Do High‐sensitivity Troponin and Natriuretic Peptide Predict Death or Serious Cardiac Outcomes After Syncope?

Clark, Carol L.; Gibson, Thomas; Weiss, Robert E.; Yagapen, Annick N.; Malveau, Susan; Adler, David; Bastani, Aveh; Baugh, Christopher W.; Caterino, Jeffrey M.; Diercks, Deborah B.; Hollander, Judd E.; Nicks, Bret A.; Nishijima, Daniel K.; Shah, Manish N.; Stiffler, Kirk A.; Storrow, Alan B.; Wilber, Scott T.; Sun, Benjamin

doi:10.1111/acem.13709

Cited by 16 publications

(6 citation statements)

References 38 publications

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“…Diagnostic imaging (such as computer tomography angiography or echocardiography) and laboratory tests (such as routine blood hematology, biochemistry) have low diagnostic yield and should not be routinely used for syncope assessment. Cardiac damage biomarkers such as troponin and brain natriuretic peptide (BNP) have proven valuable in emergency presentations offering help to busy emergency physicians to select those patients requiring hospitalization (Clark et al, 2019;du Fay de Lavallaz et al, 2019). Some still frequently employed testing should now be considered inappropriate due to lack of diagnostic yield in syncope patients, notably EEG and brain imaging.…”

Section: Why and How To Identify High-risk Syncope?mentioning

confidence: 99%

Risk stratification of syncope: Current syncope guidelines and beyond

Sutton

Ricci

Fedorowski

2022

Autonomic Neuroscience

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Syncope is an alarming event carrying the possibility of serious outcomes, including sudden cardiac death (SCD). Therefore, immediate risk stratification should be applied whenever syncope occurs, especially in the Emergency Department, where most dramatic presentations occur. It has long been known that short-and long-term syncope prognosis is affected not only by its mechanism but also by presence of concomitant conditions, especially cardiovascular disease. Over the last two decades, several syncope prediction tools have been developed to refine patient stratification and triage patients who need expert in-hospital care from those who may receive nonurgent expert care in the community. However, despite promising results, prognostic tools for syncope remain challenging and often poorly effective.Current European Society of Cardiology syncope guidelines recommend an initial syncope workup based on detailed patient's history, physical examination supine and standing blood pressure, resting ECG, and laboratory tests, including cardiac biomarkers, where appropriate. Subsequent risk stratification based on screening of features aims to identify three groups: high-, intermediate-and low-risk. The first should immediately be hospitalized and appropriately investigated; intermediate group, with recurrent or medium-risk events, requires systematic evaluation by syncope experts; low-risk group, sporadic reflex syncope, merits education about its benign nature, and discharge. Thus, initial syncope risk stratification is crucial as it determines how and by whom syncope patients are managed. This review summarizes the crucial elements of syncope risk stratification, pros and cons of proposed risk evaluation scores, major challenges in initial syncope management, and how risk stratification impacts management of high-risk/recurrent syncope.

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Section: Why and How To Identify High-risk Syncope?mentioning

confidence: 99%

Risk stratification of syncope: Current syncope guidelines and beyond

Sutton

Ricci

Fedorowski

2022

Autonomic Neuroscience

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“…[9,10] However, with the introduction of highly sensitive troponin kits, studies conducted in recent years have found a relationship between high-sensitivity troponin and syncope in terms of detecting poor outcomes in the patient group. [11–14] In our study, the cutoff value for hs-cTnT determination was determined as 7.3. Compared to previous studies, a higher diagnostic value of troponin was observed.…”

Section: Discussionmentioning

confidence: 99%

Diagnostic accuracy of high sensitivity troponin and association of electrocardiogram findings for mortality in syncope patients: A retrospective cohort study

Tatliparmak¹,

Yilmaz

2023

Medicine

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High-sensitivity cardiac troponin-T (hs-cTnT) and electrocardiogram (ECG) are commonly ordered in daily practice in emergency medicine but their value on long term mortality in syncope patients is unclear. Our aim is to determine the diagnostic accuracy of hs-cTnT and association of ECG findings for 1-year mortality in patients presenting with syncope. In this retrospective cohort study, we included patients presenting with syncope to the emergency department (ED) between May 2020 and May 2021. Patient demographics, vital parameters on admission, ECG findings, hs-cTnT level at admission and 1-year mortality status were recorded. The study included 417 patients (62.4% women) with a mean age of 41.51 (standard deviation [SD] 17.1), 21 of whom were deceased within 1 year after syncope attack (5%). Patients with an abnormal QTc, T-Axis or frontal QRS-T angle had significantly higher 1-year mortality (OR: 9.26, 95% CI: 1. OR: 5.82, 4.94, respectively). The hs-cTnT level was 21.92 pg/mL (95% CI: 3.35-40.51 pg/mL) higher in the mortality group (P = .023). An abnormal QTc, T-Axis and frontal QRS-T angle are associated with a higher 1-year mortality rate and hs-cTnT has good diagnostic accuracy in detecting 1-year mortality for patients presenting with syncope.

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“…Toxic inhaled gases such as halogens and carbon monoxide may cause cardiac hypertrophy on one hand and inhalation of other gases such as nitric oxide and hydrogen may help reverse hypertrophy caused by other agents/mechanisms 39,40 . Persistent increase in troponin and NT-proBNP is a great prognostic value for predicting serious cardiac outcomes in patients 41,42 . These key circulating heart-specific biomarkers (brain natriuretic protein, BNP and troponin) were elevated at both 14 and 28 days.…”

Section: Discussionmentioning

confidence: 99%

Chronic cardiac structural damage, diastolic and systolic dysfunction following acute myocardial injury due to bromine exposure in rats

et al. 2020

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Background: Highly reactive halogens such as bromine are more commonly utilized, leading to an increase in quantities that are stocked and transported, therefore increasing the risk of accidental or deliberate exposure. Here we describe progression and potential mechanisms of adverse effects of a single injurious insult on the heart caused by bromine inhalation. Our studies have shown that bromine inhalation causes acute myocardial ischemia-reperfusion-like injury mediated by cytosolic calcium overload and increased calpain activity due to inactivation of SERCA. However, the progression of this injury in survivors is unknown. Our working hypothesis is that the initial injury causes irreversible damage that leads to chronic left ventricular systolic and diastolic dysfunction.Methods: Sprague Dawley rats received bromine exposure of 600 ppm for 45' and the survivors were sacrificed at 14 or 28 days, with matching naïve groups at each time point. Echocardiography, hemodynamic analysis, histology, electron microscopy and biochemical analysis of cardiac tissue were performed to assess functional, structural and molecular effects.Results: At 14 and 28 days, hemodynamic and echocardiographic analysis revealed increases in RV and LV end-diastolic pressure and LV end-diastolic wall stress with increased LV fibrosis at 28 days. TEM images demonstrated myofibrillar loss, cytoskeletal breakdown and mitochondrial damage at both time points. The myofibrillar damage and increased LV wall stress was reflected by increases in cTnI and NT-proBNP at both time points. LV shortening decreased as a function of increasing LV end-systolic wall stress and was accompanied by increased SERCA modification and a striking dephosphorylation of phospholamban with a significant increase in protein phosphatase 1. There was an increased 4-hydroxynonenal content in the myocardium at 28 days suggesting increased oxidative stress. Conclusions:These results indicate that the initial insult of bromine inhalation initiates a continuous process with chronic myocardial damage and subsequent LV systolic and diastolic dysfunction and that oxidative stress and phospholamban dephosphorylation play a central role.

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Do High‐sensitivity Troponin and Natriuretic Peptide Predict Death or Serious Cardiac Outcomes After Syncope?

Cited by 16 publications

References 38 publications

Risk stratification of syncope: Current syncope guidelines and beyond

Risk stratification of syncope: Current syncope guidelines and beyond

Diagnostic accuracy of high sensitivity troponin and association of electrocardiogram findings for mortality in syncope patients: A retrospective cohort study

Chronic cardiac structural damage, diastolic and systolic dysfunction following acute myocardial injury due to bromine exposure in rats

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