Beta Thromboglobulin and Myocardial Infarction

Author(s):  
A. Hughes ◽  
S. Daunt ◽  
G. Vass ◽  
J. Wickes

Beta thromboglobulin. a platelet specific protein liberated during the release reaction, has been measured in normal individuals (n=285),and in patients presenting with acute chest pain. The latter group consisted of those with acute myocardial infarction (n=19),those with acute myocardial ischaemia (n=21),and those with chest pain of non cardiac origin (n-7). In the patient groups beta thromboglobulin was measured on admission to hospital, and thereafter daily until the patient was discharged. There was no significant difference between the normal population (mean 22.5 ng/ml),and the patients with with non cardiac chest pain (mean .24 ng/ml). There was a significant difference between the normal population and the patients with acute myocardial infarction (mean 34 ng/ml),and acute myocardial ischaemia (mean 33 ng/ml), p<0.001. There was also a significant difference between these two groups and the patients with non cardiac chest pain, p<0.01.We would conclude that platelet activation occurs in acute myocardial infarction and ischaemia, but it is not clear if this is a primary or a secondary phenomenon.

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.


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.


1992 ◽  
Vol 38 (12) ◽  
pp. 2396-2400 ◽  
Author(s):  
A H Wu ◽  
X M Wang ◽  
T G Gornet ◽  
J Ordóñez-Llanos

Abstract We measured total creatine kinase (CK), CK-MB isoenzyme, and the MB isoforms in 202 serum and plasma samples from nine groups of patients and normal individuals: 39 with acute myocardial infarction (MI), divided according to time between the onset of chest pain and blood collection (1-6 h, 7-12 h, and 13-48 h); 26 with chest pain for whom an MI was ruled out, sampled at admission; 17 undergoing bypass surgery or cardiac catheterization, sampled within 6 h after either procedure; 17 with acute skeletal muscle injury, sampled within 8 h after injury; 30 marathon runners immediately after a race; 17 runners and other athletes &gt; 12 h after training or a race; 12 with cerebral injury or seizures, sampled at admission; 8 with closed head injury, sampled at admission; and 38 normal subjects. CK-MB (relative index) and MB isoforms (MB2/MB1) were respectively increased in 15% and 75% of MI patients 1-6 h after onset, 94% and 94% after 7-12 h, and 88% and 8% after 12 h, and in 87% and 82% of cardiac surgery patients. MB isoforms were increased in most patients with acute skeletal muscle trauma and in subjects examined after exercise, but were within normal limits in patients for whom MI was ruled out, patients with cerebral trauma, and normal individuals. The relative index of MB/total CK was normal in essentially all individuals in the last groups, including those with acute skeletal muscle trauma. We concluded that the CK-MB isoform ratio is increased in both acute skeletal muscle injury and MI. The isoform ratio is most useful for distinguishing recent from old (&gt; 12 h) injury.


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 &lt; 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 &lt; 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 &gt;0.014 μg/L improve the prediction of death but not subsequent AMI in unselected patients presenting with acute chest pain.


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