Cardiac Troponin I Is Associated With Impaired Hemodynamics, Progressive Left Ventricular Dysfunction, and Increased Mortality Rates in Advanced Heart Failure

Abstract

Background-Cardiac troponin I (cTnI), a sensitive and specific marker of myocardial cell injury, is useful in diagnosing and assessing prognosis in acute coronary syndromes. Small studies report that cTnI is elevated in severe heart failure (HF) and may predict adverse outcomes. Methods and Results-The present study evaluated 238 patients with advanced HF referred for cardiac transplantation evaluation who had cTnI assay drawn at the time of initial presentation. Patients with acute myocardial infarction or myocarditis were excluded from analysis. cTnI was detectable (cTnI Ն0.04 ng/mL) in serum of 117 patients (49.1%).Patients with detectable cTnI levels had significantly higher B-type natriuretic peptide (BNP) levels (PϽ0.001) and more impaired hemodynamic profiles, including higher pulmonary wedge pressures (Pϭ0.002) and lower cardiac indexes (PϽ0.0001). A significant correlation was found between detectable cTnI and progressive decline in ejection fraction over time. Furthermore, detectable cTnI was associated with increased mortality risk (RR, 2.05; 95% CI, 1.22 to 3.43). After adjustment for other factors associated with adverse prognosis including age, sex, ejection fraction, and coronary artery disease, cTnI remained a significant predictor of death. cTnI used in conjunction with BNP further improved prognostic value. Conclusions-cTnI is associated with impaired hemodynamics, elevated BNP levels, and progressive left ventricular dysfunction in patients with HF. cTnI may be a novel, useful tool in identifying patients with HF who are at increased risk for progressive ventricular dysfunction and death.

Contribution of Renal Function Impairment to Unexplained Troponin T Elevations in Congestive Heart Failure

“…[4,7,8,28] We also observed such a relation between NYHA class and TnT; however, in light of our all findings, we can speculate another explanation that in the early stages of heart failure, patients may have normal GFR despite a reduced renal blood flow and normal TnT levels. Several limitations of the present study deserve consideration.…”

“…[1,2] Among ambulatory patients referred for cardiac transplantation, troponin I was detectable in approximately 50%, regardless of the cause (ischemic vs nonischemic) of heart failure. [3] In hospitalized patients with CHF, elevation of circulating troponin T (TnT) or troponin I levels occurs frequently. [4,5] These cardiac markers are associated with decreased left ventricular ejection fraction and poor prognosis in patients with CHF and are related to the severity of heart failure.…”

On admission serum sodium and uric acid levels predict 30 day rehospitalization or death in patients with acute decompensated heart failure

“…Accordingly, a growing body of research is trying to characterize this population of patients who are at increased risk of early post‐discharge mortality and hospitalization. Presumed prognosticators comprise a wide range of history and physical examination findings, laboratory measurements, electrocardiographic and echocardiographic indices, and ultrasound assessments and include anaemia, diabetes mellitus, new sustained arrhythmias, non‐use of neurohormonal antagonists, presence of coronary heart disease (CHD), jugular venous distension, admission systolic blood pressure, serum albumin levels, lymphocyte counts, troponin release, blood urea nitrogen (BUN) and BUN/creatinine ratio, natriuretic peptides, 6‐min walk distance (6MWD), LVEF, pulmonary capillary wedge pressure, diameter of inferior vena cava, and diuretic response and hemoconcentration during hospitalization among many others 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28. However, there is no general consensus regarding the majority of these indices, and application of most of them is subject to several disadvantages in routine clinical practice.…”

Narrative Review: Alternative Causes for Elevated Cardiac Troponin Levels when Acute Coronary Syndromes Are Excluded

“…Furthermore, in vitro experiments with myocytes established a link between myocardial wall stretch and programmed cell death (35), and troponin degradation has been demonstrated as a result of increased preload independently from myocardial ischemia in isolated rat hearts (36). It has also been hypothesized that increased myocardial wall stress may lead to decreased subendocardial perfusion, with resulting troponin elevation and decline in left ventricular systolic function (37). In the setting of acute or chronic congestive heart failure, additional factors, including the activation of the renin-angiotensin system, sympathetic stimulation, and inflammatory mediators, may be partially responsible for myocyte injury and cell death.…”

“…They have also established a relationship between troponin elevation and increased mortality during follow-up. Of 238 patients with advanced heart failure who were referred for cardiac transplantation evaluation, 49% were found to have elevated cardiac troponin levels (37). Patients with detectable troponin had significantly higher B-type natriuretic peptide levels, higher pulmonary wedge pressures, lower cardiac indices, and a twofold increase in mortality.…”