Effects of Percutaneous Coronary Intervention on Peripheral Venous Blood Circulating Endothelial Cells and Plasma Indices of Endothelial Damage/Dysfunction

SummaryMonocyte recruitment to damaged endothelium is enhanced by platelet binding to monocytes and contributes to vascular repair. Therefore, we studied whether the number of platelets per monocyte affects the recurrence of adverse events in patients after percutaneous coronary intervention (PCI). Platelet-monocytes complexes with high and low median fluorescence intensities (MFI) of the platelet marker CD42b were isolated using cell sorting. Microscopic analysis revealed that a high platelet marker MFI on monocytes corresponded with a high platelet density per monocyte while a low platelet marker MFI corresponded with a low platelet density per monocyte (3.4 ± 0.7 vs 1.4 ± 0.1 platelets per monocyte, P=0.01). Using real-time video microscopy, we observed increased recruitment of high platelet density monocytes to endothelial cells as compared with low platelet density monocytes (P=0.01). Next, we classified PCI scheduled patients (N=263) into groups with high, medium and low platelet densities per monocyte and assessed the recurrence of adverse events. After multivariate adjustment for potential confounders, we observed a 2.5-fold reduction in the recurrence of adverse events in patients with a high platelet density per monocyte as compared with a low platelet density per monocyte [hazard ratio=0.4 (95 % confidence interval, 0.2–0.8), P=0.01]. We show that a high platelet density per monocyte increases monocyte recruitment to endothelial cells and predicts a reduction in the recurrence of adverse events in patients after PCI. These findings may imply that a high platelet density per monocyte protects against recurrence of adverse events.Supplementary Material to this article is available online at www.thrombosis-online.com.

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Markers of oxidative stress in acute myocardial infarction treated by percutaneous coronary intervention

Open Medicine ◽

10.2478/s11536-009-0015-8 ◽

2009 ◽

Vol 4 (1) ◽

pp. 26-31 ◽

Cited By ~ 6

Author(s):

Eva Sedláková ◽

Oliver Rácz ◽

Eva Lovásová ◽

Roman Beòaèka ◽

Martin Kurpas ◽

...

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Percutaneous Coronary Intervention ◽

Venous Blood ◽

Plasma Lipid ◽

Coronary Intervention ◽

Control Group ◽

Coronary Syndrome ◽

Percutaneous Coronary

AbstractIn the current study, we evaluated the dynamics of oxidative stress markers in patients with acute myocardial infarction (AMI) treated by primary percutaneous coronary intervention (PCI). Thirty consecutive patients with AMI with ST elevation were included. Plasma lipid peroxidation end product malondialdehyde (MDA) and total antioxidant capacity (TAC) in blood plasma were evaluated. Peripheral venous blood samples were obtained prior to reperfusion and at five time points after reperfusion. The control group consisted of 20 ischemic patients without acute coronary syndrome. TAC in the AMI group at admission was lower than in control patients (1.26 + 0.32 vs. 1.52 + 0.24 mmol/l). Within 1 h after reperfusion, in most cases, values significantly declined (1 min, 1.10 + 0.33 mmol/l; 1 h, 1.06 + 0.21 mmol/l [p= 0.03]). After 3 h, values began to increase (1.14 + 0.29 mmol/l) and returned to basal values after 3 d (1.29 + 0.24 mmol/l). MDA levels in AMI patients at admission were higher than in control patients (1.66 + 0.55 vs. 1.44 + 0.55 mmol/l) but showed a sustained decrease over the 3 h after reperfusion of the occluded artery (1 min, 1.57 + 0.37 mmol/l; 1 h, 1.50 + 0.35 μmol/l; 3 h, 1.35 + 0.59 μmol/l [p = 0.03]). Reperfusion of the occluded coronary artery by PCI in AMI lead to an immediate decrease in TAC, suggesting formation of reactive oxygen species. However, the MDA level significantly decreased after reperfusion. This may suggests less reperfusion injury after PCI.

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Effects of percutaneous coronary intervention and stenting with different drug-eluting coatings and platforms on endothelial damage and inflammation

International Journal of Cardiology ◽

10.1016/j.ijcard.2012.01.059 ◽

2012 ◽

Vol 156 (2) ◽

pp. 242-243 ◽

Cited By ~ 1

Author(s):

Francesco Pelliccia ◽

Giuseppe Del Prete ◽

Armando Del Prete ◽

Cesare Greco ◽

Carlo Gaudio

Keyword(s):

Percutaneous Coronary Intervention ◽

Coronary Intervention ◽

Endothelial Damage ◽

Percutaneous Coronary ◽

Drug Eluting

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Angiographic dynamics of coronary flow state after percutaneous coronary intervention in carriers of polymorphic RS1800470 variants of the TGF-β1 gene

Russian Journal of Cardiology ◽

10.15829/1560-4071-2019-8-77-82 ◽

2019 ◽

pp. 77-82

Author(s):

D. A. Brusentsov ◽

S. Yu. Nikulina ◽

P. A. Shesternya

Keyword(s):

Percutaneous Coronary Intervention ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Venous Blood ◽

Coronary Intervention ◽

Flow State ◽

Gensini Score ◽

Mean Values ◽

Caucasian Race ◽

Percutaneous Coronary

Aim. To study the relationship between the angiographic dynamics of the state of the coronary bed in patients undergoing percutaneous coronary intervention (PCI) due to myocardial infarction (MI) and the carriage of polymorphic rs1800470 variants of the transforming growth factor beta-1 gene (TGF-β1).Material and methods. The study included 89 men with MI of the Caucasian race aged 32 to 65 years (52 [45,0-58,0]). Genomic deoxyribonucleic acid (DNA) was extracted from venous blood by phenol-chloroform technique. The rs1800470 polymorphism of the TGF-β1 gene was tested using real-time polymerase chain reaction (PCR) (TaqMan probes, AB 7900HT). Assessment of the severity of coronary lesions was carried out initially according to the standard coronary angiography (CAG) protocol with the calculation of the Gensini score. CAG was also conducted in the dynamics after 5-103 months (42,3±29,5 months) of the study beginning.Results. In male carriers of the rs1800470 A allele of the TGF-β1 gene, the mean values of the Gensini score statistically significantly increased (47,5±34,1 (CAG-1) and 64,5±35,5 (CAG-2), p <0,001) in comparison with carriers of the homozygous GG rs1800470 variant of the TGF-β1 gene (43,5±21,1 (CAG-1) and 46,2±23,2 (CAG2), p=0,066). In patients who had rs1800470 A allele of the TGF-β1 gene, a 20%decrease in the Gensini score was observed after 7 months (p=0,013), and 30% — after 5 months (p=0,003) of the initial CAG. The development of late stent restenoses in carriers of the rs1800470 A allele and the homozygous risk genotype AA of the TGF-β1 gene was noted at an earlier date — 8 (p=0,047) and 12 months (p=0,002), respectively.Conclusion. Currently, the conduct of CAG in dynamics in patients undergoing PCI is recommended as clinically indicated. The exception is the group of patients who underwent endoprosthesis replacement of the left coronary artery or have uncorrected stenosis of a different location from 3 to 12 months after PCI. The presented data show a possible predictor role of rG1800470 polymorphism of the TGF-β1 gene in relation to the progression of coronary atherosclerosis and the development of late stent restenoses.

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Inflammation during Percutaneous Coronary Intervention—Prognostic Value, Mechanisms and Therapeutic Targets

Cells ◽

10.3390/cells10061391 ◽

2021 ◽

Vol 10 (6) ◽

pp. 1391

Author(s):

Bradley Tucker ◽

Kaivan Vaidya ◽

Blake J. Cochran ◽

Sanjay Patel

Keyword(s):

Percutaneous Coronary Intervention ◽

Inflammatory Response ◽

Prognostic Value ◽

Coronary Intervention ◽

Endothelial Damage ◽

Acute Inflammatory Response ◽

Percutaneous Coronary ◽

Short And Long Term ◽

Anti Inflammatory

Periprocedural myocardial injury and myocardial infarction (MI) are not infrequent complications of percutaneous coronary intervention (PCI) and are associated with greater short- and long-term mortality. There is an abundance of preclinical and observational data demonstrating that high levels of pre-, intra- and post-procedural inflammation are associated with a higher incidence of periprocedural myonecrosis as well as future ischaemic events, heart failure hospitalisations and cardiac-related mortality. Beyond inflammation associated with the underlying coronary pathology, PCI itself elicits an acute inflammatory response. PCI-induced inflammation is driven by a combination of direct endothelial damage, liberation of intra-plaque proinflammatory debris and reperfusion injury. Therefore, anti-inflammatory medications, such as colchicine, may provide a novel means of improving PCI outcomes in both the short- and long-term. This review summarises periprocedural MI epidemiology and pathophysiology, evaluates the prognostic value of pre-, intra- and post-procedural inflammation, dissects the mechanisms involved in the acute inflammatory response to PCI and discusses the potential for periprocedural anti-inflammatory treatment.

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