized antiarrhythmic effect might be an important therapeutic benefit conferred by ACE inhibitors, beyond limitation of infarct size.
KW - ACE-inhibitor
KW - Acute myocardial infarction
KW - Percutaneous coronary intervention
KW - Reperfusion arrhythmia
KW - Ventricular arrhythmia
UR - http://www.scopus.com/inward/record.url?scp=33846289597&partnerID=8YFLogxK
U2 - 10.1111/j.1540-8159.2007.00629.x
DO - 10.1111/j.1540-8159.2007.00629.x
M3 - Article
C2 - 17302696
AN - SCOPUS:33846289597
SN - 0147-8389
VL - 30
SP - S160-S165
JO - Pacing and Clinical Electrophysiology
JF - Pacing and Clinical Electrophysiology
IS - SUPPL. 1
ER -