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Limitations of creatine kinase-MB (CK-MB) have led to alternative biochemical markers, including troponin T (TnT), to detect myocardial necrosis. Limited data are available regarding the predictive value of this new marker in patients with chest pain of uncertain etiology. Therefore, we prospectively compared CK-MB and TnT in a broad population with suspected acute coronary syndromes, including those admitted to a short-stay chest pain unit. CK-MB, quantitative TnT levels, and a rapid bedside assay were performed at 0, 4, 8, and 16 hours. Adverse events, including infarction, recurrent ischemia, coronary surgery, need for catheterization and/or intervention, stroke, congestive heart failure, or death, were identified by chart review and by follow-up phone call at 6 months. Of 707 patients, 104 were excluded for creatinine >2 mg/dl or incomplete data, leaving a total cohort of 603 patients. Coronary Care Unit admissions were 18%, intermediate care admissions were 14%, telemetry admissions is 21%, and admissions to 24-hour short-stay area were 47%. TnT (at 0.1 ng/ml) and CK-MB were positive in a similar proportion of patients (20.4% and 19.7%, respectively); however, the patients identified by TnT and CK-MB were not identical. In-hospital adverse events occurred in 37.1% with no differences in positive predictive value for the markers (p = NS). If CK-MB and TnT were negative, the early adverse event rate was 27%. No cardiac marker was positive by 16 hours in 54.9% of patients with an adverse event. Six-month follow-up was obtained in 576 of the 603 patients (95.5%). One hundred fifty-five late adverse events occurred in 134 patients (23.3%) at an average of 3.3+/-2.5 months after discharge. If both markers were negative, the late event rate was 20.2% and did not increase in patients with positive CK-MB or TnT >0.2 ng/ml. However, the late event rate was substantially higher (52.9%) in those with intermediate TnT levels of 0.1 to 0.2 ng/ml (p = 0.002). Thus, TnT is a suitable alternative to CK-MB in patients with suspected acute coronary syndromes. The rapid bedside assay is comparable to quantitative TnT and may enable early diagnosis and triage. A negative cardiac marker value (TnT or CK-MB) does not necessarily confer a low risk of complication in patients presenting with acute chest pain to an emergency department. [ABSTRACT FROM AUTHOR]

An increased plasma homocysteine concentration is a risk factor for atherosclerosis. Folic acid lowers homocysteine but the optimal dose in patients with coronary artery disease (CAD) is unclear. This placebo-controlled, single-blind, dose-ranging study evaluates the effect of low-dose folic acid on homocysteine levels in 95 patients aged 61 +/- 11 years (mean +/- SD) with documented CAD. Patients in each group were given either placebo or 1 of 3 daily supplements of folic acid (400 microg, 1 mg, or 5 mg) for 3 months. Each active treatment arm also received 500 microg vitamin B12 and 12.5 mg vitamin B6. Total plasma homocysteine levels were measured after 30 and 90 days. Folic acid 400 microg reduced homocysteine levels from 13.8 +/- 8.8 to 9.6 +/- 2.0 micromol/L at 90 days (p = 0.001). On 1- and 5-mg folic acid, levels decreased from 13.0 +/- 6.4 to 9.8 +/- 4.0 micromol/L (p = 0.001) and from 14.8 +/- 6.9 to 9.7 +/- 3.3 micromol/L (p < 0.001), respectively. The decrease was similar in all treatment groups. There was no significant change with placebo. Although the sample size is small, these findings suggest that daily administration of 400 microg/day folic acid combined with vitamin B12 and vitamin B6 may be equivalent to higher doses in reducing homocysteine levels in patients with CAD. [ABSTRACT FROM AUTHOR]

High-sensitivity C-reactive protein (hs-CRP) is a hepatocyte-derived inflammatory cytokine shown to be increased in the setting of acute heart failure (HF), particularly with increased intracardiac filling pressures. In the chronic HF setting, the relation between hs-CRP and echocardiographic indexes of left ventricular (LV) diastolic performance has not been examined. We measured plasma hs-CRP levels using a particle-enhanced immunonephelometry assay (Dade Behring, Inc., Deerfield, Illinois) in 136 subjects with chronic HF (LV ejection fraction [EF]

Increased oxidative stress and endothelial dysfunction are commonly observed in patients with chronic heart failure (HF). The relation between myeloperoxidase (MPO), an inflammatory marker with mechanistic links to plaque vulnerability and abnormal ventricular remodeling, and degrees of severity in chronic HF has not been reported. Plasma MPO levels were measured in 105 normal controls (no history of HF or left ventricular dysfunction) and 102 patients with chronic systolic HF (left ventricular ejection fraction <50%), and the relations among plasma MPO levels, plasma B-type natriuretic peptide levels, and the left ventricular ejection fraction were examined. Plasma MPO levels in patients with chronic systolic HF were significantly elevated compared with those of healthy controls (1,158 +/- 2,965 vs 204 +/- 139 pM, p <0.0001). Plasma MPO levels increased in parallel with increasing New York Heart Association class (p <0.0001) and were correlated with plasma B-type natriuretic peptide levels (Spearman's r = 0.39, p <0.0001). Levels of MPO were strongly associated with the prevalence of HF (unadjusted odds ratio 30.3, 95% confidence interval 11.1 to 94.5) and remained significant when adjusted for age and B-type natriuretic peptide (odds ratio 27.7, 95% confidence interval 3.6 to 371.1). In conclusion, in a cohort of patients with chronic HF, plasma MPO levels were elevated compared with those of normal controls and were associated with worsening functional class.