Inflammatory and vasoactive factors in the aspirate from the culprit coronary artery of patients with acute myocardial infarction

An increased platelet–leukocytes interaction at the culprit site of coronary artery occlusion in acute myocardial infarction: A pathogenic role for “no-reflow” phenomenon?

“…A recent study also showed increased levels of soluble CD40 ligand, IL-6, serotonin, tissue factor and factor VII in the culprit coronary artery compared to those in peripheral blood [31]. These and our data highlight the interaction between inflammation and thrombotic states at the site of ruptured plaque.…”

The impact of admission C-reactive protein levels on the development of no-reflow phenomenon after primary PCI in patients with acute myocardial infarction: The role of inflammation

“…Ko et al investigated the presence of locally increased inflammatory and vasoactive factors in culprit coronary artery in patients with AMI undergoing primary PCI with PercuSurge GuideWire system [11]. They collected blood samples from the femoral artery before PCI and from culprit coronary artery after first predilation while inflating the distal protection balloon and after completing PCI.…”

Early inflammatory cytokine response: A direct comparison between spontaneous coronary plaque destabilization vs angioplasty induced

“…Increased concentrations of IL-1 receptor antagonist and sCD40L could be found in samples drawn from the culprit coronary artery compared with those from a peripheral artery. Similarly, increased levels of soluble CD40 ligand, IL-6, serotonin, tissue factor and factor VII may be found in the culprit coronary artery compared to peripheral blood [16].…”