Circulating aggregated platelets in coronary artery disease.

Circulating aggregated platelets were assessed in 30 patients with stable angina, 22 with unstable angina and 50 with acute myocardial infarction (AMI). Fifty healthy volunteers and 20 noncardiac patients served as controls. One milliliter of venous blood was separated into 2 solutions: 1 composed of ethylenediamine tetraacetic acid (EDTA) and formalin containing reversible and aggregates and 1 composed of EDTA alone containing irreversible aggregates only. By direct microscopic readings the percentage of platelets forming aggregates/1,000 counted platelets was determined in the 2 solutions. The number of reversibly aggregated platelets was estimated by subtracting the percentage of aggregated platelets in the second solution from that in the first solution. In patients with stable angina the percentage of aggregated platelets was higher than in control subjects (15 +/- 4% vs 7 +/- 2%, p less than 0.001). Most aggregated platelets (72% and 76%, respectively) were irreversibly aggregated. In the unstable angina group the percentage of aggregated platelets was similar to that of the AMI group (24 +/- 13% and 24 +/- 10%) and significantly higher than in the stable angina group. Only 11% and 17% of aggregated platelets in patients with stable angina and AMI were irreversibly aggregated and 89% and 83% of them were reversibly aggregated. Participation of platelets in the pathogenesis of unstable angina and AMI may be related to the early reversible phase of platelet activation.

Circulating platelet aggregate size in ischemic heart disease.

Platelet aggregate size was measured in 178 patients with ischemic heart disease, among whom 56 had stable angina, 42 suffered from unstable angina, and 80 had had uncomplicated acute myocardial infarction. A group of 50 healthy volunteers and 20 hospitalized noncardiac patients served as controls. Venous blood (0.5 cc) was introduced into a solution containing 11.7 mM EDTA and 1.0 g formaldehyde. Platelet aggregate size was determined by microscopic reading as the number of platelets forming aggregates (per 1000 counted platelets) divided by the number of aggregates. Mean aggregate size was found not significantly different in both control groups, as well as in patients with stable angina and acute myocardial infarction (2.21 +/- 0.36 platelets, 2.20 +/- 0.58 platelets, 2.28 +/- 0.19 platelets, 2.76 +/- 1.07 platelets, respectively, p = NS). The highest value was found in the unstable angina group: 4.00 +/- 1.40 platelets (p less than 0.001 vs other studied groups). Platelet aggregate size was found not to be related to sex, age, medication, or coronary risk factors. Unstable angina may thus be a unique entity in ischemic heart disease concerning its platelet behavior, demonstrated in this study by the increased size of peripheral platelet aggregates, which may have pathogenetic, diagnostic, and eventual therapeutic implications.

Neuropsychological profile linked to low dopamine: in Alzheimer's disease, major depression, and Parkinson's disease.

A distinct pattern of neuropsychological deficits was associated with low homovanillic acid (HVA) in the cerebrospinal fluid of 21 patients with: Alzheimer's disease (9), Parkinson's disease (8) and major depressive disorders (4). Regardless of clinical diagnosis, patients with low HVA were slower on a test of efficiency of processing timed information, and showed greater benefit from semantic structure on a verbal fluency task than patients with high HVA. However, low HVA subjects were not significantly impaired on confrontation naming (Boston Naming Test). Across three diagnostic groups, patients with lower HVA also tended to have more extrapyramidal motor signs and were significantly more depressed. These results demonstrate a significant relationship between specific neuro-behavioural deficits and dopaminergic activity which cuts across traditional diagnostic categories.