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Volume 15, Issue 9, Pages 775-781 (November 2009)


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Role of Ischemic Preconditioning and Inflammatory Response in the Development of Malignant Ventricular Arrhythmias After Reperfused ST-Elevation Myocardial Infarction

Hidehiro Kaneko, MD1, Toshihisa Anzai, MD, FACC1Corresponding Author Informationemail address, Kotaro Naito, MD1, Takashi Kohno, MD1, Yuichiro Maekawa, MD1, Toshiyuki Takahashi, MD1, Akio Kawamura, MD1, Tsutomu Yoshikawa, MD, FACC1, Satoshi Ogawa, MD, FACC1

Received 16 January 2009; received in revised form 8 April 2009; accepted 4 May 2009. published online 29 June 2009.

Abstract 

Background

Sustained ventricular tachycardia and ventricular fibrillation (VT/VF) are major complications of ST-elevation myocardial infarction (STEMI), even in the era of reperfusion therapy. We sought to clarify the determinants of VT/VF after reperfused STEMI.

Methods and Results

Consecutive STEMI patients treated with primary percutaneous coronary intervention (n=457) were divided into 2 groups by the presence or absence of VT/VF during hospitalization. Serum C-reactive protein (CRP) level and peripheral white blood cell (WBC) count were serially measured. VT/VF was observed in 54 patients (12%). Prior infarction was more common and preinfarction angina was less in patients with VT/VF than those without. Peak CRP level (P < .0001), WBC count on admission (P=.008), and maximum WBC count (P=.0014) were higher in patients with VT/VF than those without. VT/VF, especially VT/VF later than 48hours after onset, was associated with greater left ventricular (LV) dimension during convalescence. Kaplan-Meier curves and log-rank test revealed VT/VF to be a significant determinant of long-term major adverse cardiac events. Multivariate analysis revealed that prior infarction, absence of preinfarction angina, and peak CRP ≥10mg/dL were independent determinants of VT/VF.

Conclusions

Lack of ischemic preconditioning, enhanced inflammatory response, and subsequent LV dysfunction are related to the development of VT/VF after STEMI.

1 Division of Cardiology, Department of Medicine, Keio University School of Medicine, Tokyo, Japan

Corresponding Author InformationCorrespondence to: Toshihisa Anzai, MD, Division of Cardiology, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Tel: +81-3-5363-3793; Fax: +81-3-3353-2502.

 Supported by the Global Center of Excellence (G-COE) Program at Keio University (H.K.) and the Medical School Faculty and Alumni Grant from Keio University Medical Science Fund (T.A.).

 No conflicts of interest exist in this study.

PII: S1071-9164(09)00143-2

doi:10.1016/j.cardfail.2009.05.001


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