Point-of-care testing with high-sensitivity cardiac troponin assays: the challenges and opportunities

Methods to improve the safety, accuracy and efficiency of assessment of patients with suspected acute coronary symptoms have occupied decades of study and have supported significant changes in clinical practice. Much of the progress is reliant on results of laboratory-based high-sensitivity cardiac troponin assays that can detect low concentrations with high precision. Until recently, point-of-care (POC) platforms were unable to perform with similar analytical precision as laboratory-based assays, and recommendations for their use in accelerated assessment strategies for patients with suspected acute coronary syndrome has been limited. As POC assays can provide troponin results within 20 min, and can be used proximate to patient care, improvements in the efficiency of assessment of patients with suspected acute coronary syndrome is possible, particularly with new high-sensitivity assays.

Tobacco Consumption and High‐Sensitivity Cardiac Troponin I in the General Population: The HUNT Study

Background Cardiac troponins represent a sensitive index of subclinical myocardial injury and are associated with increased risk of cardiovascular events in the general population. Despite positive associations with cardiovascular risk of both cardiac troponins and cigarette smoking, concentrations of cardiac troponin I measured by high‐sensitivity assays (hs‐cTnI) are paradoxically lower in current smokers than in never‐smokers. The impact of smoking intensity and time from smoking cessation on hs‐cTnI remains unknown. Methods and Results hs‐cTnI concentrations were measured in 32028 subjects free from cardiovascular disease enrolled in the prospective, population‐based HUNT (Trøndelag Health Study). Tobacco habits were self‐reported and classified as never (n=14 559), former (n=14 248), and current (n=3221) smokers. Current smokers exhibited significantly lower concentrations of hs‐cTnI than never‐smokers ( P <0.001). In adjusted models, both current smoking (−17.3%; 95% CI, −20.6 to −13.9%) and former smoking (−6.6%; 95% CI, −8.7 to −4.5%) were associated with significantly lower hs‐cTnI concentrations. Among former smokers, higher smoking burden (>10 pack‐years) were associated with lower concentrations of hs‐cTnI. Time since smoking cessation was associated with increasing concentrations of hs‐cTnI in a dose‐dependent manner ( P for trend<0.001), and subjects who quit smoking >30 years ago had concentrations of hs‐cTnI comparable with those of never‐smokers. Conclusions In the general population, both current and former cigarette smoking is associated with lower concentrations of hs‐cTnI. In former smokers, there was a dose‐response relationship between pack‐years of smoking, and hs‐cTnI. Time since smoking cessation was associated with increasing concentrations of hs‐cTnI, indicating a continuum of hs‐cTnI from current smoker to never‐smokers.

Biomarkers-in-Cardiology 8 RE-VISITED—Consistent Safety of Early Discharge with a Dual Marker Strategy Combining a Normal hs-cTnT with a Normal Copeptin in Low-to-Intermediate Risk Patients with Suspected Acute Coronary Syndrome—A Secondary Analysis of the Randomized Biomarkers-in-Cardiology 8 Trial

Regarding the management of suspected Non-ST-segment-elevation acute coronary syndrome (ACS), the main Biomarker-in-Cardiology (BIC)-8 randomized controlled trial study had reported non-inferiority for the incidence of major adverse cardiac events at 30 days in the Copeptin group (dual marker strategy of copeptin and hs-cTnT at presentation) compared to the standard process (serial hs-cTnT testing). However, in 349 (38.7%) of the 902 patients, high-sensitivity cardiac troponin was not available for the treating physicians. High sensitivity cardiac troponin T was re-measured from thawed blood samples collected at baseline. This cohort qualified for a re-analysis of the 30-day incidence rate of MACE (death, survived cardiac death, acute myocardial infarction, re-hospitalization for acute coronary syndrome, acute unplanned percutaneous coronary intervention, coronary bypass grafting, or documented life-threatening arrhythmias), or components of the primary endpoint including death or death/MI. After re-measurement of troponin and exclusion of 9 patients with insufficient blood sample volume, 893 patients qualified for re-analysis. A total of 57 cases were detected with high sensitivity cardiac troponin T ≥ 14 ng/L who had been classified as “troponin negative” based on a conventional cardiac troponin T or I < 99th percentile upper limit of normal. Major adverse cardiac events rates after exclusion were non-inferior in the Copeptin group compared to the standard group (4.34% (95% confidence intervals 2.60–6.78%) vs. 4.27% (2.55–6.66%)). Rates were 53% lower in the per-protocol analysis (HR 0.47, 95% CI: 0.18–1.15, p = 0.09). No deaths occurred within 30 days in the discharged low risk patients of the Copeptin group. Copeptin combined with high sensitivity cardiac troponin is useful for risk stratification and allows early discharge of low-to-intermediate risk patients with suspected acute coronary syndrome is as safe as a re-testing strategy at 3 h or later.