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Biomedical subjects

A Fernández-Ortiz

Publications and source records attributed to A Fernández-Ortiz.

At least 19 recordsLinked to original sources
PubMed2006

Magnitude and consequences of undertreatment of high-risk patients with non-ST segment elevation acute coronary syndromes: insights from the DESCARTES Registry.

OBJECTIVE: To analyse intensity of treatment of high-risk patients with non-ST elevation acute coronary syndromes (NSTEACS) included in the DESCARTES (Descripción del Estado de los Sindromes Coronarios Agudos en un Registro Temporal Español) registry. PATIENTS AND SETTING: Patients with NSTEACS (n = 1877) admitted to 45 randomly selected Spanish hospitals in April and May 2002 were studied. DESIGN: Patients with ST segment depression and troponin rise were considered high risk (n = 478) and were compared with non-high risk patients (n = 1399). RESULTS: 46.9% of high-risk patients versus 39.5% of non-high-risk patients underwent angiography (p = 0.005), 23.2% versus 18.8% (p = 0.038) underwent percutaneous revascularisation, and 24.9% versus 7.4% (p < 0.001) were given glycoprotein IIb/IIIa inhibitor. In-hospital and six-month mortality were 7.5% versus 1.1% and 17% versus 4.6% (p < 0.001), respectively. A treatment score (> or = 4, 2-3 and < 2) was defined according to the number of class I interventions recommended in clinical guidelines: aspirin, clopidogrel, beta blockers, angiotensin-converting enzyme inhibitors, statins and revascularisation. Independent predictors of six-month mortality were age (odds ratio (OR) 1.07, 95% confidence interval (CI) 1.04 to 1.10, p < 0.001), diabetes (OR 1.92, 95% CI 1.14 to 3.22, p = 0.014), previous cardiovascular disease (OR 4.17, 95% CI 1.63 to 10.68, p = 0.003), high risk (OR 2.20, 95% CI 1.30 to 3.71, p = 0.003) and treatment score < 2 versus > or = 4 (OR 2.87, 95% CI 1.27 to 6.52, p = 0.012). CONCLUSIONS: Class I recommended treatments were underused in high-risk patients in the DESCARTES registry. This undertreatment was an independent predictor of death of patients with an acute coronary syndrome.

Aged↗
PubMed2003

Effects of bosentan on neointimal response following coronary angioplasty.

BACKGROUND: Endothelins are important vasoconstrictors and cellular-growth promoters. ETA-specific antagonists have been shown to reduce neointimal response to injury in some experimental angioplasty models. However, there is little information on the effects of dual ETA/ETB receptor blockers, such as bosentan, on neointimal proliferation following experimental coronary angioplasty. MATERIALS AND METHODS: Coronary injury was achieved by directional atherectomy in the left anterior descending artery of 20 pigs. Animals were randomly assigned to receive a daily dose of oral bosentan (30 mg kg-1) (group I, n = 10) or no treatment (group II, n = 10). At 4 weeks, arteries were processed for histomorphometry and endothelin characterization. RESULTS: Vessel injury score was similar among the two groups. Overall, a linear correlation was found between injury and neointimal development (r = 0.57, P = 0.01). This correlation had a lower slope in group I compared with group II (P < 0.001), indicating a smaller amount of neointimal development for a similar degree of injury in bosentan-treated animals. Multivariate regression showed that neointimal response was reduced by oral treatment with bosentan (beta: -0.59 mm2, 95% CI: -1.11/-0.06 mm2). In addition, immunostaining revealed fewer positive endothelin areas in group I arteries. CONCLUSIONS: Oral treatment with bosentan reduces neointimal development following coronary angioplasty in this experimental model.

Administration, Oral↗
PubMed2001

[Effect of cAMP on the function of endothelial cells and fibromuscular proliferation after the injury of the carotid and coronary arteries in a porcine model].

INTRODUCTION AND OBJECTIVE: Reendothelization of damaged blood vessels protects against the vascular injury response. We evaluated in vivo whether a systemic increase in cAMP accelerates reendothelization and attenuates intimal hyperplasia in injured swine carotid and coronary arteries. METHODS: Both carotid arteries of 10 swines were subjected to balloon injury. Five animals had been treated with 2 ml (10 mg) of Forskolin, an activator of the adenylate cyclase, and another 5 with 2 ml of saline solution. These animals were sacrificed at day 8, and carotid artery reendothelization was evaluated. The descendent coronary (DC) artery of another 19 pigs was injured by atherotome. Nine animals had been treated with 2 ml of Forskolin, and another 10 with 2 ml of saline solution. These animals were sacrificed at day 28, with myointimal proliferation and arterial geometric remodelation being evaluated. Likewise, in these animals intracellular cAMP levels were measured at baseline and 28 and 60 minutes after saline solution or Forskolin administration and 90 min after arterial injury. RESULTS: Eight days after balloon injury, carotid artery reendothelization was greater in the Forskolin-treated group compared with the control group (p = 0.02), and the number of CD31 positive cells was statistically increased in the treated group (38 +/- 11 cells) versus controls (11 +/- 9 cells). Although the degree of vascular injury caused by atherotome was similar in all of the arteries in the control group, restenosis was only observed in 40% of these animals. Correlation analysis demonstrated that intracellular cAMP may condition arterial geometric remodeling and the diameter of the lumen after vascular injury. CONCLUSION: Our results suggest that cAMP may promote reendothelization and attenuate fibromuscular proliferation.

Animals↗
PubMed2001

Endogenous anti-inflammatory response after coronary injury in a porcine model.

BACKGROUND: Corticotropin-releasing hormone (CRH)/adrenocorticotropic hormone (ACTH)/cortisol is the major anti-inflammatory system. After percutaneous translumenal angioplasty, an inflammatory process is triggered. We investigate whether CRH/ACTH/cortisol axis is activated after deep vessel wall injury (DVWI). MATERIALS AND METHODS: Plasma and leukocyte CRH and ACTH, serum cortisol and IL-1beta, and leukocyte cAMP were measured (ELISA) in 16 pigs after anaesthesia (baseline), 60 min into anaesthesia without causing vascular injury and 90 min after DVWI of the left anterior descending (LAD) coronary artery induced by percutaneous directional atherectomy (Atherocath GTO 7F; DVI, Inc., Temecula, USA). Biochemical variables were also measured at baseline, 60 and 180 min into anaesthesia in six additional pigs without coronary intervention. RESULTS: MANOVA showed that CRH/ACTH/Cortisol, cAMP and IL-1beta production was not modified during anaesthesia. Post-DVWI plasma CRH (0.077 +/- 0.046 ng mL-1), and cellular cAMP (0.14 +/- 0.067 pmol 10(-6) cells) increased significantly (P = 0.001) with respect to their baseline values (CRH = 0.036 +/- 0.013 ng mL-1; cAMP = 0.081 +/- 0.034 pmol 10-6). There was also a statistically significant increase (P = 0.02) in post-DVWI IL-1beta (from 46.6 +/- 12.8 to 64.05 +/- 13.5 pg mL-1), and in serum cortisol (P = 0.05) compared to its baseline values (8.98 +/- 3.2 microgr dL-1 vs. 6.57 +/- 2.3 microgr dL-1, respectively). CONCLUSION: In our experimental model, coronary vessel wall injury-activated CRH/ACTH/cortisol axis caused a significant increase in plasma CRH, cortisol and cellular cAMP levels, which may influence the response of coronary arteries to injury.

Adrenocorticotropic Hormone↗
PubMed2000

Guidewire-induced coronary pseudostenosis as a source of error during physiological guidance of stent deployment.

Coronary pseudostenoses are a known result of the interaction between tortuous vessels and guidewires and are generally handled by the interventionalist as inocuous side effects of intracoronary instrumentation. The present report demonstrates that pseudostenosis may have hemodynamic relevance and may constitute an important source of error when physiological guidance of percutaneous procedures is performed using sensor-tipped guidewires.

Aged↗
PubMed2000

[Aspiration of large intracoronary thrombus after apparently successful angioplasty. Therapeutic implications].

We present a case in which, after performing an optimal angioplasty after an acute myocardial infarction with intracoronary thrombus, normal coronary flow was not achieved. After aspirating through the guiding catheter we obtained a large thrombus that the histopathologic study confirmed as a recent thrombus and, subsequently, normal flow was reestablished. The procedure was completed with a successful intracoronary stent implantation, with an uneventful clinical course. The therapeutic and diagnostic implications of this case are discussed.

Aged↗
PubMed2000

[Clinical practice guidelines of the Spanish Society of Cardiology on unstable angina/infarction without ST elevation].

This paper up-dates the Clinical Guidelines for Unstable Angina/Non Q wave Myocardial Infarction of the Spanish Society of Cardiology. Due to the increased efficacy of adequate management in the early phases, it has been considered necessary to include recommendations for the pre Hospital and Emergency department phase. Prehospital management. Patients with thoracic pain compatible with myocardial ischemia should be transferred to Hospital as quickly as possible and an ECG tracing performed. Initial management includes rest, sublingual nitroglycerin and aspirin. In the Emergency department. Immediate clinical attention and accessibility to a defibrillator should be available. If ECG tracing discloses ST elevation reperfusion strategy is to be implemented immediately. If no ST elevation is present, the probability of myocardial ischemia and risk factor evaluation is essential for adequate management. A simplified risk stratification classification is presented, that also determines the most adequate site for admission: Coronary Care Unit if high risk factors are present, Cardiology ward for the intermediate risk patient and ambulatory treatment if low risk. Management in Coronary Care Unit. Includes routine ECG monitoring and analgesia. Antithrombotic and anti ischemic treatment include new indication for GP IIb-IIIa and Low molecular weight heparins. Coronary arteriography and revascularisation are recommended, if refractory or recurrent angina, left ventricles dysfunction or other complications are present. Management in the ward is based on adequate chronic medical treatment, risk stratification, and secondary prevention strategy. Coronary arteriography before discharge must be considered in the light of the result of non-invasive tests.

Angina, Unstable↗
PubMed1999

Results (>6 months) of stenting of >1 major coronary artery in multivessel coronary artery disease.

Multivessel percutaneous transluminal coronary angioplasty (PTCA) is associated with a high requirement for further revascularization procedures. Although stenting can reduce restenosis and clinical events after 1-vessel intervention, little information is available after multivessel coronary stenting. We followed up 136 patients (9% of 1,481 undergoing stenting in our center) who had had stent implantation in at least 2 different major native coronary arteries and were followed-up for >6 months. Each patient had received a mean of 2.3 +/- 0.6 stents (1.13 +/- 0.4 stents per lesion) and procedural success was 95%. In-hospital complications included 1 death, 1 Q-wave infarction, 5 non-Q-wave myocardial infarctions, and 1 repeat PTCA. After a mean of 18 +/- 13 months, 7 patients died (3 of heart failure, 4 of noncardiac causes), 2 required coronary bypass surgery, 1 had a myocardial infarction, 13 target vessel repeat PTCA, and 4 non-target vessel PTCA. Survival free of major cardiac events was 75% at 3 years. A history of heart failure, dilation of a restenotic lesion, and 3-vessel dilation were independent negative predictors of event-free survival. Angiographic follow-up was available in 86 patients: 56 (65%) were restenosis free, 23 (27%) had 1-vessel restenosis, and 6 (7%) had 2-vessel and 1 patient 3-vessel restenosis. Restenosis per vessel was 23% (41 of 177). Reference diameter, past-PTCA minimal luminal diameter, and length of the stent were independent predictors of restenosis. We conclude that multivessel stenting provides good midterm results in selected patients with multivessel coronary artery disease. Midterm events are less frequent than previously reported after balloon PTCA.

Angioplasty, Balloon, Coronary↗
PubMed1999

Long-term clinical and echocardiographic follow-up after percutaneous mitral valvuloplasty with the Inoue balloon.

BACKGROUND: The objective of this study was to assess the long-term clinical outcome and valvular changes (area and regurgitation) after percutaneous mitral valvuloplasty (PMV). METHODS AND RESULTS: After PMV, 561 patients were followed up for 39 (+/-23) months and clinical/echocardiographic data obtained yearly. Kaplan-Meier and Cox regression analyses were performed to estimate event-free survival, its predictors, and the relative risks of several patient subgroups. There were several nonexclusive events: 19 (3.3%) cardiac deaths, 55 (9.8%) mitral replacements, 6 (1%) repeated PMVs, 56 (10%) cases of restenosis, and 108 (19%) cases of clinical impairment. Survival free of major events (cardiac death, mitral surgery, repeat PMV, or functional impairment) was 69% at 7 years, ranging from 88% to 40% in different subgroups of patients. Wilkins score was the best preprocedural predictor of mitral opening, but the procedural result (mitral area and regurgitation) was the only independent predictor of major event-free survival. Mitral area loss, though mild [0.13 (+/-0.21)cm2], increased with time and was >/=0.3 cm2 in 12%, 22%, and 27% of patients at 3, 5, and 7 years, respectively. Regurgitation did not progress in 81% of patients, and when it occurred it was usually by 1 grade. CONCLUSIONS: Seven years after PMV, more than two thirds of patients were in good clinical condition and free of any major event. The procedural result was the main determinant of long-term outcome, although a high score had also negative implications. Mitral area decreased progressively over time, whereas regurgitation did not tend to progress.

Aged↗
PubMed1997

Clinical and angiographic implications of coronary stenting in thrombus-containing lesions.

OBJECTIVES: This study sought to determine the results of coronary stenting in thrombus-laden lesions. BACKGROUND: The angiographic evidence of intracoronary thrombus has classically been considered a formal contraindication to stent implantation. However, with increasing use of stenting, the indications for this technique have widened to include treatment of patients who have an acute coronary syndrome or lesions with adverse anatomic features. METHODS: We studied 86 consecutive patients (mean age +/- SD 61 +/- 11 years, 14 women) undergoing coronary stenting of a thrombus-containing lesion; the procedure was performed electively in 39% and after angioplasty failure in 61%. Sixty-four patients (75%) were treated for unstable angina, and 19 (22%) underwent the procedure during an acute myocardial infarction. A specific protocol that included clinical and late angiographic follow-up was used. RESULTS: Angiographic success was obtained in 83 patients (96%). Five patients (6%) died during the hospital stay despite angiographic success; four of these had cardiogenic shock, and one (1%) had subacute stent thrombosis. Non-Q wave myocardial infarction developed in five additional patients (6%), and four of these five had data consistent with distal embolization. Of the 78 patients discharged with angiographic success, 67 (86%) were event-free and clinically improved at last follow-up visit (12 +/- 11 months). During the follow-up period, eight patients required repeat angioplasty, one patient required heart transplantation, and two patients died. Quantitative angiography demonstrated excellent angiographic results after stenting (minimal lumen diameter 0.31 +/- 0.4 vs. 2.77 +/- 0.6 mm). Late angiographic follow-up (5.5 +/- 1 months) was obtained in 50 patients with 54 lesions (93% of eligible), revealing a minimal lumen diameter of 2.0 +/- 1 mm and restenosis (lumen narrowing > 50%) in 18 lesions (33%). CONCLUSIONS: Coronary stenting constitutes an effective therapeutic strategy for patients with thrombus-containing lesions, either after failure of initial angioplasty or electively as the primary procedure. Coronary stenting in this adverse anatomic setting results in a high degree of angiographic success, a low incidence of subacute thrombosis and an acceptable restenosis rate.

Adult↗
PubMed1997

Tissue factor modulates the thrombogenicity of human atherosclerotic plaques.

BACKGROUND: The thrombogenicity of a disrupted atherosclerotic lesion is dependent on the nature and extent of the plaque components exposed to flowing blood together with local rheology and a variety of systemic factors. We previously reported on the different thrombogenicity of the various types of human atherosclerotic lesions when exposed to flowing blood in a well-characterized perfusion system. This study examines the role of tissue factor in the thrombogenicity of different types of atherosclerotic plaques and their components. METHODS AND RESULTS: Fifty human arterial segments (5 foam cell-rich, 9 collagen-rich, and 10 lipid-rich atherosclerotic lesions and 26 normal, nonatherosclerotic segments) were exposed to heparinized blood at high shear rate conditions in the Badimon perfusion chamber. The thrombogenicity of the arterial specimens was assessed by 111In-labeled platelets. After perfusion, specimens were stained for tissue factor by use of an in situ binding assay for factor VIIa. Tissue factor in specimens was semiquantitatively assessed on a scale of 0 to 3. Platelet deposition on the lipid-rich atheromatous core was significantly higher than on all other substrates (P = .0002). The lipid-rich core also exhibited the most intense tissue factor staining (3 +/- 0.1 arbitrary units) compared with other arterial components. Comparison of all specimens showed a positive correlation between quantitative platelet deposition and tissue factor staining score (r = .35, P < .01). CONCLUSIONS: Our results show that tissue factor is present in lipid-rich human atherosclerotic plaques and suggest that it is an important determinant of the thrombogenicity of human atherosclerotic lesions after spontaneous or mechanical plaque disruption.

Animals↗
PubMed1997

[The role of non-angiographic observations (IVUS, angioscopy, doppler) in coronary stenting].

Coronary stenting is increasingly used during transcatheter coronary therapy. Coronary angiography, mainly since the advent of quantitative angiography, provides an effective tool to obtain excellent clinical results with coronary stenting. However, during this procedure some limitations inherent to the angiographic techniques may become apparent. Accordingly, great enthusiasm has been generated regarding the potential value of alternative diagnostic techniques to guide coronary stenting. Intravascular ultrasound is able to study the arterial wall and provides a unique tool to assess stent expansion, apposition and symmetry. Therefore, this technique is increasingly used to optimize stent deployment. Coronary angioscopy directly visualizes stent expansion and is able to precisely recognize protrusion of redundant fronds of tissue or residual dissections within the stent struts. In addition, this technique is the procedure of choice to identify intracoronary thrombus. Intracoronary Doppler permits the application in the catheterization laboratory of sophisticated methods of functional assessment of lesion severity. Coronary stenting allows a faster and complete normalization of coronary flow reserve than balloon angioplasty. Thus, all these new techniques of intracoronary diagnosis provide unique and useful information, which is complementary to that obtained with angiography, potentially useful during coronary stenting.

Angioscopy↗
PubMed1996

Stent embolization during intracoronary stenting.

Nine patients with systemic embolization complicating intracoronary stenting (incidence 1.8%) are described. Although this rare complication was not associated with any clinical sequelae, great care should be taken to prevent this possibility, especially in patients with unfavorable anatomic characteristics, including lesions in the left circumflex artery, at bend points, and calcified lesions.

Aged↗
PubMed1996

Pathophysiology of coronary artery disease.

Atherogenic risk factors provoke chronic injury to the endothelium in certain parts of the arterial tree leading to dysfunctional endothelium. Lipid accumulation, macrophage formation, and smooth muscle cell proliferation are key events in the initial slow progression of atherosclerotic lesions (phase 1). If extracellular lipid accumulation predominates, atherosclerotic process progresses into a more clinically relevant, advance lipid-rich lesion (phase 2)--the pathogenic basis for plaque rupture and thrombus formation. Small plaque fissures and mural thrombus formation may be responsible for the rapid, clinically silent progression of lesions (phase 3). Plaque rupture with large thrombus formation may be responsible for acute coronary syndromes (phase 4). Alternatively, if smooth muscle cell proliferation and collagen matrix synthesis predominate, atherosclerotic lesions may progress into advanced, stable sclerotic lesions (phase 5).

Aged↗
PubMed1995

Role of thrombosis in atherosclerosis and its complications.

The endothelium is intact but activated and dysfunctioning during the early phase of atherogenesis. Owing to increased endothelial permeability, many blood-derived components, including hemostatic factors, are present in early as well as advanced atherosclerotic lesions. Insudated fibrin(ogen) and related degradation products and thrombin could contribute to atherogenesis by their chemotactic (attracting monocytes/macrophages) and mitogenic (stimulating cell proliferation) properties. All key cells in plaque may express thrombin receptors, indicating that thrombin may play a role in the genesis of uncomplicated atherosclerosis by mediating inflammatory and proliferative processes. Later, endothelial denudation with platelet adherence occurs over mature plaques. Then, incorporation of microthrombi and probably platelet/thrombus-derived growth factors are critical for the progressive growth of the smooth muscle cell-related plaque component. Besides transendothelial influx and incorporation of mural thrombi, blood products in atherosclerotic plaques may originate from hemorrhage through a ruptured plaque surface or from fragile newly formed vessels (neovascularization) frequently found at the base of advanced plaques. Rupture-related plaque progression due to luminal thrombosis and/or plaque hemorrhage is the most important mechanism underlying the unpredictable rapid progression of coronary lesions responsible for acute coronary syndromes. Both platelets and fibrin play a role in the dynamic thrombotic response to plaque rupture.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

[Coronary angioscopy: initial experience during coronary interventions].

BACKGROUND AND OBJECTIVE: Percutaneous coronary angioscopy (CAG) provides in vivo visual information about the luminal aspect of the vessel. In this report we describe our initial experience with CAG during coronary angioplasty (PTCA). METHODS: Fifty-five patients (age 60 +/- 9 years), 8 female, were included. Most patients, 42 (76%) were treated for unstable angina. RESULTS: In 49 patients (89%) CAG was performed prior to PTCA, and in all cases the intraluminal material responsible of the stenosis was recognized. This included plaque associated to thrombus in 29 patients (59%), isolated plaque in 15 (31%) and isolated thrombus in 5 (10%). Of these plaques, 25 (57%) were yellow, 14 (32%) were yellow and white and 5 (11%) were white. Of the 34 thrombi, 23 (68%) were mural and 11 (32%) protruding. CAG post-PTCA was performed in 43 patients (78%). CAG visualized residual plaque in 41 patients (95%) and residual thrombus in 34 (79%). In addition, CAG recognized dissections in 30 patients (70%). CAG was more sensitive than angiography for the detection of thrombus (pre-PTCA 34 [69%] vs 11 [22%]; p < 0.05, and post-PTCA 34 [79%] vs 5 [12%]; p < 0.05]) and coronary dissections (post-PTCA 30 [70%] vs 19 [44%]; p < 0.05). CAG before intervention caused angina in 39 patients (80%), ventricular fibrillation (successfully managed with DC cardioversion) in 1, and AV block in another patient. The angiographic result deteriorated in 4 patients (9%) immediately after the CAG performed following PTCA. A repeat balloon PTCA was required in these patients. CONCLUSIONS: CAG provides unique information on coronary lumen surface that complements angiographic data. As compared with angiography, CAG is more sensitive in the detection of intracoronary thrombi and dissections. Further studies are required to determine whether the additional information provided by CAG may be used, to select coronary interventions according to specific lesion characteristics, to optimize dilation results and, eventually, to improve the clinical outcome of these patients.

Aged↗
PubMed1994

Characterization of the relative thrombogenicity of atherosclerotic plaque components: implications for consequences of plaque rupture.

OBJECTIVES: The purpose of this study was to determine whether different components of human atherosclerotic plaques exposed to flowing blood resulted in different degrees of thrombus formation. BACKGROUND: It is likely that the nature of the substrate exposed after spontaneous or angioplasty-induced plaque rupture is one factor determining whether an unstable plaque proceeds rapidly to an occlusive thrombus or persists as a nonocclusive mural thrombus. Although observational data show that plaque rupture is a potent stimulus for thrombosis, and exposed collagen is suggested to have a predominant role in thrombosis, the relative thrombogenicity of different components of human atherosclerotic plaques is not well established. METHODS: We investigated thrombus formation on foam cell-rich matrix (obtained from fatty streaks), collagen-rich matrix (from sclerotic plaques), collagen-poor matrix without cholesterol crystals (from fibrolipid plaques), atheromatous core with abundant cholesterol crystals (from atheromatous plaques) and segments of normal intima derived from human aortas at necropsy. Specimens were mounted in a tubular chamber placed within an ex vivo extracorporeal perfusion system and exposed to heparinized porcine blood (mean [+/- SEM] activated partial thromboplastin time ratio 1.5 +/- 0.04) for 5 min under high shear rate conditions (1,690 s-1). Thrombus was quantitated by measurement of indium-labeled platelets and morphometric analysis. Under similar conditions, substrates were perfused with heparinized human blood (2 IU/ml) in an in vitro system, and thrombus formation was similarly evaluated. RESULTS: Thrombus formation on atheromatous core was up to sixfold greater than that on other substrates, including collagen-rich matrix (p = 0.0001) in both heterologous and homologous systems. Although the atheromatous core had a more irregular exposed surface and thrombus formation tended to increase with increasing roughness, the atheromatous core remained the most thrombogenic substrate when the substrates were normalized by the degree of irregularity as defined by the roughness index (p = 0.002). CONCLUSIONS: The atheromatous core is the most thrombogenic component of human atherosclerotic plaques. Therefore, plaques with a large atheromatous core content are at high risk of leading to acute coronary syndromes after spontaneous or mechanically induced rupture because of the increased thrombogenicity of their content.

Animals↗