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Background and Aims: Leptin is a hormone involved in the regulation of food intake. Previous studies suggested an interplay between leptin, platelet aggregation, and cardiovascular outcome but this issue was not investigated in vivo in patients treated with percutaneous coronary intervention (PCI). We designed a study to evaluate the possible relation between leptin, cardiovascular outcome, and platelet reactivity (PR) in patients undergoing PCI., Methods: 155 PCI patients had preprocedural measurements of PR and leptin plasma levels. The latter were assessed by ELISA. Hyperleptinemia was defined as leptin levels ≥14 ng/ml. PR was evaluated by the VerifyNowP2Y12 assay and expressed as P2Y12 reaction units (PRU). Patients were divided into three groups based on PR values and defined as low (LPR), normal (NPR), and high (HPR). Patients were followed for up 8 years. The primary endpoint was the incidence of Major Acute Cardiac Events (MACE) at long-term follow-up according to leptin groups. Secondary endpoints were the evaluation of leptin levels according to PR groups and the incidence of periprocedural myocardial infarction (PMI) according to leptin groups., Results: Long-term follow-up was completed in 140 patients. Patients with hyperleptinemia experienced a higher MACE rate than the normoleptinemic group (HR 2.3; CI 95% 1.14-4.6, P = 0.02). These results remained unchanged after adjusting for Body Mass Index, hypertension, and gender. Leptin levels were significantly different among groups of PR (P = 0.047). Leptin levels were higher in the HPR group (12.61 ± 16.58 ng/ml) compared to the LPR group (7.83 ± 8.87 ng/ml, P = 0.044) and NPR group (7.04 ± 7.03 ng/ml, P = 0.01). The rate of PMI was higher in hyperleptinemia patients (15.1% vs. 6.5%, P = 0.22)., Conclusions: This study suggests that high leptin levels are associated with a worse clinical outcome in patients undergoing PCI and with HPR. Further studies are needed to define better the pathophysiological pathways underlying this association., Competing Interests: Declaration of competing interest All authors have nothing to declare concerning the present manuscript., (Copyright © 2023 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.)

Percutaneous coronary intervention (PCI) is frequently complicated by type 4a myocardial infarction (MI), which is associated with an increased risk of mortality. We assessed the usefulness of the angiography-derived hemodynamic index (ADDED), which is based on the extent of myocardium at risk and on the anatomical lesion severity, in predicting type 4a MI in patients with chronic coronary syndrome (CCS) undergoing PCI. We enrolled 442 patients treated with single-vessel PCI. The ADDED index was calculated as the ratio of the Duke Jeopardy Score to the minimum lumen diameter assessed with quantitative angiography analysis. Type 4a MI was defined according to the 4th Universal Definition of MI. The overall population was divided into tertiles of ADDED index. Type 4a MI occurred in 5 patients (3.3%) in the ADDED-low tertile, 8 (5.5%) in the ADDED-mid tertile, and 26 (17.7%) in the ADDED-high tertile (p < 0.0001). At ROC curve analysis, the ADDED index could significantly discriminate between patients with and without type 4a MI (area under the curve 0.745). At multivariate analysis, an ADDED index value > 5.25 was the strongest independent predictor type 4a MI. Our results support the role of the ADDED index as a predictor of type 4a MI in patients with CCS treated with elective PCI of a single vessel. Whether a selective use of additional preventive measures in patients considered at high risk based on ADDED index values may improve peri-procedural and long-term outcomes remains to be tested in dedicated investigations., (© 2022. Springer Japan KK, part of Springer Nature.)

No comprehensive data are available on the role of platelet indexes (PI) in the periprocedural risk stratification of patients who underwent percutaneous coronary intervention (PCI). The aim of this study was to investigate the relation of PI to platelet reactivity (PR) and periprocedural myocardial infarction (PMI) in patients receiving PCI. A total of 502 PCI patients had preprocedural measurement of PI and PR, the latter assessed by VerifyNow P2Y12 assay. Study end points were incidence of PMI and high platelet reactivity (HPR) according to tertiles of PI and evaluation of PI in HPR patients. Incidence of PMI in the overall population was 6.6%. Rates of PMI were not different in PI tertiles: platelet count (I: 6.0%, II: 7.1%, III: 6.5%; p = 0.74), mean platelet volume (MPV, I: 6.6%, II: 7.3%, III: 5.8%;p = 0.86), platelet distribution width (I: 7.2%, II: 7.2%, III: 5.8%;p = 0.74), and MPV/P ratio (I: 6.6%, II: 6.0%, III: 7.1%; p = 0.91). The occurrence of PMI was significantly different in PR tertiles (I: 3%, II: 5.4%, III: 11.4%; p = 0.006). Platelet count and MPV/P ratio were significantly different in patients with and without HPR (221.8 ± 58.6 × 103/µL vs207 ± 59.4 × 103/µL, p = 0.008; 51.73 ± 15.17 vs 56.7 ± 18.3, p = 0.002).In conclusion, this study showed no relation between PI and PMI in PCI patients but confirms the association of HPR with increased incidence of PMI; thus, PI seem to be not able to identify patients at higher periprocedural risk, but monitoring PR by a bedside assay remains a useful tool for risk stratification., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Neutrophil to lymphocyte ratio (NLR) has been proposed as a marker of cardiovascular risk. The potential relation between NLR and periprocedural myocardial damage after percutaneous coronary intervention (PCI) is unclear. We enrolled 502 consecutive patients with stable coronary artery disease undergoing elective PCI. Blood samples were drawn in all patients at baseline, 6 hours, and 24 hours after PCI for complete blood cell count and cardiac biomarkers (creatine kinase-MB and troponin T [Tn-T]) assessment. NLR was calculated as the ratio between the absolute number of neutrophil over the absolute number of lymphocyte. Periprocedural myocardial infarction (PMI) was defined according to the 2012 universal definition of myocardial infarction. In the overall population, a significant postprocedural increase in NLR was observed (3.255 [2.763 to 3.995] at baseline, 4.430 [3.390 to 6.020] at 6 hours, 4.720 [3.940 to 5.750] at 24 hours, p <0.0001). PMI occurred in 33 patients (6.6%). Baseline NLR was similar in patients with and without PMI (3.250 [2.820 to 3.885] vs 3.260 [2.750 to 4.000], p = 0.898); however, patients who developed PMI showed significantly higher NLR both at 6 hours (5.750 [4.360 to 9.095] vs 4.370 [3.370 to 5.950], p <0.001) and 24 hours (5.180 [4.440 to 8.065] vs 4.670 [3.920 to 5.710], p = 0.003). Among patients who developed PMI, periprocedural NLR increase showed a moderate positive correlation with both creatine kinase-MB (rho = 0.377, p = 0.031) and troponin T increase (rho = 0.506, p = 0.003). In conclusion, preprocedural NLR values do not impact on the occurrence of PMI during elective PCI; however, PCI procedures induce a significant increase in NLR that seems to be proportional to the magnitude of periprocedural myocardial damage., (Copyright © 2016 Elsevier Inc. All rights reserved.)

The incremental predictive value of high inflammatory status and high on-treatment platelet reactivity (HPR) on the occurrence of periprocedural myocardial infarction (PMI) after percutaneous coronary intervention (PCI) has not been characterized. The aim of this study was to evaluate the correlation of elevated C-reactive protein (CRP) level and/or HPR with the incidence of PMI in patients who undergo PCI. Five hundred consecutive patients treated with clopidogrel who underwent PCI had preprocedural measurement of CRP levels and platelet reactivity using the point-of-care VerifyNow P2Y12 assay. Elevated inflammatory status was defined as CRP >3 mg/L and HPR as P2Y12 reactivity units ≥240. The primary end point was the incidence of PMI in relation to platelet reactivity and/or inflammatory status. Rates of PMI were increased in patients with CRP levels >3 mg/L (10.9% vs 4.6% in those with normal levels, odds ratio 2.4, 95% confidence interval 1.2 to 4.5, p = 0.015) and in patients with HPR (11% vs 5.5% in those without HPR, odds ratio 2.2, 95% confidence interval 1.2-4.4, p = 0.018). The occurrence of PMI was highest in the subgroup with HPR and high inflammatory status (16.6% vs 3.6% in patients with CRP ≤3 mg/L and P2Y12 reactivity units <240, odds ratio 4.3, 95% confidence interval 1.5 to 12.6, p = 0.008). HPR in association with elevated CRP levels resulted in a significant increase in the discriminatory power of a model including clinical and procedural variables in predicting PMI (area under the curve 0.811, p = 0.041). In conclusion, in patients who undergo PCI, baseline stratification according to platelet reactivity and inflammatory status may identify those at higher risk for PMI., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Objectives: We sought to evaluate the influence of platelet reactivity after clopidogrel, as assessed by the VerifyNow point-of-care assay (Accumetrics, San Diego, California), on myonecrosis in low-to-intermediate risk patients undergoing percutaneous coronary intervention (PCI)., Background: Inadequate platelet inhibition at the time of PCI is associated with a higher risk of recurrent ischemic events., Methods: A total of 250 consecutive biomarker-negative patients treated with clopidogrel and undergoing elective PCI were enrolled. Cardiac biomarkers (creatine kinase-myocardial band and troponin I) were measured before and 8 and 24 h after intervention. Platelet reactivity after clopidogrel was assessed immediately before PCI by the VerifyNow P2Y12 point-of-care assay. High platelet reactivity (HPR) after clopidogrel was defined as a platelet reaction unit value > or =240., Results: Patients with HPR (31% of the overall population) showed more frequent myonecrosis, with statistical significance with regard to creatine kinase-myocardial band elevation (35% vs. 20%; p = 0.011), and by trend with regard to troponin-I elevation (47% vs. 35%; p = 0.059). Incidence of periprocedural myocardial infarction was higher in patients with HPR, both by creatine kinase-myocardial band (13% vs. 4%; p = 0.011) and troponin-I definition (32% vs. 19%; p = 0.019). By multivariable analysis, HPR was an independent predictor of periprocedural myocardial infarction., Conclusions: Easily assessed by a point-of-care assay, HPR after clopidogrel is a frequent finding and is associated with increased risk of myonecrosis in low-to-intermediate risk patients undergoing planned PCI., (Copyright (c) 2010 American College of Cardiology Foundation.Published by Elsevier Inc. All rights reserved.)