High-Sensitivity Cardiac Troponin I Thresholds to Identify Myocardial Injury After Noncardiac Surgery: A Cohort Study.

BACKGROUND: Myocardial injury after noncardiac surgery (MINS) is common and associated with short- and long-term major cardiovascular events. Diagnostic criteria for MINS using Abbott high-sensitivity cardiac troponin I (hs-cTnI) are unknown. METHODS: We performed a prospective cohort study of adults who had in-patient noncardiac surgery and measured hs-cTnI (Abbott Laboratories) on postoperative serum samples collected up to postoperative day 3. The objective was to determine prognostically important hs-cTnI thresholds associated with major cardiac events and death at 30 days after noncardiac surgery. Using Cox proportional iterative analyses, we determined peak postoperative hs-cTnI thresholds associated with the occurrence of the 30-day composite of major cardiac events (ie, nonfatal myocardial infarction after 3 postoperative days, cardiac arrest, and congestive heart failure) and death. RESULTS: Of 3953 included patients, 66 (1.7%) experienced the primary outcome at 30 days. Peak hs-cTnI values and associated incidence of major cardiac events and death were as follows: < 60 ng/L: 1.0% (95% CI 0.7-1.3); 60 to < 700 ng/L: 8.6% (5.6-13.0); and ≥ 700 ng/L: 27.3% (16.4-41.9). Compared with peak hs-cTnI < 60 ng/L, adjusted hazard ratios were 7.54 (95% CI% 4.27-13.32) for hs-cTnI values of 60 to < 700 ng/L and 26.87 (13.27-54.41) for values ≥ 700 ng/L. CONCLUSIONS: Hs-cTnI elevation within the first 3 days after noncardiac surgery independently predicts major cardiac events and death at 30 days. A postoperative hs-cTnI ≥ 60 ng/L was associated with a > 7-fold increase in the risk of subsequent major cardiac events and mortality at 30 days.

Vitamin E modulation of C-reactive protein in smokers with acute coronary syndromes.

Acute coronary syndromes are characterized by the expression of proinflammatory cytokines such as C-reactive protein (CRP). Sustained upregulation of inflammatory markers is associated with an adverse prognosis. Vitamin E is known to have significant anti-inflammatory properties and has been associated with a reduction in cardiovascular events in some studies of high-risk patients. The mechanism of benefit remains controversial. We conducted a randomized, double-blind placebo controlled trial of vitamin E 400 IU daily for 6 months in 110 patients with acute coronary syndromes. Serum samples were collected at enrollment and at 2, 4, and 6 months. CRP, interleukin-6 and the soluble cell adhesion molecules were measured. Vitamin E levels increased significantly in the treatment group (from 31 micromol/l at baseline to 51 micromol/l, p <.0001) and were unchanged in the placebo group (32 micromol/l at baseline to 34 micromol/l, p = NS). CRP levels fell in both the vitamin E group and the placebo group over the treatment period (from 17.2 +/- 2.9 to 6.1 +/- 0.8 mg/l and from 21.5 +/- 4.9 to 5.9 +/- 0.9 mg/l, p = NS for the difference between active and placebo groups). However, vitamin E treatment was associated with significantly lower 6 month CRP levels in smokers versus smokers on placebo (4.7 +/- 0.71 mg/l vs. 8.26 +/- 1.5 mg/l, p =.02). Vitamin E reduces CRP levels in smokers with acute coronary syndromes for up to 6 months after hospitalization.