Renal Function and Scaled Troponin in Patients Presenting to the Emergency Department with Symptoms of Myocardial Infarction

2017 ◽  
Vol 45 (4) ◽  
pp. 304-309 ◽  
Author(s):  
Anupama Vasudevan ◽  
Adam J. Singer ◽  
Christopher DeFilippi ◽  
Gary Headden ◽  
Jeffrey M. Schussler ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Emergency Department ◽  
Renal Dysfunction ◽  
Myocardial Injury ◽  
Estimated Glomerular Filtration Rate ◽  
Elevated Troponin ◽  
Disease Epidemiology ◽  
Acute Myocardial Injury ◽  
Multicenter Prospective Study ◽  
Cardiac Troponins

Background: Cardiac troponins are often found to be elevated in patients with renal dysfunction, even in the absence of acute myocardial injury. The objective of this report was to characterize the scaled troponin values and proportion of adjudicated acute myocardial infarction (AMI) among patients with and without renal dysfunction. Methods: The data was from a multicenter prospective study including patients presenting to the emergency department with symptoms of AMI. Troponin measurements were standardized across various assays by calculating the observed results as multiples of the assay-specific 99th percentile upper limit of normal. Patients with an estimated glomerular filtration rate (eGFR; calculated by the Chronic Kidney Disease Epidemiology Collaboration formula) <60 mL/min/1.73 m2 were considered to have renal dysfunction. Results: Of 430 included patients, 249 (58%) were male and 181 (42%) were female, with a mean age of 55.9 ± 12.3 and 57.3 ± 12.8 years, respectively. Eighty-seven (20.2%) had renal dysfunction. The proportions of patients with at least one scaled troponin value above the 99th percentile cut-off point among patients with and without renal dysfunction were 40 (45.9%) and 81 (23.6%) respectively (p < 0.001). The proportions of patients with an adjudicated diagnosis of AMI among those with and without renal dysfunction were 20.7 and 18.7%, respectively (p = 0.67). Using scaled troponins, by the second test there was >5X and by the third test >15X separation in the excursion of troponin among those with AMI compared to those without. Conclusions: One or more elevated troponin values are common in those with renal dysfunction. Scaled troponins for eGFR groups were similar, indicating that the use of this interpretative technique is applicable in discerning AMI for those with and without renal dysfunction.

scholarly journals Copeptin Testing in Acute Myocardial Infarction: Ready for Routine Use?

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Sebastian Johannes Reinstadler ◽  
Gert Klug ◽  
Hans-Josef Feistritzer ◽  
Bernhard Metzler ◽  
Johannes Mair
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Risk Stratification ◽  
Myocardial Injury ◽  
Early Stage ◽  
Additional Information ◽  
Acute Myocardial Injury ◽  
Coronary Syndromes ◽  
Suspected Acute Myocardial Infarction ◽  
Cardiac Troponins

Suspected acute myocardial infarction is one of the leading causes of admission to emergency departments. In the last decade, biomarkers revolutionized the management of patients with suspected acute coronary syndromes. Besides their pivotal assistance in timely diagnosis, biomarkers provide additional information for risk stratification. Cardiac troponins I and T are the most sensitive and specific markers of acute myocardial injury. Nonetheless, in order to overcome the remaining limitations of these markers, novel candidate biomarkers sensitive to early stage of disease are being extensively investigated. Among them, copeptin, a stable peptide derived from the precursor of vasopressin, emerged as a promising biomarker for the evaluation of suspected acute myocardial infarction. In this review, we summarize the currently available evidence for the usefulness of copeptin in the diagnosis and risk stratification of patients with suspected acute myocardial infarction in comparison with routine biomarkers.

Troponin least significant change (z-score) is associated with poor clinical outcomes in patients presenting to the emergency department

2021 ◽  
pp. 000456322199281
Author(s):  
Joel D Smith ◽  
Kai'En Leong ◽  
Timothy Fazio ◽  
Cherie Chiang
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Emergency Department ◽  
Length Of Stay ◽  
Clinical Outcomes ◽  
Myocardial Injury ◽  
Significant Rise ◽  
Z Score ◽  
Troponin Elevation ◽  
Acute Myocardial Injury

Background A rise and/or fall in high sensitivity cardiac troponin (hs-Tn) is critical in defining acute myocardial injury and therefore the diagnosis of acute myocardial infarction. A significant rise in hs-Tn is not well defined in current guidelines. Calculation of a z-score for two consecutive hs-Tn measurements is a method-independent measure of dynamic troponin elevation. However, the association of hs-Tn z-score with outcomes for unselected emergency department admissions is unknown. Moreover, the association of non-dynamic troponin elevations, as defined by a normal z-score, with clinical outcomes remains to be assessed. Methods We retrospectively calculated z-scores for patients presenting to emergency department over 18 months who had serial troponin measurements with at least one result >99th percentile using the Abbott hs-TnI assay. We assessed the association of z-score with discharge diagnosis, cardiac interventions, inpatient mortality, length of stay and readmission rates. Results There were 2062 presentations for 1830 patients where a z-score was calculated. Z-score was elevated in 1080 presentations. Dynamic troponin elevation (z-score ≥ 2) was associated with acute myocardial infarction (OR = 9.1, P < 0.01), admission to an inpatient unit (95 vs. 88%, P < 0.01), increased inpatient length of stay (97 vs. 65 days, P < 0.01), inpatient coronary intervention (21 vs. 6%, P < 0.01) and mortality (4.4 vs. 2.4%, P < 0.05) compared with myocardial injury with a static troponin elevation. Conclusions Z-score is an assay-independent tool to alert clinicians of significant, dynamic troponin elevation and acute myocardial injury. It is associated with poorer clinical outcomes.

scholarly journals Acute myocardial injury after administration of intravenous epinephrine for allergic reaction

2020 ◽  
Vol 8 ◽  
pp. 2050313X2093310 ◽  
Author(s):  
Katerina Zakka ◽  
Sneha Gadi ◽  
Nikoloz Koshlelashvili ◽  
Noble M Maleque
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Emergency Department ◽  
Coronary Artery ◽  
Myocardial Ischemia ◽  
Intravenous Administration ◽  
Myocardial Injury ◽  
T Wave ◽  
Acute Myocardial Injury ◽  
Artery Disease

Myocardial injury or infarction in the setting of anaphylaxis can be due to anaphylaxis itself, known as Kounis syndrome, or as a result of treatment with epinephrine. Myocardial ischemia caused by therapeutic doses of epinephrine in the setting of anaphylaxis is a rare event attributed to coronary artery vasospasm. A 41-year-old female with past medical history of recurrent costochondritis, chronic thrombocytopenia, and nonspecific palindromic rheumatism presented to the emergency department with perioral numbness, flushing and throat tightness after a meal containing fish and almonds. Intramuscular epinephrine was ordered but inadvertently administered intravenously, after which she developed sharp, substernal chest pain and palpitations. Electrocardiogram showed normal sinus rhythm with QT interval prolongation. Troponin peaked at 1.41 ng/mL. She was given 324 mg of aspirin in the emergency department. Transthoracic echocardiogram showed normal ejection fraction with lateral wall motion abnormality. We present a case of a patient with no significant risk factors for coronary artery disease who developed myocardial injury following inadvertent IV administration of a therapeutic dose of epinephrine for an anaphylactic-like reaction. The development of myocardial injury after epinephrine is rare, with only six reported cases in literature and just one after intravenous administration. This is the first described case of known myocardial injury without ST-T wave changes on electrocardiogram . The proposed mechanism is an alpha-1 receptor-mediated coronary vascular spasm resulting in myocardial ischemia. The aim of this case is to raise awareness of the potential for acute myocardial injury after inadvertent intravenous administration of epinephrine for anaphylaxis, even in patients with no known risk factors for coronary artery disease, as well as to demonstrate that this clinical scenario can present regardless of troponin elevation and without ST-T wave ECG changes.

scholarly journals Adverse Cardiovascular Effects of Anti-COVID-19 Drugs

2021 ◽  
Vol 12 ◽  
Author(s):  
Dongling Liu ◽  
Xiang Zeng ◽  
Zufeng Ding ◽  
Fenghua Lv ◽  
Jawahar L. Mehta ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Adverse Effects ◽  
Myocardial Injury ◽  
Cardiovascular Effects ◽  
Cardiovascular Complications ◽  
Therapeutic Interventions ◽  
Risk Of Death ◽  
Cardiovascular Comorbidities ◽  
Global Pandemic ◽  
Acute Myocardial Injury

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or COVID-19 infection is the cause of the ongoing global pandemic. Mortality from COVID-19 infection is particularly high in patients with cardiovascular diseases. In addition, COVID-19 patients with preexisting cardiovascular comorbidities have a higher risk of death. Main cardiovascular complications of COVID-19 are myocardial infarction, myocarditis, acute myocardial injury, arrhythmias, heart failure, stroke, and venous thromboembolism. Therapeutic interventions in terms of drugs for COVID-19 have many cardiac adverse effects. Here, we review the relative therapeutic efficacy and adverse effects of anti-COVID-19 drugs.

scholarly journals Acute myocardial damage in new coronavirus infection (COVID-19)

2021 ◽  
Vol 20 (5) ◽  
pp. 98-104
Author(s):  
N. V. Izmozherova ◽  
A. A. Popov ◽  
A. I. Tsvetkov ◽  
M. A. Shambatov ◽  
I. P. Antropova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Medical Care ◽  
Myocardial Injury ◽  
Troponin I ◽  
Myocardial Damage ◽  
True Incidence ◽  
Wide Range ◽  
Acute Myocardial Injury ◽  
Coronavirus Infection

Introduction. Acute respiratory distress syndrome (ARDS) and cardiovascular events, acute myocardial injury being the most frequent of the latter, are among the leading causes of death in COVID-19 patients. The lack of consensus on acute myocardial injury pathogenesis mechanisms, the patients management, treatment an rehabilitation logistics, the anticoagulant treatment in identified SARS-CoV-2 or suspected COVID-19 patients setting indicates the need to assess, analyze and summarize the available data on the issue.Materials and methods. Scientific publications search was carried out in PubMed, Google Scholar databases for the period from December 2019 to September 2021.Results and Discussion. Cardiospecific troponin I increase beyond reference limits is reported to occur in at least every tenth patient with identified SARS-CoV-2, the elevated troponin detection rate increasing among persons with moderate to severe course of the infection. The mechanisms of acute myocardial injury in patients with COVID-19 are poorly understood. By September 2021, there are several pathogenesis theories. A high frequency viral myocarditis direct cardiomyocytes damage is explained by the high SARS-CoV-2 affinity to ACE2 expressed in the myocardium. The cytokine storm related myocardial damage is reported a multiple organ failure consequence. Coagulopathy may also trigger myocardial microvessels damage. Up to every third death of SARS-CoV-2 infected persons is related to the acute myocardial injury. At the same time, due to the high incidence of the acute myocardial injury, it is rather difficult to assess the true incidence of acute myocardial infarction in patients with COVID-19. In the pandemic setting, the waiting time for medical care increases, the population, trying to reduce social contacts, is less likely to seek medical help. In this regard, in order to provide effective medical care to patients with acute myocardial infarction, it is necessary to develop algorithms for providing care adapted to the current epidemiological situation.Conclusion. The treatment of patients with probable development of acute myocardial damage against the background of new coronavirus infection should be performed in accordance with the current clinical guidelines. Anticoagulant therapy should be administered in a prophylactic dose under control of hemostasis parameters and a wide range of biochemical parameters.

Myocardial Perfusion Studies - Direct Imaging of Acute Myocardial Injury with 99mTc-Pyrophosphate

1978 ◽  
Vol 17 (04) ◽  
pp. 157-160
Author(s):  
J. W. Keyes
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Myocardial Perfusion ◽  
Myocardial Injury ◽  
Myocardial Tissue ◽  
Direct Imaging ◽  
Perfusion Studies ◽  
Acute Myocardial Injury ◽  
Myocardial Perfusion Studies

Imaging of acute myocardial injury is possible with a large number of agents. All of these agents share similar patterns of uptake in acutely injured myocardial tissue. The technique appears to be a reliable way of ruling in or out the diagnosis of acute myocardial infarction.

Abstract 17471: Outcome of Acute Myocardial Injury in COVID-19 Patients

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Magdi Zordok ◽  
Muhammad Etiwy ◽  
Shruti Hegde ◽  
Michael Maysky
Keyword(s):  
Myocardial Injury ◽  
Average Length ◽  
Invasive Mechanical Ventilation ◽  
Morbidity And Mortality ◽  
Hospital Death ◽  
Chronic Obstructive ◽  
High Morbidity ◽  
Elevated Troponin ◽  
Obstructive Sleep ◽  
Acute Myocardial Injury

Background: Acute myocardial injury has been reported in approximately 20% of patients with Coronavirus disease 2019 (COVID-19). Little is known about the outcome of this subset of patients. We are testing the hypothesis of higher morbidity and mortality in patients with COVID-19 who have acute myocardial injury. Methods: In this retrospective study, we analyzed data from patients admitted to Steward Healthcare hospitals in Massachusetts between March 22 and April 24, who tested positive for COVID-19 confirmed by serology and found to have elevated troponin levels (>0.01). The sociodemographic information, clinical data, and outcomes of these critically ill patients were retrospectively extracted from the medical records. The primary outcome was in-hospital death. Data were analyzed using JMP statistical analysis software. Results: Two hundred eighty-three COVID-19 positive patients were found to have troponin levels >0.01 on admission. Of these 183 patients (64.6%) were males, 49.1% were Caucasian and 32.1% were African Americans. The mean age of the patients was 70.7 ± 13.8. The prevalence of comorbid conditions was as follows: hypertension, 69.7%; hyperlipidemia, 46.9%; diabetes mellitus, 42.6%; chronic kidney disease, 28.3%; heart failure, 19.3%; atrial fibrillation, 22.1%; coronary artery disease, 17.1%; cerebrovascular accident, 10.2%; obesity, 38%; chronic obstructive pulmonary disease or asthma 20.8%, obstructive sleep apnea, 4.9%. One hundred thirty-seven patients (48.4%) noted to have acute kidney injury on presentation,128 (45.2%) required ICU level of care, 41% required invasive mechanical ventilation for a mean of 10.4 ± 7.9 days, and 38.8% required vasopressors. The average length of stay (LOS) in the medical intensive care unit and the hospital was 11.5 ± 8.3 days and 11.4 ± 9.5 days respectively. The overall in-hospital mortality rate was 45.6%. Conclusion: Patients with COVID-19 and elevated Troponin levels had high morbidity and mortality

Abstract 14077: Use of Cardiac Troponin I to Identify Acute Myocardial Infarction in Patients With Impaired Renal Function

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Beatrice von Jeinsen ◽  
Stergios Tzikas ◽  
Lars Palapies ◽  
Tanja Zeller ◽  
Christoph Bickel ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Renal Function ◽  
Impaired Renal Function ◽  
Estimated Glomerular Filtration Rate ◽  
Troponin I ◽  
Reference Population ◽  
Final Diagnosis ◽  
The Difference ◽  
Cardiac Troponins

Introduction: Cardiac troponins are the gold standard to diagnose acute myocardial infarction (AMI). Troponin I (TnI) levels are known to be increased in patients with chronic kidney disease (CKD) irrespective of an AMI. The established diagnostic TnI cut-off to detect AMI is calculated based on a healthy reference population and might not be representative for CKD patients. Hypothesis: The aim of this study was to investigate TnI levels in patients with and without CKD with suspected AMI and to calculate CKD- optimized diagnostic TnI thresholds. Methods: Of 1572 patients enrolled with suspected AMI, 266 patients showed an impaired renal function with estimated glomerular filtration rate (eGFR) of less then 60ml/min and were classified as patients with CKD. N=77 (34%) of patients with CKD and n=278 (24%) without CKD had the final diagnosis AMI. TnI was measured on admission and after 3h. Based on receiver operator characterics curve analyses (AUROC) of the baseline levels CKD optimized TnI threshold were derived. Sensitivity and specifity were calculated for the 99th percentile cut-off (30.0 pg/mL), the optimized cut-off (58.0 pg/mL) and the change in TnI concentration within 3h after admission. Results: Patients with CKD had higher TnI levels then patients without CKD (6.0pg/mL vs. 20.9pg/ml; p<0.001). This difference was more pronounced in patients without AMI (median 9.1 vs. 4.4; p<0.001), whereas the difference diminished in AMI patients (median 337.4 vs. 238.6; p=0.83). In CKD patients TnI remained a strong marker to detect AMI with AUROC of 0.933 compared to 0.969 in patients without CKD. Applying the 99th percentile threshold it was associated with a relevant loss of specificity in CKD patients with 80% compared to 96% in patients without CKD. This poor specificity could be regained by use of a higher CKD-optimized threshold or use of the change in TnI concentration within 3h leading to specificities of 90% and 96%, respectively. Conclusions: Patients presenting with suspected AMI and CKD have higher TnI levels on admission compared to patients without CKD leading to a low specificity detecting AMI in CKD patients. Using an CKD-optimized TnI cut-off level on admission or using the change in TnI concentration within 3h is able to regain this lost specificity.

scholarly journals Diagnostic Implications of an Elevated Troponin in the Emergency Department

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Maame Yaa Yiadom ◽  
Petr Jarolim ◽  
Cathy Jenkins ◽  
Stacy E. F. Melanson ◽  
Michael Conrad ◽  
...  
Keyword(s):  
Emergency Department ◽  
Differential Diagnosis ◽  
Medical Records ◽  
Screening Test ◽  
Myocardial Injury ◽  
Troponin I ◽  
Type I ◽  
Elevated Troponin ◽  
Hospital Medical ◽  
Ed Visits

Objective. To determine the proportion of initial troponin (cTn) elevations associated with Type I MI versus other cardiovascular and noncardiovascular diagnoses in an emergency department (ED) and whether or not a relationship exists between the cTn level and the likelihood of Type I MI.Background. In the ED, cTn is used as a screening test for myocardial injury. However, the differential diagnosis for an initial positive cTn result is not clear.Methods. Hospital medical records were retrospectively reviewed for visits associated with an initial positive troponin I-ultra (cTnI), ≥0.05 μg/L. Elevated cTnI levels were stratified into low (0.05–0.09), medium (0.1–0.99), or high (≥1.0). Discharge diagnoses were classified into 3 diagnostic groups (Type I MI, other cardiovascular, or noncardiovascular).Results. Of 23,731 ED visits, 4,928 (21%) had cTnI testing. Of those tested, 16.3% had initial cTnI ≥0.05. Among those with elevated cTn, 11% were classified as Type I MI, 34% had other cardiovascular diagnoses, and 55% had a noncardiovascular diagnosis. Type I MI was more common with high cTnI levels (41% incidence) than among subjects with medium (9%) or low (6%).Conclusion. A positive cTn is most likely a noncardiovascular diagnosis, but Type I MI is far more common with cTnI levels ≥1.0.

scholarly journals Treatment With Cardiovascular Medications: Prognosis in Patients With Myocardial Injury

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Erik Kadesjö ◽  
Andreas Roos ◽  
Anwar J. Siddiqui ◽  
Ulrik Sartipy ◽  
Martin J. Holzmann
Keyword(s):  
Myocardial Infarction ◽  
Emergency Department ◽  
Myocardial Injury ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
University Hospital ◽  
Angiotensin Ii Receptor ◽  
Converting Enzyme Inhibitors ◽  
Risk Of Death ◽  
Cardiovascular Medications

Background There is no clinical guidance on treatment in patients with non‐ischemic myocardial injury and type 2 myocardial infarction (T2MI). Methods and Results In a cohort of 22 589 patients in the emergency department at Karolinska University Hospital in Sweden during 2011 to 2014 we identified 3853 patients who were categorized into either type 1 myocardial infarction, T2MI, non‐ischemic acute and chronic myocardial injury. Data from all dispensed prescriptions within 180 days of the visit to the emergency department were obtained concerning β‐blockers, angiotensin‐converting enzyme inhibitors/angiotensin II receptor blockers, statins, and platelet inhibitors. We estimated adjusted hazard ratios (HR) with 95% CI for all‐cause mortality in relationship to the number of medications (categorized into 0–1 [referent], 2–3 and 4 medications) in the groups of myocardial injury. In patients with T2MI, treatment with 2 to 3 and 4 medications was associated with a 50% and 56% lower mortality, respectively (adjusted HR [95% CI], 0.50 [0.25–1.01], and 0.43 [0.19–0.96]), while corresponding associations in patients with acute myocardial injury were 24% and 29%, respectively (adjusted HR [95% CI], 0.76 [0.59–0.99] and 0.71 [0.5–1.02]), and in patients with chronic myocardial injury 27% and 37%, respectively (adjusted HR [95% CI], 0.73 [0.58–0.92] and 0.63 [0.46–0.87]). Conclusions Patients with T2MI and non‐ischemic acute or chronic myocardial injury are infrequently prescribed common cardiovascular medications compared with patients with type 1 myocardial infarction. However, treatment with guideline recommended drugs in patients with T2MI and acute or chronic myocardial injury is associated with a lower risk of death after adjustment for confounders.

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