Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study

Arlati, Sergio; Brenna, Sergio; Prencipe, L; Marocchi, Alessandro; Casella, Giampaolo; Lanzani, Marta; Gandini, C.

doi:10.1007/s001340050008

Cited by 197 publications

(128 citation statements)

References 30 publications

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“…21 Troponin level is reportedly higher in patients with sepsis and hypotension: 85% and 74%, respectively. 5,22 In our study the highest troponin levels were in the patients with cor pulmonale and COPD: 67% and 66%, respectively. In another study, elevated cardiac troponin was found in 70% of patients with COPD exacerbation.…”

Section: Discussionsupporting

confidence: 46%

C-Reactive Protein Alone or Combined With Cardiac Troponin T for Risk Stratification of Respiratory Intensive Care Unit Patients

Özsu¹,

Yılmaz

Yılmaz³

et al. 2011

Respir Care

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BACKGROUND: Mortality is high among patients admitted to intensive care units (ICUs). Several prognostic markers have been described in such patients, but the literature contains no data comparing C-reactive protein (CRP) and cardiac troponin T (cTn-T), nor of a combination of CRP and cTn-T in the same patient group in the ICU. METHODS: This was a retrospective electronic data review of patients who presented to the emergency department for respiratory reasons between December 2007 and December 2009 and in whom CRP and cTn-T levels were measured. Patients with a diagnosis of pulmonary embolism and acute coronary syndrome were excluded. We recorded demographics, chronic diseases, admission diagnosis, Simplified Acute Physiology Score II (SAPS II), ICU stay, and CRP and cTn-T concentrations. RESULTS: We included the records of 158 patients. Mean ICU stay was 9.9 days (range 1-65 d), and mean hospital stay was 14.1 days (range 1-72 d). For predicting mortality, receiver operating characteristic analysis gave a CRP cutoff value of > 10 mg/dL, and a CTn-T cutoff value of > 0.01 ng/mL. For CRP the mortality area under the curve was 0.691 (95% CI 0.608 -0.775), the sensitivity was 65%, and the specificity was 70%. For cTn-T the mortality area under the curve was 0.733 (95% CI 0.655-0.812), the sensitivity was 78%, and the specificity was 56%. Of the patients who died, 65% had CRP > 10 mg/dL and 78% had cTn-T > 0.01 ng/mL. On multivariable regression analysis, CRP > 10 mg/dL was associated with 6.6-fold higher (95% CI 1.7-21.3) ICU mortality. There was no advantage for models that combined CRP and cTn-T. CRP alone was more valuable in predicting ICU mortality than in combination with troponin or SAPS II. CONCLUSIONS: Elevated CRP is an independent early prognostic marker of mortality risk in ICU patients. We suspect that a CRP-based prognosis strategy may be useful.

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Section: Discussionsupporting

confidence: 46%

C-Reactive Protein Alone or Combined With Cardiac Troponin T for Risk Stratification of Respiratory Intensive Care Unit Patients

Özsu¹,

Yılmaz

Yılmaz³

et al. 2011

Respir Care

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“…It was found that the duration of hypotension during sepsis (Arlati et al, 2000) and the vasopressors administered had been found to correlate with the plasma concentration of cTnI, a regulatory protein of the thin actin filament of cardiac muscle (Bertichant et al, 1999). cTnI is a well known diagnostic marker for myocardial injury following congestive heart failure and myocardial infarction (Turner et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Distinct cardiodynamic and molecular characteristics during early and late stages of sepsis-induced myocardial dysfunction

Chopra

Sharma

2007

Life Sciences

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We hypothesized that progressive decline in myocardial performance would correlate with upregulation of markers for apoptotic mechanisms following increased duration of polymicrobial sepsis in the rat. Male Sprague-Dawley rats (350-400 g) were randomized into sham, 1-, 3-and 7-day sepsis groups. Each septic rat received 200 mg/kg cecal inoculum intraperitoneally (i.p). The post-mortem analysis showed a severely inflamed peritoneum with the presence of pus in all septic animals that was directly proportional to the duration of sepsis. We observed 10, 33 and 42% mortality in the 1-, 3-and 7-day sepsis groups, respectively. Septic animals at 3 and 7 days exhibited an increased wet lung/total body weight and heart weight/total body weight. A significant increase in total cardiac troponin I (cTnI) and C Reactive Protein (CRP) and endothelin-1 (ET-1) was also observed with an increased duration of sepsis. Myocardial ET-1 concentration in the 7-day postsepsis group was significantly elevated compared to the sham and 1-day post-sepsis groups. Sepsis also produced a significant decrease in the mean arterial pressure in the 7-day post-sepsis group and tachycardia in the 1-, 3-, and 7-day post-sepsis groups compared to the sham group. A significant prolongation of the left ventricular isovolumic relaxation rate constant, tau, and left ventricular enddiastolic pressure in the 1-, 3-and 7-day post-sepsis groups compared to the sham group was observed. In addition, a significant decrease in the rates of left ventricular relaxation (−dP/dt) and contraction (+dP/dt) in the 3-and 7-day post-sepsis groups compared to the sham and 1-day postsepsis group was observed. Sepsis produced a significant upregulation in the expression of myocardial TRADD, cytosolic active caspase-3, the Bax/Bcl 2 ratio, and the mitochondrial release of cytochrome C in the 3-and 7-day post-sepsis groups. We observed a progressive increase in the number of TUNEL positive nuclei, cytosolic caspase-3 activation and co-localization of PARP in the nuclei at 1, 3 and 7 days post-sepsis. These data suggest that the progression of sepsis from 1 day to 3-7 days produce distinct cardiodynamic characteristics with a more profound effect during later stages. The sepsis-induced decline in myocardial performance correlates with the induction of myocardial apoptosis.

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“…Both AKI and myocardial dysfunction are also common in sepsis. [70][71][72] Data have found that 30-80% of septic patients have elevated cardiac-specific troponins [73][74][75] Hepato-Renal syndrome…”

Section: Secondary Cardio-renal Syndromes (Type 5 Crs)mentioning

confidence: 99%

Review article: Acute kidney injury in critical illness

Bagshaw

Bellomo

Devarajan

et al. 2010

Can J Anesth/J Can Anesth

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Purpose This review provides a focused and comprehensive update on emerging evidence related to acute kidney injury (AKI).Principal findings Acute kidney injury is a significant clinical problem that increasingly complicates the course of hospitalization and portends worse clinical outcome for sick hospitalized patients. The recent introduction of consensus criteria for the diagnosis of AKI (i.e., RIFLE/AKIN classification) have greatly improved our capacity not only to standardize the diagnosis and classification of severity of AKI, but also to facilitate conducting comparative epidemiologic studies in an effort to better understand the burden of adult and pediatric AKI and its syndromes (i.e., septic, cardio-renal, hepato-renal). The characterization of several novel AKI-specific biomarkers (i.e., neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, and interleukin-18) is extending our understanding of the pathophysiology of AKI. Moreover, these biomarkers appear to have clinical relevance for early detection and they provide prognostic value. These innovations are aiding in the design of epidemiologic surveys and randomized trials of therapeutic interventions. Strategies for prevention Editor's Note: This article is the first of two linked special review articles published in this issue of the Journal. The concept of these articles emerged from the scientific content of the 2010 Acute Kidney Injury (AKI) and Renal Support in Critical Illness Symposium, hosted in Edmonton, Alberta. This review (Part 1) provides a focused and comprehensive update on emerging evidence in the diagnosis and classification of AKI, on specific AKI syndromes, and on the prevention and conservative management of hospitalized patients with AKI. Abstracts presented at this meeting were selected on the basis of peer review by the Scientific Committee and were accepted for presentation at the AKI 2010 Symposium, and appear as Electronic Supplementary Material at

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Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study

Abstract: Hypotension may cause cardiac damage in critically ill patients with acute non-cardiac diseases as shown by abnormal levels of cTnI. It is likely that a high number of these myocardial necroses may go unnoticed on the ECG.

Cited by 197 publications

References 30 publications

C-Reactive Protein Alone or Combined With Cardiac Troponin T for Risk Stratification of Respiratory Intensive Care Unit Patients

C-Reactive Protein Alone or Combined With Cardiac Troponin T for Risk Stratification of Respiratory Intensive Care Unit Patients

Distinct cardiodynamic and molecular characteristics during early and late stages of sepsis-induced myocardial dysfunction

Review article: Acute kidney injury in critical illness

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