To determine the long-term prognostic value of stress imaging and clinical risk scoring for cardiovascular mortality in chest pain patients after ruling out acute coronary syndrome (ACS).

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OBJECTIVES We prospectively studied the prognostic value of predischarge dobutamine stress echocardiography (I)SE) in low-risk chest pain patients with a normal or nondiagnostic electrocardiogram (ECG) and a negative serial troponin T.BACKGROUND Noninvasive stress testing is recommended before discharge or within 72 h in patients with low-risk chest pain. The prognostic value of immediate DSE has not been studied in a blinded, prospective fashion. METHODS Patients presenting at the emergency room within 6 h of symptom onset and a normal or nondiagnostic ECG were eligible. Dobutamine stress echocardiography was performed after unstable coronary artery disease was ruled out by a standard rule-out protocol and a negative serial troponin T; the occurrence of any new wall motion abnormality was considered positive. Results were kept blinded. End points were cardiac death, myocardial infarction, rehospitalization for unstable angina or revascularization.RESULTS In total, 377 patients were included. There were 2 deaths, 2 myocardial infarctions, 8 rehospitalization for unstable angina, and 10 revascularizations at six-month follow-up. The end points occurred in 8/26 (30.8%) patients with a positive versus 14/351 (4.0%) patients with a negative DSE (odds ratio, 10.7; 95% confidence interval, 4.0 to 28.8; p < 0.0001). By multivariate analysis, DSE remained a predictor of end points (p < 0.0001).CONCLUSIONS A predischarge DSE had important, independent prognostic value in low-risk, troponin negative, chest pain patients. (J Am Coll Cardiol 2003;41:596-602) (C) 2003 by the American College of Cardiology Foundation

PURPOSE:To assess the prognostic value of markers of inflammation for rule-out purposes in patients admitted to the emergency department with troponin T-negative chest pain. METHODS:Patients presenting to the emergency department within 6 hours of symptom onset and who had a normal or nondiagnostic electrocardiogram were eligible. The standard rule-out protocol, which included serial creatine kinase and creatine kinase-MB measurements, was applied, and markers of inflammation (C-reactive protein, erythrocyte sedimentation rate, and total white blood cell count and differential count) were measured. The study group comprised patients with negative serial troponin T results (<0.06 microg/L) who were discharged home after unstable coronary artery disease was ruled out. Endpoints during the 6-month follow-up were cardiac death, myocardial infarction, or rehospitalization for unstable angina. RESULTS:A total of 382 troponin T-negative patients were discharged, of whom 2 died, 2 had a myocardial infarction, and 7 were rehospitalized for unstable angina. A positive C-reactive protein test result (>0.3 mg/dL) was associated with future clinical events (hazard risk [HR] = 4.5; 95% confidence interval [CI]: 1.2 to 17.0; P = 0.03), as was a positive test (>13 mm/h) for erythrocyte sedimentation rate (HR = 5.6; 95% CI: 1.5 to 22.2; P = 0.01). Patients with positive results for both tests were at highest risk of clinical events (9.3%) compared with patients with other combinations of test results (1.1% to 2.1%; HR = 7.5; 95% CI: 2.2 to 25.5; P = 0.001). CONCLUSION:The combination of C-reactive protein and erythrocyte sedimentation rate had prognostic value in patients with troponin T-negative chest pain and a normal or nondiagnostic electrocardiogram in whom unstable coronary artery disease was ruled out.

OBJECTIVE:To determine whether a new protocol, using a rapid and sensitive CK-MB(mass) assay and serial sampling, can rule out myocardial infarction in patients with chest pain and decrease their length of stay in the cardiac emergency room without increasing risk. DESIGN:The combined incidence of cardiac death and acute myocardial infarction at 30 days, six months, and 24 months of follow up were compared between patients discharged home from the cardiac emergency room after ruling out myocardial infarction with a CK-MB(activity) assay in 1994 and those discharged home after a rapid CK-MB(mass) assay in 1996. SETTING:Cardiac emergency room of a large university hospital. PATIENTS:In 1994 and 1996, 230 and 423 chest pain patients, respectively, were discharged home from the cardiac emergency room with a normal CK-MB and an uneventful observation period. RESULTS:The median length of stay in the cardiac emergency room was significantly reduced, from 16.0 hours in 1994 to 9.0 hours in 1996 (p < 0.0001). Mean event rates in patients from the 1994 and 1996 cohorts, respectively, were 0.9% (95% confidence interval (CI) -0.3% to 2.1%) v 0.7% (95% CI -0.1% to 1. 5%) at 30 days, 3.0% (95% CI 0.8% to 5.2%) v 2.8% (95% CI 1.2% to 4. 4%) at six months, and 7.0% (95% CI 3.7% to 10.3%) v 5.7% (95% CI 3. 5% to 7.9%) at 24 months. Kaplan-Meier survival analysis showed no difference in mean event-free survival at 30 days, six months, and 24 months of follow up. CONCLUSIONS:Using a rule-out myocardial infarction protocol with a rapid and sensitive CK-MB(mass) assay and serial sampling, the length of stay of patients with chest pain in the cardiac emergency room can be reduced without compromising safety.

BACKGROUND:Increased C-reactive protein (CRP) is an important prognostic indicator for early risk stratification in patients with an acute coronary syndrome (ACS), independent of, and in combination with, increased cardiac troponin T (cTnT). However, increases in both cTnT and CRP also occur secondary to myocardial damage.METHODS AND RESULTS:In 156 consecutive patients, early release kinetics of CRP and cTnT were analyzed. The cutoff values were 3.0 mg/L for CRP and 0.1 microgram/L for cTnT. In the 75 patients with a CRP below the cutoff on admission, there was little change in CRP until 8 h after the onset of symptoms. At 12 h after the onset of symptoms, the cumulative proportions of abnormal CRP and cTnT in non-ST elevation ACS patients were 27% and 89%, respectively (P <0.01). During the first 24 h after the onset of symptoms, the median time above the cutoff was 20 h for CRP and 5 h for cTnT (P <0.0001). CRP was below the cutoff on admission significantly more often among patients receiving thrombolytic therapy than in patients without an indication for reperfusion therapy (51% vs 28%; P = 0.004).CONCLUSIONS:Increased CRP as an early independent risk indicator should be measured as soon as possible after the onset of symptoms, whereas increased cTnT is most reliable at 12 or more hours after the onset of symptoms.

The baseline plasma level of C-reactive protein (CRP) is considered to be a parameter for risk stratification in patients with an acute coronary syndrome, independent of the level of cardiac troponin T (cTnT) or cardiac troponin I. However, myocardial tissue necrosis following prolonged arterial occlusion also induces release of CRP. Both phenomena may have their own kinetic behaviour with respect to changes in concentration of CRP. Therefore, in this study the time frame after onset of symptoms for measurement of CRP as an independent parameter is established. For this purpose, we evaluated patients with proven myocardial damage due to acute myocardial infarction (AMI) with respect to changes of creatine kinase (CK)-MB mass, cTnT and CRP during 24 hours after onset of symptoms. Our results show that two subgroups can be discerned in patients with AMI: those with initially normal and those with already elevated concentration CRP on admission. Furthermore, based on the results of this study we conclude that for use of CRP as an independent prognostic parameter in patients with acute coronary syndrome, CRP should be measured in blood samples drawn as early as possible after the onset of symptoms to avoid contribution of a process of myocardial tissue necrosis, whereas estimation of cTnT should be performed at 6-12 hours.

AIMS:We studied the diagnostic value for acute myocardial infarction of serial creatine kinase-MBmass measurements on admission and at 7 h after the onset of symptoms. METHODS AND RESULTS:Patients presenting to our chest pain unit with symptoms of <5-h duration were eligible. Patients were kept under observation at least until 12 h after onset of symptoms. Blood samples were drawn on admission and 7 and 10 h after onset of symptoms. Creatine kinase-MBmass>7.0 microg x 1(-1) (upper reference limit for acute myocardial infarction), or an increase >2.0 microg x 1(-1) (reference change value) between admission and at 7 h was considered abnormal. Of a total of 470 patients, 248 patients had acute myocardial infarction: 100 out of the 248 patients had a single creatine kinase-MBmass>7.0 microg x 1(-1) on admission (sensitivity 40%, 95% CI:34-46%), 234/248 patients at 7 h (sensitivity 94%, 95% CI:91-97%), and 240/248 at 10 h (sensitivity 97%, 95% CI:94-99%). At 7 h, 246/248 patients had either a single creatine kinase-MB >7.0 microg x 1(-1) or a significant increase between admission and 7 h (sensitivity 99%, 95% CI:98-100%). Of 222 patients without acute myocardial infarction, 214 had a normal serial creatine kinase-MBmass (specificity 96%, 95% CI:93-98%). CONCLUSION:In patients with symptoms of <5-h duration, acute myocardial infarction can be ruled out using serial creatine kinase-MBmass taken on admission and at 7 h.

Objectives: Elevated concentrations of C-reactive protein (CRP), a non-specific acute phase reactant, and troponin I (TnI), a cardiac-specific marker of myocardial damage, have been found to be associated with a higher risk for cardiac events in patients with an acute coronary syndrome. We evaluated CRP alone and in combination with TnI for predicting the incidence of major cardiac complications within 6 months in patients with unstable angina or non-Q-wave infaction (NQMI). Methods: CRP and TnI was measured on admission in patients with unstable angina or NQMI, but results were kept blinded. Patients were treated according to a conservative management strategy, and the incidence of major cardiac events within 6 months was assessed. Results: An abnormal CRP (>5 mg/l) and an abnormal TnI (>0.4 mu g/l) were more frequent in patients that suffered a major cardiac event (CRP: 93 vs. 35%, P<0.0001; TnI: 73 vs. 26%, P<0.001). The incidence of major cardiac events was higher in patients with an abnormal CRP than in patients with a normal CRP, both when TnI was abnormal (42 vs. 4.5%, P=0.003) and when TnI was normal (11 vs. 0%, P=0.014). Mean event-free survival was excellent in patients with both a normal CRP acid TnI, whereas survival was poorest in patients with both an abnormal CRP and TnI (121+/-16 vs. 180 days, P<0.0001). Conclusions: An abnormal CRP on admission in patients with unstable angina or NQMI is associated with increased incidence of major cardiac events within 6 months, both in patients with normal and abnormal TnI. CRP and TnI. have independent and additive prognostic value in this patient group, and the combination may be useful for early risk stratification. (C) 1999 Elsevier Science B.V. All rights reserved.

Severe congenital hearing impairment is an important handicap affecting 0.1% of live-born infants and 1%–2% of graduates of Neonatal Intensive Care Units. The prognosis for intellectual, emotional, language and speech development in the hearing-impaired child is improved when the diagnosis is made early and intervention is begun before the age of 6 months. The usual age at diagnosis of hearing impairment is at least 18–30 months (or even later in cases of less severe hearing impairment) where there are no screening programmes. When screening is carried out using distraction methods at the age of approximately 9 months some hearing-impaired infants are missed and those discovered are at least 15–18 months before intervention begins. Neonatal screening could give hearing-impaired children the best chances for optimal care and development. Universal neonatal hearing screening is necessary, because, when neonatal hearing screening is restricted to high risk groups 30%–50% of infants with hearing loss are not discovered. The methods available for neonatal hearing screening are discussed in this paper.