Elevated troponin i levels but not low grade chronic inflammation is associated with cardiac-specific mortality in stable hemodialysis patients

Ahsan Alam, Andrea Palumbo, I. Mucsi, Paul E. Barré, Allan D. Sniderman

Research output: Article

9 Citations (Scopus)

Abstract

Background: Elevated cardiac troponin I (TnI) levels are associated with all-cause mortality in stable hemodialysis patients. Their relationship to cardiac-specific death has been inconsistent, and the reason for their elevation is not well understood. We hypothesized that elevated TnI levels in chronic stable hemodialysis patients more specifically track with cardiac mortality, and this mechanism is independent of other contributors of cardiac mortality, such as inflammation. Methods. We conducted a single-centre, cohort study of prevalent hemodialysis patients at a tertiary care hospital. Plasma TnI levels were measured with routine monthly blood tests in clinically stable patients for two consecutive months. Plasma TnI was measured by immunoassay and a value above the laboratory reference range (0.06 μg/L) was considered elevated. The primary outcome of death was adjudicated separately for this study, and classified as cardiac, non-cardiac, or unknown. Cox proportional hazard models were used to examine the association of TnI with the all-cause and cardiac-specific mortality, adjusting for potential confounders, including C-reactive protein (CRP) as a marker of inflammation. Results: Of 133 patients followed for a median of 1.7 years, there were 38 deaths (58% non-cardiac, 39% cardiac, 3% unknown). Elevated TnI was associated with adjusted HR for all-cause mortality of 2.57 (95% CI 1.30-5.09) and an adjusted HR for cardiac death of 3.14 (95% CI 1.07-9.2), after accounting for age, time on dialysis, diabetes status, prior coronary artery disease history, and C-reactive protein. Although CRP was also independently associated with all-cause mortality, it did not add prognostic information to TnI for cardiac-specific death. Conclusion: Elevated TnI levels are independently associated with cardiac and all-cause mortality in asymptomatic hemodialysis patients. The mechanism for this risk is likely independent of inflammation, but may reflect chronic subclinical myocardial injury or unmask those with subclinical atherosclerotic heart disease. Whether those with elevated TnI levels may benefit from additional investigations or more aggressive therapies to treat cardiovascular disease remains to be determined.

Original languageEnglish
Article number247
JournalBMC Nephrology
Volume14
Issue number1
DOIs
Publication statusPublished - nov. 9 2013

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Troponin
Troponin I
Renal Dialysis
Inflammation
Mortality
C-Reactive Protein
Hematologic Tests
Tertiary Healthcare
Immunoassay
Proportional Hazards Models
Tertiary Care Centers
Coronary Artery Disease
Dialysis
Heart Diseases
Reference Values
Cohort Studies
Cardiovascular Diseases
Wounds and Injuries

ASJC Scopus subject areas

  • Nephrology

Cite this

Elevated troponin i levels but not low grade chronic inflammation is associated with cardiac-specific mortality in stable hemodialysis patients. / Alam, Ahsan; Palumbo, Andrea; Mucsi, I.; Barré, Paul E.; Sniderman, Allan D.

In: BMC Nephrology, Vol. 14, No. 1, 247, 09.11.2013.

Research output: Article

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abstract = "Background: Elevated cardiac troponin I (TnI) levels are associated with all-cause mortality in stable hemodialysis patients. Their relationship to cardiac-specific death has been inconsistent, and the reason for their elevation is not well understood. We hypothesized that elevated TnI levels in chronic stable hemodialysis patients more specifically track with cardiac mortality, and this mechanism is independent of other contributors of cardiac mortality, such as inflammation. Methods. We conducted a single-centre, cohort study of prevalent hemodialysis patients at a tertiary care hospital. Plasma TnI levels were measured with routine monthly blood tests in clinically stable patients for two consecutive months. Plasma TnI was measured by immunoassay and a value above the laboratory reference range (0.06 μg/L) was considered elevated. The primary outcome of death was adjudicated separately for this study, and classified as cardiac, non-cardiac, or unknown. Cox proportional hazard models were used to examine the association of TnI with the all-cause and cardiac-specific mortality, adjusting for potential confounders, including C-reactive protein (CRP) as a marker of inflammation. Results: Of 133 patients followed for a median of 1.7 years, there were 38 deaths (58{\%} non-cardiac, 39{\%} cardiac, 3{\%} unknown). Elevated TnI was associated with adjusted HR for all-cause mortality of 2.57 (95{\%} CI 1.30-5.09) and an adjusted HR for cardiac death of 3.14 (95{\%} CI 1.07-9.2), after accounting for age, time on dialysis, diabetes status, prior coronary artery disease history, and C-reactive protein. Although CRP was also independently associated with all-cause mortality, it did not add prognostic information to TnI for cardiac-specific death. Conclusion: Elevated TnI levels are independently associated with cardiac and all-cause mortality in asymptomatic hemodialysis patients. The mechanism for this risk is likely independent of inflammation, but may reflect chronic subclinical myocardial injury or unmask those with subclinical atherosclerotic heart disease. Whether those with elevated TnI levels may benefit from additional investigations or more aggressive therapies to treat cardiovascular disease remains to be determined.",
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AU - Barré, Paul E.

AU - Sniderman, Allan D.

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N2 - Background: Elevated cardiac troponin I (TnI) levels are associated with all-cause mortality in stable hemodialysis patients. Their relationship to cardiac-specific death has been inconsistent, and the reason for their elevation is not well understood. We hypothesized that elevated TnI levels in chronic stable hemodialysis patients more specifically track with cardiac mortality, and this mechanism is independent of other contributors of cardiac mortality, such as inflammation. Methods. We conducted a single-centre, cohort study of prevalent hemodialysis patients at a tertiary care hospital. Plasma TnI levels were measured with routine monthly blood tests in clinically stable patients for two consecutive months. Plasma TnI was measured by immunoassay and a value above the laboratory reference range (0.06 μg/L) was considered elevated. The primary outcome of death was adjudicated separately for this study, and classified as cardiac, non-cardiac, or unknown. Cox proportional hazard models were used to examine the association of TnI with the all-cause and cardiac-specific mortality, adjusting for potential confounders, including C-reactive protein (CRP) as a marker of inflammation. Results: Of 133 patients followed for a median of 1.7 years, there were 38 deaths (58% non-cardiac, 39% cardiac, 3% unknown). Elevated TnI was associated with adjusted HR for all-cause mortality of 2.57 (95% CI 1.30-5.09) and an adjusted HR for cardiac death of 3.14 (95% CI 1.07-9.2), after accounting for age, time on dialysis, diabetes status, prior coronary artery disease history, and C-reactive protein. Although CRP was also independently associated with all-cause mortality, it did not add prognostic information to TnI for cardiac-specific death. Conclusion: Elevated TnI levels are independently associated with cardiac and all-cause mortality in asymptomatic hemodialysis patients. The mechanism for this risk is likely independent of inflammation, but may reflect chronic subclinical myocardial injury or unmask those with subclinical atherosclerotic heart disease. Whether those with elevated TnI levels may benefit from additional investigations or more aggressive therapies to treat cardiovascular disease remains to be determined.

AB - Background: Elevated cardiac troponin I (TnI) levels are associated with all-cause mortality in stable hemodialysis patients. Their relationship to cardiac-specific death has been inconsistent, and the reason for their elevation is not well understood. We hypothesized that elevated TnI levels in chronic stable hemodialysis patients more specifically track with cardiac mortality, and this mechanism is independent of other contributors of cardiac mortality, such as inflammation. Methods. We conducted a single-centre, cohort study of prevalent hemodialysis patients at a tertiary care hospital. Plasma TnI levels were measured with routine monthly blood tests in clinically stable patients for two consecutive months. Plasma TnI was measured by immunoassay and a value above the laboratory reference range (0.06 μg/L) was considered elevated. The primary outcome of death was adjudicated separately for this study, and classified as cardiac, non-cardiac, or unknown. Cox proportional hazard models were used to examine the association of TnI with the all-cause and cardiac-specific mortality, adjusting for potential confounders, including C-reactive protein (CRP) as a marker of inflammation. Results: Of 133 patients followed for a median of 1.7 years, there were 38 deaths (58% non-cardiac, 39% cardiac, 3% unknown). Elevated TnI was associated with adjusted HR for all-cause mortality of 2.57 (95% CI 1.30-5.09) and an adjusted HR for cardiac death of 3.14 (95% CI 1.07-9.2), after accounting for age, time on dialysis, diabetes status, prior coronary artery disease history, and C-reactive protein. Although CRP was also independently associated with all-cause mortality, it did not add prognostic information to TnI for cardiac-specific death. Conclusion: Elevated TnI levels are independently associated with cardiac and all-cause mortality in asymptomatic hemodialysis patients. The mechanism for this risk is likely independent of inflammation, but may reflect chronic subclinical myocardial injury or unmask those with subclinical atherosclerotic heart disease. Whether those with elevated TnI levels may benefit from additional investigations or more aggressive therapies to treat cardiovascular disease remains to be determined.

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