Changes in Platelet Size and Spleen Volume in Response to Selective and Non‐selective Β‐adrenoceptor Blockade in Hypertensive Patients

Baković, Darija; Pivac, Nediljko; Eterović, Davor; Palada, Ivan; Valić, Zoran; Pauković-Sekulić, Branka; Dujić, Željko

doi:10.1111/j.1440-1681.2008.05090.x

Cited by 25 publications

(27 citation statements)

References 38 publications

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“…The medical treatment used was also similar in both groups except β-blockers which are less commonly used in CACP group (Table II). In a recent study of hypertensive patients, 15-30 days after treatment with either selective or nonselective β-blockers, an increase in MPV with contraction of spleen has been reported [17]. Even then, in our study, MPV was lower in CACP group despite less β-blocker use.…”

Section: Discussioncontrasting

confidence: 47%

Cocaine use does not affect mean platelet volume

Akkuş

Rajpal

Vargas

et al. 2015

IMAS

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Increased mean platelet volume (MPV) is a marker of platelet activation. Platelet activation with cocaine use is not well studied. We wanted to investigate MPV levels in patients with cocaine-associated chest pain (CACP) as a marker of platelet activation. Retrospectively, MPV of 82 consecutive patients with CACP (group 1) with positive urine drug screen (UDS), without acute myocardial infarction (AMI) (group 1A) and with AMI with elevated troponin (group 1B), were included in the study. The control group (group 2) consisted of 89 consecutive patients admitted during the same time period with acute chest pain (ACP) who had negative UDS and negative cardiac markers with a normal cardiac stress test or normal coronary angiogram. Analysis showed no statistically signifi cant diff erence of MPV between group 1, 8.46 ± 1.06 fL, versus group 2, 8.7 ± 1.07 fL; p = 0.142; and between group 1A, 8.46 ± 1.05 fL, and group 1B, 8.46 ± 1.09 fL; p = 0.983. By multiple linear regression analysis, MPV was not infl uenced by cocaine abuse (R = 0.269, R 2 = 0.072, adjusted R 2 = −0.009, p = 0.562). MPV is not elevated in patients with cocaine use even when they had AMI. Further studies may be necessary to investigate the role of platelet activation in patients with cocaine use and chest pain.

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Section: Discussioncontrasting

confidence: 47%

Cocaine use does not affect mean platelet volume

Akkuş

Rajpal

Vargas

et al. 2015

IMAS

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“…Circulating platelets exhibit significant heterogeneity in size, density, age and function [24][25][26][27][28][29][30][31][32][33]. In the current study, large platelets expressed more VWF, fibrinogen, and P-selectin in response to each agonist (ADP, TRAP or AA), compared with small platelets.…”

Section: Discussionmentioning

confidence: 93%

Platelet activation patterns in platelet size sub-populations: differential responses to aspirin in vitro

Mangalpally

Siqueiros-Garcia

Vaduganathan

et al. 2010

J Thromb Thrombolysis

105

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Circulating platelets are heterogeneous in size and structure. Whether this translates into differences in platelet function and efficacy of antiplatelet therapy is unclear. Hence, we decided to investigate the activation patterns among different platelet populations differentiated by size, and to compare the inhibitory effects of aspirin in these populations. Circulating platelets from 9 healthy volunteers were separated by size and stratified into the largest and smallest quintiles. Platelets were stimulated with 75 μM arachidonic acid (AA), 10 μM ADP or 25 μM TRAP. Alpha-granule protein secretion and expression (P-selectin, VWF, fibrinogen), surface-protein activation (activated integrin αIIbβ3) were assessed. Platelet thromboxane B(2) (TxB(2)) synthesis following AA stimulation was measured in vitro before and after incubation with 265 μM aspirin. Reticulated (juvenile) platelets were assessed using thiazole orange staining. A greater number of large platelets in the largest quintile were reticulated compared with the smallest quintile (6.1 ± 2.8% vs. 1.2 ± 1.5% respectively, p < 0.001). Larger platelets also synthesized more TxB(2) than small platelets both before (1348 ± 276 pg/mL vs. 1023 ± 214 pg/mL, respectively, p = 0.01) and after aspirin (1029 ± 190 pg/mL vs. 851 ± 159 pg/mL, respectively, p = 0.03). After stimulation with each agonist, a greater proportion of large platelets bound fibrinogen, VWF, P-selectin and activated integrin αIIbβ3 than small platelets both in the presence and in the absence of in vitro aspirin. In an in vitro setting, large platelets appear to be more active than small platelets and continue to be more active even after in vitro aspirin. Platelets exhibit heterogeneity in size and structure. Whether this translates into platelet function and efficacy of antiplatelet therapy is unclear. We evaluated platelet functional properties and the effects of aspirin on separated platelet subpopulations in an in vitro setting. Platelets were sorted into the largest and smallest size quintiles using flow cytometry forward scatter. Alpha-granule protein release, dense granule content, surface protein activation and thromboxane synthesis were significantly greater in large platelets compared with small platelets, before and after stimulation with arachidonic acid, ADP and TRAP. Even after incubation with aspirin, large platelets continued to be more active than small platelets. In conclusion, large platelets are more active than small platelets and aspirin fails to eliminate these differential activation properties.

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“…Beta blocker use may also explain the overall significantly lower platelet counts in patients with CAD. Catecholamine activation leading to splanchnic activation and subsequent platelet release might be suppressed due to higher incidence of chronic use of beta blockers in the CAD patients [32, 33]. …”

Section: Discussionmentioning

confidence: 99%

Pro-coagulant activity during exercise testing in patients with coronary artery disease

et al. 2017

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BackgroundStrenuous exercise may trigger myocardial infarction through increased pro-coagulant activity. We aimed to investigate whether patients referred for exercise testing, who were found to have angiographically verified coronary artery disease (CAD), have a more hypercoagulable profile during exercise testing than those without CAD.MethodsPatients with symptoms of stable CAD were examined with exercise electrocardiography on bicycle ergometer. Venous blood samples were taken at rest and within 5 min after end of exercise. The following haemostatic variables were analyzed: tissue factor pathway inhibitor (TFPI) activity and antigen, prothrombin fragment 1 + 2 (F1 + 2), D-dimer and endogenous thrombin potential (ETP). All participants underwent conventional coronary angiography. CAD was defined as having any degree of atherosclerosis.ResultsOut of the 106 patients enrolled, 70 were found to have CAD. Mean exercise duration was 10:06 ± 4:11 min, with no significant differences between the groups. A significant increase from baseline to after exercise testing was observed in all measured markers in the total population (p ≤ 0.002 for all). In patients with angiographically verified CAD, total TFPI was significantly lower at baseline compared to patients without CAD (median value 67.4 and 76.6 ng/ml respectively, p = 0.027). However, no significant differences in changes of any of the measured markers during exercise were observed between the two groups.ConclusionPro-coagulant activity increased during short-term strenuous exercise testing in patients with symptoms suggestive of CAD. However the hypercoagulable state observed, was not more pronounced in patients with angiographically verified CAD compared to patients without CAD. NCT01495091.

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Changes in Platelet Size and Spleen Volume in Response to Selective and Non‐selective Β‐adrenoceptor Blockade in Hypertensive Patients

Cited by 25 publications

References 38 publications

Cocaine use does not affect mean platelet volume

Cocaine use does not affect mean platelet volume

Platelet activation patterns in platelet size sub-populations: differential responses to aspirin in vitro

Pro-coagulant activity during exercise testing in patients with coronary artery disease

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