Automated electrocardiographic scores to estimate myocardial injury size during the course of acute myocardial infarction

1999 ◽  
Vol 83 (6) ◽  
pp. 949-952 ◽  
Author(s):  
Pekka Porela ◽  
Matti Luotolahti ◽  
Hans Helenius ◽  
Kari Pulkki ◽  
Liisa-Maria Voipio-Pulkki
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Myocardial Injury

scholarly journals Pattern of serum cardiac troponin-I in symptomatic acute myocardial infarction patients in national institute of cardiovascular disease in Bangladesh

2014 ◽  
Vol 42 (1) ◽  
pp. 3-6
Author(s):  
SS Shahina ◽  
JU Ahmed ◽  
S Ahmed ◽  
E Shahriar ◽  
MN Uddin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Acute Myocardial Infarction ◽  
Myocardial Injury ◽  
Troponin I ◽  
Clinical Symptoms ◽  
Cardiac Injury ◽  
Circadian Variation ◽  
Assay Method ◽  
Ctni Level

Troponin I (cTnI) isoform is cardiac muscle specific protein and shown to have several features as a preferred marker of myocardial injury. It rises early in acute myocardial infarction (AMI) and attains levels that are clearly separated from baseline values. It remains elevated for several days providing a long window for detection of cardiac injury. The objective of the study was to evaluate for the profile of cTnI level among symptomatic AMI patients. The study was conducted at National Institute of Cardiovascular Disease, Dhaka, Bangladesh from July 2007 to June 2008 and total 9552 patients with type 1 or type 2 MI were included. Blood Sample was taken within 3 days of symptoms and cTnI was measured by chemiluminescent immunometric assay method. cTnI was considered positive when the value was >1ng/ml and study population was divided as per age, sex and cTnI level. The mean (+ SD) age of all patients was 55(+ 12.8) years and majority was males (82.20%). Seasonal variation showed highest positive cases in winter. In case of circadian variation positive cTnI results were suggestive of morning peak of AMI. Positive results were obtained in 32.3% of Cases. cTnI is now considered as a better indicator of myocardial injury. Further study in depth is necessary to correlate with clinical symptoms and other diagnostic tests to make a complete profile of AMI according to the latest subtypes. DOI: http://dx.doi.org/10.3329/bmj.v42i1.18969 Bangladesh Med J. 2013 Jan; 42 (1): 3-6

Biochemical Markers of Myocardial Injury Test Turnaround Time: A College of American Pathologists Q-Probes Study of 7020 Troponin and 4368 Creatine Kinase–MB Determinations in 159 Institutions

2004 ◽  
Vol 128 (2) ◽  
pp. 158-164 ◽  
Author(s):  
David A. Novis ◽  
Bruce A. Jones ◽  
Jane C. Dale ◽  
Molly K. Walsh
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Biochemical Markers ◽  
Myocardial Injury ◽  
Turnaround Time ◽  
Test Results ◽  
Cardiac Marker ◽  
Laboratory Personnel ◽  
Creatine Kinase Mb

Abstract Context.—Rapid diagnosis of acute myocardial infarction in patients presenting to emergency departments (EDs) with chest pain may determine the types, and predict the outcomes of, the therapy those patients receive. The amount of time consumed in establishing diagnoses of acute myocardial infarction may depend in part on that consumed in the generation of the blood test results measuring myocardial injury. Objective.—To determine the normative rates of turnaround time (TAT) for biochemical markers of myocardial injury and to examine hospital and laboratory practices associated with faster TATs. Design.—Laboratory personnel in institutions enrolled in the College of American Pathologists Q-Probes Program measured the order-to-report TATs for serum creatine kinase–MB and/or serum troponin (I or T) for patients presenting to their hospital EDs with symptoms of acute myocardial infarction. Laboratory personnel also completed detailed questionnaires characterizing their laboratories' and hospitals' practices related to testing for biochemical markers of myocardial injury. ED physicians completed questionnaires indicating their satisfaction with testing for biochemical markers of myocardial injury in their hospitals. Setting.—A total of 159 hospitals, predominantly located in the United States, participating in the College of American Pathologists Q-Probes Program. Results.—Most (82%) laboratory participants indicated that they believed a reasonable order-to-report TATs for biochemical markers of myocardial injury to be 60 minutes or less. Most (75%) of the 1352 ED physicians who completed satisfaction questionnaires believed that the results of tests measuring myocardial injury should be reported back to them in 45 minutes or less, measured from the time that they ordered those tests. Participants submitted TAT data for 7020 troponin and 4368 creatine kinase–MB determinations. On average, they reported 90% of myocardial injury marker results in slightly more than 90 minutes measured from the time that those tests were ordered. Among the fastest performing 25% of participants (75th percentile and above), median order-to-report troponin and creatine kinase–MB TATs were equal to 50 and 48.3 minutes or less, respectively. Shorter troponin TATs were associated with performing cardiac marker studies in EDs or other peripheral laboratories compared to (1) performing tests in central hospital laboratories, and (2) having cardiac marker specimens obtained by laboratory rather than by nonlaboratory personnel. Conclusion.—The TAT expectations of the ED physicians using the results of laboratory tests measuring myocardial injury exceed those of the laboratory personnel providing the results of those tests. The actual TATs of myocardial injury testing meet the expectations of neither the providers of those tests nor the users of those test results. Improving TAT performance will require that the providers and users of laboratory services work together to develop standards that meet the needs of the medical staff and that are reasonably achievable by laboratory personnel.

scholarly journals Thrombolytic treatment in acute myocardial infarction: neutrophil activation, peripheral leucocyte responses, and myocardial injury.

Heart ◽  
1991 ◽  
Vol 66 (1) ◽  
pp. 10-14 ◽  
Author(s):  
K Ranjadayalan ◽  
V Umachandran ◽  
S W Davies ◽  
D Syndercombe-Court ◽  
C N Gutteridge ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Myocardial Injury ◽  
Neutrophil Activation ◽  
Thrombolytic Treatment

Neutrophil activation precedes myocardial injury in patients with acute myocardial infarction

2009 ◽  
Vol 47 (1) ◽  
pp. 79-83 ◽  
Author(s):  
Britta U. Goldmann ◽  
Volker Rudolph ◽  
Tanja K. Rudolph ◽  
Ann-Katrin Holle ◽  
Matthias Hillebrandt ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Myocardial Injury ◽  
Neutrophil Activation

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.

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