[Thrombocyte aggregation and serum thromboxane in patients with acute myocardial infarction]. / Trombocytaggregation og serum-tromboxan hos patienter med akut myokardieinfarkt.

Treatment with acetylsalicylic acid reduces the mortality following acute myocardial infarction (AMI). The mode of action is unknown but studies of patients with unstable angina pectoris have revealed that acetylsalicylic acid inhibits the platelet aggregating and vessel-constricting metabolite thromboxane B2. In the present investigation, we have examined ten patients with AMI. Platelet aggregation induced by arachidonic acid and serum thromboxane B2 were compared with findings in patients with unstable angina pectoris and healthy control persons. The investigation reveals that the platelet aggregateability is increased significantly already on the first day after AMI and increases in all cases for 14 days (p less than 0.001). Serum thromboxane B2 concentration is normal on the first day and increases gradually in the course of 14 days (p less than 0.05) to values which are not significantly different from those observed in patients with unstable angina pectoris. Patients with AMI have significantly increased platelet aggregation and increasing concentrations in the blood of thromboxane B2. Acetylsalicylic acid inhibits platelet aggregation and lowers thromboxane B2 concentration in the blood which may explain the effect of this preparation in reducing the mortality after AMI.

[Thrombocyte aggregation and serum thromboxane B2 in patients with unstable angina pectoris treated with diltiazem or verapamil]. / Trombocytaggregation og serum-tromboxan-B2 hos patienter med ustabil angina pectoris behandlet med diltiazem eller verapamil.

Patients with unstable angina pectoris have increased thrombocyte aggregation and disturbances in serum prostaglandin balance. As a pilot project, we conducted a single-blind investigation of 24 patients with unstable angina pectoris treated with dilthiazem (n = 12, 240-360 mg) or verapamil (n = 12, 240-360 mg) for ten days. At the commencement of the investigation, both patient groups had hyperaggregating thrombocytes and increased serum-thromboxan-B2 (TXB2) as compared to healthy individuals (p < 0.01). In the patient group treated with dilthiazem, the aggregation threshold rose (p < 0.01), and the serum TXB2 values fell to approximately normal (p < 0.05). In the patient group treated with verapamil, no significant changes were observed in the measurements registered. The difference between the two groups remained significant during the entire therapeutic period (p < 0.01). Thus, dilthiazem appears to counteract thrombocyte aggregation in patients with unstable angina pectoris.

High density lipoprotein cholesterol and arteriography in intermittent claudication.

Overnight fasting plasma lipoprotein and lipid concentrations were measured in a group of 76 patients with peripheral arterial disease (PAD)--main symptom: intermittent claudication--and compared to those of 21 controls, matched with the patients according to age, sex, body-mass index, alcohol and tobacco consumption, but without any signs of peripheral arterial disease. Significantly lower median values of high density lipoprotein cholesterols (HDL-C) (P less than 0.01), and significantly higher median values of low density lipoprotein cholesterols (LDL-C) (P less than 0.05) were found in the PAD group. The results also showed significantly lower ratios of HDL-C/LDL-C and HDL-C/total cholesterol in the PAD group when compared to the controls (both P less than 0.005). No significant differences were demonstrated concerning very low density lipoprotein, total cholesterol, or triglyceride plasma concentrations. Evaluation of arteriograms showed a significant negative correlation between HDL-C concentrations and the extent of arteriosclerotic lesions in the lower extremities (P less than 0.05). Thus, not only were the HDL-C and LDL-C levels different in the PAD group, but we also found a correlation between HDL-C and the severity of vascular disease.

Unstable angina pectoris. Platelet behavior and prognosis in progressive angina and intermediate coronary syndrome.

Platelet behavior was compared in two groups of patients with unstable angina: 13 patients with rest pain and ST depression on the electrocardiogram (the intermediate coronary syndrome), 14 patients with progressive angina without rest pain, and 20 healthy controls. Both patient groups had hyperaggregating platelets when compared with the controls (p less than 0.01). Platelet aggregation was measured ex vivo in the presence of arachidonic acid. Serum thromboxane B2, plasma beta-thromboglobulin, and platelet factor 4 were all temporarily increased in the group with intermediate coronary syndrome (p less than 0.01), whereas measurements in patients with progressive angina were not significantly different from the controls. Thus, patients with the intermediate coronary syndrome, who have a high frequency of suboccluding coronary artery thrombus and a very serious prognosis, had severely altered platelet behavior in contrast to patients with progressive angina.

The influence of fenflumizole on platelet aggregation in patients with unstable angina pectoris.

We have studied the antiaggregatory effect of fenflumizole, a new non-steroidal antiinflammatory imidazole derivative, in ten patients with unstable angina pectoris. We have measured the aggregation induced by arachidonic acid (AA), ADP, and collagen, and serum or plasma concentrations of beta-thromboglobulin (beta-TG), platelet factor 4 (PF-4), thromboxane B2 (TXB2), and fenflumizole before, during, and after treatment with fenflumizole in two different regimens either as 10 mg b.i.d. for four days followed by 10 mg daily for six days (Group I, n = 5), or as 20 mg b.i.d. for four days followed by 20 mg daily for six days (Group II, n = 5). The threshold concentration of AA-induced platelet aggregation increased in both groups by the first day of treatment, the mean increase being significantly higher in Group II than in Group I. There was close correlation between serum fenflumizole and the threshold concentration of AA-induced platelet aggregation (r = 0.95). A significant fall in TXB2 occurred in both groups. In group I TXB2 concentrations subsequently increased to initial values during treatment, whereas it remained significantly reduced in Group II. There were no significant changes in collagen and ADP aggregation, and beta-TG and PF-4 concentrations remained unchanged during and after the administration of fenflumizole.

Arachidonic Acid-induced Platelet Aggregation ex vivo in Patients with Acute Ischaemic Heart Disease.

The threshold concentrations of arachidonic acid (AA) required to induce platelet aggregation were measured in platelet-rich plasma (PRP) from patients with acute ischaemic heart disease and healthy controls. The analytical precision of the test was very good (coefficient of variation 0-4%). Analytical accuracy was evaluated by comparing the results with threshold values for collagen-induced platelet aggregation, and a significant correlation was found (r = 0.56; p<0.01). When comparing the serum levels of thromboxane B(2) to threshold values for AA-induced platelet aggregation an inverse relationship was found (r = -0.37; p<0.01). In the clinical study significantly increased aggregability to AA was seen in patients with unstable angina pectoris (n = 13) compared to patients with stable angina pectoris (n = 14), (p<0.01), and both groups had hyperaggregating platelets compared to healthy controls (n = 27), (p<0.01). The patients with acute myocardial infarction (n = 10) had nearly normoaggregating platelets for the first 2-3 days after admission, but after a week and at day 14 their platelets showed significant hyperaggregability compared to healthy controls (p<0.01). Thus studies of AA-induced aggregation ex vivo suggest that patients with unstable angina pectoris and acute myocardial infarction, in whom coronary thrombus is frequently present, have increased platelet aggregability compared to patients with stable angina pectoris and healthy controls.

High-density lipoprotein cholesterol assay by magnesium dextransulphate precipitation.

A method for determination of high-density lipoprotein cholesterol (HDL-C) is evaluated: after precipitation of low and very low lipoprotein cholesterol in serum by magnesium dextransulphate, HDL-C is determined by an enzymatic method. The precision of the method was good: coefficient of variation 4%. The accuracy was good, evaluated by correlating HDL-C results from the present assay to the results obtained from three other HDL-C assays (n = 17): ultracentrifugation r = 0.91, phosphotungstate/MgCl2 r = 0.98, and alpha-lipoprotein determination by electrophoresis r = 0.91 (p less than 0.01). Repeated analysis showed that serum may be kept at 4 degrees C for 1 month, at -20 degrees C for 2 months, and requires -80 degrees C for longer storage. Ten patients with acute myocardial infarction showed significantly lower HDL-C from day 4 in the acute phase and during the first 3 months follow up (p less than 0.05). Eighty patients with peripheral vascular disease, who were compared to a group of matched controls, also showed significantly decreased serum HDL-C (p less than 0.01). The present HDL-C assay is easy, fast and reliable and is considered a valuable clinical test.