Blood Levels Of Cardiac Troponin Research Articles

Biomarkers of myocardial injury in surgical treatment of lung cancer: perioperative dynamics and prognostic value

Aim. To study the perioperative dynamics of myocardial injury biomarkers and determine their significance in assessing the postoperative mortality risk in patients with nonsmall cell lung cancer.Methods. The study included 82 male patients with non-small cell lung cancer undergoing pneumonectomy. The median age was 64 (59; 67) years. The blood levels of cardiac troponin I (cTnI), N-terminal pro b-type natriuretic peptide (NT-proBNP) and fatty acid-binding protein (FABP) were noted before and after surgery. The rate of myocardial injury after non-cardiac surgery (MINS) was determined. The postoperative cTnI level above 0.023 μg/L was considered as MINS criterion. The significance of the studied biomarkers in predicting the total mortality within 6 months after surgery was assessed using the univariate and multivariate Cox regression and ROC analysis.Results. Compared to baseline levels, all myocardial injury biomarkers increased in 24 and 48h after surgery: cTnI by 120 and 85%, NT-proBNP by 128 and 129%, FABP by 207 and 31%, respectively. The postoperative cTnI levels met the MINS criterion in 45.1% of patients. During the follow-up period 12 patients died, 9 (75%) of those were diagnosed with MINS. Based on the results of the univariate Cox regression overall postoperative mortality was associated with NTproBNP levels before and after the surgery, cTnI growth rate after the surgery and MINS. According to the multivariate Cox regression (adjusted for age and other clinical parameters), preoperative NT-proBNP and atrial fibrillation proved to be the independent predictors of postoperative mortality. The cut-off value of preoperative NT-proBNP was 225 pg/mL; relative risk of death above that value was 5.9 and 95% confidence interval of 1.74–20.0.Conclusion. In patients with non-small cell lung cancer the increase of cTnI, NT-proBNP and FABP mean levels was observed in 24 and 48 hours after pneumonectomy. MINS was diagnosed in 45.1% of patients. According to the univariate regression analysis, MINS and preoperative and postoperative NT-proBNP levels were associated with the risk of total six-month postoperative mortality. The preoperative NT-proBNP was proved to be an independent predictor of adverse outcome.

Relationship of magnesemia with myocardial damage and mortality in patients with COVID-19.

Magnesium (Mg) is the second most abundant intracellular cation and plays a significant role in immune system and cardiac protection. Mg deficiency contributes to chronic low-grade inflammation leading to cardiovascular diseases, and low Mg level exacerbates virus-induced inflammation. The aim of the study was to investigate whether serum magnesium level is associated with myocardial damage and prognosis of COVID-19. This was a single-center, observational retrospective study of patients with COVID-19. The study population was divided into two groups according to in-hospital mortality: a survivor group (SG) and a non-survivor group (NSG). Myocardial damage was defined as blood levels of cardiac troponin I (cTnI) above the 99th percentile upper reference limit. Magnesium, variables regarding inflammation, and myocardial damage were compared between the groups. A total of 629 patients with COVID-19 were included. Mortality rate was 11.85% (n = 82). There were 61 (74.4%) and 294 male patients (53.7%) in NSG and SG, respectively (p = 0.001). The median age of NSG was 64.5 years (min-max: 37-93) and the median age of SG was 56.0 years (min-max: 22-92) (p < 0.001). Median serum magnesium levels of NSG and SG were 1.94 mg/dL (min-max: 1.04-2.87) and 2.03 mg/dL (min-max: 1.18-2.88), respectively (p = 0.027). Median cTnI levels of NSG and SG were 25.20 pg/mL (min-max: 2.10-2240.80) and 4.50 pg/mL (min-max: 0.50-984.3), respectively (p < 0.001). The cTnI levels were lower in those patients whose serum Mg levels were higher than 1.94. Although serum magnesium level was not a predictor for in-hospital mortality, there was a significant negative correlation between magnesemia and myocardial damage.

Different predictive value for short-term all-cause mortality with commonly used biomarkers regarding the cause of pulmonary embolism

Background/Aim. The evaluation of blood levels of cardiac troponin I (cTnI), D-dimer, B-type natriuretic peptide (BNP), and C-reactive protein (CRP) on admission and during the treatment of pulmonary embolism (PE) are the part of routine diagnostic process and estimation of mortality risk. The aim of this study was to evaluate the predictive value of these biomarkers on admission for all-cause 30-day mortality in consecutive PE patients regarding whether they classified as spontaneous, transiently provoked, or permanently provoked PE. Methods. This retrospective analysis was gained from the data of 590 PE patients from the Serbian University Multicenter Pulmonary Embolism Registry (SUPER). Patients had at least one of these biomarkers (BNP, CRP, cTnI, and D-dimer) measured during the first 24 hours upon admission. Results. Receiver operating characteristic (ROC) curve analyses demonstrated that BNP had the highest prognostic accuracy for 30-day mortality in patients (n = 219) who had data for all examined biomarkers. BNP provided an AUC of 0.785 (p &lt; 0.001). Separately, BNP had the highest c-statistic for all three groups of patients. CRP had a modest predictive value for the 30-day all-cause mortality in the group with transient provoked PE. Troponin I had a very modest predictive value for the 30-day all-cause mortality only in patients with spontaneous PE, and D-dimer was a very weak predictor of this end-point only in patients with persistent provoked PE. Conclusion. Patients with spontaneous, transient provoked, and persistent provoked PE have a significantly different pro-file of blood biomarkers level with different prognostic significance for early all-cause mortality.

Activation of complement factor B contributes to murine and human myocardial ischemia/reperfusion injury.

The pathophysiology of myocardial injury that results from cardiac ischemia and reperfusion (I/R) is incompletely understood. Experimental evidence from murine models indicates that innate immune mechanisms including complement activation via the classical and lectin pathways are crucial. Whether factor B (fB), a component of the alternative complement pathway required for amplification of complement cascade activation, participates in the pathophysiology of myocardial I/R injury has not been addressed. We induced regional myocardial I/R injury by transient coronary ligation in WT C57BL/6 mice, a manipulation that resulted in marked myocardial necrosis associated with activation of fB protein and myocardial deposition of C3 activation products. In contrast, in fB-/- mice, the same procedure resulted in significantly reduced myocardial necrosis (% ventricular tissue necrotic; fB-/- mice, 20 ± 4%; WT mice, 45 ± 3%; P < 0.05) and diminished deposition of C3 activation products in the myocardial tissue (fB-/- mice, 0 ± 0%; WT mice, 31 ± 6%; P<0.05). Reconstitution of fB-/- mice with WT serum followed by cardiac I/R restored the myocardial necrosis and activated C3 deposition in the myocardium. In translational human studies we measured levels of activated fB (Bb) in intracoronary blood samples obtained during cardio-pulmonary bypass surgery before and after aortic cross clamping (AXCL), during which global heart ischemia was induced. Intracoronary Bb increased immediately after AXCL, and the levels were directly correlated with peripheral blood levels of cardiac troponin I, an established biomarker of myocardial necrosis (Spearman coefficient = 0.465, P < 0.01). Taken together, our results support the conclusion that circulating fB is a crucial pathophysiological amplifier of I/R-induced, complement-dependent myocardial necrosis and identify fB as a potential therapeutic target for prevention of human myocardial I/R injury.

Activation of Complement Factor B Contributes to Murine and Human Myocardial Ischemia/Reperfusion Injury

Abstract The pathophysiology of myocardial injury resulting from cardiac ischemia and reperfusion (I/R) is incompletely understood. Experimental evidence from murine models indicates that innate immune mechanisms including complement activation via the classical and lectin pathways are crucial. Whether factor B (fB), a component of the alternative complement pathway required for amplification of complement cascade activation, participates in the pathophysiology of myocardial I/R injury has not been addressed. We induced regional myocardial I/R injury by transient coronary ligation in WT mice, a manipulation that resulted in marked myocardial necrosis associated with upregulated myocardial expression of fB gene, activation of fB protein, and myocardial deposition of C3 activation products. In contrast, in fB−/− mice, the same procedure resulted in significantly reduced myocardial necrosis and diminished deposition of C3 activation products in the myocardial tissue. To extend the analysis to humans we measured levels of activated fB (Bb) in intracoronary blood samples obtained during cardio-pulmonary bypass surgery before and after aortic cross clamping (AXCL), during which global heart ischemia was induced. Intracoronary Bb increased immediately after AXCL, the levels were directly related to the length of the AXCL and correlated with peripheral blood levels of cardiac troponin I, an established biomarker of myocardial necrosis. Taken together, our results support the conclusion that fB is a crucial pathophysiological amplifier of I/R-induced, complement-dependent myocardial necrosis and identify fB as a potential therapeutic target for prevention of human myocardial I/R injury.

Percutaneous Coronary Intervention in a Patient with Acute Thrombosis of Saphenous Vein Graft and Patent Native Coronary Artery: Which is the Vessel to Approach?

We describe a case of a patient with a clinical history of coronary artery disease, previously treated by coronary surgery and, one year later, by percutaneous coronary intervention plus stenting for sub-occlusive disease of the saphenous vein graft to first obtuse marginal (OM) branch. The patient, admitted to our emergency room with chest pain, nausea, hypotension and diaphoresis, had elevated blood levels of cardiac troponin T and EKG showed elevation of the ST segment in the in lateral leads, suggesting a diagnosis of ST elevated myocardial infarction (STEMI). Thus, coronary angiography was immediately performed, showing the massive thrombosis of the saphenous vein graft previously treated by stenting and the slight patency of the native vessel. We decided to approach the native vessel instead of clashing to the massive thrombus of the saphenous vein graft, overcoming the actual guidelines indications.

Sodium Nitrite Fails to Limit Myocardial Infarct Size: Results from the CAESAR Cardioprotection Consortium (LB645)

The CAESAR Consortium was established in 2010 to test promising cardioprotective agents in a manner analogous to clinical trials. This consortium features highly standardized murine, leporine, and porcine models of myocardial ischemia and reperfusion (MI/R). These models are conducted at two sites per species, in a randomized and blinded manner, and in combination with core laboratories to assess myocardial infarct size, measure cardiac troponin I levels, and perform unbiased statistical analyses. After validating the Consortium with an ischemic preconditioning study, we evaluated several putative potent cardioprotective agents (e.g. sodium nitrite). We performed preliminary studies to determine appropriate dosing and pharmacokinetics of sodium nitrite in mice and rabbits. MI/R was performed in mice (n=29-36/group), rabbits (n=20-22/group), and pigs (n=8/group); sodium nitrite was administered intravenously 5 min before reperfusion. We observed no differences in hemodynamics or myocardial area-at-risk (AAR) in any species. Sodium nitrite failed to attenuate myocardial infarct size (INF) per AAR or reduce peak blood levels of cardiac troponin I in any species.Thus, sodium nitrite does not afford acute protection during MI/R when investigated under rigorous experimental conditions that mimic clinical trials. Grant Funding Source: National Institutes of Health (NIH)-Heart Lung and Blood Institute (NHLBI) CAESAR Consortium-1U24 HL 094373

Intrathecal sufentanil for coronary artery bypass grafting

ContextCardiac surgery patients undergoing coronary artery bypass grafting with cardiopulmonary bypass. ObjectiveEvaluate the effect of adding intrathecal sufentanil to general anesthesia on hemodynamics. DesignProspective, randomized, not blinded study, after approval by local ethics in Research Committee. SettingMonocentric study performed at Dante Pazzanese Institute of Cardiology, Sao Paulo, Brazil. Patients40 consenting patients undergoing elective coronary artery bypass, both genders. Exclusion criteriaChronic kidney disease; emergency procedures; reoperations; contraindication to spinal block; left ventricular ejection fraction less than 40%; body mass index above 32kg/m2 and use of nitroglycerin. InterventionsPatients were randomly assigned to receive intrathecal sufentanil 1μg/kg or not. Anesthesia induced and maintained with sevoflurane and continuous infusion of remifentanil. Main outcome measuresHemodynamic variables, blood levels of cardiac troponin I, B-type natriuretic peptide, interleukin-6 and tumor necrosis factor alfa during and after surgery. ResultsPatients in sufentanil group required less inotropic support with dopamine when compared to control group (9.5% vs 58%, p=0.001) and less increases in remifentanil doses (62% vs 100%, p=0.004). Hemodynamic data at eight different time points and biochemical data showed no differences between groups. ConclusionsPatients receiving intrathecal sufentanil have more hemodynamical stability, as suggested by the reduced inotropic support and fewer adjustments in intravenous opioid doses.

Letter to the Editor

I read with interest the article entitled: “Cardiac Troponin I in Calves with Congenital Heart Disease” (Suzuki, et al., JVIM, 2012 DOI: 10.1111/j.1939-1676.2012.00953.x).1 This study deals with an understudied area of internal medicine: cardiology in food animals. Adding evidence-based studies is of great importance but can be challenging especially for unfrequent diseases. The authors concluded that the blood levels of cardiac troponin I (cTnI) can be of interest in for diagnosing congenital heart disease (CHD) in calves. They also state that “using a cutoff value of ≥ 0.035 ng/mL, cTnI in plasma may distinguish calves with and without significant CHD with reasonnable sensitivity and specificity.” Designing of diagnostic accuracy studies is challenging not only in veterinary medicine but also in human medicine.2 The case selection of control group to assess the specificity of the cTnI levels needs to be discussed since it may certainly overestimate test accuracy. Using healthy control subjects in case-control studies commonly led to overestimation of diagnostic accuracy compared with cohort study.3 As discussed by the authors, the clinical diagnosis of CHD in calves is challenging without echocardiography since the clinical signs especially cardiac murmur can be found in calves without CHD (anemia, excitement or fever) as well as various signs of respiratory distress. It has been shown that cTnI can be increased in cattle due to various thoracic diseases4, 5 or endotoxemia.6 Such animals may represent a better group to establish the specificity of the diagnostic accuracy of cTnI in calves with heart murmur and CHD to calves with heart murmur due to various cardiorespiratory condition or endotoxemia/sepsis. Another concern that has not been addressed in that study is that the test accuracy has been determined in only 12 cases with various CHD and 19 healthy control animals. With this small sample although the receiver operating characteristic lead to interesting Se/Sp of this test in their sample of calves, the authors did not mention that before doing any inference of their best Se/Sp value of cTnI, they need to calculate the 95% confidence interval (CI) for their values. Such a small sample of animals would lead to a wider imprecision of their Se/Sp estimate to extrapolate to the general population that needs to be known by any clinician attempting to include cTnI determination in their diagnostic workup for suspected calves with CHD. Morerover, determining a threshold (here 0.035 ng/mL) although interesting, needs to be discussed in regard with the method of determination of cTnI. Previous studies in dogs7 have shown that normal ranges should be established for every technique/analyzer used for establishing cTnI levels since difference in the antibodies used in the assays could lead to differences in results obtained with different analyzers. Moving from this point, it is difficult to extrapolate the proposed threshold without comparisons of other point of care cTnI analyzers that could be used in the farm with portative analyzers that may be used for cTnI determination. Finally, despite having a threshold for diagnosing CHD in calves could be interesting, from a practical perspective, it would have been interesting to know if the cTnI values were quite different depending on the exact nature of CHD. The impact of the heart defect on cardiomyocytes oxygen delivery may (or may not) be different in a case of early VSD without any cardiac chamber modification whereas hypoxemia due to intracardiac shunt may lead to increased cTnI due to myocardial hypoxia in cyanotic heart disease (Tetralogy of Fallot or double outlet right ventricle which represent 6 of 12 cases investigated in the present study1). This study raises interesting points concerning potential interest of cTnI in the diagnosis of CHD in calves. However, the authors did not convince me that it could replace transthoracic echocardiography which is more specific in living animals and more sensitive (for experienced user) especially for commonly encountered CHD such as VSD. Having higher number of CHD calves and calves with various conditions that could clinically mimick CHD would be of great interest to investigate more accurately Se/Sp of this cardiac biomarker. Using the proposed threshold to diagnose CHD in calves without other confirmatory test would certainly lead to overdiagnosing CHD in calves with simple infectious respiratory conditions or endotoxemic condition.

CALCITONIN GENE RELATED PEPTIDE IS ELEVATED IN PATIENTS WITH ACUTE CORONARY SYNDROME

IntroductionElevated blood levels of cardiac troponin (cTn) released during myocardial ischaemia/infarction define acute coronary syndrome (ACS). However, cTn is not detectable for 3–4 h after symptom onset. The peptide Calcitonin...

Abstract P012: Cardiac Biomarkers of Newborn Myocardial Injury, Cardiomyopathy and Inflammation are Associated with Indicators of Premature Cardiovascular Disease in Childhood: The National Institutes of Health Project VIVA Study

Objective: To examine associations of cord blood cardiac biomarker levels in normal newborns with cardiovascular outcomes and adiposity in childhood. Methods: Among a sample (N=49) from 1120 Project Viva pediatric participants, selected to be ∼1/3 white, 1/3 black, 1/3 Hispanic, and whose gestational age at birth was ≥34 wks, we examined relations of cord blood levels of cardiac troponin T (cTnT, a biomarker for myocyte injury), high sensitivity C-reactive protein (hsCRP, a generalized marker of systemic inflammation) &amp; N-terminal pro-brain natriuretic peptide (NT-proBNP, a biomarker of LV pressure or volume overload, cardiomyopathy, cardiac neurohormonal activation) with child outcomes at ages 3 &amp; 7 years. Results: Forty six percent (22 of 49) were female. Mean cTnT was 47.0 pg/mL (range=15.1-87.3 pg/mL; detection limit=10 pg/ml). Mean NT-proBNP was 663 pg/mL (range=166-2042 pg/mL; normal &lt;150 pg/ml) and mean hsCRP was 0.07 mg/L (range=0.03-0.18 mg/L; normal &lt;1mg/L). For each 100 pg/mL increase in NT-pro-BNP, the ratio of subscapular: triceps skinfolds (central fat distribution) at 3 yrs was slightly higher (0.98 [95% CI -0.20, 2.16], P=0.10) and fat mass/m2 (DXA) at 7 yrs was higher (0.18 [95% CI 0.03, 0.33], P=0.02). For each 0.1 mg/L increase in hsCRP, the heart rate was 8.7 beats per minute lower (95% CI -15.8, -1.6, P=0.02) at age 7 years. Conclusions: Biomarkers of cardiomyopathy, inflammation, and cardiac injury are commonly elevated at birth. In this pilot study, cardiomyopathy and inflammation biomarkers were associated with higher central fat distribution and fat mass and lower resting pulse rate up to 7 years later. Larger cohort studies are needed to further examine cardio-metabolic outcomes related to these cord blood cardiac biomarkers.

Ischemia/Reperfusion of the Liver Induces Heart Injury in Rats

Objective We evaluated the cardiovascular injury induced by ischemia and reperfusion (I/R) of the liver by measuring changes in blood levels of cardiac troponin I (cTNI), an index of cardiovascular injury, as well as levels of selected indicators of an inflammatory response. Materials and Methods Ischemia was induced in the rat liver by clamping the common hepatic artery and portal vein for 40 minutes, after which flow was restored, and the liver reperfused for 90 minutes. Blood samples were collected prior to ischemia and after reperfusion. cTNI as well as levels of tumor necrosis factor α (TNFα), hydroxyl radical (· OH), nitric oxide (NO), and alanine transferase (ALT) were measured. Results I/R of the liver induced a significant increase in ALT ( P < .001). Increased cTNI levels ( P < .05) were associated with inflammatory responses, such as elevated levels of TNFα ( P < .001), · OH ( P < .001), and NO ( P < .001). After administration of 3-aminobenzamide, a poly(ADP-ribose) polymerase (PARP) inhibitor, liver and heart injuries were significantly attenuated ( P < .05). Conclusions I/R-induced liver injury was associated with cardiovascular injury, perhaps resulting from inflammatory responses triggered by elevated levels of reactive radical species of nitric oxide, superoxide, and peroxynitrite, by which PARP was activated. 3-Aminobenzamide, significantly attenuated I/R-induced liver and heart injuries.

Clinical significance of a single measurement of troponin-I and C-reactive protein at admission in 1773 consecutive patients with acute coronary syndromes

Background The clinical significance of biochemical markers of myocardial damage or inflammation has not been prospectively established in populations representing the whole spectrum of acute coronary syndromes. We investigated whether the elevation of these biomarkers at admission has a prognostic value that is independent and incremental to baseline clinical variables and quantitative electrocardiographic ischemia. Methods We measured blood levels of cardiac troponin I (cTnI) and C-reactive protein (CRP) in 1773 consecutive patients admitted to 31 Italian coronary care units within 12 hours from an episode of acute coronary syndrome. Primary and secondary outcomes were (1) 30-day incidence of death or nonfatal (re)infarction and (2) death alone. Results In a multivariate model, cTnI was independently associated with the risk of death or (re)infarction (OR, 1.8; 95% CI, 1.2 to 2.6; P = .002) and death (OR, 2.2; 95% CI, 1.4 to 3.4; P < .001), whereas CRP was of borderline significance for the primary outcome but was associated with death (OR, 1.4; 95% CI, 1.0 to 2.1; P = .06, and OR, 1.7; 95% CI, 1.1 to 2.6; P = .01, respectively). However, the inclusion of the biomarkers did not increase the prognostic capacity of the clinical risk model (C-index of both models with and without biomarkers was 0.73 for the primary outcome measures and 0.80 for the secondary outcome measures). CRP further stratified cTnI-negative patients. The prognostic significance of the biomarkers was similar in patients with and in those without persistent ST-segment elevation. Conclusions In acute coronary syndromes, the elevation of cTnI and CRP at admission has an independent prognostic value that is not incremental to baseline clinical variables and quantitative electrocardiographic ischemia.

Detection of myocardial injury during radiofrequency catheter ablation by measuring serum cardiac troponin I levels: procedural correlates

OBJECTIVESIn the present prospective controlled study, we measured blood levels of cardiac troponin I (cTnI) in patients undergoing radiofrequency (RF) catheter ablation (RFA), and we sought to investigate the degree of myocardial injury incurred by the application of RF energy and determine its procedural correlates.BACKGROUNDMeasurement of serum creatine kinase (CK) levels after RFA may underestimate the degree of myocardial injury due to its thermal inactivation by RFA. Cardiac troponin I is a newer, more specific marker of myocardial injury, which may circumvent this limitation; its use in this setting has rarely been studied.METHODSIn 118 consecutive patients, 67 men and 51 women aged 38 ± 19 years undergoing RFA for a variety of arrhythmias, cTnI and creatine kinase isoenzyme (CK-MB) levels were measured before, immediately after and 4 to 24 h after RFA. Cardiac troponin I was also measured in 39 patients (control group) having only electrophysiologic studies (EPS) without RFA.RESULTSAll RFA procedures were uncomplicated, lasted 3.2 ± 2.0 h and included delivery of 16 ± 22 (median: 9) RF current applications. Baseline cTnI levels averaged 0.17 ± 0.18 ng/ml, rose to 0.88 ± 1.12 at the end of RFA and to 2.19 ± 2.46 at 4–24 h later. Creatine kinase isoenzyme was found to be elevated (>6 μg/l) in 32 patients (27%), while cTnI levels were increased (≥1 ng/ml) in 80 patients (68%) (p = 0.0001). Cardiac troponin I levels correlated with the number of RF lesions applied (r = 0.53, p < 0.0001), the site of RFA, being higher with ventricular > atrial > annular lesions (p = 0.012) and the approach to the mitral annulus (transaortic > transseptal, p = 0.004). In a control group of 39 patients undergoing EPS, all but one patient had normal cTnI or CK-MB.CONCLUSIONSThe degree of myocardial injury incurred by RFA is far more accurately assessed by cTnI levels rather than by CK-MB measurements. Cardiac troponin I levels correlate with the number of RF lesions applied, the site of RFA and the approach to the mitral annulus.

Clinically Recognized Cardiac Dysfunction: An Independent Determinant of Mortality Among Critically III Patients: Is There a Role for Serial Measurement of Cardiac Troponin I?

To determine the relative importance of clinically recognized cardiac dysfunction and unrecognized cardiac injury to hospital mortality. Prospective, blinded, single-center study. Medical ICU of Barnes-Jewish Hospital, St. Louis, a university-affiliated teaching hospital. Two hundred sixty adult patients requiring admission to the medical ICU. Daily blood collection. The presence of cardiac dysfunction (myocardial infarction, unstable angina, cardiac arrest, or congestive heart failure) as determined by the physicians responsible for the care of the patient. Daily measurement of levels of cardiac troponin I, a sensitive, highly specific, and long-lived marker of myocardial injury. Fifty-five (21.2%) patients had clinical evidence of cardiac dysfunction, among whom 22 (40%) had an elevated level of cardiac troponin I. A total of 41 (15.8%) patients had evidence of acute myocardial injury based on elevated levels of cardiac troponin I. Patients with clinically recognized cardiac dysfunction had a significantly greater hospital mortality rate compared to patients without clinically recognized cardiac dysfunction (45.5% vs 10.2%; p < 0.001). Similarly, patients with elevated blood levels of cardiac troponin I had a greater hospital mortality rate compared to patients without elevated blood levels of cardiac troponin I (26.8% vs 16.0%; p = 0.095). Multiple logistic-regression analysis controlling for potential confounding variables demonstrated that the presence of clinically recognized cardiac dysfunction was independently associated with hospital mortality (adjusted odds ratio = 3.0; 95% confidence interval = 1.9 to 4.8; p = 0.016). However, having an elevated blood level of cardiac troponin I was not found to be an independent determinant of hospital mortality. Among critically ill medical patients, clinically recognized cardiac dysfunction is an independent determinant of hospital mortality. The identification of unrecognized cardiac injury, using serial measurements of cardiac troponin I, did not independently contribute to the prediction of hospital mortality.