The distributions of platelet volume and density were measured in 15 men suffering myocardial infarction and in 22 healthy controls. The method used separated 93% of the total platelet population from whole blood. Mean platelet volume of the study group compared with that of controls was increased by a mean of 0 98 fl (p < 0-001) in the first 12 hours after myocardial infarction, and by 1 24 fl six weeks later (p < 0 001). Distribution of platelet volume remained log normal after myocardial infarction. Modal platelet density was increased by a mean of 25 g/l (p < 0-05) after myocardial infarction. Platelet volume is probably chronically large in men suffering myocardial infarction and may be related to changes in megakaryocytes. It is suggested that the increase in platelet volume occurs before infarction.

Platelet count and volume were measured in man (n = 51) and rat (n = 9). Bone marrow megakaryocyte nuclear and megakaryocyte planimetric areas were measured in man (n = 11) and rat (n = 9). Megakaryocyte cytoplasmic volumes were computed from the planimetric areas. Rat had a significantly higher (p less than 0.001) mean megakaryocyte cytoplasmic volume than man and a significantly wider range (p less than 0.01). Rat mean platelet volume was significantly lower (p less than 0.001) than man while the rat platelet count was significantly higher (p less than 0.001) than man. A computer simulation of the random binary sequential division of megakaryocyte cytoplasm was used to explain these observations. Transmission electron microscopy shows that the site of this binary sequential division is probably the pulmonary circulation. The number of circulating megakaryocytes ml-1 of blood which would maintain the observed platelet counts was computed. The ellipses of constant density associated with the bivariate Gaussian distribution of platelet count and mean volume were computed. Platelet volume distributions of 13 men within two standard deviations of the composite mean of platelet count and mean volume were used to construct the platelet volume distribution signature in normal man. A similar platelet volume distribution signature for rat was constructed. The two distributions were significantly different. Neither rat nor man had a log Gaussian platelet volume distribution, however the measured volume distributions tended towards a log Gaussian curve.

SummaryMegakaryocyte cytoplasmic volumes were studied in 13 subjects 18 ± 2 days after admittance to the coronary care unit. Seven had suffered a myocardial infarction (MI group) while six had chest pain but no recent infarction. Megakaryocytes were also studied in 10 subjects suffering coronary sudden unexpected death (CSD group) and 11 subjects suffering sudden unexpected un-natural death. There was no significant difference between the megakaryocyte cytoplasmic volume distributions of the MI and CSD groups, although they had a significantly greater mean (p <0.01) and range (p <0.001) than theirrespectivecontrolgroups.There was no significant difference in platelet volumes observed within 24 hr of the infarct and 18 ± 2 days later. Mean platelet volume was significantly correlated (r = 0.89, p <0.006) to mean megakaryocyte cytoplasmic volume in the MI group. A computer simulation of platelet production showed no significant difference between platelet volumes observed in the MI group and those estimated to be circulating before death in the CSD group.

IntroductionDetermination of the QT interval dispersion by means of a standard ECG at rest has been widely used for cardiovascular risk assessment during the last 15 years as one of the recent explanations for the development of life threatening ventricular arrhythmias. However, little is known about the relation between QT dispersion and the severity of coronary artery atherosclerosis as defined by SYNTAX score.Aim of work:The present study was done to assess the correlation between QTc dispersion and the severity of coronary artery disease in acute ST elevation myocardial infarction (STEMI) detected by SYNTAX score.Patients and methodsIt included 50 patients who were non-diabetic, non-hypertensive and diagnosed as acute STEMI within 6 months undergoing coronary angiography in the cath. lab. of Assiut University Hospital. QT dispersion was calculated as the difference between the longest (QT max) and the shortest QT (QTmin) interval recorded by standard 12 lead ECG. The QT interval was corrected by using Bazett’s formula (QTc = QT/square root of R-R interval in seconds). Corrected QT dispersion (QTcd) was defined as the difference between the maximum and minimum QTc for a given heart rate. The SYNTAX score is calculated by syntax calculator, a new tool to grade the complexity of coronary artery disease.ResultsOut of 50 participating patients, there were 43 (86%) males with mean age 53.9 ± 12.1 years. The mean QTc dispersion was 83.1 ± 20.3 ms, while mean SYNTAX score was 11.6 ± 6.1. There is a strong positive correlation between QTc dispersion and SYNTAX score. This was not related to age, gender, risk factors or family history of ischemic heart disease. Of note, there was a relationship between QTc dispersion and serum creatinine.ConclusionsOur study concluded that there is a significant positive correlation between corrected QT dispersion and severity of coronary artery disease as assessed by SYNTAX score.

Rabbits were fed either 2 g cholesterol in 10 ml olive oil daily with normal diet (n = 5) or normal diet alone (n = 5). After 12 weeks, the cholesterol-fed animals had developed fatty plaques involving 24% ± 4% of the surface area of the aorta; the control animals had none. Mean platelet volume was significantly smaller (p < 0.04) in the cholesterol-fed animals (4.1 ± 0.3 fl) compared with the controls (4.8 ± 0.4 fl). The heterogeneity of the average volume distributions of the two groups, characterized by the statistical parameters of the coefficient of variation, skewness, and kurtosis, was also significantly different. Platelet count was significantly higher (p < 0.001) in the cholesterol-fed group (7.48 ± 1.06 x 10" platelets/liter blood) compared to the control group (4.86 ± 0.60 x 10 11 platelets/liter blood). Mean megakaryocyte cytoplasmic volume was significantly larger (p < 0.001) in the cholesterol-fed rabbits (12,262 ± 1485 fl) compared with controls (6,814 ± 761 fl). The range of cytoplasmic volumes was also significantly increased in the cholesterol-fed rabbits. A significant (p < 0.01) increase in mean megakaryocyte nuclear volume in the cholesterol-fed animals was accompanied by a nonsignificant increase in mean nuclear DNA content: 30.2 ± 3.7 N compared with a control value of 23.6 ± 4.0 N. This evidence indicates that a high cholesterol diet in rabbits is associated with changes in platelet production from megakaryocytes as well with as the development of atherosclerosis. (Arteriosclerosis 5:604-612, November/December 1985) P latelets in vascular disease have increased reactivity in both human and animal models. 12 The cause of this increased reactivity may either be an effect of vessel wall changes on normal platelets or be related to an intrinsic change in the platelets themselves. In humans, the increased platelet reactivity has been associated with platelet size changes 1 which have been confirmed in recent studies.3 " 5 This evidence suggests that there may be alterations in platelet production in vascular disease. Two further observations support this hypothesis. Men who suffered sudden cardiac death associated with atheromatous arteries had larger megakaryocytes than a control group who died unexpectedly from unnatural causes.6 Similar large megakaryocytes, which produced larger than normal platelets, were also observed in men with acute myocardial infarction.