Chronic lymphocytic leukemia involving the coronary arteries with accompanying acute myocardial infarction

2005 ◽  
Vol 14 (6) ◽  
pp. 324-326 ◽  
Author(s):  
Ali H. Assiri ◽  
Manisha Lamba ◽  
John P. Veinot
1993 ◽  
Vol 70 (06) ◽  
pp. 0978-0983 ◽  
Author(s):  
Edelmiro Regano ◽  
Virtudes Vila ◽  
Justo Aznar ◽  
Victoria Lacueva ◽  
Vicenta Martinez ◽  
...  

SummaryIn 15 patients with acute myocardial infarction who received 1,500,000 U of streptokinase, the gradual appearance of newly synthesized fibrinogen and the fibrinopeptide release during the first 35 h after SK treatment were evaluated. At 5 h the fibrinogen circulating in plasma was observed as the high molecular weight fraction (HMW-Fg). The concentration of HMW-Fg increased continuously, and at 20 h reached values higher than those obtained from normal plasma. HMW-Fg represented about 95% of the total fibrinogen during the first 35 h. The degree of phosphorylation of patient fibrinogen increased from 30% before treatment to 65% during the first 5 h, and then slowly declined to 50% at 35 h.The early rates of fibrinopeptide A (FPA) and phosphorylated fibrinopeptide A (FPAp) release are higher in patient fibrinogen than in isolated normal HMW-Fg and normal fibrinogen after thrombin addition. The early rate of fibrinopeptide B (FPB) release is the same for the three fibrinogen groups. However, the late rate of FPB release is higher in patient fibrinogen than in normal HMW-Fg and normal fibrinogen. Therefore, the newly synthesized fibrinogen clots faster than fibrinogen in the normal steady state.In two of the 15 patients who had occluded coronary arteries after SK treatment the HMW-Fg and FPAp levels increased as compared with the 13 patients who had patent coronary arteries.These results provide some support for the idea that an increased synthesis of fibrinogen in circulation may result in a procoagulant tendency. If this is so, the HMW-Fg and FPAp content may serve as a risk index for thrombosis.


RSC Advances ◽  
2020 ◽  
Vol 10 (17) ◽  
pp. 10245-10253 ◽  
Author(s):  
Mochao Xiao ◽  
Daifeng Lu ◽  
Jiali Tian ◽  
Yang Yu ◽  
Qin Zhang ◽  
...  

Acute myocardial infarction (AMI) is a complication of atherosclerosis that takes place in coronary arteries.


1980 ◽  
Vol 99 (4) ◽  
pp. 506-509 ◽  
Author(s):  
Edward H. Schuster ◽  
Stephen C. Achuff ◽  
William R. Bell ◽  
Bernadine H. Bulkley

1997 ◽  
Vol 152 (3) ◽  
pp. 489-493 ◽  
Author(s):  
C J Charles ◽  
S J Rogers ◽  
R A Donald ◽  
H Ikram ◽  
T Prickett ◽  
...  

Although previous studies have described the hypothalamo–pituitary–adrenal (HPA) response to the stress of acute myocardial infarction, it is not possible to study the hormone changes immediately after infarction in humans. Accordingly, we have examined the HPA response to microembolization of coronary arteries in 13 sheep compared with 5 sham control sheep. Plasma vasopressin (AVP; P<0·001), ACTH (P=0·005) and cortisol (P=0·005) were all increased 2 h (first sample time) after embolization. Plasma ACTH and cortisol levels returned to baseline levels by 6 h but plasma AVP levels did not return to baseline levels until more than 12 h after embolization. Plasma corticotrophin-releasing hormone (CRH) showed no significant change in response to embolization. In a subset of six animals which were sampled more frequently, the peak responses for plasma AVP, ACTH and cortisol occurred at 40 min after embolization. The maximum responses in any individual sheep observed at this time point were 744 pmol/l for AVP, 144 pmol/l for ACTH and 492 nmol/l for cortisol. CRH levels tended to increase across the first hour but these changes were not statistically significant. In conclusion, the stress hormone responses to microembolization of the coronary arteries have been defined in an ovine model of myocardial infarction. This model is suitable for studying the effects of novel treatments to reduce the stress of myocardial infarction. Journal of Endocrinology (1997) 152, 489–493


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