Myocardial injury in critically ill patients with community-acquired pneumonia

AbstractBackgroundMyocardial injury, as reflected by elevated cardiac troponin levels in plasma, is common in patients with community-acquired pneumonia (CAP), but its temporal dynamics and etiology remain unknown. Our aim was to determine the incidence of troponin release in patients with CAP and identify risk factors which may point to underlying etiologic mechanisms.MethodsWe included consecutive patients admitted with severe CAP to two intensive care units in the Netherlands between 2011 and 2015. High-sensitivity cardiac troponin I was measured daily during the first week. We used multivariable linear regression to identify variables associated with troponin release on admission, and mixed-effects regression to model the daily rise and fall of troponin levels over time.ResultsAmong 200 eligible patients, 179 were included, yielding 792 observation days. A total of 152 (85%) patients developed raised troponin levels >26 ng/L. Baseline factors independently associated with troponin release included coronary artery disease (160% increase, 95% CI 7–529), smoking (304% increase, 95% CI 59-924), and higher APACHE IV score (2% increase, 95% CI 0.7-3.3), whereasStaphylococcus aureusas a causative pathogen was protective (67% reduction, 95% CI 9-88). Time-dependent risk factors independently associated with daily increase in troponin concentrations included reduced platelet count (1.7% increase, 95% CI 0.1-3.4), tachycardia (1.6% increase, 95% CI 0.3-3), hypotension (5.1% increase, 95% CI 1-9.4) and dobutamine use (38.4% increase 95% CI 8.8-76).ConclusionsCardiac injury develops in a majority of patients with severe CAP. Myocardial oxygen supply-demand mismatch and activated coagulation are potential causes of this injury.

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Myocardial Injury and the Release of Troponins I and T in the Blood of Patients

Clinical Chemistry ◽

10.1093/clinchem/hvaa281 ◽

2020 ◽

Author(s):

Ivan A Katrukha ◽

Alexey G Katrukha

Keyword(s):

Cardiac Disease ◽

Cardiac Troponin ◽

Myocardial Injury ◽

Clinical Evidence ◽

Troponin I ◽

High Sensitivity ◽

Clinical Settings ◽

Diagnostic Systems ◽

Troponin Release

Abstract Background Cardiac troponin I (cTnI) and cTnT are the established biomarkers of cardiomyocyte damage and the recommended biomarkers for the diagnosis of acute myocardial infarction (MI). High-sensitivity immunochemical diagnostic systems are able to measure the cTn concentrations in the blood of a majority of healthy people. At the same time, the concentration of cTn may be increased not only after MI but also because of other pathologies that might affect myocardium. This effect reduces the clinical specificity of cTn for MI and may complicate the diagnosis. Content This review summarizes the existing information regarding the causes and mechanisms that lead to the increase of cTn concentration in blood and the forms of cTn that are present in circulation after MI or other types of myocardial injury. Summary Different etiologies of disease associated with increases of cTn above the 99th percentile and various mechanisms of troponin release from myocardium could result in the appearance of different forms of cTn in blood and provide the first clinical evidence of injury. Additional research is needed for the careful characterization of cTn forms that are present in the blood in different clinical settings. That knowledge may lead to the development of immunochemical systems that would differentiate certain forms of troponins and possibly certain types of cardiac disease.

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High-sensitivity cardiac troponin I and T methods for the early detection of myocardial injury in patients on chemotherapy

Clinical Chemistry and Laboratory Medicine (CCLM) ◽

10.1515/cclm-2020-0362 ◽

2020 ◽

Vol 0 (0) ◽

Cited By ~ 1

Author(s):

Aldo Clerico ◽

Daniela Maria Cardinale ◽

Martina Zaninotto ◽

Nadia Aspromonte ◽

Maria Teresa Sandri ◽

...

Keyword(s):

Early Detection ◽

Cardiac Troponin ◽

Myocardial Injury ◽

Troponin I ◽

Cardiac Injury ◽

Cost Benefit ◽

High Sensitivity ◽

High Price ◽

Cost Benefit Ratio ◽

The Cost

AbstractImportant advances achieved in pharmacological cancer treatment have led progressively to a reduction in mortality from many forms of cancer, and increasing numbers of previously incurable patients can now hope to become cancer-free. Yet, to achieve these improved outcomes a high price has been paid in terms of untoward side effects associated with treatment, cardio-toxicity in particular. Several recent studies have reported that cardiac troponin assay using high-sensitivity methods (hs-cTn) can enable the early detection of myocardial injury related to chemotherapy or abuse of drugs that are potentially cardiotoxic. Several authors have recently suggested that changes in hs-cTn values enable the early diagnosis of cardiac injury from chemotherapy, thus potentially benefitting cancer patients with increased troponin values by initiating early cardioprotective therapy. However, large randomised clinical trials are needed in order to evaluate the cost/benefit ratio of standardised protocols for the early detection of cardiotoxicity using the hs-cTn assay in patients treated with chemotherapy.

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Myocardial injury is associated with in-hospital mortality of confirmed or suspected COVID-19 in Wuhan, China: A single center retrospective cohort study

10.1101/2020.03.21.20040121 ◽

2020 ◽

Cited By ~ 13

Author(s):

Fan Zhang ◽

Deyan Yang ◽

Jing Li ◽

Peng Gao ◽

Taibo Chen ◽

...

Keyword(s):

Risk Factors ◽

Hospital Mortality ◽

Cardiac Troponin ◽

Troponin I ◽

Cox Regression ◽

Cardiac Injury ◽

High Sensitivity ◽

Hospital Death ◽

Cox Regression Analysis ◽

D Dimer

AbstractBackgroundSince December 2019, a cluster of coronavirus disease 2019 (COVID-19) occurred in Wuhan, Hubei Province, China and spread rapidly from China to other countries. In-hospital mortality are high in severe cases and cardiac injury characterized by elevated cardiac troponin are common among them. The mechanism of cardiac injury and the relationship between cardiac injury and in-hospital mortality remained unclear. Studies focused on cardiac injury in COVID-19 patients are scarce.ObjectivesTo investigate the association between cardiac injury and in-hospital mortality of patients with confirmed or suspected COVID-19.MethodsDemographic, clinical, treatment, and laboratory data of consecutive confirmed or suspected COVID-19 patients admitted in Wuhan No.1 Hospital from 25th December, 2019 to 15th February, 2020 were extracted from electronic medical records and were retrospectively reviewed and analyzed. Univariate and multivariate Cox regression analysis were used to explore the risk factors associated with in-hospital death.ResultsA total of 110 patients with confirmed (n=80) or suspected (n=30) COVID-19 were screened and 48 patients (female 31.3%, mean age 70.58±13.38 year old) among them with high-sensitivity cardiac troponin I (hs-cTnI) test within 48 hours after admission were included, of whom 17 (17/48, 35.4%) died in hospital while 31 (31/48, 64.6%) were discharged or transferred to other hospital. High-sensitivity cardiac troponin I was elevated in 13 (13/48, 27.1%) patents. Multivariate Cox regression analysis showed pulse oximetry of oxygen saturation (SpO2) on admission (HR 0.704, 95% CI 0.546-0.909, per 1% decrease, p=0.007), elevated hs-cTnI (HR 10.902, 95% 1.279-92.927, p=0.029) and elevated d-dimer (HR 1.103, 95%CI 1.034-1.176, per 1mg/L increase, p=0.003) on admission were independently associated with in-hospital mortality.ConclusionsCardiac injury defined by hs-cTnI elevation and elevated d-dimer on admission were risk factors for in-hospital death, while higher SpO2 could be seen as a protective factor, which could help clinicians to identify patients with adverse outcome at the early stage of COVID-19.

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Misclassification of Myocardial Injury by a High-Sensitivity Cardiac Troponin I Assay

Canadian Journal of Cardiology ◽

10.1016/j.cjca.2021.01.004 ◽

2021 ◽

Cited By ~ 1

Author(s):

Peter A. Kavsak ◽

Shawn Mondoux ◽

Andrew Worster ◽

Janet Martin ◽

Vikas Tandon ◽

...

Keyword(s):

Cardiac Troponin ◽

Myocardial Injury ◽

Troponin I ◽

High Sensitivity ◽

Cardiac Troponin I

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Abstract 19710: Causes for Increased Cardiac Troponin I Using Gender-Specific 99th Percentiles From a High Sensitivity Assay in a US Population

Circulation ◽

10.1161/circ.130.suppl_2.19710 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Yader Sandoval ◽

Stephen W Smith ◽

Karen M Schulz ◽

MaryAnn M Murakami ◽

Fred S Apple

Keyword(s):

Myocardial Ischemia ◽

Cardiac Troponin ◽

Myocardial Injury ◽

Troponin I ◽

Plaque Rupture ◽

High Sensitivity ◽

The United States ◽

Universal Definition ◽

Definition Of ◽

Gender Specific

Introduction: High-sensitivity cardiac troponin (hs-cTn) assays have not yet been FDA cleared for clinical use in the United States (US). Pending expected approval of hs-cTn assays, which will use gender-specific cutoffs (GSC), it is relevant to recognize the causes of cTn increases using hs-cTnI assays in a US population. Our purpose was to describe the frequency of distinct etiologies of hs-cTnI assay increases using GSC. Methods: Retrospective study of 310 patients with serial hs-cTnI (Abbott ARCHITECT, 99th percentiles: F:16 ng/L; M:34 ng/L) measurements. Patients with an increased hs-cTnI were adjudicated into categories according to the 3rd Universal Definition of MI. Categories included, A: primary myocardial ischemia (i.e. plaque rupture); B: injury secondary to supply/demand imbalance; C: injury not related to myocardial ischemia (i.e. cardiac contusion, ablation, shock, surgery); D: multifactorial or indeterminate myocardial injury (i.e. heart failure, critically ill, pulmonary HTN, sepsis, stroke, renal failure, pulmonary embolism); E: Unknown. Results: 127 (41%) had an increased hs-cTnI above the GSC 99th percentile, whereas 183 (59%) had a normal hs-cTnI. The most common causes of hs-cTnI increases were: a) multifactorial or indeterminate injury - 43% among all patients and 52% in males, and b) supply/demand imbalance - 39% in women (Table). Injury related to primary myocardial ischemia was present in 10% (n=13). Females had more injury related to supply/demand ischemia than males (39% vs. 18%, p=0.01), whereas males had more multifactorial or indeterminate injury (52% vs. 33%, p=0.05). Conclusions: Most increased hs-cTnI values were explained by non-plaque rupture conditions. Males tended to have hs-cTnI increases due to multifactorial/indeterminate causes, whereas in women supply/demand imbalance was the most common etiology. Investigations are needed to better understand if etiologies of myocardial injury have gender differences.

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Markers of Myocardial Stress, Myocardial Injury, and Subclinical Inflammation and the Risk of Sudden Death

Circulation ◽

10.1161/circulationaha.120.046947 ◽

2020 ◽

Vol 142 (12) ◽

pp. 1148-1158

Author(s):

Brendan M. Everett ◽

M.V. Moorthy ◽

Jani T. Tikkanen ◽

Nancy R. Cook ◽

Christine M. Albert

Keyword(s):

Cardiovascular Disease ◽

High Density Lipoprotein ◽

Cardiac Troponin ◽

Myocardial Injury ◽

Troponin I ◽

Density Lipoprotein ◽

High Sensitivity ◽

C Reactive Protein ◽

Cholesterol Ratio ◽

Reactive Protein

Background: The majority of sudden cardiac deaths (SCDs) occur in low-risk populations often as the first manifestation of cardiovascular disease (CVD). Biomarkers are screening tools that may identify subclinical cardiovascular disease and those at elevated risk for SCD. We aimed to determine whether the total to high-density lipoprotein cholesterol ratio, high-sensitivity cardiac troponin I, NT-proBNP (N-terminal pro-B-type natriuretic peptide), or high-sensitivity C-reactive protein individually or in combination could identify individuals at higher SCD risk in large, free-living populations with and without cardiovascular disease. Methods: We performed a nested case-control study within 6 prospective cohort studies using 565 SCD cases matched to 1090 controls (1:2) by age, sex, ethnicity, smoking status, and presence of cardiovascular disease. Results: The median study follow-up time until SCD was 11.3 years. When examined as quartiles or continuous variables in conditional logistic regression models, each of the biomarkers was significantly and independently associated with SCD risk after mutually controlling for cardiac risk factors and other biomarkers. The mutually adjusted odds ratios for the top compared with the bottom quartile were 1.90 (95% CI, 1.30–2.76) for total to high-density lipoprotein cholesterol ratio, 2.59 (95% CI, 1.76–3.83) for high-sensitivity cardiac troponin I, 1.65 (95% CI, 1.12–2.44) for NT-proBNP, and 1.65 (95% CI, 1.13–2.41) for high-sensitivity C-reactive protein. A biomarker score that awarded 1 point when the concentration of any of those 4 biomarkers was in the top quartile (score range, 0–4) was strongly associated with SCD, with an adjusted odds ratio of 1.56 (95% CI, 1.37–1.77) per 1-unit increase in the score. Conclusions: Widely available measures of lipids, subclinical myocardial injury, myocardial strain, and vascular inflammation show significant independent associations with SCD risk in apparently low-risk populations. In combination, these measures may have utility to identify individuals at risk for SCD.

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