Perioperative platelet and monocyte activation in patients with critical limb ischemia

Burdess, Anne; Nimmo, A. F.; Campbell, Neil; Harding, Scott; Garden, O. James; Dawson, A. R. W.; Newby, David E.

doi:10.1016/j.jvs.2010.04.024

Cited by 16 publications

(18 citation statements)

References 33 publications

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“…Another limitation is the fact that blood samples were drawn from the arterial sheath, which may potentially dilute any local effect caused by the FFR-positive lesion. Systemic blood sampling may not recognize local PLC formation in the coronary circulation, although previous research have also found differences in PLCs in systemic blood samples of patients with localized arterial pathology [9], [29].…”

Section: Discussionmentioning

confidence: 90%

“…Increased systemic platelet reactivity was described in patients with documented coronary artery disease immediately after peak exercise [27]; [28], however no relationship with ischemia was found [27]. In critical limb ischemia, increased PMCs and expression of P-selectin was observed, implying an ischemic mechanism of platelet activation [29]. Conversely, other investigators found an inverse relationship between coronary obstruction and platelet reactivity [30], although all patients investigated had severe single-vessel disease.…”

Section: Discussionmentioning

confidence: 95%

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The Relationship between Fractional Flow Reserve, Platelet Reactivity and Platelet Leukocyte Complexes in Stable Coronary Artery Disease

et al. 2013

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BackgroundThe presence of stenoses that significantly impair blood flow and cause myocardial ischemia negatively affects prognosis of patients with stable coronary artery disease. Altered platelet reactivity has been associated with impaired prognosis of stable coronary artery disease. Platelets are activated and form complexes with leukocytes in response to microshear gradients caused by friction forces on the arterial wall or flow separation. We hypothesized that the presence of significantly flow-limiting stenoses is associated with altered platelet reactivity and formation of platelet-leukocyte complexes.MethodsOne hundred patients with stable angina were studied. Hemodynamic significance of all coronary stenoses was assessed with Fractional Flow Reserve (FFR). Patients were classified FFR-positive (at least one lesion with FFR≤0.75) or FFR-negative (all lesions FFR>0.80). Whole blood samples were stimulated with increasing concentrations of ADP, TRAP, CRP and Iloprost with substimulatory ADP. Expression of P-selectin as platelet activation marker and platelet–leukocyte complexes were measured by flowcytometry. Patients were stratified on clopidogrel use. FFR positive and negative patient groups were compared on platelet reactivity and platelet-leukocyte complexes.ResultsPlatelet reactivity between FFR-positive patients and FFR-negative patients did not differ. A significantly lower percentage of circulating platelet-neutrophil complexes in FFR-positive patients and a similar non-significant decrease in percentage of circulating platelet-monocyte complexes in FFR-positive patients was observed.ConclusionThe presence of hemodynamically significant coronary stenoses does not alter platelet reactivity but is associated with reduced platelet-neutrophil complexes in peripheral blood of patients with stable coronary artery disease.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 95%

The Relationship between Fractional Flow Reserve, Platelet Reactivity and Platelet Leukocyte Complexes in Stable Coronary Artery Disease

et al. 2013

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“…Local ischemic preconditioning attenuates platelet activation and aggregation (182). In humans, marked systemic platelet activation has been demonstrated in patients with acute coronary syndromes (183) or acute limb ischemia (184). In animal models, the extent of platelet activation is related to the extent of subsequent tissue injury after reperfusion (185).…”

Section: Clinical Evidence For Ricmentioning

confidence: 99%

Remote Ischemic Conditioning

Heusch

Bøtker

Przyklenk

et al. 2015

Journal of the American College of Cardiology

544

531

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In remote ischemic conditioning (RIC) brief, reversible episodes of ischemia with reperfusion in one vascular bed, tissue or organ confer a global protective phenotype and render remote tissues and organs resistant to ischemia/reperfusion injury. The peripheral stimulus can be chemical, mechanical or electrical and involves activation of peripheral sensory nerves. The signal transfer to the heart or other organs is through neuronal and humoral communications. Protection can be transferred, even across species, with plasma-derived dialysate and involves nitric oxide, stromal derived factor-1α, microRNA-144, but also other, not yet identified factors. Intracardiac signal transduction involves: adenosine, bradykinin, cytokines, and chemokines, which activate specific receptors; intracellular kinases; and mitochondrial function. RIC by repeated brief inflation/deflation of a blood pressure cuff protects against endothelial dysfunction and myocardial injury in percutaneous coronary interventions, coronary artery bypass grafting and reperfused acute myocardial infarction. RIC is safe and effective, noninvasive, easily feasible and inexpensive.

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“…MPAs are increased in numerous conditions associated with ischemia and thrombosis, such as acute MI, 7,15 limb ischemia, 16 and stroke. 17 However, an interaction between monocytes (and their individual subsets) and platelets has not been studied in HF, and the possible impact on clinical outcome is unknown.…”

Section: Clinical Perspective On P 135mentioning

confidence: 99%

Increased Formation of Monocyte-Platelet Aggregates in Ischemic Heart Failure

Wrigley

Shantsila

Tapp

et al. 2013

Circ: Heart Failure

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Background— Cross-talk between monocytes and platelets is reflected by the formation of monocyte-platelet aggregates (MPAs). It is not known whether MPAs are affected in heart failure (HF), and we examined differences in patients with acute HF (AHF), stable HF (SHF), stable coronary artery disease (CAD) without HF, and healthy controls (HCs). Methods and Results— MPAs were analyzed by flow cytometry for the 3 monocyte subsets (CD14++CD16-CCR2+ [Mon1], CD14++CD16+CCR2+ [Mon2] and CD14+CD16++CCR2– [Mon3]) in patients with AHF (n=51), SHF (n=42), stable CAD (n=44), and HCs (n=40). Counts of total MPA and MPAs associated with Mon1 and Mon2 were significantly higher in AHF compared with SHF, CAD, and HCs ( P <0.001 for all). The proportion of Mon1 aggregated with platelets was increased in AHF compared with SHF ( P =0.033), CAD ( P <0.001), and HCs ( P <0.001). A higher percentage of Mon3 aggregated with platelets was also seen in AHF compared with SHF ( P =0.012) and HCs ( P <0.001) but not compared with CAD ( P =0.647). MPAs associated with Mon2 were significantly lower in patients who experienced adverse clinical outcomes of death or rehospitalization compared with those who remained free of events ( P =0.03). Mon2 count remained an independent negative predictor of combined death and rehospitalization after adjustment for age, left ventricular ejection fraction, creatinine, and brain natriuretic peptide (hazard ratio, 0.58 [95% CI, 0.34–0.98]; P =0.043). Conclusions— MPA formation in patients with both acute and stable HF is increased and seems to be confined to monocytes from Mon1 and Mon2 subsets. MPAs associated with Mon2 seem to be negatively predictive of a worse prognosis in AHF.

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Perioperative platelet and monocyte activation in patients with critical limb ischemia

Cited by 16 publications

References 33 publications

The Relationship between Fractional Flow Reserve, Platelet Reactivity and Platelet Leukocyte Complexes in Stable Coronary Artery Disease

The Relationship between Fractional Flow Reserve, Platelet Reactivity and Platelet Leukocyte Complexes in Stable Coronary Artery Disease

Remote Ischemic Conditioning

Increased Formation of Monocyte-Platelet Aggregates in Ischemic Heart Failure

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