Spontaneous platelet aggregation in normal subject assessed by a laser light scattering method: an attempt at standardization.

Platelet aggregometry by the laser light scattering (LS) method is sufficiently sensitive to detect small platelet aggregates that form spontaneously in vitro in the absence of agonists. Platelet aggregation without agonists is named spontaneous platelet aggregation (SPA). Since SPA has been suggested to be associated with various thrombotic diseases, it is essential to measure SPA and to establish a standard range of SPA values. In this study, we measured SPA in 167 healthy subjects by the LS method and attempted to clarify various factors influencing SPA, including the blood collection procedure. We also attempted to establish a tentative standard range of SPA values. SPA was quantitatively measured in terms of the maximum total LS intensity, which reflects small aggregates formed over 10 minutes (SMAX) and the area under the total LS intensity curve of small aggregates (SAUC). Since both the values of SMAX and SAUC were skewed and the log SMAX and log AUC values showed a normal distribution, the statistical analyses were performed using log SMAX and log SAUC. The log SMAX and log SAUC were significantly higher in the samples collected using a tourniquet and/or a 21 G needle, than in those collected without a tourniquet and/or with an 18 G needle. The log SAUC values were significantly lower in samples obtained with a syringe and/or 3.8% sodium citrate than in those obtained in vacuum sampling tubes and/or 3.13% or 3.14% sodium citrate. The Ht and plasma glucose concentration influenced the log SMAX values. We propose that to standardize SPA measurements, the measurements should be completed within two hours of blood sample collection and collected using the regular concentration of citrate. The standard range of SMAX values measured in samples obtained using a tourniquet and a 21 G needle was 2.0-23.99 (*10(3) mV*count). The standard range of SAUC values measured under same conditions was 0.58-9.12 (*10(6) mV*count*min). The standard range of SMAX values measured in samples obtained using a tourniquet, 21 G needle and a vacuum tube was 1.7-29.51 (*10(3) mV*count). The standard range of SAUC values measured under same conditions was 0.59-9.33 (*10(6) mV*count*min).

Hypertensive patients with carotid artery plaque exhibit increased platelet aggregability.

BACKGROUND: Platelets play an important role in myocardial infarction and ischemic stroke events, but whether platelet aggregability is related to early stage arteriosclerosis remains unclear. METHODS: We used a novel platelet counting system which makes it possible to detect spontaneous platelet aggregation, to evaluate the relationship between platelet aggregability and carotid artery arteriosclerosis in 125 outpatients with primary hypertension (46-73 years old: 65 men, 60 women). All subjects underwent carotid artery ultrasonography to determine whether plaque was present and to estimate intima-media thickness. RESULTS: Patients with carotid artery plaques (Plaque(+), n=63) were older and had higher systolic blood pressures than patients without plaques (Plaque(-), n=62), but no significant differences in sex, body mass index, diastolic blood pressure, plasma concentrations of glucose, total cholesterol, triglyceride, lipoprotein cholesterol, fibrinogen or the platelet count in whole blood were observed between Plaque(+) and Plaque(-) groups. Plaque(+) subjects showed greater spontaneous platelet aggregability and platelet aggregation induced by 2 microM or 0.5 microM of ADP or 0.3 microM of epinephrine than the Plaque(-) group. When age and systolic blood pressure were matched (n=52 in both groups), the Plaque(+) subjects exhibited greater platelet aggregability than the Plaque(-) subjects. Platelet aggregation induced by 2 microM of ADP showed statistical significant positive correlation coefficients with age, HbA1c and diastolic blood pressure. CONCLUSION: Our results indicate that hypertensive patients with carotid artery plaque have increased platelet aggregability. A prospective study is recommended to clarify whether this increase in platelet aggregability promotes the progression of arteriosclerosis.

A case of familial hypercholesterolemia; secession from LDL-apheresis by the drug treatment with potent statin and resin.

Low density lipoprotein (LDL)-apheresis is a useful tool for the treatment of familial hypercholesterolemia (FH) with coronary artery disease (CAD). However, it gives economic, physical and mental burdens for the patients. We reports a case of FH in whom LDL-apheresis treatment was seceded with drug treatment with a potent statin and bile acid-sequestering resin. A 54-year-old woman was admitted for evaluation of atherosclerotic lesion after 4 years of LDL-apheresis and 1 year of drug medication with a potent statin, atorvastatin and resin, cholestimide with coronary angiography. She had been diagnosed as heterozygous FH when she was 46 years old. Oral medication was initiated at the outpatient clinic. LDL-cholesterol (C) level was not successfully controlled despite the administration of a statin, pravastatin, a fibrate, clinofibrate and probucol at maximum doses Concomitantly. Therefore, as combination therapy, LDL-apheresis was introduced in May 1997. However, the patient strongly complained of the economic, physical, and mental burdens of LDL-apheresis and requested discontinuation of apheresis. Therefore, LDL-apheresis was discontinued in July 2000, and oral medication was subsequently changed to a combination of atorvastatin and cholestimide, resulting in successful control of serum LDL-C level by oral medication alone. We compared coronary arteriographic findings between 1997 and 2001. No advancement of lesions was observed. We think that strong drug treatment can secede from the LDL-apheresis for treatment of patients with FH.