scholarly journals Effect of cigarette smoking on platelet aggregation in arteriosclerosis

1977 ◽  
Vol 8 (4) ◽  
pp. 524-528
Author(s):  
Yuzo NAGAKAWA ◽  
Toshio OZAWA ◽  
Masaki YOSHIKAWA
Keyword(s):  
Platelet Aggregation ◽  
Cigarette Smoking

Abstract 3473: The Effect of Cigarette Smoking on the Antiplatelet Effect of Clopidogrel: The Smokers Paradox

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Paul Gurbel ◽  
Joseph Dichiara ◽  
Kevin P Bliden ◽  
Mark J Antonino ◽  
Lawal Lookman
Keyword(s):  
Platelet Aggregation ◽  
Cigarette Smoking ◽  
Metabolic Activation ◽  
Adenosine Diphosphate ◽  
Platelet Inhibition ◽  
Response Variability ◽  
Light Transmittance ◽  
Prior History ◽  
Platelet Response ◽  
Clopidogrel Therapy

Background: Wide response variability to clopidogrel therapy has been reported. Clopidogrel is a prodrug that requires metabolic activation by hepatic cytochromes (CYP). Cigarette smoking is an inducer of CYP1A2 and may, therefore, enhance the metabolism of clopidogrel. We sought to examine the effect of cigarette smoking on the platelet response to clopidogrel. Methods: Three hundred thirteen consecutive patients undergoing elective coronary stenting were studied. Platelet aggregation (PA) was assessed by light transmittance aggregometry (LTA) stimulated by 5 and 20μ M adenosine diphosphate. One hundred fourteen patients were on chronic clopidogrel therapy, were not reloaded, and had pre-stenting PA measurements. Pre-and post-stenting PA was measured in 199 patients: 60 were loaded with 300mg and 139 were loaded with 600mg. There were 120 current smokers (smoking within 2 weeks of PCI) and 193 non-smokers (no prior history of smoking). Low PA was defined as the lowest two quartiles of 5μM ADP-induced platelet aggregation (≤ 40%). Results: PA was significantly lower (p ≤ 0.008) in smokers on long term chronic clopidogrel treatment (Table ). Relative platelet inhibition (RPI) was higher in smokers treated with either 300mg or 600mg clopidogrel measured by 5 and 20μM ADP-induced PA. In a multivariate analysis, cigarette smoking was an independent predictor of low PA in patients on chronic clopidogrel therapy and in patients loaded with clopidogrel (r=0.3, p=0.0001). Conclusion: Clopidogrel therapy in smokers is associated with increased platelet inhibition and lower aggregation as compared to non-smokers. The mechanism of the smoking effect deserves further study and may be another cause of response variability to clopidogrel. RPI = 100 x ((baseline aggregation-post-treatment aggregation)/(baseline aggregation))

scholarly journals Circulating Platelet Aggregates During Emotional Stress and Cigarette Smoking

1977 ◽  
Author(s):  
G.F. Gensini ◽  
R. Abbate ◽  
D. Prisco ◽  
G.G. Neri Serneri
Keyword(s):  
Platelet Aggregation ◽  
Medical Students ◽  
Cigarette Smoking ◽  
Cigarette Smoke ◽  
Emotional Stress ◽  
Predictive Value ◽  
Normal Values ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Clinically Significant

Increased platelet aggregation has been observed in various hypercoagulable states, but its predictive value for thrombosis is so far uncertain. We studied the effect of emotional stress and of cigarette smoking on circulating platelets by platelet aggregates ratio (PAR) according to Wu and Hoak (1974.) in medical students aged 20-22 years. The emotional stress was undergoing a University examination.PAR was measured immediately before the examination, at the end and 15 and 30 min after the examination.PAR was significantly lowered in all the subjects at the end (P<0.0l) and after 15 min (P<0.0l) but returned toward normal values after 30 min. The decrease of PAR suggests the production of reversible circulating platelet aggregates. The effect of smo=king a cigarette has been investigated in 8 students. PAR has been determined before smoking, at the end and after 2,5 and 10 min. Smoking lasted 4 min. In 5 subjects we observed a decrease of PAR at 2 min (P< 0. 01), whereas at 5 and 10 min PAR value became normal. Lettuce cigarette smoke did not affect PAR value. Our results indicate that: 1) – Platelet aggregates are very easily produced in circulating blood; 2)- A low value of PAR does not necessarily indicate a platelet hy=peraggregability clinically significant.

Abstract 347: Cigarette Smoking Associated Changes on Platelet Surface

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Curtis L Lowery ◽  
James D Marsh ◽  
Fusun Kilic
Keyword(s):  
Nervous System ◽  
Plasma Membrane ◽  
Platelet Aggregation ◽  
Cigarette Smoking ◽  
Membrane Trafficking ◽  
Platelet Surface ◽  
Pharmacological Targets ◽  
The Us ◽  
Novel Biomarkers ◽  
Pharmacological Blockade

Thirty percent of all deaths from coronary heart disease each year in the US are attributable to cigarette smoking. The acute effects of smoking on the cardiovascular systems are associated with arterial thrombosis. Cigarette smoking produces central nervous system-mediated activation of the sympathetic nervous system, which stimulates secretion of pro-thrombotic molecules, serotonin (5-HT) and catecholamines into the blood at supraphysiological levels. 5-HT and catecholamines activate their platelet-specific receptors in an additive manner to change the platelet biology and physiology. Our studies of blood samples from smokers (collected just after smoking) showed several-fold elevation in plasma 5-HT and catecholamines, and platelet aggregation. To explore smoking-associated changes on platelets, the plasma membrane glycans and proteins were eluted and analyzed in MALDI-MS and LC-MS, respectively. The surface glycans of nonsmokers’ platelets were high-mannose-type but those of smokers’ platelets were on smokers’, sialylated N-glycans. Removing the N-glycan counteracted smoking-mediated platelet aggregation, suggesting that N-glycans play a role in adhesiveness of the platelet surface. MS analysis of the membrane proteins identified enzymes and proteins exclusively on smokers’ platelet plasma membrane. These included enzymes involved in glycan biosynthesis and proteins important in membrane trafficking of secretory vesicles. We hypothesize that, upon smoking, glycosylation enzymes normally sequestered in intracellularly, are translocated to the plasma membrane to induce changes in surface glycans. Interestingly, we showed that treating nonsmokers’ platelets with 5-HT and catecholamines predisposed them to a prothrombotic state. Furthermore, pharmacological blockade of receptors for 5-HT or catecholamines counteracted the 5-HT-catecholamine-mediated aggregation and alterations in level and composition of surface glycans. Achieving our proposed aims potentially will provide novel biomarkers and pharmacological targets for preventing and treating smoking-associated thrombosis.

Effect of Cigarette Smoking on Platelet Aggregation

2011 ◽  
Vol 17 (6) ◽  
pp. E175-E180 ◽  
Author(s):  
Burak Pamukcu ◽  
Huseyin Oflaz ◽  
Imran Onur ◽  
Arif Cimen ◽  
Yilmaz Nisanci
Keyword(s):  
Platelet Aggregation ◽  
Cigarette Smoking ◽  
Platelet Function ◽  
Adenosine Diphosphate ◽  
Platelet Activity ◽  
Paired Samples ◽  
Function Analyzer ◽  
Regular Aspirin ◽  
Increase Platelet Aggregation ◽  
The Impact

Background: Cigarette smoking may increase platelet aggregation and cause atherothrombotic cardiovascular events. We aimed to investigate the impact of cigarette smoking on platelet function in patients with ischemic coronary heart disease (CHD).Methods: Twenty patients with ischemic stable CHD under aspirin therapy (300 mg/d), who continue to smoking despite all warnings, and 20 nonsmokers with CHD are enrolled in the study. Platelet function is studied at the morning, before and 15 minutes after the first cigarette, by the Platelet Function Analyzer (PFA)-100, with collagen and epinephrine and collagen and adenosine diphosphate cartridges. Post aspirin platelet hyperactivity is defined as having a closure time (CT) shorter than 186 seconds despite regular aspirin intake. Serial CT measurements are analyzed by paired samples t test.Results: Persistent platelet activity was present in 4 smoker (20%) and 3 nonsmoker (15%) patients at the beginning. Platelet activity measured by the PFA-100 is been increased significantly after cigarette smoking ( P = .004). Shorter CTs were determined after smoking in all patients with and without baseline persistent platelet activity, and 4 more participants became aspirin nonresponder ( P = .004). No significant differences in demographic, hematological, and biochemical parameters were determined between aspirin responders and nonresponders.Conclusions: We determined that cigarette smoking may increase platelet aggregation in patients with ischemic CHD in an aspirin nonresponsive manner. Our results emphasize the importance of quitting cigarette smoking in patients with CHD.

scholarly journals PENGARUH MEROKOK SIGARET PADA PEMERIKSAAN RESISTEN ASPIRIN

2018 ◽  
Vol 20 (2) ◽  
pp. 141
Author(s):  
D.I.S Siregar ◽  
Z. Lubis ◽  
H. Hariman
Keyword(s):  
Cardiovascular Disease ◽  
Platelet Aggregation ◽  
Cigarette Smoking ◽  
Blood Sample ◽  
Aspirin Resistance ◽  
Framingham Study ◽  
Anti Platelet Drug

Based on the Framingham study, it was revealed that cigarette smoking can cause athero- thrombotic cardiovascular disease (CVD).Aspirin is the most widely used anti platelet drug in CVD; it reduces the risk of the secondary events by about 25% in cardiovasculardisease. Lately, it was reported that 5–45% of these patients are resistant to aspirin. The researchers aimed to investigate in this study theimpact of cigarette smoking on aspirin resistance. Twenty two smokers and 18 non-smokers were enrolled in this study. The researchersrequired all of the 40 subjects to take 160 mg of aspirin after the first blood sample was taken. The first sample was taken in the morning,while the second one was obtained two (2) hours after the aspirin intake. Platelet aggregation was performed using a light transmittanceaggregometry (LTA). Aspirin resistance was found in two (2) of 22 smokers (9.09%) and two (2) of 18 non-smokers (11.11%). There wereno significant differences (p>0.05) before or after taking aspirin in either both smokers or non smokers as seen from the aggregationresults. The researchers concluded that cigarette smoking does not cause aspirin resistance at all.

Cigarette-Smoking Effect on Platelet Function

1977 ◽  
Vol 37 (03) ◽  
pp. 423-428 ◽  
Author(s):  
G Grignani ◽  
G Gamba ◽  
E Ascari
Keyword(s):  
Platelet Aggregation ◽  
Young People ◽  
Cigarette Smoking ◽  
Cerebrovascular Disease ◽  
Platelet Function ◽  
Normal Subjects ◽  
Platelet Adhesiveness ◽  
Platelet Activity ◽  
Heavy Smokers

SummaryThe immediate effect of cigarette-smoking on ADP-induced platelet aggregation and on platelet adhesiveness was investigated in 12 normal subjects aged 20 to 40, in 10 normal subjects aged 43 to 72 and in 10 patients with cerebrovascular disease aged 45 to 75.All the subjects were heavy smokers (more than 20 cigarettes a day).After smoking 2 cigarettes a significant increase in ADP aggregation and platelet adhesiveness was found in the group of young heavy smokers, while in the old subjects with or without cerebrovascular disease the increase in platelet activity was never significant.These data were discussed and some hypotheses for this higher reactivity of platelets from young people were suggested.

Fine Structure of Platelet Interaction with a New Microcrystalline Collagen Preparation

1974 ◽  
Vol 32 ◽  
pp. 58-59
Author(s):  
W. H. Zucker ◽  
R. G. Mason
Keyword(s):  
Fine Structure ◽  
Platelet Aggregation ◽  
Hydrochloric Acid ◽  
Whole Blood ◽  
Platelet Adhesion ◽  
Hemostatic Agent ◽  
Native Collagen ◽  
Fibrillar Morphology ◽  
Clinical Interest ◽  
New Form

Platelet adhesion initiates platelet aggregation and is an important component of the hemostatic process. Since the development of a new form of collagen as a topical hemostatic agent is of both basic and clinical interest, an ultrastructural and hematologic study of the interaction of platelets with the microcrystalline collagen preparation was undertaken.In this study, whole blood anticoagulated with EDTA was used in order to inhibit aggregation and permit study of platelet adhesion to collagen as an isolated event. The microcrystalline collagen was prepared from bovine dermal corium; milling was with sharp blades. The preparation consists of partial hydrochloric acid amine collagen salts and retains much of the fibrillar morphology of native collagen.

Sign in / Sign up

Export Citation Format

Share Document