Cardiac troponin T for risk stratification in decompensated chronic heart failure

Abstracts

FUNDAMENTO: As troponinas cardíacas são marcadores altamente sensíveis e específicos de lesão miocárdica. Esses marcadores foram detectados na insuficiência cardíaca (IC) e estão associadas com mau prognóstico. OBJETIVO: Avaliar a relação da troponina T (cTnT) e suas faixas de valores com o prognóstico na IC descompensada. MÉTODOS: Estudaram-se 70 pacientes com piora da IC crônica que necessitaram de hospitalização. Na admissão, o modelo de Cox foi utilizado para avaliar as variáveis capazes de predizer o desfecho composto por morte ou re-hospitalização em razão de piora da IC durante um ano. RESULTADOS: Durante o seguimento, ocorreram 44 mortes, 36 re-hospitalizações por IC e 56 desfechos compostos. Na análise multivariada, os preditores de eventos clínicos foram: cTnT (cTnT > 0,100 ng/ml; hazard ratio (HR) 3,95 intervalo de confiança (IC) 95%: 1,64-9,49, p = 0,002), diâmetro diastólico final do ventrículo esquerdo (DDVE >70 mm; HR 1,92, IC95%: 1,06-3,47, p = 0,031) e sódio sérico (Na <135 mEq/l; HR 1,79, IC95%: 1,02-3,15, p = 0,044). Para avaliar a relação entre a elevação da cTnT e o prognóstico na IC descompensada, os pacientes foram estratificados em três grupos: cTnT-baixo (cTnT < 0,020 ng/ml, n = 22), cTnT-intermediário (cTnT > 0,020 e < 0,100 ng/ml, n = 36) e cTnT-alto (cTnT > 0,100 ng/ml, n = 12). As probabilidades de sobrevida e sobrevida livre de eventos foram: 54,2%, 31,5%, 16,7% (p = 0,020), e 36,4%, 11,5%, 8,3% (p = 0,005), respectivamente. CONCLUSÃO: A elevação da cTnT está associada com mau prognóstico na IC descompensada, e o grau dessa elevação pode facilitar a estratificação de risco.

Insuficiência cardíaca congestiva; prognóstico; troponina T; sódio

FUNDAMENTO: Las troponinas cardíacas son marcadores altamente sensibles y específicos de lesión miocárdica. Se las detectaron en la insuficiencia cardiaca (IC) y están asociadas con mal pronóstico. OBJETIVO: Evaluar la relación de la troponina T (cTnT) y sus franjas de valores con el pronóstico en la IC descompensada. MÉTODOS: Se estudiaron a 70 pacientes con empeoramiento de la IC crónica que necesitaron hospitalización. Al ingreso, se empleó el modelo de Cox para evaluar las variables capaces de predecir el desenlace conformado por muerte o rehospitalización en razón de empeoramiento de la IC durante un año. RESULTADOS: Durante el seguimiento, ocurrieron 44 muertes, 36 rehospitalizaciones por IC y 56 desenlaces compuestos. En el análisis multivariado, los predictores de eventos clínicos fueron: cTnT (cTnT > 0,100 ng/ml; hazard ratio (HR) 3,95 intervalo de confianza (IC) 95%: 1,64-9,49, p = 0,002), diámetro diastólico final del ventrículo izquierdo (DDVI >70 mm; HR 1,92, IC95%: 1,06-3,47, p = 0,031) y sodio sérico (Na <135 mEq/l; HR 1,79, IC95%: 1,02-3,15, p = 0,044). Para avaluar la relación entre la elevación de la cTnT y el pronóstico en la IC descompensada, se dividieron a los pacientes en tres grupos: cTnT-bajo (cTnT < 0,020 ng/ml, n = 22), cTnT-intermediario (cTnT > 0,020 y < 0,100 ng/ml, n = 36) y cTnT-alto (cTnT > 0,100 ng/ml, n = 12). Las probabilidades de sobrevida y sobrevida libre de eventos fueron: 54,2%, 31,5%, 16,7% (p = 0,020), y 36,4%, 11,5%, 8,3% (p = 0,005), respectivamente. CONCLUSÃO: La elevación de la cTnT está asociada con mal pronóstico en la IC descompensada, y el grado de esa elevación puede facilitar la estratificación de riesgo.

Insuficiencia cardiaca congestiva; pronóstico; troponina T; sodio

ORIGINAL ARTICLE

^IInstituto do Coração do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, SP - Brazil

^IIDepartamento de Epidemiologia da Faculdade de Saúde Pública da Universidade de São Paulo, São Paulo, SP - Brazil

Maling address

SUMMARY

BACKGROUND: The cardiac troponins are highly sensitive and specific markers of myocardial injury. They have been detected in heart failure (HF) and are associated with a bad prognosis.

OBJECTIVE: To evaluate the association of cardiac troponin T (cTnT) and its ranges with prognosis in decompensated HF.

METHODS: A total of 70 patients with chronic HF worsening that needed hospitalization were studied. Cox model was used to evaluate the variables at admission capable of predicting the combined outcome that consisted of death or re-hospitalization due to HF worsening during a 1-year follow-up.

RESULTS: During the follow-up, there were 44 deaths, 36 re-hospitalizations due to HF and 56 combined outcomes. At the multivariate analysis, the predictors of clinical events were the cTnT (cTnT >0.100 ng/mL; hazard ratio [HR] 3.95 95% confidence interval [CI]: 1.64-9.49, p = 0.002), left ventricular end diastolic diameter (LVDD >70 mm; HR 1.92, 95%CI: 1.06-3.47, p = 0.031) and serum sodium (Na <135 mEq/L; HR 1.79, 95%CI: 1.02-3.15, p = 0.044). To evaluate the association between the cTnT increase and the prognosis in decompensated HF, the patients were stratified in three groups: low-cTnT (cTnT <0.020 ng/ml, n = 22), intermediate-cTnT (cTnT >0.020 and <0.100 ng/ml, n = 36), and high-cTnT (cTnT >0.100 ng/ml, n = 12).The probabilities of survival and event-free survival were 54.2%, 31.5%, 16.7% (p = 0.020) and 36.4%, 11.5%, 8.3% (p = 0.005), respectively.

CONCLUSION: The increase in cTnT is associated with a bad prognosis in decompensated HF and the degree of this increase can help the risk stratification.

Key words: Heart failure, congestive; prognosis; troponin T; sodium.

Introduction

Heart failure (HF) represents an important public health problem in modern society, due to its increasing incidence and prevalence, low survival and economic overload caused by prolonged and repeated hospitalizations^1-3. Thus, the identification of patients with a worse prognosis is essential for the appropriate allocation of health resources, as well as the planning of new researches and therapeutic strategies to improve patient care and the outcome of this life-threatening and debilitating disease.

The cardiac troponins are highly sensitive and specific biomarkers of myocardial injury, which are broadly used for risk stratification in acute coronary syndromes⁴. The detection of troponins in patients with advanced HF by Missov et al⁵, has attracted the interest of physicians aiming at prognostic assessment.

Many prognostic indicators have been described in patients with compensated and decompensated HF^6-10, with several studies focusing on the association between an increase in troponin levels and the HF prognosis, which showed an association of troponin increase with worse clinical outcome^11-22.

Although the current guidelines for the treatment of decompensated HF recommend the routine assessment of troponins in this situation, there are no indications of how these markers should be interpreted regarding patient management²³. The use of troponins in the risk stratification for decompensated HF can help improve patient care by identifying those with a worse prognosis. Thus, the objective of this study was to evaluate the prognostic value of cTnT levels and the association between its ranges in a cohort of patients that had been hospitalized with chronic decompensated HF and the clinical outcomes after a one-year follow-up.

Methods

Studied population

The studied population consisted of 70 patients with HF that were prospectively admitted at the Emergency Department (ER) of Instituto do Coraçao - The Heart Institute (InCor) - HCFMUSP, Sao Paulo - SP, Brazil and needed to be hospitalized due to decompensated symptoms of HF and NYHA functional class, between January and September 1999. The study included 62 patients that had participated in a previously published study¹⁷.

The study methods had been previously published¹⁷; however, in summary, the patients with chronic decompensated HF were eligible for this study if they did not have a recent history of acute myocardial infarction, unstable angina or surgery in the previous 30 days. Patients with chronic renal disease, non-controlled arterial hypertension or active myocarditis were also excluded from the study. The patients included in the study had blood samples collected for laboratory assessment and measurement of serum cardiac troponin T (cTnT) and creatine-phosphokinase fraction -MB mass (CKMB-mass) levels. The levels of cTnT and CKMB-mass were analyzed at the end of the study, so that the patients would receive the conventional treatment for decompensated HF, while the physicians were blinded to the serum levels of these markers.

The present study is according to the principles stated in the Declaration of Helsinki. The study protocol was approved by the Ethics Committee in Research of InCor-HCFMUSP and all patients signed the informed consent form prior to the study participation.

Clinical outcome and patient follow-up

The primary outcome of the present study was a combined outcome, consisting of death or the need for re-hospitalization due to a new episode of HF decompensation during the 1-year follow-up (clinical event). The studied population was followed through contacts every three months to determine the vital status of the patients. The type of death was classified as death by pump failure, myocardial infarction or sudden death.

Analysis of cardiac troponin T and creatine phosphokinase Fraction-MB Levels

The blood samples for the measurement of cTnT and CK-MB levels were obtained at the hospital admission (median: 3 days; interquartiles: 2 to 4 days). cTnT was quantified by a third-generation immunoassay (Elecsys^® Troponin T STAT Immunoassay, Roche Diagnostics, Germany). The lower range of detection is 0.010 ng/mL, and cTnT levels that are below this detection threshold were considered as zero. The serum levels of CK-MB mass were analyzed through another immunoassay (Elecsys^® CK-MB STAT Immunoassay, Roche Diagnostics, Germany). This assay has a detection threshold of 0.1 ng/mL, with a reference range of 0 a 5.0 ng/mL.

Statistical analysis

The comparisons between the continuous variables were carried out by the Mann-Whitney U-test. The Chi-square test or Fisher's exact test were used to evaluate the categorical variables.

To estimate the probability of clinical events in relation to the ranges of cTnT increase during the 1-year follow-up period (primary outcome), the patients were retrospectively stratified in groups based on the cTnT levels. The low-cTnT group was defined based on the cutoff value below the level determined by the ROC (receiver operating characteristic) curve. The cTnT level >0.100 ng/mL was selected to define the high-cTnT group. The intermediate-cTnT group was defined as having cTnT levels above the cutoff and <0.100 ng/mL. The Kruskal-Wallis and the Chi-square tests were used to compare the characteristics among the three groups (low, intermediate and high). The survival and event-free survival probabilities, stratified for the cTnT groups, were estimated by the Kaplan-Meier method.

The analysis of univariate and multivariate regression for the primary outcome predictors were carried out by Cox Proportional Hazard method. The variables with p<0.200 at the univariate analysis were selected for the multivariate model. The final model was constructed with the stepwise-forward procedure and included only the variables with p<0.050. All the statistical analyses were carried out with the SPSS software and a p value < 0.050 was considered statistically significant.

Results

Basal characteristics and results

The basal characteristics of the studied population are shown in Table 1. The follow-up was complete in all patients with a median of 262 days (range: 3 to 393 days). During the follow-up period there were 44 (62.9%) deaths, 36 (51.4%) re-hospitalizations due to HF, 56 (80.0%) combined outcomes consisting of death or re-hospitalization (clinical event) and 2 (2.9%) heart transplants. Figure 1 shows the natural history of HF, in relation to the events analyzed during the follow-up. The patients that presented clinical events were more hypotensive, presented a more dilated left ventricle, lower levels of serum sodium, more frequently needed the administration of intravenous inotropic drugs (dobutamine) and had a tendency to present more elevated levels of cTnT.

Detection of cardiac troponin t and its prognostic role in decompensated chronic heart failure

Elevated levels of cTnT (>0.010 ng/mL) were detected in 58 patients (82.9%) with decompensated HF and 12 patients (17.1%) presented cTnT >0.100 ng/mL. The mean concentration of this marker was 0.062±0.089 ng/mL and Table 2 shows the mean concentration of cTnT and the range (minimum-maximum) according to the HF etiology. The area under the ROC curve was 0.66 and identified a cutoff for cTnT >0.020 ng/mL, for the prediction of clinical events (sensitivity = 0.76, specificity = 0.62). When the patients were stratified based on this cutoff, higher rates of clinical events and deaths were observed among patients with levels of cTnT >0.020 ng/mL (Figure 2).

To evaluate the association between the ranges of cTnT increase and their prognostic value, the studied population was retrospectively stratified in the groups based on the previously described cTnT levels. A progressive and significant decrease in survival and event-free survival (Figures 3 and 4) was observed with the increase in cTnT levels. The cumulative probabilities of survival and event-free survival in the low, intermediate and high-cTnT groups were, respectively: 54.2%, 31.5% and 16.7% (p = 0.020) and 36.4%, 11.5% and 8.3% (p = 0.005).

At the multivariate analysis (Table 3), the independent predictors for clinical events, considering only the patients' basal clinical and laboratory variables, were: elevated cTnT levels (cTnT >0.100 ng/mL; hazard ratio [HR] = 3.95, 95% confidence interval [CI] = 1.64 - 9.49; p = 0.002), increased left ventricular end-diastolic diameter (LVDD >70 mm; HR = 1.92, 95% CI= 1.06 - 3.47; p = 0.031) and low serum sodium levels (Na <135 mEq/L; HR = 1.79, 95%CI = 1.02 - 3.15; p = 0.044). When the need to use dobutamine was introduced in the multivariate analysis, the independent predictors for clinical events were dobutamine (HR = 2.33; 95%CI = 1.27 - 4.26; p = 0.006) and troponin T >0.100 ng/mL (HR = 3.07; 95%CI = 1.30 - 7.28; p = 0.001). We did not observe any difference in cTnT levels between patients that received and those that did not receive dobutamine during the hospitalization (0.062 ± 0.094 vs. 0.062 ± 0.084 ng/mL, p = 0.094). At the final analysis (Table 3), we considered only the clinical and laboratory variables at the patients' admission for the risk stratification.

The comparison of the clinical characteristics among the three groups of patients in relation to cTnT levels (Table 4) showed that the patients in the high-cTnT group had a tendency to present older mean age (p=0.071), more frequently presented the ischemic etiology (p=0.004), had a previous history of acute myocardial infarction (p=0.001) and presented lower estimated glomerular filtration rates (p=0.010).

Discussion

This study showed that the cTnT was detected in approximately 83% of the patients with decompensated chronic HF and was a long-term independent predictor for clinical events. It was also possible to demonstrate that the degree of cTnT elevation was useful in the one-year prognostic stratification of these patients in three risk groups, based on the cTnT levels: low (cTnT <0.020 ng/mL), intermediate (cTnT >0.020 ng/mL and <0.100 ng/mL) and high (cTnT >0.100 ng/mL).

The troponins are reliable markers that are broadly used to detect myocardial injury; additionally, several studies^11-22 have associated the presence of these markers with adverse outcomes in HF. In the present study, the minimal myocardial cell injury, detected through the cTnT release, was associated with a bad prognosis in HF. Additionally, it was possible to observe a progressive increase in death and clinical event risk with the increase in cTnT levels. This association had been previously reported for cardiac troponin I²².

Other authors have described different cutoffs to predict adverse events for troponins in HF, ranging from 0.02 to 0.1 ng/mL for troponin T^{11,13-15,18-21} and from 0.04 to 0.5 ng/mL for troponin I^12,16,22. Three studies^13,18,19 described the same cutoff observed in the present study.

The mechanism through which the troponins are released in HF is not completely understood; however, there are several factors that can explain the detection of these biomarkers in this clinical situation. The physiopathological process responsible for the destruction of the contractile apparatus in the HF progression to the terminal stage can be responsible for the release of troponins²⁴, as follows: ventricular remodeling, apoptosis, endothelial dysfunction, alterations in the coronary microcirculation, recurrent ischemia episodes or infarction.

Additionally, the increase in the pre-load and the decrease in the diastolic perfusion time, which are commonly observed in patients with decompensated HF, facilitate the degradation of troponin I and this finding can also probably be valid for cTnT. The stretching of cardiomyocytes through the pre-load increase and the activation of endogenous proteases leading to the degradation of troponin I seem to be related to the ischemia of the inner layers of the myocardial wall^25,26. We observed the presence of increased cTnT levels (>0.01 ng/mL) in 16 of the 19 patients with HF due to Chagasic etiology (84,2%), with 3 patients presenting cTnT levels >0.100 ng/mL. This increase can be the consequence of a chronic inflammatory process in Chagasic cardiopathy, leading to myocardial injury and resulting in troponin release.

Thus, the detection of troponins in HF seems to indicate the continuous destruction of cardiomyocytes, with the HF progression to its final stage, which consequently indicates a bad prognosis.

Elevated troponin levels were detected in patients with renal failure in the absence of acute myocardial ischemia. In spite of the uncertainties regarding the mechanisms of serum troponin increase in renal function decrease, the detection of these markers seems to reflect the myocardial necrosis²⁷. There is evidence to indicate that the renal function contributes to the elimination of cardiac troponins²⁸. However, in acute coronary syndromes, the cTnT levels were strong short-term prognostic predictors, even when the decrease in renal function was present²⁹. In the present study, the mechanisms of myocardial injury in decompensated HF associated with the decrease in the cTnT clearance due to renal dysfunction can explain the increased concentrations of this marker in the high-cTnT group.

The worst prognosis associated with the administration of dobutamine must be interpreted with care, as its use probably reflects more advanced disease and consequently, a bad prognosis, instead of a direct effect of this medication on the clinical results.

Study limitations

The sample size of this cohort was relatively small; however, due to the high rates of adverse clinical outcomes in this population with advanced disease, it was possible to demonstrate the association between cTnT levels and prognosis in these patients. Furthermore, this study only included patients with systolic dysfunction and therefore, the prognostic value of the cTnT in HF with preserved systolic function is unknown. Additionally, we did not analyze the serum levels of other prognostic markers in HF, such as the brain natriuretic peptide (BNP or NT-ProBNP), as these markers were not available in our country when the present study was carried out.

However, two studies^14,21 demonstrated that the combination of the levels of cTnT and BNP were capable of stratifying the prognosis of hospitalized patients with decompensated HF. A previous study³⁰ by our group showed that elevated levels of NT-proBNP were associated with a 3.6-fold higher risk of death within 90 days in patients with decompensated HF.

Another potential limitation of this study was that the coronary angiography was not routinely carried out in these patients. Thus, the undiagnosed coronary artery disease and the presence of micro-infarctions are possible explanations for the increase in cTnT levels. Indeed, the association between the HF of ischemic etiology and previous myocardial infarctions in patients from the high-cTnT group (Table 4) corroborates this hypothesis.

Clinical implications

The present study provides evidence confirming that increases in the cTnT levels are associated with lower survival and event-free survival rates in decompensated HF. Additionally, this study demonstrated that not only the cTnT increase, but also the degree of this marker increase allowed the stratification of the patients with decompensated HF in risk groups for adverse clinical outcomes.

At an age of frugality, the use of biochemical markers and other prognostic indicators for the identification of patients with HF and high risk of death or adverse events can optimize the allocation of resources and stimulate the development of cost-effective therapeutic strategies to improve the outcomes.

Having observed that troponin-T was detected in patients with Chagasic cardiopathy, we concluded that this marker could be used in the follow-up of these patients together with other biomarkers, such as BNP or NT-ProBNP. Additionally, in the patients with the undetermined form of Chagas' disease, the detection of troponins could indicate those at risk for the development of cardiopathy. However, these hypotheses need further studies to be confirmed.

The use of biomarkers of myocardial injury can help the physicians to perfect the clinical decision-making in individual decisions on therapeutic procedures for patients with decompensated HF. Until more data are available, patients with decompensated HF and increased cTnT levels must be submitted to an intensive evidence-based investigation of the HF.

Acknowledgements

We thank Roche Diagnostics for kindly providing the reagents and tools necessary to perform the cardiac troponin and CK-MB assays.

Potential Conflict of Interest

No potential conflict of interest relevant to this article was reported.

Sources of Funding

There were no external funding sources for this study.

Study Association

This article is part of the thesis of Doctoral submitted by Carlos Henrique Del Carlo, from Faculdade de Medicina da Universidade de São Paulo.

References

• 1. O'Connell JB, Bristow M. Economic impact of heart failure in the United States: time for a different approach. J Heart Lung Transplant. 1993; 13: S107-S112.
• 2. Berry C, Murdoch DR, McMurray JJV. Economics of chronic heart failure. Eur J Heart Failure. 2001; 3 (3): 283-91.
• 3. Rosamond W, Flegal K, Friday G, Furie K, Go A, Greenlund K, et al. Heart disease and stroke statistics-2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2007; 115 (5): e69-171.
• 4. Ohman EM, Armstrong PW, Christenson RH, Granger CB, Katus HA, Hamm CW, et al. Cardiac troponin T levels for risk stratification in acute myocardial ischemia. GUSTO IIA Investigators. N Engl J Med. 1996; 335 (18): 1333-41.
• 5. Missov E, Calzolari C, Pau B. Circulating cardiac troponin I in severe congestive heart failure. Circulation. 1997; 96 (9): 2953-8.
• 6. Eichhorn E. Prognosis determination in heart failure. Am J Med. 2001; 110 (Suppl 7A): 14S-36S.
• 7. Kearney MT, Fox KA, Lee AJ, Prescott RJ, Shah AM, Atin PD, et al. Predicting death due to progressive heart failure in patients with mild to moderate chronic heart failure. J Am Coll Cardiol. 2002; 40 (10): 1801-8.
• 8. Brophy JM, Dagenais GR, McSherry F, Williford W, Yusuf S. A multivariate model for predicting mortality in patients with heart failure and systolic dysfunction. Am J Med. 2004; 116 (5): 300-4.
• 9. Felker GM, Leimberger JD, Califf RM, Cuffe MS, Massie BM, Adams KF Jr, et al. Risk stratification after hospitalization for decompensated heart failure. J Card Fail. 2004; 10 (6): 460-6.
• 10. Fonarow GC, Adams KF, Abraham WT, Yancy CW, Boscardin WJ. Risk stratification for in-hospital mortality in acutely decompensated heart failure. JAMA. 2005; 293 (5): 572-80.
• 11. Setsuta K, Seino Y, Takahashi N, Ogawa T, Sasaki K, Harada A, et al. Clinical significance of elevated levels of cardiac troponin T in patients with chronic heart failure. Am Heart J. 1999; 84 (5): 608-11.
• 12. La Vecchia L, Mezzena G, Zanolla L, Paccanaro M, Varotto L, Bonanno C, et al. Cardiac troponin I as diagnostic and prognostic marker in severe heart failure. J Heart Lung Transplant. 2000; 19 (7): 644-52.
• 13. Sato Y, Yamada T, Taniguchi R, Nakai K, Makiyama T, Okada H, et al. Persistently increased serum concentrations of cardiac troponin T in patients with idiopathic dilated cardiomyopathy are predictive of adverse outcomes. Circulation. 2001; 103 (3): 369-74.
• 14. Ishii J, Nomura M, Nakamura Y, Naruse H, Mori Y, Ishikawa T, et al. Risk stratification using a combination of cardiac troponin T and brain natriuretic peptide in patients hospitalized for worsening chronic heart failure. Am J Cardiol. 2002; 89 (6): 691-5.
• 15. Perna ER, Macin SM, Parras JI, Pantich R, Farías EF, Badaracco JR, et al. Cardiac troponin T levels are associated with poor short- and long-term prognosis in patients with acute cardiogenic pulmonary edema. Am Heart J. 2002; 143 (5): 814-20.
• 16. Horwich T, Patel J, MacLellan WR, Fonarow GC. Cardiac troponin I is associated with impaired hemodynamics, progressive left ventricular dysfunction, and increased mortality rates in advanced heart failure. Circulation. 2003; 108 (7): 833-8.
• 17. Del Carlo CH, Pereira-Barretto AC, Strunz CC, Latorre MRDO, Ramires JAF. Serial measure of cardiac troponin T levels for prediction of clinical events in decompensated heart failure. J Card Fail. 2004; 10 (1): 43-8.
• 18. Hudson MP, O'Connor CM, Gattis WA, Tasissa G, Hasselblad V, Holleman CM, et al. Implications of elevated cardiac troponin T in ambulatory patients with heart failure: a prospective analysis. Am Heart J. 2004; 147 (3): 546-52.
• 19. Perna ER, Macin SM, Canella JP, Augier N, Stival JL, Cialzeta JR, et al. Ongoing myocardial injury in stable severe heart failure: value of cardiac troponin T monitoring for high-risk patient identification. Circulation. 2004;110 (16): 2376-82.
• 20. Perna ER, Macin SM, Cimbaro Canella JP, Alvarenga PM, Ríos NG, Pantich R, et al. Minor myocardial damage detected by troponin T is a powerful predictor of long-term prognosis in patients with acute decompensated heart failure. Int J Cardiol. 2005; 99 (2): 253-61.
• 21. Perna ER, Macin SM, Cimbaro Canella JP, Szyszko A, Franciosi V, Vargas Morales W, et al. Importance of early combined N-terminal pro-brain natriuretic peptide and cardiac troponin T measurements for long-term risk stratification of patients with decompensated heart failure. J Heart Lung Transplant. 2006; 25 (10): 1230-40.
• 22. You JJ, Austin PC, Alter DA, Ko DT, Tu JV. Relation between cardiac troponin I and mortality in acute decompensated heart failure. Am Heart J. 2007; 153 (4): 462-70.
• 23. Nieminen MS, Bohm M, Cowie MR, Drexler H, Filippatos GS, Jondeau G, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology. Eur Heart J. 2005; 26 (4): 384-416.
• 24. Del Carlo CH, O'Connor CM. Cardiac troponins in congestive heart failure. Am Heart J. 1999; 138 (4 Pt 1): 646-53.
• 25. Logeart D, Beyne P, Cusson C, Tokmakova M, Leban M, Guiti C, et al. Evidence of cardiac myolysis in severe nonischemic heart failure and the potential role of increased wall strain. Am Heart J. 2001; 141 (2): 247-53.
• 26. Feng J, Schaus BJ, Fallavollita JA, Lee TC, Canty JM Jr. Preload induces troponin I degradation independently of myocardial ischemia. Circulation. 2001; 103 (16): 2035-7.
• 27. Freda BJ, Tang WH, Van Lente F, Peacock WF, Francis GS. Cardiac troponins in renal insufficiency: review and clinical implications. J Am Coll Cardiol. 2002; 40 (12): 2065-71.
• 28. Ziebig R, Lun A, Hocher B, Priem F, Altermann C, Asmus G, et al. Renal elimination of troponin T and troponin I. Clin Chem. 2003; 49 (7): 1191-3.
• 29. Aviles RJ, Askari AT, Lindahl B, Wallentin L, Jia G, Ohman EM, et al. Troponin T levels in patients with acute coronary syndromes, with or without renal dysfunction. N Engl J Med. 2002; 346 (26): 2047-52.
• 30. Pereira-Barretto AC, de Oliveira Jr MT, Strunz CC, Del Carlo CH, Scipioni AR, Ramires JA. Serum NT-proBNP levels are a prognostic predictor in patients with advanced heart failure. Arq Bras Cardiol. 2006; 87 (2): 174-7.

Cardiac troponin T for risk stratification in decompensated chronic heart failure

Carlos Henrique Del Carlo^I; Antonio Carlos Pereira-Barretto^I; Célia Maria Cassaro-Strunz^I; Maria do Rosário Dias de Oliveira Latorre^II; Múcio Tavares de Oliveira Junior^I; José Antonio Franchini Ramires^I

Publication Dates

• Publication in this collection
  20 July 2009
• Date of issue
  May 2009

History

• Accepted
  01 Apr 2008
• Reviewed
  07 Mar 2008
• Received
  29 Jan 2008