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

Author(s):  
N. V. Izmozherova ◽  
A. A. Popov ◽  
A. I. Tsvetkov ◽  
M. A. Shambatov ◽  
I. P. Antropova ◽  
...  

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.

2021 ◽  
Vol 99 (5-6) ◽  
pp. 369-374
Author(s):  
V. N. Ardashev ◽  
A. V. Nagovitsyn ◽  
N. V. Zakaryan ◽  
O. P. Donetskaya ◽  
G. E. Kubenskiy ◽  
...  

New facts suggest that COVID-19 coronavirus infection is partly mediated by hypercoagulability reactions characterized by micro- and macrovascular thrombotic angiopathy, which leads to acute myocardial injury, myocarditis, arrhythmias and numerous cases of pulmonary thromboembolic disease . The article presents a clinical observation of acute myocardial infarction development as a result of early thrombosis of an implanted coronary stent in a patient diagnosed with a new coronavirus infection COVID-19.


2014 ◽  
Vol 42 (1) ◽  
pp. 3-6
Author(s):  
SS Shahina ◽  
JU Ahmed ◽  
S Ahmed ◽  
E Shahriar ◽  
MN Uddin ◽  
...  

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


Cardiology ◽  
2016 ◽  
Vol 136 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Georgios Giannopoulos ◽  
Dimitrios A. Vrachatis ◽  
Georgios Oudatzis ◽  
Georgios Paterakis ◽  
Christos Angelidis ◽  
...  

Objectives: Red blood cell microparticles (RBCm) have potential adverse vascular effects and they have been shown to be elevated in ST elevation myocardial infarction (STEMI). The purpose of this study is to investigate their relationship with biochemical infarct size. Methods: RBCm were quantified with flow cytometry in blood drawn from 60 STEMI patients after a primary angioplasty. The creatine kinase-myocardial brain fraction (CK-MB) was measured at predefined time points and the area under the curve (AUC) was calculated. Results: RBCm count was correlated with CK-MB AUC (Spearman's ρ = 0.83, p < 0.001). The CK-MB AUC values per RBCm quartile (lower to upper) were: 3,351 (2,452-3,608), 5,005 (4,450-5,424), 5,903 (4,862-10,594), and 8,406 (6,848-12,782) ng × h/ml, respectively. From lower to upper quartiles, the maximal troponin I values were: 42.2 (23.3-49.3), 49.6 (28.8-54.1), 59.2 (41.4-77.3), and 69.1 (48.0-77.5) ng/ml (p = 0.005). In multivariable analysis, RBCm remained a significant predictor of CK-MB AUC (standardized β = 0.63, adjusted p = 0.001). Conclusions: Erythrocyte microparticles appear to be related to the total myocardial damage biomarker output. The exact pathophysiologic routes, if any, for this interaction remain to be identified. However, these results suggest that erythrocytes may be a - thus far virtually ignored - player in the pathogenesis of ischemic injury.


2021 ◽  
Vol 10 (3) ◽  
pp. 6-14
Author(s):  
A. A. Garganeeva ◽  
V. A. Aleksandrenko ◽  
E. A. Kuzheleva ◽  
V. V. Ryabov ◽  
T. Yu. Rebrova ◽  
...  

Aim.      To investigate the relationship between the osmotic fragility of erythrocytes and the course of acute myocardial infarction (MI).Methods.           An analysis of the osmotic fragility of erythrocytes was conducted using beta-blocker-based osmotic fragility test in sixty-two patients within the first 6 hours after onset of MI symptoms.Results. The results revealed that the patients with increased erythrocyte osmotic fragility experienced more complications after acute MI, such as left ventricular failure and cardiac arrhythmias (ventricular extrasystoles and ventricular tachycardia) (p = 0.026). Moreover, these patients exhibited greater myocardial injury - the concentration of biomarkers of myocardial necrosis, such as creatine phosphokinase, creatine phosphokinase MB and Troponin I was increased - p = 0.009, p = 0.032 and p = 0.001, respectively. In addition to that, the patients with high osmotic fragility had a larger number of hypokinetic and akinetic segments, high impaired myocardial contractility index, and low ejection fraction. The impaired myocardial contractility index was significantly higher in patients with increased erythrocyte osmotic fragility (1.5 (1.22; 1.75) vs 1.12 (1.0; 1.56), U = 157.5, p = 0.032).Conclusion. Increased erythrocyte osmotic fragility in patients was associated with greater myocardial injury, manifesting through the higher concentration of biomarkers of myocardial necrosis in blood, as well as higher number of hypokinetic segments.


1978 ◽  
Vol 17 (04) ◽  
pp. 157-160
Author(s):  
J. W. Keyes

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.


Author(s):  
Simona Ferraro ◽  
Patrizia Boracchi ◽  
Matteo Santagostino ◽  
Giuseppe Marano ◽  
Chiara Vendramin ◽  
...  

2012 ◽  
Vol 38 (1) ◽  
pp. 9-13 ◽  
Author(s):  
N Alam ◽  
HILR Khan ◽  
AW Chowdhury ◽  
MS Haque ◽  
MS Ali ◽  
...  

The objective of the present study is to find out whether the increased serum homocysteine level is associated with the increased serum troponin I as a surrogate marker of extent of myocardial injury in acute myocardial infarction patients. Elevated homocysteine levels are associated with increased thrombosis. In patients presenting with Acute Coronary Syndrome (ACS), it is not known whether this association is reflected in the degree of myocardial injury. This was a cross sectional study conducted among the patients with acute myocardial infarction in the Department of Cardiology, Dhaka Medical College Hospital during the period of October 2009 to September 2010 and which included 194 consecutive patients with acute myocardial infarction. The mean (±SD) serum homocysteine level was 20.2±14.3 ?mol/L with range from 7.4 to 129.1 ?mol/L. Mean serum troponin-I level was classified according to normal (<15?mol/L) and high (?15?mol/L) levels of serum homocysteine values. The mean serum troponin-I level was 8.9±8.6 ng/ml in the patients having normal serum homocysteine level and 18.4±6.5 ng/ml in the patients having high serum homocysteine level. A significant positive correlation (r=0.273; p<0.001) was found between serum troponin-I level with homocysteine level. Patients with moderate hyperhomocysteinemia (?15 ?mol/L) was found to be 7.09 times more likely to have increased serum troponin-I (a surrogate marker of extent of myocardial injury). The main observation of the present study was that elevated serum homocysteine level has a positive correlation with serum cardiac troponin-I in patients with acute myocardial infarction. So serum homocysteine is associated with increased extent of myocardial injury as measured by serum cardiac troponin-I level, a surrogate marker in patients with acute myocardial infarction.  DOI: http://dx.doi.org/10.3329/bmrcb.v38i1.10445  Bangladesh Med Res Counc Bull 2012; 38: 9-13


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Sebastian Johannes Reinstadler ◽  
Gert Klug ◽  
Hans-Josef Feistritzer ◽  
Bernhard Metzler ◽  
Johannes Mair

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.


2016 ◽  
Vol 7 (2) ◽  
pp. 120-128 ◽  
Author(s):  
Yader Sandoval ◽  
Fred S Apple ◽  
Stephen W Smith

The term unstable angina has been conventionally applied to patients with myocardial ischemia without myocardial necrosis. However, while the clinical context has remained constant over time, the biomarkers of myocardial injury and acute myocardial infarction have evolved. High-sensitivity cardiac troponin assays have several key analytical differences from prior cardiac troponin assay generations, which may alter the diagnosis and frequency of unstable angina, as well as affect our understanding of previously developed risk stratification strategies. This document reviews the current challenges in regards to unstable angina when using high-sensitivity cardiac troponin I and T assays.


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