Enhanced Platelet Aggregation As A Risk Factor For Vascular Disease And Its Thromboembolic Complications

Pulmonary vascular disease is a risk factor for the surgical management of common arterial trunk. Surgical repair, therefore, is usually performed in early infancy, before irreversible changes can occur in the epulmonary vasculature. Because of this, there has been an increasing tendency to dispense with cardiac catheterisation as a means of assessing pulmonary vascular disease. Cardiac catheterisation, nonetheless, is still performed when there is a risk of pulmonary vascular disease, such as in older children. There are no clear guidelines, however, as to who should be catheterised. We have developed a simple screening test to help make this decision.

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Spontaneous platelet aggregation as a predictive risk factor for vascular occlusions in healthy volunteers? Results of the HAPARG Study

Atherosclerosis ◽

10.1016/s0021-9150(99)00056-8 ◽

1999 ◽

Vol 144 (1) ◽

pp. 211-219 ◽

Cited By ~ 27

Author(s):

H Breddin

Keyword(s):

Risk Factor ◽

Platelet Aggregation ◽

Healthy Volunteers ◽

Predictive Risk Factor ◽

Predictive Risk ◽

Spontaneous Platelet Aggregation ◽

Vascular Occlusions

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Abstract P676: Rates of Preventable Thrombectomy in Acute Ischemic Stroke

Stroke ◽

10.1161/str.52.suppl_1.p676 ◽

2021 ◽

Vol 52 (Suppl_1) ◽

Author(s):

Rakhee Lalla ◽

Ryan Dunlow ◽

Karen L Yarbrough ◽

Prachi Mehndiratta ◽

Michael S Phipps ◽

...

Keyword(s):

Risk Factors ◽

Risk Factor ◽

Vascular Disease ◽

Antiplatelet Agent ◽

Left Ventricular ◽

Vascular Risk Factors ◽

Large Vessel ◽

Favorable Outcome ◽

Vascular Risk ◽

History Of

Introduction: The AHA notes that more than 76% of strokes are the first occurrence. There are class 1 recommendations for the management of common risk factors such as atrial fibrillation (AF), hyperlipidemia (HLD), hypertension (HTN), diabetes (DM), and vascular disease. The purpose of this study is to investigate the percentage of large vessel strokes that are potentially preventable with adequate management of vascular risk factors. Methods: A retrospective chart review was conducted on all patients undergoing endovascular therapy (EVT) from 2012-2019. Data was collected on vascular risk factors present prior to admission including HTN, DM, HLD, AF, and smoking. Preventable stroke was defined as having at least one of the following: untreated AF, untreated HLD, poorly controlled HTN (presence of left ventricular hypertrophy on transthoracic echo), history of vascular disease not on an antiplatelet agent, poorly controlled DM (A1c>10), current smoking. Groups were compared based on age, sex and 90 day functional outcomes, with favorable outcome defined as mRS ≤ 2. Results: Our sample included 396 patients who underwent EVT (mean age 65, 50% female). 42% of patients with Afib were not on anticoagulation, 31% of patients with HLD were untreated, 39% of patients with HTN were poorly controlled, 27% of patients with a history of vascular disease were not on an antiplatelet, 14% of patients with DM were poorly controlled, and 46% of all patients were smokers. In total, 78% of patients had at least 1 poorly controlled risk factor and 37% had at least 2. There was no difference in rates of preventable stroke between males and females (48% vs 52%, p=0.30) and between age groups above and below 70 (40% vs 60%, p=0.68). 64% of patients with well controlled risk factors had a favorable outcome compared to 51% with at least one poorly controlled risk factor (p=0.03). Conclusions: Our data suggests that despite guidelines on management of vascular risk factors, a large number of these are poorly controlled prior to admission for large vessel stroke, leading to a potentially preventable procedure. Not only could improved primary prevention save the wide array of resources utilized in EVT, but it could also influence long term outcomes in this cohort of patients.

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Plasma Total Cysteine as a Risk Factor for Vascular Disease

Circulation ◽

10.1161/01.cir.103.21.2544 ◽

2001 ◽

Vol 103 (21) ◽

pp. 2544-2549 ◽

Cited By ~ 151

Author(s):

Lina El-Khairy ◽

Per M. Ueland ◽

Helga Refsum ◽

Ian M. Graham ◽

Stein E. Vollset

Keyword(s):

Risk Factor ◽

Vascular Disease

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Diabetic Retinopathy And Thromboxane Like Substance

10.1055/s-0038-1652115 ◽

1981 ◽

Author(s):

M A Lazzari ◽

M Gimeno ◽

N M Sutton ◽

J R Lopez

Keyword(s):

Diabetes Mellitus ◽

Arachidonic Acid ◽

Diabetic Retinopathy ◽

Risk Factor ◽

Platelet Aggregation ◽

Platelet Rich Plasma ◽

Thromboxane A2 ◽

Initial Step ◽

Platelet Activity

Diabetes Mellitus (DM) is a risk factor in the development of vasculopathies and its complications. It produces also its own microangiopathy. Evidence was reported of increased platelet activity in DM in different assays. Platelets aggregation and the arachidonic cycle could play a key role in the increased tendency to thrombosis. A disorder of ratio TXA2/PGI2, two opposing prostaglandin derivatives, could be the initial step. We intended to evaluate a thromboxane like substance (TLS) produced from platelet rich plasma (PRP) and to compare between normals and diabetic retinopathy (DR) patients. TLS was measured in 16 controls and 16 patients. Assay was done with the aggregating activity developed in PRP (considered TLS) after addition of arachidonic acid (f.c. 2 mM). The supernatant of the PRP (100 μl) was taken 40 sec. after the aggregation started and were added to a normal PRP treated with aspirin (f.c. 40 μl/ml) adjusted to 250.000 - 300.000 pl/μl and the degree of platelet aggregation measured in a Chrono Log Aggregometer. TLS was inactivated after its incubation during 2 min. at 37°C. This finding suggests this activity is due to TXA2.The results obtained (expressed in % of platelet aggregation) were: controls x 16.37% ± 6.28 and DR x 36.00% ± 9.72.The increase detected in the DR group supports previous experimental reports suggesting the role of the thromboxane A2 in vaso occlusive complication of diabetes mellitus.

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Homocysteine—a novel risk factor for vascular disease

Journal of the Royal Society of Medicine ◽

10.1177/014107680109400103 ◽

2001 ◽

Vol 94 (1) ◽

pp. 10-13 ◽

Cited By ~ 16

Author(s):

John C Chambers ◽

Michael D I Seddon ◽

Sapna Shah ◽

Jaspal S Kooner

Keyword(s):

Risk Factor ◽

Vascular Disease

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The Influence of Red Blood Cell Hemolysate (RBCH) on Platelet Aggregation (PA) and Release of Serotonin and β-Thromboglobulin (β-TG) in Heparinized Platelet Rich Plasma (PRP)

10.1055/s-0039-1684838 ◽

1979 ◽

Author(s):

L.J. Wurzinger ◽

P. Blasberg ◽

E. Jüngling ◽

H. Schmid-Schönbein

Keyword(s):

Platelet Aggregation ◽

Blood Cell ◽

Red Blood Cell ◽

Platelet Rich Plasma ◽

Dense Granule ◽

Thromboembolic Complications ◽

Internal Organs ◽

Physiological Conditions ◽

Granule Release ◽

Control Samples

As hemolysis occurs preferentially in artificial internal organs (AIO), and thromboembolic complications are frequently seen in AIO, the influence of liberated RBC-contents on PA was investigated. To perform the experiments under the most physiological conditions, heparin was used as anticoagulant and the platelets were kept at 37°C during withdrawal, preparation, storage and aggregometry. The lysed RBC were freed of membranes and stored at 0°C until use. PA was quantitatively monitored in a defined homogenous shear field in a Couette-chamber by turbidimetry. Dense granule release was assayed using 14C-Serotonin labelled platelets. Alpha granule release was assessed via β-TG radioimmunoassay. PRP samples with added RBCH were compared with samples with ADP added in doses equivalent to that of the samples with RBCH. PA, Serotonin, and β-TG release were found to be positively correlated to the concentration of RBCH In PRP, An increase of PA and release as compared to control samples was observed above RBCH-concentratlons of ea. 0.3 g/L hemoglobin, a concentration frequently found during use of AIO. The addioion of ADP in hemolysate-equivalent doses proved to be less effective. Chromatographic assays showed that ATP, which is found in concentration about tenfold of ADP In the RBC, is broken down to ADP in PRP, thus augmenting the ADP-pool acting on platelets.

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