Perioperative Platelet Reactivity and the Effects of Clonidine

Rosenfeld, Brain A.; Faraday, Nauder; Campbell, David L.; Dorman, Todd; Clarkson, Kevin; Siedler, Alex; Breslow, Michael J.; Bell, William

doi:10.1097/00000542-199308000-00010

Cited by 43 publications

(15 citation statements)

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“…Given the numerous plaque destabilizing and thrombogenic factors that are present in the perioperative period, troponin elevation may be a consequence of coronary plaque rupture with distal embolization of thrombus or, alternatively, thrombosis of small coronary arteries. [22][23][24][25][26][27] In these patients, further myocardial damage may be prevented by adequate treatment during the time interval between troponin elevation and death. Although many studies have addressed prevention of postoperative myocardial injury and death, a major shortcoming is the insufficiently resolved pathophysiology of such myocardial injury and POMI.…”

Section: Discussionmentioning

confidence: 99%

Myocardial Injury After Noncardiac Surgery and its Association With Short-Term Mortality

et al. 2013

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Background— To identify patients at risk for postoperative myocardial injury and death, measuring cardiac troponin routinely after noncardiac surgery has been suggested. Such monitoring was implemented in our hospital. The aim of this study was to determine the predictive value of postoperative myocardial injury, as measured by troponin elevation, on 30-day mortality after noncardiac surgery. Methods and Results— This observational, single-center cohort study included 2232 consecutive intermediate- to high-risk noncardiac surgery patients aged ≥60 years who underwent surgery in 2011. Troponin was measured on the first 3 postoperative days. Log binomial regression analysis was used to estimate the association between postoperative myocardial injury (troponin I level >0.06 μg/L) and all-cause 30-day mortality. Myocardial injury was found in 315 of 1627 patients in whom troponin I was measured (19%). All-cause death occurred in 56 patients (3%). The relative risk of a minor increase in troponin (0.07–0.59 μg/L) was 2.4 (95% confidence interval, 1.3–4.2; P <0.01), and the relative risk of a 10- to 100-fold increase in troponin (≥0.60 μg/L) was 4.2 (95% confidence interval, 2.1–8.6; P <0.01). A myocardial infarction according to the universal definition was diagnosed in 10 patients (0.6%), of whom 1 (0.06%) had ST-segment elevation myocardial infarction. Conclusions— Postoperative myocardial injury is an independent predictor of 30-day mortality after noncardiac surgery. Implementation of postoperative troponin monitoring as standard of care is feasible and may be helpful in improving the prognosis of patients undergoing noncardiac surgery.

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Section: Discussionmentioning

confidence: 99%

Myocardial Injury After Noncardiac Surgery and its Association With Short-Term Mortality

et al. 2013

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“…Plasma fibrinogen concentrations and platelet counts are increased in the first 24 h postoperatively [8]. There is increased platelet aggregation, presumably in response to release of a variety of aggregation-promoting agonists [9]. The second alteration, an initial enhancement of fibrinolysis, is followed by a decrease of its activity [10].…”

Section: Discussionmentioning

confidence: 99%

“…Most studies evaluating the perioperative alterations of hemostasis concern open surgery [7][8][9][10][11]. The risk of developing deep venous thrombosis after open surgery can be as high as 40-80%, while the incidence of fatal pulmonary embolism is 1-5% [1,12].…”

Section: Discussionmentioning

confidence: 99%

Fibrinolytic and coagulation pathways after laparoscopic and open surgery: a prospective randomized trial

et al. 2009

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“…Stimulation of a2 receptors on the surface of platelets inhibits adenylate cyclase, thus decreasing platelet cyclic adenosin monophosphate, and depressed levels of cyclic adenosin monophosphate are thought to activate platelets [28]. However, no effect of clonidine on perioperative platelet reactivity could be demonstrated as well [29]. Hypercoagulability persists beyond the known duration of tissue damage after surgery and seems to be caused predominantly by platelet activation [14].…”

Section: Discussionmentioning

confidence: 99%