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

• Published in: Journal of Echocardiography Vol. 3; no. 2; pp. 83 - 90
• Main Authors: Nishida, Yuya, Ito, Hiroshi, Iwakura, Katsuomi, Tanaka, Kouji, Kawano, Shigeo, Okamura, Atsunori, Maekawa, Yoshinori, Inoue, Kouichi, Hori, Masatsugu, Fujii, Kenshi
• Format: Journal Article
• Language: English
• Published: Japanese Society of Echocardiography 2005
• Subjects: Inflammation; Microcirculation; Monocyte; Myocardial infarction; No-reflow
• ISSN: 1349-0222; 1880-344X
• DOI: 10.2303/jecho.3.83

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.