Coronary Microvascular Dysfunction and Diastolic Load Correlate With Cardiac Troponin T Release Measured by a Highly Sensitive Assay in Patients With Nonischemic Heart Failure
What are the factors associated with cardiac troponin T (cTnT) release from failing myocardium?
The investigators evaluated serum cTnT levels in aortic root (Ao) and coronary sinus (CS) using a highly sensitive assay in 90 nonischemic heart failure (HF) patients and 47 non-HF patients. Transcardiac cTnT and plasma B-type natriuretic peptide (BNP) release were described as the differences between CS and Ao cTnT levels [ΔcTnT (CS-Ao)] and BNP levels [ΔBNP (CS-Ao)], respectively. Coronary flow reserve (CFR) was measured in 68 HF patients using an intracoronary Doppler guidewire. Linear relationships between ΔcTnT (CS-Ao) levels and key variables were first analyzed by univariate analysis, followed by stepwise multivariate analysis.
ΔcTnT (CS-Ao) levels were available in 76 HF patients and 28 non-HF patients (84% vs. 60%; p = 0.001), and higher in HF patients than non-HF patients (p < 0.001). Among HF patients, log [ΔcTnT (CS-Ao)] correlated with log [ΔBNP (CS-Ao)] (r = 0.368, p = 0.001), pulmonary capillary wedge pressure (r = 0.253, p = 0.03), and left ventricular end-diastolic pressure (LVEDP) (r = 0.321, p = 0.005). Multivariate regression analysis identified LVEDP as an independent parameter that correlated with ΔcTnT (CS-Ao). ΔcTnT (CS-Ao) levels were available in 58 HF patients who were evaluated for CFR. Coronary microvascular dysfunction, diagnosed by CFR <2.0, was observed in 18 HF patients. ΔcTnT (CS-Ao) was higher in patients with coronary microvascular dysfunction [4.8 (2.0-8.1) ng/L] than those without [2.0 (1.2-4.6) ng/L; p = 0.04].
The authors concluded that cTnT release from failing myocardium correlated with diastolic load and coronary microvascular dysfunction in nonischemic HF patients.
This study reported high ΔcTnT (CS-Ao) levels in nonischemic HF patients compared with non-HF patients and LVEDP and the presence of coronary microvascular dysfunction (CMVD) as significant and independent determinants of ΔcTnT (CS-Ao) levels. Together, these findings indicate that increased diastolic load and CMVD seem to be the causes of persistent and modest cTnT release from the failing myocardium. Because increased LVEDP and CMVD are modifiable targets that can reduce cTnT release, interventions aimed at improving these factors may prevent exacerbation of HF and worsening prognosis. This needs to be further studied in prospective trials.