Heparin Neutralizing Activity in the Diagnosis of Acute Myocardial Infarction

1975 ◽  
Author(s):  
J. R. O’Brien ◽  
M. D. Etherington ◽  
S. Jamieson ◽  
J. Sussex

We have previously demonstrated that, relative to controls, patients long after myocardial infarction and patients with atherosclerosis have highly significantly shorter heparin thrombin clotting times (HTCT) using platelet poor plasma; but there was considerable overlap between the two groups.We have now studied 89 patients admitted with acute chest pain. In 54 of these a firm diagnosis of acute myocardial infarction (ac-MI) was made and the HTCT was very short (mean 12.8 sees) and in 48 it was less than 16 sees. In 34 patients, ac-MI was excluded and the diagnosis was usually “angina”; the HTCT was much longer (mean 25.1 sees) and in 32 it was over 16 sees. Thus there was almost no overlap between these two groups. It is suggested that this test should be adopted as a quick and reliable further test to establish a diagnosis of ac-MI (providing other reasons for very short HTCTs can be excluded, e.g. D. I. C., and provinding the patient’s thrombin clotting time is normal).This HTCT measures non-specific heparin neutralizing activity; nevertheless the evidence suggests that it is measuring platelet factor 4 liberated from damaged or “activated” platelets into the plasma. These findings underline the probable important contribution of platelets in ac-MI.

1980 ◽  
Vol 44 (02) ◽  
pp. 096-099 ◽  
Author(s):  
John R O'Brien ◽  
Michael D Etherington ◽  
Robert D Shuttleworth ◽  
William H Calwell

SummaryA considerable number of tests were carried out comparing 33 patients with acute myocardial infarction (MI), 13 patients with chest pain (CP) and 47 controls. There was some evidence that the plasma platelet factor 4 (PF4) was different in the three groups. The heparin neutralizing activity (HNA) of platelet poor plasma was increased in the MI patients relative to the controls and the intra-platelet HNA was decreased. Malondialdehyde (MDA) formation by platelets maximally stimulated by thrombin was decreased in MI whilst the plasma 5-hydroxyindoles (5HIs) in MI was greatly increased. The acute phase proteins α1 acid glycoprotein and fibrinogen were significantly raised in MI. The results in the CP group were intermediate between the MI and the controls. These findings define more precisely the changes in acute MI and are relevant to the concept of exhausted platelets.


Author(s):  
Mahir Abdulkadhum Khudhair Alzughaibi ◽  
Ammar Waheeb Obeiad ◽  
Nassar Abdalaema Abdalhadi Mera ◽  
Mohammed Sadeq Hamzah Al-Ruwaiee

Background: Cardiac Troponins-I (CTNI) are myoregulatory polypeptides that control the actin-myosin interface, considered specific to cardiomyocytes. Age and sex variances in the extent of CTNI levels have arisen a recent debatable emphasis. Existing revisions do not display a reliable clinical power of sex-specific CTNI 99th centiles, which actually might mirror procedural aspects. Nevertheless, from a biochemical viewpoint, the trends of sex-specific CTNI 99th centiles seem sensible for the ruling-in of acute myocardial infarction AMI. Vulnerable females may be missed when applying the male sex-specific threshold. This study aimed to determine whether gender differences in CTNI exist in patients with AMI presented with chest pain. Methodology: The study was a cross-sectional, single-center, included 236-patients with AMI diagnosis by cardiologists at Merjan teaching hospital during the period from April to July 2020 from patients attending the hospital for cardiac consultation complaining of acute chest pain suggestive of AMI. Blood analysis had initiated at the time of admission included serum creatinine, blood urea, R/FBS, WBCs, PCV, and serum CTNI. A p-value below 0.05 specifies statistical significance. All statistical bioanalyses had performed by IBM-SPSS, version-25 for Windows. Results: The mean age of participants was 67.5 years, the men were dominant 76.2%. The incidence of DM and hypertension were significantly high and 24.5% of the patients were current smokers. Biochemical serum analysis revealed mean creatinine, urea, sugar, and STI values were 79.8±4.2 mmol/l, 15.9±1.7 mmol/l, 10.9±0.9 mmol/l, and 7.9±0.6 ng/ml separately. Both hypertension and smoking were significantly (p-0.001) more among males compared to the females, which is not the case for the prevalence of DM. The males were heavier significantly than females (p-0.001). Almost, there was no impact of gender on most of the other study variables other than serum TNI levels, which were significantly higher among the males (p-0.001). Conclusion: In patients with AMI presented with acute chest pain, the routine of CTNI in the diagnosis of AMI is based on the patient's gender. The application of gender-dependent cutoff levels for CTNI analyses appears to be highly suggested.


2013 ◽  
Vol 12 (3) ◽  
pp. 150-153 ◽  
Author(s):  
Mahmoud C. Assaad ◽  
Carlos Calle-Muller ◽  
Musa Dahu ◽  
Richard M. Nowak ◽  
Michael P. Hudson ◽  
...  

2016 ◽  
Vol 43 (3) ◽  
pp. 258-260 ◽  
Author(s):  
Jonathan Winkler ◽  
Sunit-Preet Chaudhry ◽  
Philip H. Stockwell

Acute myocardial infarction from septic embolization is a rare initial presentation of endocarditis. We report the case of a 67-year-old man who presented with acute chest pain, in whom emergency cardiac catheterization revealed findings that suggested coronary embolism. The patient was found to have Gemella endocarditis, with its initial presentation an embolic acute ST-segment-elevation myocardial infarction. We suggest that endocarditis be considered among the potential causes of acute myocardial infarction.


2011 ◽  
Vol 57 (9) ◽  
pp. 1318-1326 ◽  
Author(s):  
Willibald Hochholzer ◽  
Tobias Reichlin ◽  
Raphael Twerenbold ◽  
Claudia Stelzig ◽  
Kirsten Hochholzer ◽  
...  

BACKGROUND High-sensitivity cardiac troponin assays have better analytical precision and sensitivity than earlier-generation assays when measuring cardiac troponin at low concentrations. We evaluated whether use of a high-sensitivity assay could further improve risk stratification compared with a standard cardiac troponin assay. METHODS We enrolled consecutive patients presenting with acute chest pain, 30% of whom were diagnosed with acute coronary syndrome. Blood samples were drawn at the time of presentation. We measured cardiac troponin T with a standard fourth-generation assay (cTnT) and a high-sensitivity assay (hs-cTnT) (both Roche Diagnostics) and followed the patients for 24 months. RESULTS Of the 1159 patients, 76 died and 42 developed an acute myocardial infarction (AMI). Prognostic accuracy of hs-cTnT for death was significantly higher [area under ROC curve (AUC) 0.79, 95% CI 0.74–0.84] than that of cTnT (AUC 0.69, 95% CI 0.62–0.76; P < 0.001). After adjustment for Thrombolysis in Myocardial Infarction (TIMI) risk score (that included the cTnT assay result), hs-cTnT above the 99th percentile (0.014 μg/L) was associated with a hazard ratio for death of 2.60 (95% CI 1.42–4.74). Addition of hs-cTnT to the risk score improved the reclassification of patients (net reclassification improvement 0.91; 95% CI 0.67–1.14; P < 0.001). Subgroup analyses showed that this effect resulted from the better classification of patients without AMI at time of testing. hs-cTnT outperformed cTnT in the prediction of AMI during follow-up (P=0.02), but was not independently predictive for this endpoint. CONCLUSIONS Concentrations of hs-cTnT >0.014 μg/L improve the prediction of death but not subsequent AMI in unselected patients presenting with acute chest pain.


Sign in / Sign up

Export Citation Format

Share Document