Diagnosis and risk stratification of patients with anginal pain and non-diagnostic electrocardiograms

Abstract

Patients with acute chest pain suggestive of myocardial ischaemia, and normal or non-diagnostic electrocardiograms, form a difficult subgroup for diagnosis and early risk stratification. We prospectively evaluated the role of troponin T (cTnT), troponin I (cTnI), CKMB mass and myoglobin, in the diagnosis and risk stratification of 214 patients with acute chest pain of < or = 24 h and non-diagnostic or normal ECGs admitted directly to the Cardiac Unit of the Royal Victoria Hospital Belfast from the Mobile Coronary Care Unit or the Accident/Emergency Department. This was a single-centre prospective study, and follow-up (3 months) was complete for all patients. Blood was assessed for quantitative cTnT, cTnI, CKMB mass and myoglobin, and qualitative cTnT on admission and at 12 h. Diagnosis of index event and incidence of new cardiac events (death, non-fatal myocardial infarction, revascularization, or readmission for unstable angina) over 3 months were assessed. Based on standard criteria, myocardial infarction occurred in 37/214 (17%), and unstable angina in 72/214 (34%). At 12 h from admission, cardiac troponins had higher sensitivity for the diagnosis of acute coronary syndromes (myocardial infarction and unstable angina) than conventional markers (cTnI 48%, cTnT 38%, CKMB mass 30% or myoglobin 27%). At 3 months, a new cardiac event had occurred in 42/214 (20%). Significantly higher event rates occurred when any of the biochemical markers was elevated, but the statistical significance was highest for patients with elevated cTnI (p < 0.0001). Whilst gender, history of ischaemic heart disease (IHD), stress test response, cTnT, cTnI, CKMB mass and myoglobin were univariate predictors, cTnI at 12 h and stress test response were the only two independent significant predictors for a subsequent cardiac event at 3 months. Raised cTnI at 12 h after admission had the highest sensitivity for the diagnosis of acute coronary syndromes, and was independently associated with a 2-3 times increased risk of future cardiac events within 3 months among patients with acute chest pain suggestive of myocardial ischaemia but with normal or non-diagnostic ECGs.

Risk Stratification in Non‐ST Segment Elevation Acute Coronary Syndromes with Special Focus on Recent Guidelines

“…80 Like troponin T, troponin I can accurately predict adverse cardiovascular events like death and myocardial infarction during follow-up. 66,[69][70][71][72][73] In addition, one study 69 demonstrated a trend toward more vessel occlusions in the patients with positive troponin I (p=0.07) compared with those with negative troponin I. In that study, positive troponin I was associated with higher mortality than in those with negative troponin I (2.6% vs 0.4%; RR 3.1, 95% CI 0.8-12.2), among patients with a baseline negative CK-MB.…”

“…44 Table 5 demonstrates the value of CK-MB, troponin T, and troponin I in risk stratification. [57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72][73] Troponin T Troponin mediates the interaction of actin and myosin. Troponin T is found in skeletal and cardiac muscle, but not normally in the serum.…”

“…Several studies compared troponins T and I for risk stratification, and their results also appear in Table 5. 66,71,72 In one study, 71 the authors reported a meta-analysis of troponin T (2847 patients from 12 studies) and troponin I (1901 patients from 9 studies) in patients with unstable angina, evaluating the 30-day end point of myocardial infarction and cardiac death.…”

“…7 Another marker for myocardial necrosis is myoglobin. 52,72,85 This marker is a low-molecular-weight heme protein that peaks rapidly (< 2 hrs), but it loses its sensitivity due to rapid clearance and is not cardiac specific. Myoglobin or CK-MB subforms are recommended for patients presenting within 6 hours of chest pain onset.…”

Prevalence, Characteristics and Outcomes of People Aged 65 Years and Over with an Incidental Rise in Cardiac Troponin I

“…Furthermore, the degree of rise in troponin I has been associated with a matched increase in mortality risk [5]. There have also been studies evaluating the value of cTnI in patients with chest pain, but without ECG evidence of acute cardiac damage [6, 7]. …”