Tissue Inflammation Impairs Tissue-Level Perfusion and Promotes Left Ventricular Remodeling in Patients With Acute Myocardial Infarction

Yuya Nishida, Hiroshi Itoh, Katsuomi Iwakura, Kouji Tanaka, Shigeo Kawano, Atsunori Okamura, Yoshinori Maekawa, Kouichi Inoue, Kenshi Fujii, Masatsugu Hori

Research output: Contribution to journalArticle

Abstract

Background. C-reactive protein (CRP) level and monocytosis are associated with left ventricular (LV) remodeling in patients with AMI. Methods. One hundred twenty-nine consecutive patients with the first acute myocardial infarction (AMI) underwent myocardial contrast echocardiography (MCE) 2 weeks after successful reperfusion. Results. LV end-diastolic volume index (LVEDVI) at pre-discharge was significantly higher in the no-reflow group than the reflow group (64±17 vs. 58±11 mL/m2, p< 0.01). The no-reflow group had a higher CRP level and peak monocyte counts than the reflow group (9.5±5.2 vs. 5.8±3.5 mg/dl, p<0.0001; and 1026±400 vs. 824±278/μl, p<0.001, respectively). Peak CRP (relative risk [RR] 1.21, 95% confidence interval [CI] 1.01-1.45, p<0.05) and peak monocyte counts (RR 1.003, 95% CI 1.001-1.006, p<0.01) were independent determinants of the no-reflow phenomenon. Conclusion. Microvascular dysfunction following tissue inflammation may play an important role in the LV remodeling after AMI.

Original languageEnglish
Pages (from-to)83-90
Number of pages8
JournalJournal of Echocardiography
Volume3
Issue number2
DOIs
Publication statusPublished - 2005
Externally publishedYes

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Ventricular Remodeling
C-Reactive Protein
Perfusion
Myocardial Infarction
Inflammation
Monocytes
No-Reflow Phenomenon
Confidence Intervals
Stroke Volume
Reperfusion
Echocardiography

Keywords

  • Inflammation
  • Microcirculation
  • Monocyte
  • Myocardial infarction
  • No-reflow

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

Cite this

Tissue Inflammation Impairs Tissue-Level Perfusion and Promotes Left Ventricular Remodeling in Patients With Acute Myocardial Infarction. / Nishida, Yuya; Itoh, Hiroshi; Iwakura, Katsuomi; Tanaka, Kouji; Kawano, Shigeo; Okamura, Atsunori; Maekawa, Yoshinori; Inoue, Kouichi; Fujii, Kenshi; Hori, Masatsugu.

In: Journal of Echocardiography, Vol. 3, No. 2, 2005, p. 83-90.

Research output: Contribution to journalArticle

Nishida, Yuya ; Itoh, Hiroshi ; Iwakura, Katsuomi ; Tanaka, Kouji ; Kawano, Shigeo ; Okamura, Atsunori ; Maekawa, Yoshinori ; Inoue, Kouichi ; Fujii, Kenshi ; Hori, Masatsugu. / Tissue Inflammation Impairs Tissue-Level Perfusion and Promotes Left Ventricular Remodeling in Patients With Acute Myocardial Infarction. In: Journal of Echocardiography. 2005 ; Vol. 3, No. 2. pp. 83-90.
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AU - Itoh, Hiroshi

AU - Iwakura, Katsuomi

AU - Tanaka, Kouji

AU - Kawano, Shigeo

AU - Okamura, Atsunori

AU - Maekawa, Yoshinori

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N2 - Background. C-reactive protein (CRP) level and monocytosis are associated with left ventricular (LV) remodeling in patients with AMI. Methods. One hundred twenty-nine consecutive patients with the first acute myocardial infarction (AMI) underwent myocardial contrast echocardiography (MCE) 2 weeks after successful reperfusion. Results. LV end-diastolic volume index (LVEDVI) at pre-discharge was significantly higher in the no-reflow group than the reflow group (64±17 vs. 58±11 mL/m2, p< 0.01). The no-reflow group had a higher CRP level and peak monocyte counts than the reflow group (9.5±5.2 vs. 5.8±3.5 mg/dl, p<0.0001; and 1026±400 vs. 824±278/μl, p<0.001, respectively). Peak CRP (relative risk [RR] 1.21, 95% confidence interval [CI] 1.01-1.45, p<0.05) and peak monocyte counts (RR 1.003, 95% CI 1.001-1.006, p<0.01) were independent determinants of the no-reflow phenomenon. Conclusion. Microvascular dysfunction following tissue inflammation may play an important role in the LV remodeling after AMI.

AB - Background. C-reactive protein (CRP) level and monocytosis are associated with left ventricular (LV) remodeling in patients with AMI. Methods. One hundred twenty-nine consecutive patients with the first acute myocardial infarction (AMI) underwent myocardial contrast echocardiography (MCE) 2 weeks after successful reperfusion. Results. LV end-diastolic volume index (LVEDVI) at pre-discharge was significantly higher in the no-reflow group than the reflow group (64±17 vs. 58±11 mL/m2, p< 0.01). The no-reflow group had a higher CRP level and peak monocyte counts than the reflow group (9.5±5.2 vs. 5.8±3.5 mg/dl, p<0.0001; and 1026±400 vs. 824±278/μl, p<0.001, respectively). Peak CRP (relative risk [RR] 1.21, 95% confidence interval [CI] 1.01-1.45, p<0.05) and peak monocyte counts (RR 1.003, 95% CI 1.001-1.006, p<0.01) were independent determinants of the no-reflow phenomenon. Conclusion. Microvascular dysfunction following tissue inflammation may play an important role in the LV remodeling after AMI.

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