cTn Release Research Articles

The impact of intermittent exercise in a hypoxic environment on redox status and cardiac troponin release in the serum of well-trained marathon runners.

To investigate the effects of hypoxic training on redox status and cardiac troponin (cTn) release after intermittent exercise. Nine well-trained male marathon runners (age, 21.7±2.3year; body mass, 64.7±4.8kg; height, 177.9±3.8cm; and VO2max, 64.3±6.7mlkg(-1)min(-1)) completed intermittent exercise under normoxic [trial N; fraction of inspiration oxygen (FIO2), 21.0%] and hypoxic (trial H; FIO2, 14.4%) conditions in random order. Each bout of intermittent exercise included hard run (16.2±0.8kmh(-1)) at 90% VO2max for 2min followed by easy run (9.0±0.4kmh(-1)) at 50% VO2max for 2min and 23 bouts in 92min totally. Malondialdehyde, reduced glutathione (GSH), superoxide dismutase, an estimate of total antioxidant capacity (T-AOC), high-sensitivity cardiac troponin T (hs-cTnT), and cardiac troponin I (cTnI) were measured before, immediately after (0h), and 2, 4, and 24h after the completion of trials N and H. GSH was increased immediately after trial N. T-AOC was lower 4h after trial H than trial N. Hs-cTnT was elevated from 0 to 4h and returned to baseline 24h after both trials. CTnI was increased after trial H; peaked at 2-4h and returned to below the detection by 24h. The overall redox status was balanced under normoxic conditions, and exercise-induced cTn release did not deviate. However, the protective effects of antioxidant were weaker in the hypoxic state than normoxic, and the stress on the myocardium induced by intermittent exercise was transiently aggravated.

Cardiac Troponin T and I Release After a 30-km Run

Prolonged endurance-type exercise is associated with elevated cardiac troponin (cTn) levels in asymptomatic recreational athletes. It is unclear whether exercise-induced cTn release mirrors a physiological or pathological underlying process. The aim of this study was to provide a direct comparison of the release kinetics of high-sensitivity cTnI (hs-cTnI) and T (hs-cTnT) after endurance-type exercise. In addition, the effect of remote ischemic preconditioning (RIPC), a cardioprotective strategy that limits ischemia-reperfusion injury, was investigated in a randomized controlled crossover manner. Twenty-five healthy volunteers completed an outdoor 30-km running trial preceded by RIPC (4× 5 min 220mm Hg unilateral occlusion) or control intervention. hs-cTnT, hs-cTnI, and sensitive cTnI (s-cTnI) concentrations were examined before, immediately after, 2 and 5 hours after the trial. The completion of a 30-km run resulted in a significant increase in circulating cTn (time: all p <0.001), with maximum hs-cTnT, hs-cTnI, and s-cTnI levels of 47 ± 27, 69 ± 62, and 82 ± 64ng/L (mean ± SD), respectively. Maximum hs-cTnT concentrations were measured in 60% of the participants at 2 hours after exercise, compared with maximum hs-cTnI and s-cTnI concentrations at 5 hours in 84% and 80% of the participants. Application of an RIPC stimulus did not reduce exercise-induced cTn release (time× trial: all p >0.5). In conclusion, in contrast to acute myocardial infarction, maximum hs-cTnT levels after exercise precede maximum hs-cTnI levels. Distinct release kinetics of hs-cTnT and hs-cTnI and the absence of an effect of RIPC favors the concept that exercise-induced cTn release may be mechanistically distinct from cTn release in acute myocardial infarction.

Experimental determination of diagnostic window of cardiac troponins in the development of chronic anthracycline cardiotoxicity and estimation of its predictive value

BackgroundCardiac troponins (cTns) seem to be more sensitive for the detection of anthracycline cardiotoxicity than the currently recommended method of monitoring LV systolic function. However, the optimal timing of blood sampling remains unknown. Hence, the aims of the present study were to determine the precise diagnostic window for cTns during the development of chronic anthracycline cardiotoxicity and to evaluate their predictive value. MethodsCardiotoxicity was induced in rabbits with daunorubicin (3mg/kg, weekly, for 8weeks). Blood samples were collected 2–168h after the 1st, 5th and 8th drug administrations, and concentrations of cTns were determined using highly sensitive assays: hs cTnT (Roche) and hs cTnI (Abbott). ResultsThe plasma levels of cTns progressively increased with the rising number of chemotherapy cycles. While only a mild non-significant increase in both cTn levels occurred after the first daunorubicin dose, a significant rise was observed after the 5th and 8th administrations. Two hours after these administrations, a significant increase occurred with a peak between 4–6h and a decline until 24h. Discrete cTn release continued even after cessation of the therapy. While greater variability of cTn levels was observed around the peak concentrations, the values did not correspond well with the severity of LV systolic dysfunction. Unlike AMI in cardiotoxicity, cTn elevations may be better associated with cumulative dose and concentrations at steady state than cmax. ConclusionsTo the best of our knowledge, this is the first study to precisely describe the diagnostic window and predictive value of cTns in anthracycline cardiotoxicity.

Polyphenol Supplementation Improves Cardiomyocyte Recovery After Marathon Running

PURPOSE: The liberation and increase in concentration of cardiac troponin (cTn) during and after strenuous exercise are known phenomena. Polyphenols have anti-inflammatory and anti-oxidative effects that may counteract cTn release and inflammation-associated alterations of the cardiovascular system. Therefore, we investigated, whether supplementation with polyphenols has cardiomyocyte protective effects in marathon runners competing in the Munich Marathon. METHODS: We examined the effects of polyphenol supplementation in 277 male marathon runners (age 42±9yrs.) in a randomized, double-blind and placebo-controlled manner with regard to levels of cTnT and inflammatory biomarker levels before a marathon race, and immediately, 24 and 72hrs afterwards. Per-protocol (PP) population was defined as all participants who finished the race successfully and ingested ≥ 1L (≥ 326mg gallic acid equivalents (GAE) per 100g) of the supplementation per day. 149 participants (70 verum group (V=polyphenol supplementation), 79 placebo group (PL=identically with V except for polyphenols)) were in PP population. RESULTS: We observed no significant difference between V and PL regarding cTnT concentration immediately post-race (median [IQR]: V: 33.7 [19.2-54.6]ng/L vs. PL: 37.0 [21.0-51.0]ng/L, p=0.85). However, there was a significantly larger decrease in cTnT 24 hrs post-race in V (4.2 [2.8-6.0]-fold) compared to PL (3.4 [2.3-5.0]-fold) (p=0.02), resulting in lower cTnT levels 72 hrs post-race (24h-post: V: 8.0 [3.1-15.4]ng/L vs. PL: 11.0 [6.2-16.1]ng/L, p=0.08; 72h-post: V: 3.0 [3.0-6.3]ng/L vs. PL: 5.7 [3.0-8.7]ng/L, p=0.04). CONCLUSIONS: Supplementation with a polyphenolic mixture was linked to enhanced cardiomyocyte recovery after prolonged and strenuous exercise.

ASSOCIATION OF ALBUMIN AND HIGH SENSITIVE CARDIAC TROPONIN T AND I LEVELS AMONG CHEST PAIN PATIENTS PRESENTING TO EMERGENCY DEPARTMENT

Proteins often bind with albumin and exist as unbound and bound forms. However it is unknown whether albumin levels correlate with cardiac troponin (cTn), and whether it can be used to differentiate between acute and chronic etiologies of cTn release among chest pain patients presenting to emergency

Cardiac troponin in ischemic cardiomyocytes: Intracellular decrease before onset of cell death

AimCardiac troponin I (cTnI) and T (cTnT) are the most important biomarkers in the diagnosis of acute myocardial infarction (AMI). Nevertheless, they can be elevated in the absence of AMI. It is unclear if such elevations represent irreversible cardiomyocyte-damage or leakage from viable cardiomyocytes. Our objective is to evaluate whether cTn is released from viable cardiomyocytes in response to ischemia and to identify differences in the release of cTn and its molecular forms. Methods and resultsHL-1 cardiomyocytes (mouse) were subjected to ischemia (modeled by anoxia with glucose deprivation). The total contents and molecular forms of cTn were determined in culture media and cell lysates. Cell viability was assessed from the release of lactate dehydrogenase (LDH). Before the release of LDH, the intracellular cTn content in ischemic cells decreased significantly compared to control (52% for cTnI; 23% for cTnT) and was not matched by a cTn increase in the medium. cTnI decreased more rapidly than cTnT, resulting in an intracellular cTnT/cTnI ratio of 25.5 after 24h of ischemia. Western blots revealed changes in the relative amounts of fragmented cTnI and cTnT in ischemic cells. ConclusionsHL-1 cardiomyocytes subjected to simulated ischemia released cTnI and cTnT only in combination with the release of LDH. We find no evidence of cTn release from viable cardiomyocytes, but did observe a significant decrease in cTn content, before the onset of cell death. Intracellular decrease of cTn in viable cardiomyocytes can have important consequences for the interpretation of cTn values in clinical practice.

Cardiac troponin T elevation associated with transient global amnesia: another differential diagnosis of ‘troponosis’

Elevated cardiac troponin (cTn) levels can be detected in a variety of diseases with or without signs of myocardial ischaemia. Acute neurological disorders such as subarachnoid haemorrhage, stroke, transient ischaemic attack, epileptic seizures, and traumatic head injury can cause cTn elevation with and without myocardial wall motion abnormalities. We report a case of transient global amnesia with elevation and dynamic rise of highly sensitive troponin T (hsTnT) without clinical symptoms or signs of ischaemia. Cardiac work up was otherwise normal, with no signs of atherosclerotic coronary artery disease on coronary angiogram. Myocardial systolic function was also normal. In the era of highly sensitive cTn assays, dynamic elevations of cTn are seen in a number of acute conditions unrelated to myocardial ischaemia. Transient global amnesia should be added to the list of acute neurological disorders where cTn release can be present, even in the absence of stress-induced cardiomyopathy.

The effects of exercise at high altitude on high-sensitivity cardiac troponin release and associated biventricular cardiac function

It has been consistently shown that heavy exercise leads to cardiac troponin (cTn) release and variable changes in post exercise cardiac function. This relationship has not been explored at increasing or significant high altitude (HA). This study assessed the effects of exercise at progressively increasing HA on high-sensitivity (hs)-cTnT levels and their relationship to biventricular cardiac function and severity of acute mountain sickness (AMS). Transthoracic echocardiograms, hs-cTnT levels and AMS scores were measured at rest at 1,300m then repeated post exercise and 12h later after progressive trekking to 3,440, 4,270m and at 5,150m (after trekking to 5,643m) on 19 healthy subjects (age 35.4±years, 52.6% males). There was a detectable increase (>5ng/L) in post exercise hs-cTnT with exercise at HA which became significant at 5,150m (5.84% at 3,440m, 5.2% at 4,270m and 56.3% at 5,150m; p=0.0005). Compared with baseline, HA to 5,150m led to a significant rise in post exercise Lake Louis AMS scores (p<0.001) pulmonary artery systolic pressure (PASP) (23.7±3.8 vs 37.9±11.7mmHg: p<0.001), cardiac output (5.2±1.2 vs 7.5±1.3l/min; p<0.001) and a fall in SpO2 (96.1±vs 77.4±12.0%; p<0.001). There was no change in stroke volume (p=0.10) or estimated filling pressures (E/E') of the left (p=0.50) and right ventricles (p=0.4). On multivariate analysis increasing cardiac output (p=0.02) and PASP (p=0.04) and decreasing SpO2 (p=0.01) were the only independent predictors of increasing cTnT levels (overall R (2)=0.23, p<0.0001). Moderate intensity exercise at significant HA influences the post exercise increase in hs-cTnT without overt deleterious effects on cardiac function.

Cardiac troponin level elevations not related to acute coronary syndromes

Over the past 2 decades, cardiac troponins (cTn) have emerged as the preferred biomarkers for the noninvasive detection of myocardial injury. In conjunction with typical clinical findings of ischaemia, elevated cTn levels in blood confirm a diagnosis of myocardial infarction. However, neither cTnT or cTnI are exclusively released as a result of ischaemic myocardial cell necrosis, but also with numerous nonischaemic acute and chronic cardiac conditions, such as myopericarditis, toxic injury, or severe cardiac overload. With the advent of high-sensitivity assays, causes of cTn elevation not related to an acute coronary syndrome (ACS) have become common findings in patients with chest pain and in those with acute or chronic systemic disorders. Elevated cTn levels in blood are associated with increased rates of cardiac events and mortality, independently of the underlying disease. However, the clinical conditions leading to cTn release in patients who do not have ACS, and the appropriate diagnostic and therapeutic strategies for these individuals, are largely unknown. Here, we provide an overview of the many causes and the prognostic importance of the release of cTn not related to ACS. We also recommend strategies to discriminate between ischaemic and nonischaemic cTn elevation, and describe the clinical evaluation of these patients.

High altitude exposure, high-sensitivity cardiac troponin and biventricular cardiac function

Background: It has been consistently shown that heavy exercise leads to cardiac troponin (cTn) release and variable changes in post-exercise cardiac function. However its relationship to symptoms of acute mountain sickness (AMS) severity and exercise at significant (>4300m) and increasing high altitude (HA) has not been investigated. Purpose/study design: Transthoracic echocardiograms, hs-cTnT and Lake-Louis AMS scores were measured at rest at 1300m then repeated post-exercise and 12 hours later after progressive trekking to 3440 m, 4270m and at 5150m on 19 healthy subjects aged 35.4±8.3 years (52.6% males). Results: There was a significant and detectable increase in post-exercise hs-cTnT with increasing exercise (29.4% at 3440m, 15.8% at 4270m and 68.8% at 5150m; p=0.02). Compared with baseline, HA to 5150m led to a significant rise in AMS scores (0.1±0.3 vs 3.0±3.2; p<0.001) pulmonary artery systolic pressure ([PASP] 23.7±3.8 vs 37.9±11.7 mmHg: p<0.001), cardiac output (CO; 5.2±1.2 vs 7.5±1.3 l/minute; p<0.001) and a fall in SpO2 (96.1± vs 77.4±12.0%; p<0.001). There was no change in stroke volume (75.6± vs 77.3±12.3ml; p=0.10) or estimated filling pressures (E/E') of the left (5.9±1.1 vs 6.3±1.0; p=0.50) and right ventricles (4.5±1.5 vs 4.6±1.1; p=0.4). On multivariate analysis increasing CO (β-0.50, CI 0.024 to 0.98; p=0.040) and PASP (β0.07, 0.001 to 0.13; p=0.04) and decreasing SpO2 (β-0.07; -0.1 to 0.007; p=0.03) were the only independent predictors of increasing cTnT levels (overall R2=0.24; p=0.0004). Conclusions: Moderate intensity exercise at significant HA influences the post-exercise increase in hs-cTnT without overt deleterious effects on cardiac function.

122 HIGH ALTITUDE EXPOSURE, CARDIAC TROPONIN AND BIVENTRICULAR CARDIAC FUNCTION

<h3>Background</h3> It has been consistently shown that heavy exercise leads to cardiac troponin (cTn) release and variable changes in post exercise cardiac function. This relationship has not be explored at increasing or significant HA exposure (&gt;4300 m). <h3>Aims</h3> This study aimed to assess, for the first time, the effects of exercise at progressively increasing high altitude (HA) on high-sensitivity (hs) cardiac cTnT levels and their relationship to cardiac function and severity of acute mountain sickness (AMS). <h3>Methods</h3> Transthoracic echocardiograms, hs-cTnT levels and acute mountain sickness scores were measured at rest at 1300 m then repeated post exercise and 12 h later after moderate-intensity progressive trekking to 3440 m, 4270 m and at 5150 m (after trekking to 5643 m) on 19 healthy subjects (age 35.4±years; 52.6% males). <h3>Results</h3> There was a significant and detectable&nbsp;increase in post exercise hs-cTnT with increasing exercise (29.4% at 3440 m, 15.8% at 4270 m and 68.8% at 5150 m; p=0.02) with the rise only being significant on post test at 5150 m. No values exceed the cut of for observed with myocardail infarction (≥30 ng/l). Increasing HA led to a significant rise in AMS scores, pulmonary artery systolic pressure, cardiac output and a fall in SpO2 without changes in stroke volume. There were no changes in estimated left (E/E9; p=0.5) or right ventricular (E/E9; p=0.43) filling pressures. On multivariate analysis increasing cardiac output (p=0.040) and right ventricular systolic pressures (p=0.046) and decreasing SpO₂ (p=0.03) were the only independent predictors of increasing cTnT levels (overall R2=0.24; p=0.0004). <h3>Conclusions</h3> Moderate intensity exercise at significant HA does influence the post exercise increase in hs-cTnT without overt deleterious effects on cardiac function.

Interpretation of Serum Troponin Elevation

Interpretation of Serum Troponin Elevation

Interpretation of Serum Troponin Elevation

Interpretation of Serum Troponin Elevation

Antioxidant supplementation does not attenuate exercise-induced cardiac troponin release

Clinically, cardiac troponins (cTn) are used as sensitive markers ofcardiomyocyte damage [1,2] with any elevation in cTn being related topoor prognosis [3]. Recently, however, exercise has also been shown tostimulate the release of cTn [4–6]. The mechanism responsible forexercise-induced cTn release is not known, and is currently a matter ofdebate [7]. Notwithstanding this, it has been proposed, due to therelatively low post-exercise cTn concentrations and its rapid clearance,that cTn is likely released from the cytosolic pool and not from thebreakdownofcontractileapparatus.Previousauthors[8]havesuggestedthatoxidativestressassociatedwithprolongedexercisemaydamagethecardiomyocyte membrane, resulting in cTn release from the cytosol.Antioxidant supplementation has been shown to attenuate oxidativestress, inflammation and muscle damage indices following strenuousexercise [9]; therefore, if post-exercise cTn release is related tocardiomyocyte membrane damage we hypothesised that antioxidantsupplementation would reduce cTn release following marathonrunning.The institutional ethics committee approved all procedures [11].Followinghealth-screeningandgainingconsent,16marathonrunners(11 male and 5 female), a subset from a previous study [9], free fromnutritional supplements and medication, volunteered to participate.Runners were assigned to either a placebo or antioxidant group in adouble-blind, randomised fashion. Antioxidant or placebo supple-mentation was administered each day from 5 days prior to 48 hfollowing the marathon. Indices of cardiac damage (cTnI), inflamma-tion (IL-6 and C-RP), muscle damage (CK), and total antioxidativecapacity (TAC) were taken before supplement (TAC only), before therace, immediately post, 24 and 48 h following completion of themarathon.The antioxidant supplement (tart cherry juice, Cherrypharm, Inc,Geneva, NY) has previously been shown to reduce skeletal muscledamage [10], reduce lipid peroxidation and aid recovery followingrunning [9]. Two servings (morning and afternoon) of approximately225 mL (equating to ~50–60 cherries) were consumed per day; thejuice contained ~600 mg of phenolic compounds such as anthocya-nins and other flavonoids (quercetin, kaempferol and isoramnetin)and ~55 mmol L

Antioxidant Supplementation and Exercise-induced Cardiac Troponin Release

It has been suggested that oxidative stress and inflammation associated with strenuous physical activity may damage the cardiomyocyte membrane, and thus stimulate the release of cardiac troponin (cTn) from the cytosol. PURPOSE: Accordingly, the purpose of the study was to investigate the influence of antioxidant supplementation upon exercise-induced cTn release. METHODS: Sixteen recreational Marathon runners volunteered to participate. Volunteers were equally, but randomly assigned to two groups and consumed 16 fl oz of a tart Montmorency cherry juice (AO) or placebo (PL) everyday for 5 days prior to, and for 24 h following the Marathon. Measures of cardiac damage, (cardiac troponin, cTn), muscle damage (creatine kinase, CK) and MVC, acute inflammation (IL-6), and total antioxidant capacity (TAC) were taken pre-supplement (TAC only), pre-race, immediately post-race, 24 h post-race. A repeated measures ANOVA was used to ascertain differences over time and between groups. RESULTS: cTn and CK were elevated post-exercise in both groups (P < 0.001), but were not different between AO and PL groups (cTn = 0.521 vs. 0.632 μg·L-1; CK = 525 vs 1007 IU·L-1, respectively). MVC decreased post-exercise in both groups and returned faster in the AO group (92% vs. 81% at 24 h, P = 0.003). There were elevations in IL-6 post-exercise that were significantly less in the AO group (40 vs. 93 pg·mL-1, P = 0.003). TAC was significantly elevated by ∼10% post-supplementation in the AO group only (P = 0.007). CONCLUSIONS: Despite there being evidence of an increase in TAC, a reduction in post-exercise inflammation and a faster return of muscle function with antioxidant supplementation, there were no differences between conditions in cTn release or indeed CK activity. These pilot data suggest that the release of cTn following strenuous physical activity might not be associated with exercise-induced oxidative stress or inflammation.

From Creatine Kinase-MB to Troponin

From Creatine Kinase-MB to Troponin

Whose heart will get broken? Troponin testing and future heart failure

After the introduction of troponin T (cTnT) and later troponin I (cTnI) as useful markers of myocardial necrosis,1 their testing has quickly redefined clinical cardiology. Indeed, the importance of troponin (cTn) for the diagnosis of myocardial injury has recently been reaffirmed in the ‘Universal Definition of Myocardial Infarction’: ‘if biomarkers have been measured … and are normal, the determinations of these take precedence over … imaging criteria’.2 This well illustrates that despite all technological developments in imaging techniques over the last two decades, cTn testing remains the gold standard for the identification of acute myocardial injury. There is, however, a potential weakness in cTn testing that is widely acknowledged: notwithstanding the superior accuracy of detecting myocardial injury, an elevated cTn concentration does not provide any insight into the mechanism of heart injury, and a broad differential diagnosis to explain cTn release in the absence of regional myocardial infarction (including cardiomyopathies, pulmonary embolism, renal failure, and even acute cerebral pathologies) should be routinely considered when using these valuable tests.2 While the foregoing differential diagnosis is well understood in the application of cTn in those with acute symptoms, what remains less well understood is the significance of cTn elevation—even at low levels—among ‘apparently well’ subjects. Providing some answer to this question, in a previous study, Wallace and colleagues demonstrated, in a population cohort, that measurable concentrations of cTnT were extremely uncommon, but, … *Corresponding author. Tel: +1 617 726 3443, Fax: +1 617 643 1620, Email: jjanuzzi{at}partners.org

Clinical significance of cardiac troponins I and T in acute heart failure

Elevated cardiac troponin (cTn) levels are relatively common in acute heart failure (AHF). To evaluate the prevalence and prognostic significance of elevated cTnI and cTnT in AHF. FINN-AKVA is a prospective, multicenter study in AHF. In this analysis, 364 non-ACS patients with measurements of cTnI and cTnT taken on admission and 48 h thereafter were analyzed. Of the 364 AHF patients, 51.1% had cTnI and 29.7% cTnT levels above the cut-off value. Six-month all-cause mortality was 18.7%. Both cTnI (OR 2.0, 95% CI 1.2-3.5, p=0.01) and cTnT (OR 2.6, 95% CI 1.5-4.4, p=0.0006) were associated with adverse outcome. The mortality risk was proportional to the magnitude of cTn release. On multivariable analysis, Cystatin C (OR 6.3, 95% CI 3.2-13, p<0.0001), logNT-proBNP (OR 1.4, 95% CI 1.0-1.8, p=0.03) and systolic blood pressure on admission (/10 mm Hg increase, OR 0.9, 95% CI 0.8-0.9, p=0.0004) were independent risk markers, whereas the troponins were not significantly associated with increased mortality. cTn elevations are frequent in AHF patients without ACS. cTnI is more often elevated than cTnT. Both cTnI and cTnT elevations are associated with increased mortality proportional to the degree elevation but they do not act as independent risk markers.

The Pilot Randomized Study of Nesiritide Versus Dobutamine in Heart Failure (PRESERVD-HF)

Acute heart failure syndromes (AHFS) are related to several diseases affecting not only the heart but also the kidneys and blood vessels. Emerging evidence indicates that myocardial injury may also play a role in the pathophysiology of AHFS, as suggested by increased levels of markers of injury, such as cardiac troponin (cTn). Although cTn is a known prognostic marker, the release of cTn during hospitalization has not been evaluated prospectively with serial measures. We prospectively evaluated patterns of cTn release by conducting serial measures of cTnI and cTnT in patients hospitalized for AHFS. This study enrolled 51 patients with AHFS who were admitted with worsening heart failure (HF) and a history of coronary artery disease (CAD) in whom an acute coronary event was not suspected. Levels of cTnI and cTnT were measured at 8, 32, 56, and 80 hours after study entry. At baseline, 73.9% of patients had detectable cTnI, and 43.5% had detectable cTnT levels. The median concentrations of cTnI and cTnT were unchanged from 0 to 32 hours, increased from 32 to 56 hours, then either plateaued (cTnT) or decreased to baseline (cTnI). Of the 26 patients who had no detectable cTn levels at baseline, 2 (7.7%) developed detectable cTnT and 5 (41.7%) developed detectable cTnI release during hospitalization. Detectable levels of cTn at baseline were related to short-term clinical events. In this study of patients with CAD in whom an acute coronary event was not suspected, most had detectable levels of cTn present at admission, and some patients developed cTn release during hospitalization. Because cTn release may be a marker for myocardial injury, this study raises the possibility that injury occurred in most patients admitted with AHFS. Therefore, the goal of therapy for AHFS should be not only to improve symptoms and hemodynamics but also to salvage myocardium. Accordingly, therapies for AHFS that are aimed at improving hemodynamics may affect long-term prognosis by either injuring or salvaging myocardium.