Summary
Platelet aggregation (PA), platelet thromboxane B2 (TXB2) generation and 14C 5-hydroxytryptamine (5HT) release were studied in 13 patients with unstable angina,
and compared to 14 patients with stable angina and 16 healthy controls. A typical
pattern, distinct in 4 aspects from stable angina patients or controls, was observed
in the unstable angina patients. ADP or collagen induced shape change was 3-4 times
greater, the extent of epinephrine induced PA was nil or very low, the extent of collagen
induced 14C 5HT release was also reduced while collagen induced platelet TXB2 generation was increased in spite of a reduced extent of PA. The extent of ADP or
collagen induced PA was also significantly reduced. These results indicate a platelet
membrane abnormality occurring presumably during contact of the circulating platelets
with a non-occlusive thrombus observed at sites of ruptured plaques in unstable angina
patients. Since also the pattern (20-30% overlap with control values) was distinct
from that of stable angina patients, it might indicate an active thrombotic process.
Plasma β-thromboglobulin (βTG) and TXB2 levels and serum TXB2 generation were also studied in the cardiac patients and controls and in another
10 patients with advanced peripheral occlusive arterial disease (POAD). Plasma βTG
and TXB2 levels were slightly elevated in the unstable angina patients and markedly elevated
in the POAD patients. Serum TXB2 generation was, however, elevated in the stable angina patients (p <0.002) and more
so in the unstable angina patients (p <0.001) compared to controls or to POAD patients.
This was presumably mediated through enhanced thrombin generation. These results suggest
that the measured plasma βTG variable in the unstable angina patients is not useful
in the assessment of in vivo platelet activation. It is presumably reflecting the
sum of local enhanced platelet activation (at sites of ruptured plaques) and of reduced
function of the “defective” circulating platelets. The ability of the platelets of
unstable angina patients to generate large amounts of TXB2 if occurring in vivo might induce an intense coronary vasospasm.
Keywords
Unstable angina - Thromboxane generation - Thrombosis
