Serum Cardiac Troponin-I is Superior to Troponin-T as a Marker for Left Ventricular Dysfunction in Clinically Stable Patients with End-Stage Renal Disease

Abstract

BackgroundSerum troponin assays, widely used to detect acute cardiac ischemia, might be useful biomarkers to detect chronic cardiovascular disease (CVD). Cardiac-specific troponin-I (cTnI) and troponin-T (cTnT) generally detect myocardial necrosis equally well. In dialysis patients however, serum cTnT levels are often elevated, unlike cTnI levels. The present study aims to elucidate the associations of cTnI and cTnT with CVD in clinically stable dialysis patients.MethodsTroponin levels were measured using 5th generation hs-cTnT assays (Roche) and STAT hs-cTnI assays (Abbott) in a cohort of dialysis patients. Serum troponin levels were divided into tertiles with the lowest tertile as a reference value. Serum troponins were associated with indicators of CVD such as left ventricular mass index (LVMI), left ventricular ejection fraction (LVEF) and the presence of coronary artery disease (CAD). Associations were explored using regression analysis.ResultsWe included 154 consecutive patients, 68±7 years old, 77% male, 70% hemodialysis. Median serum cTnT was 51ng/L (exceeding the 99th percentile of the healthy population in 98%) and median serum cTnI was 13ng/L (elevated in 20%). A high cTnI (T3) was significantly associated with a higher LVMI (Beta 31.60; p=0.001) and LVEF (Beta -4.78; p=0.005) after adjusting for confounders whereas a high serum cTnT was not. CAD was significantly associated with a high cTnT (OR 4.70 p=0.02) but not with a high cTnI. Unlike cTnI, cTnT was associated with residual renal function (Beta:-0.09; p=0.006).ConclusionIn the present cohort, serum cTnI levels showed a stronger association with LVMI and LVEF than cTnT. However, cTnT was significantly associated with CAD and residual renal function, unlike cTnI. Therefore, cTnI seems to be superior to cTnT as a marker of left ventricular dysfunction in asymptomatic dialysis patients, while cTnT might be better suited to detect CAD in these patients.

Effect of haemodialysis and residual renal function on serum levels of galectin‐3, B‐type natriuretic peptides and cardiac troponin T

“…Where it has been reported, in the Implantable Cardioverter Defibrillators in Dialysis patients (ICD2) Trial, RRF correlated negatively with hs-TnT. 15 Levels of other biomarkers were not reported in this study. We also assessed residual kidney function as daily urine volume, a more practical method in practice.…”

“…12,13 The plasma concentrations of cardiac troponins I and T are frequently elevated in haemodialysis patients due to cardiac factors and/or dialysis-related factors. 14,15 Regardless of the reason, elevated cardiac troponin in haemodialysis patients is associated with adverse outcomes. 16,17 We aimed to determine how measures of cardiac structure and function assessed by echocardiography and measures of residual kidney function were associated with levels of these biochemical markers of cardiac disease in haemodialysis patients.…”

Diurnal variation in admission troponin concentrations in patients with chest pain in the emergency department

“…Studies have reported that haemodialysis may reduce hs-cTnT levels by at least 10%, and in some cases up to 50%, in stable patients with ESRD, which suggest at least a partial renal clearance of cTnT (99,100). The magnitude of elevated hs-cTnT levels observed with declining renal function seem to be more pronounced than that for hs-cTnI levels (55), and hs-cTnT levels are higher in patients ESRD (101). Intact cTnT has a molecular weight of 37 kDa, which suggest a low degree of filtration through the glomerular membrane.…”

Effects of Acute Resistance Training on Biochemical Markers of Myocardial Injury (cTnT, cTnI, CK-MB) in Non-Athlete Women

“…Cardiac troponin T and I are the proteins in actin filaments that regulate the speed and force of contraction in cardiac cells. These are highly specific and sensitive markers for cardiac cell damage, and are extensively released into blood plasma following cardiac damage or fatigue (9,10). CTn-T, cTn-I, creatine kinase (CK) and its iso-enzyme (CK-MB) are appropriate tools for diagnosis of damage to cardiac muscle cells, ischemia, and cardiac muscle infarction (11).…”