Changes in Platelet Functions, Coagulation and Fibrinolysis in Uncomplicated Cases of Acute Myocardial Infarction

Knudsen, J Bjerre; Gormsen, J; Skagen, Knud; Amtorp, Ole

doi:10.1055/s-0038-1657053

Cited by 6 publications

(6 citation statements)

References 11 publications

(12 reference statements)

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“…Although the association between CK and platelet function or bleeding risk was not assessed, distinct hypoaggregability of platelets or increased bleeding risk were reported after myocardial infarction. 17,25 In addition, the ill-understood “trauma-induced coagulopathy” may ensue after major trauma of CK-rich tissue (muscle or brain), associated with inhibition of ADP-dependent platelet aggregation and intractable bleeding. 26 Also, bleeding events occur more frequently in population subgroups with relatively high tissue and plasma CK, such as in persons of (West-)African ancestry.…”

Section: Discussionmentioning

confidence: 99%

Creatine Kinase is Associated with Bleeding after Myocardial Infarction

Brewster¹,

Fernand²

2019

Preprint

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Background: Highly elevated plasma activity of the ADP scavenging enzyme creatine kinase (CK) might reduce ADP and ADP-dependent platelet activation. Therefore, we studied, whether high CK after myocardial infarction (MI) is associated with bleeding. Method: Data of the Thrombolysis In Myocardial Infarction Study Group phase II trial on the efficacy of angioplasty following intravenous recombinant tissue-type plasminogen activator (rt-PA), are used to assess whether peak plasma CK (CKmax) is independently associated with adjudicated fatal or non-fatal bleeding (primary) and combined bleeding/all-cause mortality (secondary) in multivariable binomial logistic regression analysis, adjusting for baseline and treatment allocation covariates. Results: The included patients (N=3339, 82% men, 88% white, mean age 57 y, SE 0.2), had a history of angina pectoris (55%), hypertension (38%), and/or diabetes mellitus (13%). CKmax ranged between 16 and 55 890 IU/L (mean 2389 IU/L; SE 41), reached within 8 h in 51% of the patients (93% within 24 h). Adjudicated fatal/non-fatal bleeding occurred in 30% of the patients (respectively 26% in the low vs 34% in the high CK tertile), and bleeding/all-cause mortality in 35% (29% in the low, vs 40% in the high CK tertile). The adjusted odds ratio for fatal/non-fatal bleeding (vs not bleeding and survival) was 2.6 [95% CI, 1.8 to 3.7]/log CKmax increase, and 3.1 [2.2 to 4.4] for bleeding/all-cause mortality). Conclusion: Highly elevated plasma CK after MI might be a hitherto overlooked independent indicator of bleeding and hemorrhagic death. This biologically plausible association warrants prospective study of the potential role of CK in hemorrhagic diathesis, and the risk of severe, potentially fatal bleeding with antithrombotic or thrombolytic therapy in the presence of high plasma CK.

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Section: Discussionmentioning

confidence: 99%

Creatine Kinase is Associated with Bleeding after Myocardial Infarction

Brewster¹,

Fernand²

2019

Preprint

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“…In two early studies [65,66] on the changes of FXIII levels during the acute phase of MI a depression of FXIII activity, with a nadir on day 4, was demonstrated [66]. Surprisingly, no changes in FXIII-A and FXIII-B plasma levels were detected by electro-immunoassay.…”

Section: Factor XIII Levels In Thrombotic Vascular Diseasesmentioning

confidence: 96%

Fibrin Stabilization (Factor XIII), Fibrin Structure and Thrombosis

Bereczky

Katona

Muszbek

2003

Pathophysiol Haemos Thromb

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“…Furthermore, there was a significant negative correlation between the ADP-induced platelet aggregation by ADP (Mills & Robert, 1965). Higher concentrations of epinephrine (10-6M), however, cause a single phase aggregation unaccompanied by a shape change, which is slower and less extensive than primary aggregation induced by ADP, and do not reverse spontaneously (O'Brien, 1964 (O'Brien et aL, 1971), stressfu1 condition (Arkel et al, 1977Haft & Arkel, 1976), and in an acute phase of myocardial infarction (Knudsen et at., 1979; Aosaki, I981), In this paper, we report that such decreased platelet aggregation occurrs in variant angina. Clin.…”

Section: Resultsmentioning

confidence: 99%

Platelet Aggregation in Variant Angina : Its Relation to Plasma Catecholamines

Takahara

Nakashima

Takei

et al. 1984

J UOEH

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We concurrently measured plasma catecholamine levels and platelet aggregation in patients with variant angina, effort angina and old myocardial infarction. Platelet aggregability was lower in variant angina than in effort angina and old myocardial infarction. Plasma concentrations of epinephrine and norepinephrine in the variant angina group showed higher values than those in the effort angina group and the old myocardial infarction group. Moreover, there was a statistically significant negative correlation between plasma catecholamine concentration and ADP-induced platelet aggregation. These findings suggest that the lower platelet aggregation is related to the higher concentration of plasma catecholamine in variant angina.

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Changes in Platelet Functions, Coagulation and Fibrinolysis in Uncomplicated Cases of Acute Myocardial Infarction

Cited by 6 publications

References 11 publications

Creatine Kinase is Associated with Bleeding after Myocardial Infarction

Creatine Kinase is Associated with Bleeding after Myocardial Infarction

Fibrin Stabilization (Factor XIII), Fibrin Structure and Thrombosis

Platelet Aggregation in Variant Angina : Its Relation to Plasma Catecholamines

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