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

Hidehiro Kaneko, Toshihisa Anzai, Kotaro Naito, Takashi Kohno, Yuichiro Maekawa, Toshiyuki Takahashi, Akio Kawamura, Tsutomu Yoshikawa, Satoshi Ogawa

Research output: Contribution to journalArticle

19 Citations (Scopus)

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 48 hours 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 ≥10 mg/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.

Original languageEnglish
Pages (from-to)775-781
Number of pages7
JournalJournal of Cardiac Failure
Volume15
Issue number9
DOIs
Publication statusPublished - 2009 Nov

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Ischemic Preconditioning
Ventricular Fibrillation
Ventricular Tachycardia
Cardiac Arrhythmias
Leukocyte Count
C-Reactive Protein
Unstable Angina
Infarction
ST Elevation Myocardial Infarction
Left Ventricular Dysfunction
Percutaneous Coronary Intervention
Reperfusion
Blood Proteins
Hospitalization
Multivariate Analysis

Keywords

  • ischemic preconditioning
  • post-infarction inflammation
  • Ventricular arrhythmia

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Role of Ischemic Preconditioning and Inflammatory Response in the Development of Malignant Ventricular Arrhythmias After Reperfused ST-Elevation Myocardial Infarction. / Kaneko, Hidehiro; Anzai, Toshihisa; Naito, Kotaro; Kohno, Takashi; Maekawa, Yuichiro; Takahashi, Toshiyuki; Kawamura, Akio; Yoshikawa, Tsutomu; Ogawa, Satoshi.

In: Journal of Cardiac Failure, Vol. 15, No. 9, 11.2009, p. 775-781.

Research output: Contribution to journalArticle

Kaneko, Hidehiro ; Anzai, Toshihisa ; Naito, Kotaro ; Kohno, Takashi ; Maekawa, Yuichiro ; Takahashi, Toshiyuki ; Kawamura, Akio ; Yoshikawa, Tsutomu ; Ogawa, Satoshi. / Role of Ischemic Preconditioning and Inflammatory Response in the Development of Malignant Ventricular Arrhythmias After Reperfused ST-Elevation Myocardial Infarction. In: Journal of Cardiac Failure. 2009 ; Vol. 15, No. 9. pp. 775-781.
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AU - Maekawa, Yuichiro

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AU - Ogawa, Satoshi

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N2 - 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 48 hours 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 ≥10 mg/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.

AB - 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 48 hours 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 ≥10 mg/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.

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