scholarly journals Association between the osmotic fragility of erythrocytes and the course of acute myocardial infarction

2021 ◽  
Vol 10 (3) ◽  
pp. 6-14
Author(s):  
A. A. Garganeeva ◽  
V. A. Aleksandrenko ◽  
E. A. Kuzheleva ◽  
V. V. Ryabov ◽  
T. Yu. Rebrova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Myocardial Contractility ◽  
Myocardial Injury ◽  
Creatine Phosphokinase ◽  
Troponin I ◽  
Osmotic Fragility ◽  
Myocardial Necrosis ◽  
Left Ventricular ◽  
Erythrocyte Osmotic Fragility

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.

High-sensitivity cardiac troponin assays and unstable angina

2016 ◽  
Vol 7 (2) ◽  
pp. 120-128 ◽  
Author(s):  
Yader Sandoval ◽  
Fred S Apple ◽  
Stephen W Smith
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Unstable Angina ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
Myocardial Necrosis ◽  
High Sensitivity ◽  
Clinical Context ◽  
Over Time

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.

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

Abstract 2832: Which Cardiac Marker is Most Useful to Predict Final Infarct Size and Cardiac Function Following Primary Percutaneous Coronary Intervention For Acute Myocardial Infarction?

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stanley Chia ◽  
O. Christopher Raffel ◽  
Faisal Merchant ◽  
Frans J Wackers ◽  
Fred Senatore ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Troponin I ◽  
Troponin T ◽  
Coronary Intervention ◽  
Left Ventricular ◽  
Cardiac Biomarkers ◽  
Primary Pci ◽  
Percutaneous Coronary

Background: Assessment of cardiac biomarker release has been traditionally used to estimate the size of myocardial damage after acute myocardial infarction (AMI). However, the significance of cardiac biomarkers in the setting of primary percutaneous coronary intervention (PCI) has not been systematically studied in a large patient cohort. We evaluated the usefulness of serial and single time-point measures of various cardiac biomarkers (creatine kinase (CK), CK-MB, troponin T and I) in predicting infarct size and left ventricular ejection fraction (LVEF) after primary PCI. Methods: EVOLVE (Evaluation of MCC-135 for Left Ventricular Salvage in AMI) was a randomized double-blind, placebo-controlled trial comparing the efficacy of intracellular calcium modulator as an adjunct to primary PCI in patients with first large AMI. Levels of cardiac biomarkers (CK, CK-MB mass, troponin T and I) were determined in 375 patients at baseline before PCI and 2, 4, 12, 24, 48 and 72 hours thereafter. Single photon emission computed tomography imaging was performed to measure infarct size and LVEF on day 5. Results: Area under curve and peak concentrations of all cardiac markers: CK, CK-MB mass, troponin T and troponin I were significantly correlated with myocardial infarct size and LVEF determined on day 5 (Spearman correlation, all P< 0.001; Table ). Troponin I, however provided the best predictor and a single measure at 72 hr was a strong indicator of both infarct size and LVEF. Using receiver operator characteristics curve, troponin I cutoff value of >55 pg/mL at 72 hr has 90% sensitivity and 70% specificity for detection of large infarct size≥10% ( c =0.88; P< 0.001). Conclusions: Plasma levels of CK, CK-MB, troponin T and troponin I remain useful predictors of infarct size and cardiac function in the era of primary PCI for AMI. A single measurement of circulating troponin I at 72 hours can provide an effective and convenient indicator of infarct size and LVEF in clinical practice. Correlation of cardiac biomarkers with Day 5 SPECT determined infarct size and LVEF

Abstract 18996: Impact of Infarct Size on Left Ventricular Diastolic Function Following Acute Myocardial Infarction

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Andrew Lin ◽  
Christopher Kwan ◽  
Kristyan Guppy-Coles ◽  
Joanne Sippel ◽  
John Atherton ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Troponin I ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Ventricular Diastolic Function ◽  
St Elevation

Introduction: Severe left ventricular diastolic dysfunction is associated with worse prognosis after acute myocardial infarction (MI). Twenty percent of patients have a restrictive filling pattern (RFP) following MI, and this is associated with a fourfold increase in mortality. The determinants of diastolic function in this setting are not well defined. Aim: We sought to determine the correlation between enzymatic infarct size and RFP in patients with a first ever MI. We hypothesized that a larger infarct size would result in greater impairment of left ventricular diastolic function. Methods: Data analysis was performed on consecutive patients admitted with first ever non-ST elevation MI (NSTEMI) or ST-elevation MI (STEMI) to a single large tertiary referral hospital from January 2013 to December 2014. All patients underwent coronary angiography during the index admission. Infarct size was determined by peak troponin I. Doppler transmitral flow pattern was obtained from the initial transthoracic echocardiogram performed within 48 hours of admission. RFP was defined as: E/A ratio >2.0 and/or E-wave deceleration time <160ms (American Society of Echocardiography Guidelines 2009). Results: Data were available on 645 consecutive patients who underwent coronary angiography for MI. We excluded 160 patients with a previous MI. Of the remaining 485 patients (mean age 62±13 years; mean left ventricular ejection fraction (LVEF) 53±12%), there were 338 NSTEMIs (70%) and 147 STEMIs (30%). PCI was performed in 360 (74%) patients (single vessel (82%), ≥2 vessels (18%)); coronary artery bypass surgery in 58 (13%); and medical management in 67 (13%). Sixty-nine patients (14.4%) had RFP; 52% of these had a LVEF ≥45%. Peak troponin I levels were higher in the RFP group (31.8±30.9μg/L vs 16.8±25.2μg/L, p=<0.001). On multivariate analysis, infarct size by peak troponin I (OR 1.02, 95%CI 1.00-1.03, p=0.026) and low LVEF (OR 0.95, 95%CI 0.91-0.99, p=0.015) were the only independent predictors of RFP. Conclusion: Infarct size was a major determinant of diastolic dysfunction following first ever MI. Whilst LV systolic dysfunction was strongly associated with impaired diastolic function, 52% of patients with severe diastolic dysfunction had relatively preserved LVEF.

scholarly journals The chronic periodontitis in patients with acute coronary syndromes. The inflammation link between periodontal disease and coronary atherosclerosis

2020 ◽  
Author(s):  
Agnieszka Wojtkowska ◽  
Tomasz Zapolski ◽  
Joanna Wysokinska-Miszczuk ◽  
Andrzej P. Wysokinski
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Periodontal Disease ◽  
Systemic Inflammation ◽  
Coronary Atherosclerosis ◽  
Troponin I ◽  
Left Ventricular ◽  
Treatment Needs ◽  
Pocket Depth ◽  
Periodontal Index

Abstract Background Coronary atherosclerosis and periodontal disease, due to their prevalence, are a serious epidemiological problem. Pathophysiological evidence points to their possible common inflammatory etiopathological background. The aim of the study was to analyze the relationship between the presence and severity of periodontitis, systemic inflammation and selected parameters of myocardial injury and heart function in patients with acute myocardial infarction. Methods The study group consisted of 71 patients 54.22(7.05) - year - old hospitalized due to acute myocardial infarction. The patients underwent a coronary angiographic examination and echocardiography. The following laboratory parameters were determined: blood morphology, hsCRP, ESR, fibrinogen, troponin I, CK-MB, BNP, lipidogram, glucose, creatinine, GFR, TSH, HbA1c. Dental assessment of the patients was performed and the following indicators were included: the number of teeth preserved, approximal plaque index (API), bleeding on probing (BoP), pocket depth (PD), the number of bleeding periodontal pockets ≥ 4 mm in depth (NoPD ≥ 4 mm), the percentage of bleeding periodontal pockets ≥ 4 mm in depth (%PD ≥ 4 mm), clinical attachment loss (CAL). The severity of periodontal disease and periodontological treatment needs were determined using the Community Periodontal Index of Treatment Needs (CPITN). Results The BI (bleeding index) significantly correlated with fibrynogen. All indices regarding the pocket depth (PD, NoPD ≥ 4 mm,% PD4 ≥ mm) correlated significantly with the number of leukocytes. PD and NoPD ≥ 4 mm were also associated significantly with the level of hsCRP. The BI is correlated closely with the levels of BNP. The multifactorial analysis showed that significant predictors of myocardial infarction are API and BI. The analysis showed that API and BI are important predictors of troponin levels. Linear regression analysis showed that only CAL is a significant predictor of BNP. Conclusions Patients with acute myocardial infarction have worse periodontal status in the AAP and CPITN classification compared to people without coronary heart disease. Higher severity of periodontal disease, poorer oral hygiene and increased activity of the periodontitis leads to greater manifestation of systemic inflammation in patients with acute myocardial infarction. Periodontitis is a risk factor for myocardial infarction and also affects the degree of post-infarction left ventricular damage, which means that there is an inflammatory link between these two diseases.

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.

Ultra-sensitive troponin I levels to exclude acute myocardial infarction from myocardial injury

2012 ◽  
Vol 50 (1) ◽  
Author(s):  
Simona Ferraro ◽  
Patrizia Boracchi ◽  
Matteo Santagostino ◽  
Giuseppe Marano ◽  
Chiara Vendramin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Myocardial Injury ◽  
Troponin I

scholarly journals Elevated serum homocysteine level has a positive correlation with serum cardiac troponin I in patients with acute myocardial infarction

2012 ◽  
Vol 38 (1) ◽  
pp. 9-13 ◽  
Author(s):  
N Alam ◽  
HILR Khan ◽  
AW Chowdhury ◽  
MS Haque ◽  
MS Ali ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Myocardial Injury ◽  
Troponin I ◽  
Homocysteine Level ◽  
Surrogate Marker ◽  
Cardiac Troponin I ◽  
Serum Homocysteine ◽  
Serum Cardiac Troponin

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

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