Publications by authors named "Fridolin Sy"

5 Publications

  • Page 1 of 1

A Single Controlled Exposure to Secondhand Smoke May Not Alter Thrombogenesis or Trigger Platelet Activation.

Nicotine Tob Res 2016 May 22;18(5):580-4. Epub 2015 Jun 22.

Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA

Introduction: Chronic secondhand smoke (SHS) exposure increases cardiovascular events, particularly acute thrombotic events. There are little human data on acute SHS exposure. The 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/m(3)) 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 leukocyte 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: There was no effect of acute exposure to SHS on platelet activation or thrombogenesis. Also, intra group (smokers [n = 19] and nonsmokers [n = 31]) comparisons of LPA and TEG parameters did not show changes with SHS exposure.

Conclusions: While there are abundant data showing enhanced thrombogenesis and platelet activation following repeated exposure to SHS, our study suggests that a single exposure does not appear to significantly alter thrombin kinetics nor result in platelet activation. The effects of SHS on thrombogenesis might be nonlinear.
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May 2016

Frequency of Takotsubo cardiomyopathy in postmenopausal women presenting with an acute coronary syndrome.

Am J Cardiol 2013 Aug 16;112(4):479-82. Epub 2013 May 16.

Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA, USA.

Takotsubo cardiomyopathy (TC) may be more common than previously reported in postmenopausal women (PMW) presenting with acute coronary syndrome (ACS). TC often masquerades as an ACS with electrocardiographic changes, elevated troponins, and/or chest discomfort. Its exact incidence in ACS is unknown but most studies suggest it is 1% to 2.2%. As most patients with TC are PMW, it was hypothesized that the incidence would be greater in this population. A prospective evaluation was carried out in all middle-aged and older women (≥45 years of age) presumed to be peri- or postmenopausal with an elevated troponin presenting to a community hospital over a 1-year period (July 2011 to July 2012). Troponin results above the upper limit of normal were screened on a daily basis through a computerized system. The patients' in-hospital charts were reviewed and determined if they fulfilled the criteria for acute myocardial infarction according to the universal definition of myocardial infarction. Prespecified criteria were used to identify all patients with TC. Of the 1,297 PMW screened for positive troponins, 323 patients (24.9%) fulfilled the criteria for acute myocardial infarction and of these, 19 (5.9%) met the prespecified criteria for TC. Three additional patients with TC had acute neurologic events. Most patients (81.8%) had the apical variant. In conclusion, TC may be more common than reported in PMW with clinical and laboratory criteria suggesting acute myocardial infarction. Heightened awareness of TC in this population appears warranted.
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August 2013

Acute cigarette smoke exposure reduces clot lysis--association between altered fibrin architecture and the response to t-PA.

Thromb Res 2010 Nov 1;126(5):426-30. Epub 2010 Sep 1.

Division of Cardiovascular Medicine, University of California San Francisco, Fresno, CA 93721, USA.

Background: Enhanced thrombolysis is a proposed mechanism for reduced mortality in cigarette smokers with STEMI ("smoker's paradox"). The mechanisms remain unclear but studies suggest fibrin architecture (FA) may affect thrombolysis. Our group has previously shown that acute cigarette smoke exposure (CSE) alters FA. This study was done to evaluate the association between FA, thrombolysis and CSE.

Methods And Results: Otherwise healthy smokers (n=22) were studied before and after smoking two cigarettes. Non-smokers (n=22) served as controls. Two ex-vivo models were used to evaluate clot lysis of venous blood and these data were compared to FA as determined by SEM. In the first model, clot lysis in a glass tube at 60minutes after addition of t-PA was measured. The second model quantified lysis utilizing thromboelastography. With the latter, after a clot reached maximum strength, t-PA was added and clot lysis at 60min was noted. SEM studies were performed on platelet poor plasma mixed with thrombin and FA was examined at 20K. Clot lysis was similar in both groups except that post-smoking, TEG showed a significantly lower lysis compared to pre- and non-smoking clots. SEM analysis showed significantly thinner fibers and denser clots post-smoking.

Conclusions: Venous clots from smokers failed to show an enhanced lysis when exposed to t-PA. In fact, acute CSE was associated with changes in FA and increased resistance to thrombolysis. These findings in part may explain enhanced thrombogenicity but suggest that mechanisms other than enhanced fibrinolysis are likely to be responsible for "smoker's paradox."
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November 2010

Effects of cigarette smoke exposure on clot dynamics and fibrin structure: an ex vivo investigation.

Arterioscler Thromb Vasc Biol 2010 Jan 8;30(1):75-9. Epub 2009 Oct 8.

Division of Cardiovascular Medicine, University of California San Francisco, Fresno, 2823 N Fresno Street, Fresno, CA 93721, USA.

Objective: The purpose of this study was to examine the effect of cigarette smoke exposure (CSE) on clot dynamics and fibrin architecture and to isolate the relative contribution of platelets and fibrinogen to clot dynamics.

Methods And Results: From young healthy males smokers (n=34) and nonsmokers (n=34) a baseline blood was drawn, and smokers had another blood draw after smoking 2 regular cigarettes. Using thromboelastography (TEG) the degree of platelet-fibrin interaction was measured. In additional experiments, abciximab (20 microg/mL) was added to the smokers samples (n=27) to reduce the effects of platelet function from the TEG parameters. The maximum clot strength (G) obtained with abciximab measured mainly the contribution of fibrinogen to clot strength (GF). By subtracting GF from G, the contribution of platelets to clot strength (GP) was presumed. A significant difference was found for all TEG parameters between nonsmokers versus postsmoking and pre- versus postsmoking samples. Postsmoking both GF and GP were significantly higher as compared to presmoking. On electron microscopy and turbidity analysis, postsmoking fibrin clots were significantly different compared to presmoking and nonsmoking samples.

Conclusions: Acute CSE changes clot dynamics and alters fibrin architecture. Both functional changes in fibrinogen and platelets appear to contribute to heightened thrombogenicity after acute CSE.
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January 2010

Frequency of elevated troponin I and diagnosis of acute myocardial infarction.

Am J Cardiol 2009 Jul 4;104(1):9-13. Epub 2009 May 4.

Division of Cardiology, UCSF Fresno Medical Education Program, Fresno, CA, USA.

This study evaluated the incidence and type of acute myocardial infarction (AMI) in a consecutive population with increased troponin I (TnI). AMI has recently been redefined and subclassified. Incidence, demographic data, angiographic findings, and hospital mortality of patients with various AMI subtypes or an increased TnI in the absence of AMI have not been previously reported in a prospective study. Over a 3-month period, all patients admitted from an emergency room or from in-patient services with >1 TnI level >0.04 ng/ml were evaluated and subclassified in AMI subgroups. In-hospital or recent coronary angiograms were reviewed. In-hospital mortality was noted. Of 2,944 patients with serial TnI measurements, 728 had an increased TnI and 701 (23.8%) were evaluated. Two hundred sixteen (30.8% with increased TnI and 42.7% with "rule-out MI" on admission) met criteria for AMI. One hundred forty-three (20.4%) had type 1, 64 (9.1%) had type 2, whereas 461 (65.8%) did not meet criteria for AMI. On multivariate analysis, use of angiography, peak TnI level, hyperlipidemia, and illicit drug use were independently associated with the diagnosis of AMI. TnI of 0.28 ng/ml had a 70% sensitivity and specificity for AMI diagnosis. In conclusion, a minority admitted with increased TnI have AMI by the universal definition. Type 1 is the most common AMI and is associated with higher TnI values and these patients are more likely to undergo angiography. Type 2 AMI is often associated with illicit drug use.
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July 2009