Increased platelet deposition on atherosclerotic coronary arteries (original) (raw)
Related papers
The role of platelets in the pathophysiology of atherosclerosis (Review)
Molecular Medicine Reports, 2008
The physiopathology of atherothrombosis is complex. The development and progression of this vascular disease involves the interactive processes of atherosclerotic lesions and the formation of thrombi. In and of itself, atherosclerosis is not deadly; the actual risk lies in the vulnerability of the arteriolosclerotic plaque to breakage. An ulceration, which is the rupture or breakage of the covered plaque, constitutes a complication that favors thrombosis. During these processes platelets are relevant factors, acting with the endothelial and inflammatory cells even at the premature stages of atherogenesis. The interaction of platelets with the endothelial cells (ECs) can occur in two ways: activated platelets joining intact ECs, or resting platelets joining activated ECs. Platelet molecules such as GPIIb-IIIa, CD40, CD40L and P-selectin, as well as microparticle platelets, are important in this process. In this review, the most important mechanisms by which platelets participate in the genesis of atherosclerotic lesions are described. Contents 1. Introduction 2. Platelet physiology 3. Platelets and atherogenesis 4. Conclusion
Platelet activation in stable coronary artery disease
The American Journal of Cardiology, 1994
To elucidate the rote of physical acttvtty in the pathogenesis of acute ischemic syndromes in patii wfth coronary artery disease (CAD), we hypothesized that platetet actfvation occurs wben coronary blood flowveloct and shear stress increase across an atherosclerotic vascular bed. We measured platelet aggwgation by using angiolo@c catheterfzation to obtain simultaneous samples of whole biood from the coronary shfus and the aorta while at rest, 2 minutes after the onset of rapid atrial pacing, and 10 mtnutes after termination of pacing. of 82 consecuttve patients inchuled in our study, 26 had stenosis of the left coronary artery, l2 had stenosis of the right coronary artery only, and 24 had no evidence of CAD. Samples taken at rest revealed no arteriovenous difference in platelet -ion between patients wfth CAD and those without CAD. In patients with signfficant stenosis (~50%) of the left coronary artery, atrial pacing caused platelet aggregation to increase in sampfes from the coronary sinus (64 + 9% increase; p cO.01) butnotinbkwdfromtheaorta(2 *S%dewea!q diince not significant). Thii increase was transient, wtth aggwgatlon returning almost to resting values 10 minutes after pacing ended. Atrial pacing elk&d no change in platelet aggregatton in samptes from either the coronary sinus or aorta of patients wtth nonsignificant stenosis (40%) of the left coronary artery, patients with signtficant stenosis of the right coronary artery only, and patiints free of CAD. Thus, under resting conditions, no evklence of platelet acttvatiin across the coronary bed was seen regardless of CAD status. However, signtfiwnt steno& was associated with heightened platefet acttvation and -ion when coronary blood flow was Increased with atrial pacing.
Role of Platelets in the Pathogenicity of Atherosclerosis and Thrombosis in Coronary Heart Diseases
Sokoto Journal of Medical Laboratory Science
Atherosclerosis is a chronic inflammatory process that results in coronary artery disease, peripheral artery disease and in many cases of stroke. It is a disease that involves multiple inflammatory cytokine which is regarded as the primary underlying cause of cardiovascular diseases (CVD). CVD is the leading cause of death in the developed and developing countries like Nigeria. From pathological perspective, the chronic inflammatory condition of atherosclerosis occurs due to interplay between platelets, monocytes, macrophages. Physiologically platelets play a significant role in coagulation and repair of endothelial injury. Pathologically, studies have shown that activated platelets release multiple inflammatory cytokines and chemokines that serve as positive mediators of atherosclerosis. This chemokine is (RANTES, P-selectin and PF-4). Activated platelet release p-selectin that mediate platelet adhesion and rolling to injured endothelial cell, RANTES trigger the recruitment of mono...
Platelet deposition in remote cardiac regions after coronary occlusion
European Journal of Clinical Investigation, 2007
Background Activated platelets might contribute to endothelial dysfunction in non-ischaemic territories during acute myocardial infarction. We assessed platelet deposition, coronary flow reserve and contractile function in remote cardiac regions after transient coronary occlusion and their association with systemic platelet activation.Materials and methods In 10 pigs (series A) subjected to 48-min occlusion of the left anterior descending coronary artery (LAD), 99mTc-platelet content in the right coronary artery (RCA) and its dependent myocardium was counted after reflow. In 10 pigs (series B) receiving the same occlusion of the RCA, the hyperaemic response at the LAD and systolic shortening in LAD-dependent myocardium were monitored after reperfusion. P-selectin expression on circulating platelets was assessed in both series by flow cytometry.Results In series A, platelet counts in the RCA and non-ischaemic myocardium were correlated with platelet content, polymorphonuclear leukocyte infiltration and infarct size in the reperfused zone, as well as with the percentage of P-selectin-positive platelets after reflow. In series B, a transient reduction in peak hyperaemic response in the LAD and sustained contractile dysfunction in non-ischemic myocardium were observed after releasing the RCA occlusion, these changes being also correlated with platelet activation status.Conclusions Ischaemic injury triggers macro- and microvascular platelet deposition and causes an impairment in coronary flow reserve and contractile function in distant regions of the heart, which are related to activation of circulating platelets.
Immature platelets in patients with acute coronary syndromes
Thrombosis and Haemostasis, 2008
Platelets newly released from the bone marrow are RNA-containing and more haemostatically active than mature platelets. Immature platelets are reliably quantified by flow cytometry, and the immature platelet fraction (IPF) reflects platelet production and the rate of platelet turnover. It was the objective of this study to evaluate the presence of immature platelets in healthy subjects, patients with stable coronary artery disease (CAD) and patients with acute coronary syndromes. Flow cytometric determination of immature platelets was performed with an automated analyzer (Sysmex XE-2100) using RNA fluorescent dyes. IPF was determined in 420 individuals: 22 healthy subjects, 39 patients with stable CAD, 182 patients with unstable angina/ non-ST-segment elevation myocardial infarction (non-STEMI) Keywords Atherothrombosis, arterial thrombosis, aspirin resistance, myocardial infarction, thrombopoiesis and 177 patients with acute STEMI. The geometric mean [95% confidence interval] of IPF was 2.51 [2.04-3.10] in healthy subjects, 2.87 [2.45-3.36] in CAD patients, 2.93 [2.72-3.15] in the non-STEMI/unstable angina group and 3.71 [3. 45-3.99] in patients with STEMI (ANOVA: p < 0.0001). This difference remained significant after adjusting for baseline characteristics (p = 0.0003). In active smokers, IPF was 18% higher than in nonsmoking individuals (p = 0.007), and IPF was 16% higher in diabetics compared with non-diabetics (p = 0.060). In conclusion, the fraction of immature platelets is increased in acute coronary syndromes, especially in the acute phase of STEMI. Immature platelets with an increased haemostatic potential may contribute to coronary thrombus formation.
Platelet activation and atherothrombosis
New England Journal of Medicine, 2007
P latelets are essential for primary hemostasis and repair of the endothelium, but they also play a key role in the development of acute coronary syndromes and contribute to cerebrovascular events. In addition, they participate in the process of forming and extending atherosclerotic plaques. Atherosclerosis is a chronic inflammatory process, 1 and inflammation is an important component of acute coronary syndromes. 2 The relation between chronic and acute vascular inflammation is unclear, but platelets are a source of inflammatory mediators, 3 and the activation of platelets by inflammatory triggers may be a critical component of atherothrombosis. 4 This review article describes the role of platelets in atherothrombosis by integrating our knowledge of basic mechanisms with the results of mechanistic studies in humans and clinical trials of inhibitors of platelet function.
The role of platelets in atherothrombosis
Hematology / the Education Program of the American Society of Hematology. American Society of Hematology. Education Program, 2011
Platelets have evolved highly specialized adhesion mechanisms that enable cell-matrix and cell-cell interactions throughout the entire vasculature irrespective of the prevailing hemodynamic conditions. This unique property of platelets is critical for their ability to arrest bleeding and promote vessel repair. Platelet adhesion under conditions of high shear stress, as occurs in stenotic atherosclerotic arteries, is central to the development of arterial thrombosis; therefore, precise control of platelet adhesion must occur to maintain blood fluidity and to prevent thrombotic or hemorrhagic complications. Whereas the central role of platelets in hemostasis and thrombosis has long been recognized and well defined, there is now a major body of evidence supporting an important proinflammatory function for platelets that is linked to host defense and a variety of autoimmune and inflammatory diseases. In the context of the vasculature, experimental evidence indicates that the proinflamma...
Atherosclerosis, 1998
PTCA is a well-established intervention to reduce the severity of atherosclerotic coronary stenosis. Its primary success rate is seriously handicapped by the high incidence of late restenosis. Given the clinical and social importance of this proliferative process, new strategies are needed to prevent or reduce restenosis. Several animal models as well as different arteries have been used to study neointimal proliferation after arterial injury. A number of agents have shown to reduce neointimal proliferation after arterial injury in the carotids and iliac arteries of rodent models. Unfortunately, these results have not been replicated in humans. We have compared the acute and late response to vascular injury of the carotid and coronary arteries in the pig. Arterial injury was induced by performing balloon angioplasty of the carotid (elastic) and coronary (muscular) arteries in swine. Acute platelet-thrombus formation was evaluated by quantitation of Indium-labeled platelets deposited on the injured segments 1 h after procedure. Measurement of intimal area was performed by morphometry of the most stenotic cross-section at 28 days after balloon angioplasty. Platelet deposition after mild and severe injury in carotids (4 91 and 56 913× 10 6 platelets/cm 2 , respectively) and coronaries (15 95 and 141 9 20 × 10 6 platelets/cm 2 , respectively) are significantly greater in deep, than in mild injury (P B0.005), and significantly greater in coronary than in carotid arteries after deep injury (PB0.05). Likewise, late neointima formation was significantly greater (PB 0.05) after mild and severe injury in coronary (17 9 0.5 and 56 9 2%, respectively) than in carotid arteries (590.5 and 1291%, respectively). Acute platelet-thrombus formation and late neointimal thickening are modulated by the degree of injury induced during the interventions; and after disruption of the internal elastic lamina, coronary arteries always had significantly more acute thrombus and neointimal thickening. This study emphasizes the importance of the animal species, the type of injury and the artery chosen for studies on restenosis post interventions.