HEPARIN AND ACETYLSALICYLIC ACID (ASA) 75 MG/DAY IN UNSTABLE CORONARY ARTERY DISEASE - EFFECTS ON PLATELET REACTIVITY

Long Term Treatment ◽

Artery Disease ◽

One Year

In unstable coronary artery disease (UCAD), i.e. unstable angina pectoris (UAP) or non-Q-myocardial infarction (NMI), treatment with heparin or ASA have given encouraging results. The present study attempts to verify the effects of i.v. heparin (5 days) and to evaluate the utility of ASA 75 mg/day (one year). Patients, admitted because of chest pain, who either develops NMI or signs of ischemia in resting or exercise ECG.s are included. Within 72 hours patients are randomized to obtain Heparin+ASA, Heparin+Placebo, Placebo + ASA or Placebo+Placebo . Platelet reactivity is studied in vitro in platelet rich plasma (PRP) in a subgroup of patients.The aggregation response is studied after addition of collagen and ADP and after preincubation with prostacyclin before aggregation with ADP. The figures present results from 85 randomized patients tested before, 5 days, one month and one year after start of therapy.Conclusion: In patients with unstable CAD long term treatment with ASA 75 mg/day inhibits collagen induced platelet aggregation and hampers the ADP response. I.v. heparin tends to raise platelet reactivity and reduce the inhibitory effect of prostacyclin. Heparin induced platelet activation is reduced by simultaneous ASA therapy.

Platelet Reactivity in Unstable Coronary Artery Disease

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651121 ◽

1987 ◽

Vol 57 (03) ◽

pp. 302-305 ◽

Cited By ~ 13

Author(s):

Eva Swahn ◽

Lars Wallentin

Keyword(s):

Myocardial Infarction ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Acute Phase ◽

Platelet Reactivity ◽

Platelet Rich Plasma ◽

Control Group ◽

Platelet Factor ◽

SummaryUnstable coronary artery disease (CAD) might be related to obstructions of coronary blood flow by platelet aggregates. In 121 men and 43 women admitted to the coronary care unit with suspected unstable CAD, blood samples for tests of platelet function were obtained within 24 hours after admission. Platelet reactivity was tested in vitro in platelet rich plasma as the aggregability towards ADP 1 μM and collagen 1 mg/ml and as the sensitivity to prostacyclin (PSP). The levels of beta-thrombo-globulin and platelet factor 4 were determined ex vivo in platelet poor plasma. Patients who developed a nontransmural myocardial infarction (n = 39) or had signs of myocardial ischemia at an exercise test performed within a week (n = 39) were considered to have unstable CAD while patients without signs of ischemia constituted the control group. In the acute phase the PSP was reduced in patients with unstable CAD without any difference between genders. The aggregability towards ADP was higher in women than men but otherwise there were no differences between groups or sexes in any other test in the acute phase. After 12 months there were no differences in PSP between the groups but women had a lower PSP than men. Thus, in the acute phase of unstable CAD, the platelet sensitivity to the inhibitory effects of prostacyclin was reduced which might contribute to the risk for further platelet aggregation, coronary occlusion and myocardial infarction.

PLATELET REACTIVITY AND FIBRINOGEN LEVELS IN UNSTABLE CORONARY ARTERY DISEASE(UCAD)

10.1055/s-0038-1643008 ◽

1987 ◽

Author(s):

E Swahn ◽

H von Schenck ◽

L Wallentin

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Acute Phase ◽

Fibrinogen Level ◽

Platelet Reactivity ◽

Control Group ◽

Predisposing Factor ◽

Unstable Phase ◽

Artery Disease ◽

One Year

Unstable angina and non-Q-wave myocardial infarction represents the unstable phase Of coronary artery disease (CAD). In UCAD a thrombosis in a coronary artery could be the triggering factor of the unstable phase. Increased platelet reactivity and hypercoagulability could be the predisposing factor for developing this condition. Therefore, in patients with UCAD the platelet reactivity was measured as the aggregation response to ADP and collagen, the platelet sensitivity to PgI2 and the release of platelet derived proteins. As an indicator of hypercoagulability the fibrinogen level in plasma was analysed. The control group consisted of patients with chest pain but without CAD. Blood samples for platelet tests and fibrinogen analysis were obtained in the acute phase and after one year.Results.: The only difference in platelet reactivity between cases and controls was noted in their sensitivity to PgI2. The difference remained in the females but not in the male UCAD group after one year.In the acute phase a diagnosis of UCAD, elevated weight index and smoking contributed independently to increased fibrinogen levels.Conclusion: The increased fibrinogen level and decreased platelet sensitivity to PgI2 might reflect a hypercoagulable state in patients with UCAD.

Platelet-Derived PCSK9 Is Associated with LDL Metabolism and Modulates Atherothrombotic Mechanisms in Coronary Artery Disease

International Journal of Molecular Sciences ◽

10.3390/ijms222011179 ◽

2021 ◽

Vol 22 (20) ◽

pp. 11179

Author(s):

Álvaro Petersen-Uribe ◽

Marcel Kremser ◽

Anne-Katrin Rohlfing ◽

Tatsiana Castor ◽

Kyra Kolb ◽

...

Keyword(s):

Coronary Artery Disease ◽

Platelet Count ◽

Coronary Artery ◽

Platelet Function ◽

Platelet Reactivity ◽

Clinical Effects ◽

Monocyte Migration ◽

Artery Disease ◽

Pcsk9 Inhibition

Platelets play a significant role in atherothrombosis. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is critically involved in the regulation of LDL metabolism and interacts with platelet function. The effect of PCSK9 in platelet function is poorly understood. The authors of this article sought to characterize platelets as a major source of PCSK9 and PCSK9’s role in atherothrombosis. In a large cohort of patients with coronary artery disease (CAD), platelet count, platelet reactivity, and platelet-derived PCSK9 release were analyzed. The role of platelet PCSK9 on platelet and monocyte function was investigated in vitro. Platelet count and hyper-reactivity correlated with plasma LDL in CAD. The circulating platelets express on their surface and release substantial amounts of PCSK9. Release of PCSK9 augmented platelet-dependent thrombosis, monocyte migration, and differentiation into macrophages/foam cells. Platelets and PCSK9 accumulated in tissue derived from atherosclerotic carotid arteries in areas of macrophages. PCSK9 inhibition reduced platelet activation and platelet-dependent thrombo-inflammation. The authors identified platelets as a source of PCSK9 in CAD, which may have an impact on LDL metabolism. Furthermore, platelet-derived PCSK9 contributes to atherothrombosis, and inhibition of PCSK9 attenuates thrombo-inflammation, which may contribute to the reported beneficial clinical effects.

Influence on Platelet Function by Heparin in Men with Unstable Coronary Artery Disease

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646479 ◽

1991 ◽

Vol 66 (06) ◽

pp. 648-651 ◽

Cited By ~ 7

Author(s):

Ulf Berglund ◽

Lars Wallentin

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Platelet Function ◽

Ex Vivo ◽

Inhibitory Effect ◽

Controlled Study ◽

Concomitant Treatment ◽

Double Blind ◽

SummaryNinetyseven men with unstable coronary artery disease (CAD), i.e. unstable angina or a non Q-wave myocardial infarction, entered a double-blind placebo-controlled study with heparin intravenously 30,000-40,000 U daily. Platelet function was evaluated as ex vivo aggregation toward collagen and ADP and as the platelet inhibitory effect of prostacyclin, before and after 5 days of treatment. Heparin increased aggregation induced by ADP 1 εM from 39.6 ± 3.1% to 52.1 ± 4.1% (p = 0.014) and reduced the inhibition of aggregation by prostacyclin 1.0 ng/ml from 59.6 ± 3.7% to 39.3 ± 5.6% (p <0.001). No changes occurred in the placebo group.Thus, treatment with heparin enhances the platelet sensitivity to ADP and decreases the platelet inhibitory effect of prostacyclin in men with unstable CAD. Concomitant treatment with acetylsalicylic acid abolishes the increased reponse to ADP, but does not seem to influence the interaction between heparin and prostacyclin.

Persistent inhibition of platelet function during long-term treatment with 75 mg acetylsalicylic acid daily in men with unstable coronary artery disease

European Heart Journal ◽

10.1093/oxfordjournals.eurheartj.a059912 ◽

1991 ◽

Vol 12 (3) ◽

pp. 428-433 ◽

Cited By ~ 28

Author(s):

U. BERGLUND ◽

L. WALLENTIN

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Acetylsalicylic Acid ◽

Platelet Function ◽

Term Treatment ◽

Long Term Treatment ◽

Aldosterone Modulates Blood Homocysteine and Cholesterol in Coronary Artery Disease Patients – a Possible Impact on Atherothrombosis?

Physiological Research ◽

10.33549/physiolres.933668 ◽

2018 ◽

pp. 197-207 ◽

Cited By ~ 3

Author(s):

K. KAROLCZAK ◽

P. KUBALCZYK ◽

R. GLOWACKI ◽

R. PIETRUSZYNSKI ◽

C. WATALA

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Cardiovascular Diseases ◽

Adrenal Glands ◽

Ex Vivo ◽

Platelet Reactivity ◽

Control Subjects ◽

Aldosterone plays a key role in maintaining the homeostasis of the whole organism. Under some circumstances, aldosterone can contribute to the progression of cardiovascular diseases, including coronary artery disease. This study demonstrates that aldosterone associates negatively with some lipidogram parameters and positively with the concentration of homocysteine. These associations are characteristic for coronary artery disease and are not present in control subjects. The findings also indicate that in vitro aldosterone stimulates homocysteine production by rat adrenal glands, which may explain the associations observed with coronary artery disease. Moreover, we have found that aldosterone significantly modulates in vitro platelet reactivity to arachidonate and collagen – aldosterone increases the pro-aggregatory action of collagen, but decreases the pro-aggregatory potential of arachidonate. Therefore, the findings of these in vitro and ex vivo experiments indicate the existence of new pathways by which aldosterone modulates lipid- homocysteine- and platelet-dependent atherogenesis.