Platelet Reactivity in Acute Coronary Syndromes: Evidence for Differences in Platelet Behaviour between Unstable Angina and Myocardial Infarction

2001 ◽  
Vol 85 (06) ◽  
pp. 989-994 ◽  
Author(s):  
Anthony Mathur ◽  
Monique Robinson ◽  
James Cotton ◽  
John Martin ◽  
Jorge Erusalimsky
Keyword(s):  
Myocardial Infarction ◽  
Platelet Count ◽  
Unstable Angina ◽  
Mean Platelet Volume ◽  
Acute Coronary Syndromes ◽  
Platelet Reactivity ◽  
Fundamental Difference ◽  
Platelet Volume ◽  
Platelet Size ◽  
Coronary Syndromes

SummaryPrevious work has shown that P-selectin and mean platelet volume, two markers associated with platelet reactivity, are elevated in acute coronary syndromes. This study investigated the possibility that these markers may define unstable angina (UA) and acute myocardial infarction (MI) as two separate conditions based on platelet behaviour. Mean platelet volume (MPV) was higher in UA patients (n = 15) than in those diagnosed with MI (n = 15) (10.7 ± 0.25 fL, vs. 9.8 ± 0.27 fL, P = 0.005). Platelet count was lower in UA than in MI (215 ± 13 × 109/L vs. 271 ± 20 × 109/L, P = 0.03). The percentage of platelets expressing P-selectin was higher in MI than in UA (9.1 ± 1.9% vs. 4.2 ± 0.85%, P = 0.03). This parameter was positively correlated with MPV in UA (r = 0.5, P = 0.04) but negatively correlated in MI (r = -0.6, P = 0.01), with no correlation for ACS as a whole (r = –0.32, P = 0.1). Our results suggest that in MI there is an acute process of generalised platelet activation that is unrelated to changes in MPV, whereas in UA there is an ongoing process of platelet consumption that leads to an increase in platelet size to compensate for a persistent decrease in platelet count. This study suggests that there is a fundamental difference in platelet biology between these two diseases.

scholarly journals Increased Mean Platelet Volume (MPV) in Patients with ST Elevation Myocardial Infarction (STEMI) Compared to Non-ST Elevation Myocardial Infarction (NSTEMI) Patients

2020 ◽  
Vol 6 (2) ◽  
pp. 145
Author(s):  
Tri Ratnaningsih ◽  
Istiqomah Istiqomah
Keyword(s):  
Myocardial Infarction ◽  
Risk Factor ◽  
Mean Platelet Volume ◽  
Acute Coronary Syndromes ◽  
St Elevation Myocardial Infarction ◽  
Platelet Volume ◽  
Cross Sectional ◽  
Coronary Syndromes ◽  
St Elevation ◽  
Vascular Mortality

Platelets are known to have a role major in the pathogenesis of atherothrombosis. More giant and hyperreactive platelets accelerate the formation of an intracoronary thrombus. An increased MPV as an indicator of larger and more reactive platelets represents a risk factor for overall vascular mortality, including myocardial infarction. This study aimed to identify the increase of Mean Platelet Volume in Patients with Acute Coronary Syndromes, especially in ST-elevation myocardial infarction and Non-ST-elevation myocardial infarction. Thus this parameter can be used as consideration for diagnosis and treatment decisions. This research is an analytic observational with a cross-sectional method. The subjects were patients with STEMI and NSTEMI who were hospitalized in ICCU Dr.Sardjito Hospital Yogyakarta. Thirty-four subjects STEMI and NSTEMI patients at Dr. Sardjito Hospital, consisting of 28 males (82,35%) and six women (17,65%) with a mean age of 55,5 ± 10,3 years. The results showed that MPV in AMI was higher in patients with STEMI than NSTEMI, but this difference is not significant (p = 0,091). This study concludes that MPV to be higher in patients with STEMI compared to NSTEMI. MPV may be used as a marker of myocardial infarction in clinically appropriate situations.

OP-116 PLATELET COUNTS AND MEAN PLATELET VOLUME IN PATIENTS WITH ACUTE CORONARY SYNDROMES

2013 ◽  
Vol 163 (3) ◽  
pp. S46
Author(s):  
M. Yalçın ◽  
Z. Işılak ◽  
O. Uz ◽  
M. Atalay ◽  
E. Kardeşoglu ◽  
...  
Keyword(s):  
Mean Platelet Volume ◽  
Acute Coronary Syndromes ◽  
Platelet Volume ◽  
Platelet Counts ◽  
Coronary Syndromes

scholarly journals Platelet-associated immunoglobulin, platelet size, and the effect of splenectomy in the Wiskott-Aldrich syndrome

Blood ◽  
1985 ◽  
Vol 65 (6) ◽  
pp. 1439-1443 ◽  
Author(s):  
L Corash ◽  
B Shafer ◽  
RM Blaese
Keyword(s):  
Platelet Count ◽  
Mean Platelet Volume ◽  
Critical Role ◽  
Volume Distribution ◽  
Normal Range ◽  
Platelet Volume ◽  
Wiskott Aldrich Syndrome ◽  
Platelet Size ◽  
Number Of Patients ◽  
Effect Of Splenectomy

Abstract Wiskott-Aldrich syndrome (WAS) thrombocytopenia is frequently improved by splenectomy, although the mechanism of the thrombocytopenia and its resolution are unknown. Previous studies in two patients have shown that mean platelet volume, which is characteristically reduced in WAS, increased along with platelet count postsplenectomy. Additional studies in a limited number of patients have also demonstrated that platelet- associated immunoglobulin G (PAIgG) is elevated presplenectomy, but to date no postsplenectomy data have been reported. The present study was performed to more fully evaluate the effect of splenectomy on platelet volume and PAIgG in WAS. Before splenectomy, mean platelet volume was reduced but platelet size was broadly distributed with substantial overlap of the normal range. PAIgG was significantly elevated in 13 of 14 presplenectomy WAS patients (means = 78.9 fg per platelet) and fell to normal levels postoperatively (means = 4.0 fg per platelet). Platelet count and clinical status improved postsplenectomy, and mean platelet volume and platelet volume distribution returned to the normal range. WAS subjects who relapsed with recurrent thrombocytopenia redeveloped elevated PAIgG but maintained normal platelet size. The spleen appears to play a critical role in a process that may be immunologically mediated and results in reduced platelet size.

Platelet volume subpopulations in acute myocardial infarction: an investigation of their homogeneity for smoking, infarct size and site

1985 ◽  
Vol 68 (4) ◽  
pp. 419-425 ◽  
Author(s):  
Y. T. Kishk ◽  
E. A. Trowbridge ◽  
J. F. Martin
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Count ◽  
Heart Disease ◽  
Ischaemic Heart Disease ◽  
Mean Platelet Volume ◽  
Control Group ◽  
Disease Group ◽  
Platelet Volume ◽  
Asymptomatic Group

1. Mean platelet volume and count were measured in three groups: patients with acute myocardial infarction, a control group with myocardial ischaemia but no infarction and an asymptomatic group of young males. 2. Mean platelet volume was significantly larger in the myocardial infarction group compared with the ischaemic heart disease group or the asymptomatic group. 3. Two subpopulations were present within the myocardial infarction group. One subgroup had a large mean platelet volume and low count. The other subpopulation was indistinguishable, with regard to platelet count and mean volume, from the ischaemic heart disease group. 4. Over 60% of the myocardial infarction group lay in the area of high platelet volume and low count compared with 13% of the ischaemic heart disease control group and 38% of the asymptomatic group. Acute myocardial infarction is likely to be associated with a large mean platelet volume and low count compared with the ischaemic heart disease group. There is no statistical evidence that this condition is related to smoking or size and site of infarct. 5. This evidence suggests that large mean platelet volume and low platelet count could be a major risk factor for myocardial infarction.

Evidence of Phylogenetic Canalisation of the Circulating Platelet Mass in Man

1972 ◽  
Vol 27 (01) ◽  
pp. 159-172 ◽  
Author(s):  
W. E von Behrens
Keyword(s):  
Platelet Count ◽  
Mean Platelet Volume ◽  
Total Mass ◽  
Prognostic Significance ◽  
Platelet Volume ◽  
Platelet Size ◽  
Biochemical Function ◽  
Objective Classification ◽  
The Mean ◽  
Platelet Mass

SummaryPhylogenetically mammalian platelets are an apocrine secretion from nucleated thrombocytes, and biologically the number of circulating fragments is irrelevant compared with their total mass and biochemical function. The literature on human genetic derangements affecting the circulating platelet mass is reviewed. The product of platelet count and platelet volume is shown to be “canalised” since many congenital forms of thrombocytopenia are associated with a reciprocal increase in the mean platelet volume. Considerations of platelet size are essential since macrothrombocytopenia is a racial characteristic of many Mediterranean peoples and probably also occurs frequently in others races. The location of platelet disorders in relation to the phylogenetic canal provides an objective classification which has diagnostic, therapeutic and prognostic significance.

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