TY - JOUR. T1 - Molecular imaging identifies regions with microthromboemboli during primary angioplasty in acute coronary thrombosis. AU - Sakuma, Tadamichi. AU - Sklenar, Jiri. AU - Leong-Poi, Howard. AU - Goodman, Norman C.. AU - Glover, David K.. AU - Kaul, Sanjiv. PY - 2004/7/1. Y1 - 2004/7/1. N2 - Microthromboemboli (MTE) may contribute to the no-reflow phenomenon in acute myocardial infarction (AMI) either spontaneously or after primary percutaneous transluminal coronary angioplasty (PTCA). We hypothesized that myocardial MTE in acute coronary syndromes can be identified on imaging by in vivo 99mTc labeling of the coronary thrombus with a compound that binds to the glycoprotein IIb/IIIa present on activated platelets (DMP-444). Methods: Fifteen dogs underwent left anterior descending coronary artery (LAD) injury in to produce thrombus, whereas 5 control dogs had LAD ligation. Before recanalization, the risk area (RA) and myocardial blood flow (MBF) were measured, and in vivo thrombus ...
Plaque erosion is suspected in the presence of an acute luminal thrombus that is in direct contact with the underlying intima comprising smooth muscle cells and proteoglycan with an absence of endothelial lining (1). The erosive plaques are rich in versican, hyaluronan, and type III collagen, unlike rupture or stable plaques, which are rich in type I collagen (2). The erosion lesions are more often eccentric and infrequently calcified; they show minimal inflammation with a few or absent macrophages and T-lymphocytes (2). The media underneath plaque erosions are similar to plaques with mild stenosis, rich in smooth muscle cell actin, which is also highly expressed in intimal smooth muscle cells in erosions. Plaque erosions often show negative remodeling. It is likely that spasm may play an important role in plaque erosion.. Plaque erosion accounts for 25% to 35% of coronary thrombi in patients dying of acute myocardial infarction and/or sudden coronary death (1). Plaque erosions occur in ...
The Academic Research Consortium (ARC) divides stent thrombosis (ST) into early (within 30 days), late (30 days to 1 year), and very late (beyond 1 year). Intravascular imaging studies, to date mostly using intravascular ultrasound (IVUS), have provided clues with regard to the causes of ST-primarily by focusing on either early or very late ST, although each study usually includes a small number of patients with events between 30 days and 1 year. In this issue of JACC: Cardiovascular Interventions, the current study is similar in that 15 of 18 patients have very late ST with only 3 patients presenting earlier than 1 year (and those 3 at least 172 days) after implantation (1).. The distinction between patients with early versus very late ST is important, especially after drug-eluting stent (DES) implantation. Studies should not combine these 2 groups of patients, because their fundamental mechanisms seem to be different.. The IVUS-identified causes or predictors of early ST are mechanical and ...
The changes in the final ventricular complex, the T-wave, and in the S-T segment of the electrocardiogram in coronary thrombosis have been extensively studied, both experimentally and clinically, since the early works of Herrick,1 Smith,2 and Pardee.3 As a result, it has been generally accepted that characteristic changes do occur in the majority of the cases, following an attack of coronary thrombosis.. In contrast, the changes in the initial ventricular complex have, up to recent years, received much less attention. Smith2 and Wearn4 observed that in coronary thrombosis the initial ventricular complex may not rarely be of a very small ...
To the Editor:. There are questions regarding long-term safety of drug-eluting stents (DES), especially concern about an increased rate of late DES thrombosis compared with bare-metal stents. Numerous intravascular ultrasound (IVUS) studies have reported an increased frequency of late stent malapposition (LSM) in patients with DES (1-3), speculating that there may be a relationship between LSM and late stent thrombosis. The present study reports the long-term (,2 years) follow-up after the diagnosis of LSM was made using serial IVUS examination after DES implantation.. We previously reported 82 patients (85 lesions) with LSM from an overall cohort of 557 patients (705 native lesions) who underwent DES implantation (mean interval between baseline and follow-up IVUS of 6.1 ± 2.1 months). No intervention was performed in 542 patients (683 lesions) at 6-month follow-up (3). At least 2-year follow-up was available for all but 10 patients (12 lesions). Therefore, the present study reports 532 ...
Coronary thrombosis definition, a coronary occlusion in which there is blockage of a coronary arterial branch by a blood clot within the vessel, usually at a site narrowed by arteriosclerosis. See more.
Medical literature has recently focused on very late stent thrombosis (VLST) after drug-eluting stent implantation, while its mechanistic issue was not fully explored in the bare-metal stent (BMS) era. The first case is a 59-year-old man presenting with inferior non-ST-segment elevation myocardial infarction, 4 years after BMS implantation (NIR 3.5/18 mm, Boston Scientific, Galway, Ireland) for a chronic total occlusion lesion in the proximal right coronary artery. Coronary angiograms showed Thrombolysis In Myocardial Infarction (TIMI) flow grade 1 and filling defects in the BMS deployed previously, and massive red thrombi attaching to uncovered stent struts were found by angioscope (Fig. 1,Online Video 1). Thrombectomy and adjunctive balloon angioplasty were performed based on the angioscopic findings, and TIMI flow grade 3 was obtained. The second case is a 71-year-old man who was admitted for a diagnosis of inferior non-ST-segment elevation myocardial infarction 10 years after a treatment ...
The present study showed that the thrombi of ruptured plaques were more significantly rich in fibrin and that more tissue factor and CRP were expressed in ruptured than in eroded plaques.. Acute coronary thrombosis leading to acute myocardial infarction may arise from a difference in underlying plaque morphology, namely rupture and superficial erosion.2-6 In acute coronary death with coronary thrombosis, two necropsy studies have found plaque rupture in 75% of cases and that erosion accounted for the remainder.2,6 Kojima and colleagues5 found plaque rupture in 81% and erosion in 19% of Japanese patients who died of acute myocardial infarction.5 The findings of the present study agree with these previous results. In contrast, Farb and colleagues3 and Burke and associates4 have reported that 56% of such deaths are associated with plaque rupture and 44% with erosion. In addition, they found plaque erosion in 69% of women who died of sudden ischaemic heart disease.3,4 These reports emphasised a high ...
A number of risk factors for stent thrombosis have been identified by previous investigators. Persistent dissection, longer stent length, and final lumen diameter within the stent were identified as independent multivariable predictors of stent thrombosis in a meta-analysis of 6,186 patients enrolled in six major clinical trials of coronary stenting (17). Other studies have identified balloon size ≤2.5 mm, bail-out situations, unstable angina or acute MI (15), ejection fraction, use of a combination of different stents, postprocedural dissections, and slow flow (16)as predictive of stent thrombosis.. Multivariate analysis of correlates of stent thrombosis is difficult to perform in even a study as large as this because of the low incidence of the primary end point. A common method of avoiding over-fitting is bootstrap model selection. It involves creating random data sets from the patient population, selecting correlates with stepwise model selection for each bootstrap sample, and counting the ...
Background Clinical evidence suggests that intracoronary thrombus formation is associated with a high incidence of late restenosis after successful coronary intervention in patients with myocardial infarction. However, little is known about the mechanism by which intracoronary thrombi play pathological roles.. Methods and Results We analyzed the cellular constituents of 108 thrombi aspirated from coronary lesions with a thrombectomy device in 62 patients who underwent emergent coronary intervention for the treatment of acute (,24 hours) or recent (24∼72 hours) ST-segment-elevation myocardial infarction (44 male, 18 female, age 68.0±19.3 years). Immunohistological analysis of aspirated thrombotic materials revealed that the content of platelets, as determined by immunostaining for CD42a, had a negative correlation with the time after the onset of chest pain (correlation coefficient: −0.683, p,0.01). Immunofluorescent staining for CD34 and breast cancer resistant protein-1 (bcrp-1) detected ...
Percutaneous coronary intervention (PCI) and coronary stent insertion has become commonplace and is ubiquitous in the treatment of myocardial infarction. Use of dual antiplatelet therapy or "DAPT" (ASA plus clopidogrel, ASA plus prasugrel, ASA plus ticagrelor) is critical post PCI and coronary stent insertion to prevent stent thrombosis. The incidence of early stent thrombosis ranges around 1-2% while on DAPT while late stent thrombosis ranges from 0.2-0.6%.1 While the incidence may be low, acute stent thrombosis often presents as a STEMI and is associated with mortality rates of 20-45%. While several factors influences the rates of stent thrombosis, the most common cause of acute stent thrombosis is nonadherence to DAPT.2. ...
Another name for Coronary Thrombosis is Heart Attack. The treatment of a heart attack focuses on reducing pain, improving blood flow to the heart muscle ...
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Coronary thrombi in patients who die suddenly are more likely to display signs of healing if they are caused by a plaque erosion rather than a rupture, researchers found.
The pathophysiological model for the occurrence of STEMI describes sudden vessel closure, mostly due to plaque rupture or erosion and subsequent intracoronary occlusive thrombosis at the onset of symptoms.3 Plaque disruption results in exposure of the lipid-rich core of the plaque to the bloodstream, which causes activation and aggregation of platelets. As a result, a luminal thrombus occurs, which prevents normal blood supply to the myocardium. This explains why in many patients with acute transmural myocardial infarction, a platelet-rich, fresh thrombus can be found.12-15 The aspiration of thrombi in 95% of patients in general and fresh thrombi in particular in patients with STEMI in the present study confirms these perspectives and other studies with regard to the pathogenesis of this event. The fact that fresh thrombus could not be identified in all patients may be explained in part by disintegration of the very fragile fresh material by passage through the catheter or in the collection ...
Coronary thrombus in patients undergoing primary PCI for STEMI: Prognostic significance and management.: Acute ST-elevation myocardial infarction (STEMI) usuall
Coronary thrombosis is now widely recognised as a major cause of sudden cardiac death, acute myocardial infarction, and unstable angina pectoris. Inflammation is an important component of the atherosclerotic lesion. In this review we will discuss inflammatory mechanisms in relation to atherosclerosis and clinical coronary thrombosis.. The "response to injury" hypothesis postulates that endothelial dysfunction represents the initial step of atherogenesis and can be induced by haemodynamic forces, by a variety of vasoactive substances, by mediators from blood cells, and directly from risk factors for atherosclerosis.1 Upon activation, endothelial cells express various cellular adhesion molecules, cytokines, chemokines, and growth factors. Focal arterial inflammatory activity is one of the most prominent characteristics of the atherosclerotic process.2,3 Inflammation is also implicated in the pathogenesis of acute syndromes, as suggested by histological findings in unstable coronary plaques,4-6 ...
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trigger the formation of a clot causing a coronary thrombosis. This stops the flow of blood through the vessel and the capillary network it supplies causing a heart attack. The portion of the heart muscle deprived of oxygen dies quickly of oxygen starvation. If the area is not too large, the undamaged part of the heart can, in time, compensate for the damage. Coronary bypass surgery uses segments of leg veins to bypass the clogged portions of the coronary arteries. ...
Project plan. Modeling rat bloodstream using fluorescence imaging data. Alander et al. (2012). The Research Project. Rats with artificial coronary thrombosis Chest blood vessel to heart muscle Replace bypass for people with bad coronary vessels ?. Team. Slideshow 6945525 by...
Stent thrombosis (ST) is an acute thrombotic occlusion in the stented segment of a coronary artery. It is a serious complication that frequently presents as an acute myocardial infarction and/or sudden death. The most recently accepted definition established by the Academic Research Consortium classifies ST as: early (occurring within 30 days), late (30 days to 1 year) or very late (after 1 year). Very late ST has been reported following drug-eluting stent implantation with rates up to 0.6% per year. However, very late ST is unusual after bare-metal stent (BMS) implantation. Here we report a case of patient presenting with ST-elevation myocardial infarction due to very late ST occurring 2 years after BMS implantation. Keywords: Stent thrombosis, Percutaneous coronary intervention, Bare metal stent, Drug eluting stent
Case Reports in Critical Care is a peer-reviewed, Open Access journal that publishes case reports in all areas of critical care medicine.
For the past 15 years evidence has stacked up showing patients with acute coronary thrombosis improve their survival chances by 50-82
Pre-discharge transthoracic echocardiography revealed the left ventricle with normal dimensions and overall systolic function (left ventricular ejection fraction 56%), and hypokinesis of the basal inferior wall. The patient was discharged on the fifth day, medicated with aspirin 100 mg once daily, ticagrelor 90 mg twice daily, atorvastatin 40 mg once daily, ramipril 2.5 mg once daily, ivabradine 5 mg twice daily, colchicine 1 mg once daily and pantoprazole 20 mg once daily.. After discharge the patient was referred for a cardiology consultation in addition to previous medical consultations. Prednisone was introduced three months after the event by the rheumatology team. At the six-month cardiology consultation, the patient presented free of angina with good functional capacity, and no new cardiovascular events have been reported.. Discussion. Coronary artery disease is extremely uncommon in BD, with a reported prevalence of 0.5%.4 As in the case presented, most BD patients with coronary events ...
coronary (artery) occlusion. coronary (artery) rupture. cardiac infarction. infarction of heart, myocardium, or ventricle. rupture of heart, myocardium, or ventricle. acute myocardial infarction occurring within four weeks (28 days) of a previous acute myocardial infarction, regardless of site. subsequent type 1 myocardial infarction. reinfarction of myocardium. coronary (artery) embolism. coronary (artery) thrombosis. recurrent myocardial infarction. ...
Current trial protocol definitions of stent thrombosis. CEC process for adjudication of definite/confirmed ST has been the same for all major trials of DES Acute myocardial ischemia (ECG major ST abnormality or any biomarker elevation) ANDAngiographic or autopsy evidence of stent occlusion or thrombusAbsence of intervening TLRPossible/presumed STMI in target vessel territory without angiographic evidence of thrombus or other culpritVariably reported among different devices and within studi31646 Slideshow 1281571 by mardi
Almost all heart attacks occur when a blood clot suddenly and completely blocks a coronary artery. This condition is called a coronary thrombosis, or simply a coronary. The part of the heart muscle nourished by the blocked artery becomes damaged by lack of oxygen.
s body exhumed in order to prove her case. We were told that my sister had died of coronary artery thrombosis, but she didnt have a history of heart disease, she said this week. There was no trace of alcohol or barbiturates in her system, but there was this brown cereal-type substance which was never identified. I believe she was killed because someone wanted to silence her. But who? Maxine admits that she has privately confronted the man she suspects of being responsible for her sisters death. ...
... , according to results from the PRESTIGE study presented at ESC Congress1 and published in European
As per investigate information distributed by the American Journal of Clinical Nutrition, people that incorporate general day by day admission of Omega 3 can diminish the danger of heart assault (coronary thrombosis) by up to 70%. Such reassuring news has produced a decent arrangement of enthusiasm for Omega 3 recently. What is Omega 3? Omega 3 is, truth be told, a polyunsaturated unsaturated fat which, as it goes through the limentary channel (stomach related tract through the human body), separates existing cholesterol and stores a minutely thin obstruction to keep its transformation. Omega 3 attempts to battle again the main cholesterol offender that causes thickening of the blood. These coagulations at that point square veins causing heart assaults or, on the off chance that they achieve the mind, strokes. Omega 3 is most regularly connected with the oils found in angle. Best known sources are mackerel, trout and salmon in spite of the fact that the oils can be removed from white fish; and ...
Wells Carl CLINGMAN - Yavapai County Arizona - b. March 6, 1899, Ft. Worth, Tx. d. Jan. 27, 1955, Cottonwood, Az. COD: Coronary thrombosis h/o Hattie Louise Clingman s/o Charles Mmagne & Atlanta E. (Stevens) Clingman Occ: Farm laborer Wagoner, Med. Dept. - WW I Enlisted: June 4, 1917 Discharged: Aug. 21, 1919 Note: Resided in Az. 50 years. Site # A/166 Westcott Funeral Home, Cottonwood, Az. Burial: Jan. 20, 1955 Az. death records /Military records Picture taken by Kelley Townsend
Alma Mae ORTWINE - Yavapai County Arizona - Alta M.(Troutwine) Ortwine b. Feb. 2, 1900, Pidgion, Mich. d. July 9, 1964, Prescott, Az. COD: Coronary thrombosis w/o Frank Simon Ortwine d/o Adolph & Amelia M. (Wagoner) Troutman Site # S/010/H Hampton Funeral Home, Prescott, Az. Buried July 13, 1964
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DESs have dramatically decreased the need for coronary artery bypass graft (CABG) surgery and repeated PCI. However, late stent thrombosis is a small but important risk with DESs because it is commonly associated with sudden death or acute MI. The clinical occurrence of stent thrombosis after stent implantation can be defined as acute (, 24 h), subacute (1 to 30 d), late (30 d to 1 y), or very late (, 1 y). The clinical diagnosis of stent thrombosis can be defined as "definite" if proven angiographically or pathologically, "probable" if an MI occurs in the distribution of the stented artery, or "possible" if death is unexplained (1). Risk for subacute stent thrombosis is about 1% for both DESs and BMSs, but risk for very late stent thrombosis continues for at least 4 years with DESs at a rate of 2 to 4 events/1000 patients per year (1−3). The presumed cause is delayed or incomplete endothelialization of the stent struts. The unanswered question is whether the decrease in risk for death and MI ...
Most physicians believe that acute coronary syndromes (ACS) are due to coronary artery thrombosis resulting from plaque rupture of a metabolically active inflamed lesion characterized by a thin fibrous cap (thin-cap fibroatheroma [TCFA]), overlying a large necrotic core containing rich concentrations of cholesterol, cholesterol esters, and senescent macrophages (1). Such lesions also demonstrate spotty calcification and neovascularization arising from the vasa vasorum with plaque hemorrhage. Indeed, the chemical structure and morphology of the TCFA is so distinctive that numerous invasive and noninvasive imaging modalities have been developed to search for the mischievous TCFA prior to its becoming unstable, to improve prognostic discrimination and perhaps guide systemic or focal therapies.. However, although pathologic studies have demonstrated that the majority of thrombotic lesions responsible for acute myocardial infarction (AMI) and sudden cardiac death have a ruptured fibrous cap (RFC) ...
Lines of Zahn are a characteristic of thrombi that appear particularly when formed in the heart or aorta. They have visible and microscopic alternating layers (laminations) of platelets mixed with fibrin, which appear lighter and darker layers of red blood cells. Their presence implies thrombosis at a site of rapid blood flow that happened before death. In veins or smaller arteries, where flow is not as constant, they are less apparent. They are named after German-Swiss pathologist Friedrich Wilhelm Zahn. "Atherosclerosis". Lee R, Adlam D, Clelland CA, Channon KM (2012). "Lines of Zahn in coronary artery thrombus". Eur Heart J. 33 (9): 1039. doi:10.1093/eurheartj/ehs028. PMID 22345124. Stegman, JK, ed. (2006), Stedmans Medical Dictionary (28th ed.), Baltimore, MD: Lippincott, Williams, & Wilkins Kumar, V. et al. (2005). Hemodynamic Disorders, Thromboembolic Disease, and Shock. Robbins and Cotran Pathologic Basis of Disease. 7th edition. Elsevier Saunders: Pennsylvania. Simon S. Cross (ed.). ...
Novel nanostructured biomaterials: implications for coronary stent thrombosis Varvara Karagkiozaki,1,2 Panagiotis G Karagiannidis,1 Nikolaos Kalfagiannis,1 Paraskevi Kavatzikidou,1 Panagiotis Patsalas,3 Despoina Georgiou,1 Stergios Logothetidis11Lab for Thin Films – Nanosystems and Nanometrology (LTFN), Physics Department, Aristotle University of Thessaloniki, Thessaloniki, 2AHEPA Hospital, Aristotle University of Thessaloniki, Thessaloniki, 3Department of Materials Science and Engineering, University of Ioannina, Ioannina, Epirus, GreeceBackground: Nanomedicine has the potential to revolutionize medicine and help clinicians to treat cardiovascular disease through the improvement of stents. Advanced nanomaterials and tools for monitoring cell–material interactions will aid in inhibiting stent thrombosis. Although titanium boron nitride (TiBN), titanium diboride, and carbon nanotube (CNT) thin films are emerging materials in the biomaterial field, the effect of their surface properties on
To explore effective and convenient rescue therapy options for coronary artery aneurysms (CAA) with thrombosis in Kawasaki disease (KD). A total of
This study reports a significantly lower risk of ST during the first year after PCI with both n-DES and o-DES compared with BMS, but a higher risk of very late ST up to 3 years in the o-DES group compared with the BMS group; and a similar risk of very late ST in the n-DES and BMS groups. Although BMS have been proven to be safe in STEMI patients and the improvements of the new stent platforms have reduced restenosis rates, DES are superior in terms of a decrease in restenosis occurrence. This study suggests that n-DES are associated with a low risk of ST even on long-term follow-up and may be the preferred stent type in STEMI patients compared to BMS and o-DES. ...
The study by den Heijer and colleagues is of interest to both interventional cardiologists and internists. The availability of low-profile, flexible, and steerable angioscopic systems has allowed the routine percutaneous application of this technology. Interpretable images can now be obtained in most patients having interventional procedures, although the technique still has important limitations. Problems remain with aiming the angioscope, and a clear imaging field cannot always be obtained. The widespread availability of second-generation interventional technologies, including stents, atherectomy catheters, and local drug delivery systems, give the interventionist a choice of therapies. Precise knowledge of coronary morphology may have an important effect on the decision of which technique to use to treat a given lesion. The study by den Heijer and colleagues suggests that, in a few patients, the angioscopic information was useful to the clinician. These results, however, cannot be ...
Myocardial infarction. Theres a mouthful. Its a tongue-twiser, isnt it? And it sounds serious.. Well, it is.. Myocardial infarction is medical language for a heart attack. It means the death of tissue (an infarct) in the muscular wall of the heart (the myocardium).. Heart attack is known by several names. coronary thrombosis is a heart attack caused by a clot in the coronary arteries. Sometimes, it is caused by snoring. Coronary occlusion is a blocked artery that could have a number of causes. Myocardial infarction refers to the end result-the damage or death of a part of the heart muscle.. The heart never stops working. In contrast to the muscles in our arms and legs, the heart muscle never rests, although it does slow down when we sleep.. to do its important job of keeping us alive, the heart must have a regular and adequate supply of oxygen and nutrients for energy. For this reason, the heart receives its own supply of oxygen-rich blood by way of the coronary arteries. The sole purpose of ...
Shah, N., Garg, J., Agarwal, V., Mehta, K., Jacobs, L., Patel, N., Freudenberger, R. Stent Thrombosis is Not Increased in Cardiac Arrest Patients Undergoing Therapeutic Hypothermia: An Analysis of 15,079 Procedures. Poster presented at: American College of Cardiology, San Diego, CA.. ...
Review of the recent literature reveals little dealing with the effects of large doses of quinidine on ventricular tachycardia. No series comparable in size to this one has been noted within the past 15 years. McMillan1 recently reported two cases following coronary thrombosis treated successfully with quinidine. Reich2 reported a cure with a total of 185 grains given in a period of two and a half days, a dosage believed by him and also by Levine3 and Gold4 to be the largest dose given in a period of 60 hours. Some of the cases in this series had quinidine in ...
Feng QZ, Wang SW, Zhao YS, Zheng XQ.Subacute stent thrombosis happening at discharge. International Journal of Cardiology 119: E59-E62, No. 2, 10 Jun 2007 - ChinaGoogle Scholar ...
Thrombosis yw tolchenni gwaed a all fod yn farwol syn ffurfio yn y rhedweli (thrombosis rhedwelïol) neu yn y wythïen (thrombosis gwythiennol). Ar ôl i dolchen ffurfio, gall arafu neu rwystro llif gwaed a hyd yn oed gwahanu ei hun a theithio i organ. Gelwir tolchen syn teithio ir system gylchrediad yn emboledd.. Gan amlaf, mae modd atal thrombosis ac maen batholeg o drawiadau ar y galon, strociau thrombo-embolig a thrombo-emboledd gwythiennol (VTE) - sef y tri phrif achos o farwolaethau cardiofasgwlaidd.. Maer Bartneriaeth Effeithiau Gofal Iechyd Cyngor Ymchwil Peirianneg ar Gwyddorau Ffisegol ar Ddiagnosteg a Rheoli Tolchennu Gwaed a arweinir gan Brifysgol Abertawe yn cynnwys athrawon, darlithwyr, ymchwilwyr ôl-ddoethurol, a myfyrwyr o Goleg Peirianneg ac Ysgol Feddygaeth y Brifysgol yn ogystal â phartneriaid ym maes diwydiant a phartneriaid o dramor. Bydd y Bartneriaeth yn cynnal digwyddiad codi arian a chodi ymwybyddiaeth ar Gampws y Bae y Brifysgol ddydd Iau 13 Hydref lle y byddant ...
Thrombosis: Thrombosis,, formation of a blood clot in the heart or in a blood vessel. Factors that play a role in the formation of clots (thrombi) include injury to a blood vessel and
Although almost 10% of middle-aged persons who have major operations afterward develop thrombosis* a serious disease caused by clots which jam the blood vessels they dont need to....
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