[Autonomic nerve function expressed by the baroreflex sensitivity (BRS) in elderly adults].

We examined 24 hour heart rate variability (HRV) components and baroreflex sensitivity (BRS) in elderly adults. Forty-eight subjects, aged 65-69 years old (24 men, 24 women) were examined in this study. BRS was measured in the morning (8:00-9:00) using noninvasive cross spectral analysis. There were significant correlations between BRS and low-frequency (LF) power (r = 0.593, p < 0.001) of HRV, and between BRS and high-frequency (HF) power (r = 0.402, p < 0.005). BRS values were lower in women compared with men (p < 0.01), and LF/HF was significantly lower in women than in men (p < 0.05).

[A case of heterozygous familial hypercholesterolemia showing the regression of coronary atherosclerosis by LDL-apheresis].

A case showing the regression of coronary atherosclerosis by the treatment with LDL-apheresis, was reported. The patient was a 67-year old female with heterozygous familial hypercholesterolemia. She had noticed the xanthelasma or left cubital xanthoma at the age of 50 years old. She was informed about her high serum cholesterol level (greater than 350 mg/dl), and the abnormal thickness of her bilateral achilles tendon at the age of 61 years. As her serum cholesterol level did not decrease sufficiently with several lipid-lowering drugs, she was referred to our hospital in order to obtain treatment for it by LDL-apheresis at the age of 66 years. LDL-apheresis was performed once every two weeks with drugs such as probucol, cholestyramine and pravastatin. Her coronary angiogram after two and half years of LDL-apheresis showed a decrease of the coronary narrowing in segment 1 and segment 13 (from 96.8% to 74.6% in segment 1, and from 81.5% to 61.7% in segment 13, respectively). The thickness of her bilateral achilles tendons had also decreased from 18 mm in the right and 19 mm in the left to 14 mm in both, after receiving LDL-apheresis for two and half years. It is suggested from the result of this case that the regression of coronary atherosclerosis could be expected after treatment with LDL-apheresis in hypercholesterolemic patients.

Proteoglycan obtained from bovine aorta suppress thrombin-induced platelet aggregation.

Proteoglycan (PG), isolated and purified from bovine aorta (intima-media), consisted of 68.6% chondroitin 4/6-sulfate (CS 4/6-S), 30% dermatan sulfate (DS), 1.4% heparan sulfate (HS), and a trace of hyaluronic acid (HA). PG did not affect platelet aggregation induced by ADP, collagen, and epinephrine, but inhibited that induced by thrombin. Of the standard GAGs investigated, hyaluronic acid (HA) and CS-4/6-S slightly inhibited only thrombin-induced platelet aggregation. However, PG and standard GAGs did not affect the thrombin induced aggregation of washed platelets. The effect of PG after papain digestion on thrombin-induced platelet aggregation was less potent than that before. It is suggested by the results of this study that PG in the aorta inactivates plasma thrombin, probably by inhibiting thrombin activators or potentiating substances which inactivate thrombin and that these effect of PG would be mainly due to PG-DS and partly due to PG-HS.

Heparin-releasable platelet factor 4 in patients with coronary artery disease.

Recently, platelet factor 4 (PF4) release by heparin (heparin-releasable PF4) has been examined as a useful marker of the interaction between the substances liberated from circulating platelets and the vascular endothelium. We compared the plasma levels of PF4 and beta-thromboglobulin (beta-TG) after intravenous heparin injection in patients with coronary artery disease (CAD) and normal control subjects. We also studied the effects of low-dose aspirin (81 mg/day) on the plasma level of heparin-releasable PF4 in the CAD patients. Blood samples were obtained before and 5 min after the intravenous injection of heparin (1,000 IU) from 23 patients with CAD and 15 normal control subjects. Although the plasma beta-TG level remained unchanged after heparin injection, the plasma PF4 level markedly increased in both groups. There was a significant difference in plasma PF4 levels at 5 min after heparin injection between the CAD group (100.1 +/- 38.1) and the control group (61.0 +/- 24.0) (p less than 0.01). The PF4/beta-TG ratio after heparin injection was also higher in the CAD group than in the control group (p less than 0.01). There was a correlation between the PF4/beta-TG ratio after heparin and the Gensini CAD score, which defines the severity of coronary atherosclerosis (r = 0.489, n = 23, p less than 0.01). Low-dose aspirin was administered to 11 CAD patients for 246.0 +/- 28.8 days. Blood samples for the assay of PF4 and beta-TG were obtained as stated above, and platelet aggregation, thromboxane B2 (TxB2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) levels were also measured before and during aspirin administration.(ABSTRACT TRUNCATED AT 250 WORDS)