Myocardial infarction causes inflammation and leukocyte recruitment at remote sites in the myocardium and in the renal glomerulus

Abstract

Rationale and ObjectiveAcute myocardial infarction (AMI) results in the recruitment of leukocytes to injured myocardium. Additionally, myocardium remote to the infarct zone also becomes inflamed and is associated with adverse left ventricular remodelling. Renal ischaemic syndromes have been associated with remote organ inflammation and impaired function. Here, we tested the hypothesis that AMI results in remote organ (renal) inflammation.MethodsMice were subjected to either AMI, sham procedure or no procedure and the inflammatory response in peripheral blood, injured and remote myocardium, and kidneys was studied at 24 h.ResultsAMI resulted in increased circulating neutrophils (P < 0.001) and monocytes (P < 0.001). mRNA for inflammatory mediators significantly increased in infarcted myocardium and in remote myocardium. VCAM-1 mRNA was increased in both infarcted and remote myocardium. VCAM-1 protein was also increased in the kidneys of AMI mice (P < 0.05) and immunofluorescence revealed localisation of VCAM-1 to glomeruli, associated with leukocyte infiltration and increased local inflammatory mRNA expression.ConclusionsWe conclude that in addition to local inflammation, AMI results in remote organ inflammation evidenced by (1) increased expression of mRNA for inflammatory cytokines, (2) marked upregulation of VCAM-1 in renal glomeruli, and (3) the recruitment and infiltration of leukocytes in the kidney.Electronic supplementary materialThe online version of this article (doi:10.1007/s00011-013-0605-4) contains supplementary material, which is available to authorized users.

Predictive Value of Monocyte to High-Density Lipoprotein Cholesterol Ratio for Contrast-Induced Nephropathy in Patients with ST-Segment Elevation Myocardial Infarction Who Underwent Primary Percutaneous Coronary Intervention

“…Monocytes are the key players in this inflammatory damage and mediate a negative effect on myocardial remodelling. Furthermore, remote organ inflammation is evidenced by the upregulation of VCAM-1 in renal glomeruli and by the recruitment and infiltration of leukocytes throughout the kidney 24 h following myocardial infarction (9) . Karasawa et al showed that the inflammatory subset of peripheral monocytes accumulates in injured renal tissue and contributes to renal damage.…”

Characterizing the Inflammatory Tissue Response to Acute Myocardial Infarction by Clinical Multimodality Noninvasive Imaging

“…Summed FDG score was 19 (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25) and correlated significantly with the global scores for LE (ρ=0.54; P=0.04; Figure 3A) and edema (ρ=0.76; P=0.002; Figure 3B). Consistently, the mean FDG score was significantly elevated in segments with LE compared with those without In patients with chronic MI, a reverse pattern was observed.…”

“…to a lesser degree, 7,13 providing a rationale for remote remodeling. 14 But the use of FDG is complicated by the fact that its uptake may also reflect the presence of ischemically compromised, viable myocytes after AMI.…”

“…20,21 Also, dynamic 13 N-ammonia PET rest and stress images were quantitatively analyzed by generating myocardium and blood time-activity curves and applying a validated 3-compartment model to determine myocardial blood flow (MBF) at stress and rest, as previously described.…”

“…CMR showed transmural LE in the infarct region in 3 of 5 patients, with a summed LE score of 15 (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24). No edema or MVO was identified.…”