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A SINGLE CONTROLLED EXPOSURE TO SECOND HAND SMOKE DOES NOT ALTER THROMBOGENESIS OR CAUSE PLATELET ACTIVATION
E557 JACC March 27, 2012 Volume 59, Issue 13
Acute Coronary Syndromes A SINGLE CONTROLLED EXPOSURE TO SECOND HAND SMOKE DOES NOT ALTER THROMBOGENESIS OR CAUSE PLATELET ACTIVATION ACC Moderated Poster Contributions McCormick Place South, Hall A Sunday, March 25, 2012, 11:00 a.m.-Noon
Session Title: Acute Coronary Syndromes: Clinical XIII Abstract Category: 6. Acute Coronary Syndromes: Basic Presentation Number: 1174-507 Authors: Sundararajan Srikanth, Kamal Kotak, Richard Kiel, Rahat Bajwa, Eldon Swanson, Fridolin Sy, Waqas Aftab, Abhishek Tandon, John Ambrose, University of California San Francisco, Fresno, CA, USA Background: Chronic second hand smoke (SHS) exposure increases cardiovascular events, particularly acute thrombotic events. There are little human data on acute SHS exposure. Aim of this study was to determine whether a single controlled exposure of humans to SHS increased thrombogenesis. Methods: After 6-8 hours fast, subjects (n= 50) were exposed to constant dose SHS (particulate level of 500 μg/m3) for 120 minutes in a temperature-regulated and ventilated, simulated bar environment. Blood was drawn before and immediately after SHS exposure for thromboelastography (TEG) and flow cytometry. Maximum clot strength (MA) was measured using TEG and platelet leucocyte aggregates (LPA) were measured as an index of platelet activation. Anti-CD 14 antibodies were used as leukocyte markers and anti-CD 41 antibodies as platelet markers for cytometry. Data were analyzed using students’ T test for paired samples. Results: (table) There was no effect of acute exposure to SHS on platelet activation or thrombogenesis. Varying duration of exposure from 30 to 240 min did not show any effect either. Also, intra group (smokers [n=19] and non-smokers [n=31]) comparisons of LPA and TEG parameters did not show changes with SHS exposure.
Parameter MA (pre-SHS exposure) MA (post-SHS exposure) Platelet-Monocyte aggregates (pre-SHS exposure) Platelet-Monocyte aggregates (post-SHS exposure) Platelet-PMN aggregates (pre-SHS exposure) Platelet-PMN aggregates (post-SHS exposure)
Mean ± SEM 53.68 ± 1.76 53.52 ± 1.09 7.18 ± 0.42 7.66 ± 1.03 4.88 ± 0.39 4.88 ± 0.55
p value 0.33 0.66 0.99
Conclusion: While there are data showing enhanced thrombogenesis, and platelet activation following repeated exposure to SHS our study suggests that a single exposure does not alter thrombin kinetics nor result in platelet activation. The effects of SHS on thrombogenesis might be non-linear.
Acute Coronary Syndromes A SINGLE CONTROLLED EXPOSURE TO SECOND HAND SMOKE DOES NOT ALTER THROMBOGENESIS OR CAUSE PLATELET ACTIVATION ACC Moderated Poster Contributions McCormick Place South, Hall A Sunday, March 25, 2012, 11:00 a.m.-Noon
Session Title: Acute Coronary Syndromes: Clinical XIII Abstract Category: 6. Acute Coronary Syndromes: Basic Presentation Number: 1174-507 Authors: Sundararajan Srikanth, Kamal Kotak, Richard Kiel, Rahat Bajwa, Eldon Swanson, Fridolin Sy, Waqas Aftab, Abhishek Tandon, John Ambrose, University of California San Francisco, Fresno, CA, USA Background: Chronic second hand smoke (SHS) exposure increases cardiovascular events, particularly acute thrombotic events. There are little human data on acute SHS exposure. Aim of this study was to determine whether a single controlled exposure of humans to SHS increased thrombogenesis. Methods: After 6-8 hours fast, subjects (n= 50) were exposed to constant dose SHS (particulate level of 500 μg/m3) for 120 minutes in a temperature-regulated and ventilated, simulated bar environment. Blood was drawn before and immediately after SHS exposure for thromboelastography (TEG) and flow cytometry. Maximum clot strength (MA) was measured using TEG and platelet leucocyte aggregates (LPA) were measured as an index of platelet activation. Anti-CD 14 antibodies were used as leukocyte markers and anti-CD 41 antibodies as platelet markers for cytometry. Data were analyzed using students’ T test for paired samples. Results: (table) There was no effect of acute exposure to SHS on platelet activation or thrombogenesis. Varying duration of exposure from 30 to 240 min did not show any effect either. Also, intra group (smokers [n=19] and non-smokers [n=31]) comparisons of LPA and TEG parameters did not show changes with SHS exposure.
Parameter MA (pre-SHS exposure) MA (post-SHS exposure) Platelet-Monocyte aggregates (pre-SHS exposure) Platelet-Monocyte aggregates (post-SHS exposure) Platelet-PMN aggregates (pre-SHS exposure) Platelet-PMN aggregates (post-SHS exposure)
Mean ± SEM 53.68 ± 1.76 53.52 ± 1.09 7.18 ± 0.42 7.66 ± 1.03 4.88 ± 0.39 4.88 ± 0.55
p value 0.33 0.66 0.99
Conclusion: While there are data showing enhanced thrombogenesis, and platelet activation following repeated exposure to SHS our study suggests that a single exposure does not alter thrombin kinetics nor result in platelet activation. The effects of SHS on thrombogenesis might be non-linear.