Silverio Sbrana

Monitoring of monocyte functional state after extracorporeal circulation: a flow cytometry study.

Cardiovascular surgery with cardiopulmonary bypass (CPB) induces systemic inflammation and postoperative complications depending on pro‐ and anti‐inflammatory mechanisms. Activated polymorphonuclear cells and monocytes may be responsible for morbidity associated with CPB. Knowledge of the monocyte functional state in particular may help to develop protective interventions.

Relationships Between Optical Aggregometry (Type Born) and Flow Cytometry in Evaluating ADP-Induced Platelet Activation

Platelet response to activating agents is used to monitor the efficacy of anti‐aggregation therapies. The aim of our study has been to demonstrate the existence of relationships between early events of ADP‐induced platelet activation, measured by flow cytometry and platelet‐rich plasma aggregation, quantified by optical aggregometry.

Post-reperfusion changes of monocyte function in coronary blood after extracorporeal circulation.

Neutrophil and mononuclear cell functional changes represent a hallmark of inflammation during cardiopulmonary bypass and cardiovascular surgery. Knowledge of mechanisms underlying monocyte functional modulation in coronary blood may be useful to develop protective interventions that can limit ischemia/reperfusion injury.

Granulocyte- and Monocyte-Platelet Adhesion Index in Coronary and Peripheral Blood After Extracorporeal Circulation and Reperfusion

Neutrophil‐granulocyte and mononuclear‐cell functional changes occur during cardiopulmonary bypass and cardiovascular surgery. In particular, leukocyte–platelet interaction, leading to generation of heterotypic coaggregates, represents an amplification mechanism of the local inflammatory response and tissue damage.

Stromal cell-derived factor-1-3'A polymorphism is associated with decreased risk of myocardial infarction and early endothelial disturbance.

Aim Genome-wide association studies have identified single-nucleotide polymorphisms at the 10q11 locus as risk factors for myocardial infarction (MI). This locus lies upstream (∼80 kb) of the stromal cell-derived factor-1 (SDF1) gene that codify for a chemokine with protective atherogenetic effects and with a major role in the mobilization, homing, and differentiation of endothelial progenitor cells (EPCs). The purpose of this study was to investigate the possible association of SDF1–3′A polymorphism, that upregulates SDF1 protein expression, with MI and early endothelial dysfunction and atherosclerosis in young healthy subjects. Methods 200 patients (181 men age 57.3 ± 7.7 years) and 230 healthy controls (96 men, age 52 ± 11.9 years) were recruited to investigate the association between MI and SDF1–3′A polymorphism. The relationship between SDF1–3′A polymorphism and brachial artery flow-mediated dilation and the number of circulating EPCs was examined in 50 healthy young adults. Results A significant difference in SDF1–3′A genotype distribution was observed between patients and controls (P = 0.006). Patients carrying the A allele had a significantly reduced MI risk compared with subjects with GG genotype (odds ratio = 0.5, 95% CI = 0.3–0.9, P = 0.001). SDF1–3′A polymorphism presented a significant interaction with other cardiovascular risk factors (Pinteraction < 0. 0001). Controls carrying the A allele showed significantly higher flow-mediated dilation (13.9 ± 4.9 vs 10.8 ± 4.3, P = 0.03) and significantly higher values of EPCs (0.029 ± 0.009 vs 0.022 ± 0.008, P = 0.02) compared with GG homozygotes. Conclusion SDF1–3′A polymorphism is associated with a decreased risk of MI and early endothelial dysfunction, strongly confirming the important atherogenic role of SDF1 gene at clinical level.