ライフサイエンスコーパス: coronary thrombosis

1 or the use of statins to prevent or modulate coronary thrombosis.

2 s offers the potential for direct imaging of coronary thrombosis.

3 y associated with plaque rupture, leading to coronary thrombosis.

4 progression of atherosclerosis and prevents coronary thrombosis.

5 known whether it also increases the risk of coronary thrombosis.

6 f these drugs in settings that involve acute coronary thrombosis.

7 ported association of the Pl(A2) allele with coronary thrombosis.

8 lerotic regions and thus could contribute to coronary thrombosis.

9 ntegrins is reported to be a risk factor for coronary thrombosis.

10 akdown product of bradykinin prevents canine coronary thrombosis.

11 which are usually due to plaque rupture and coronary thrombosis.

12 icrog x kg(1) x min(-1) completely abolished coronary thrombosis.

13 cal disruption of atheroma frequently causes coronary thrombosis.

14 iven plasminogen activators for treatment of coronary thrombosis.

15 A) in a canine model of electrically induced coronary thrombosis.

16 ue thrombus suggests that TF plays a role in coronary thrombosis.

17 important role in the pathogenesis of acute coronary thrombosis.

18 roxemic SSO(2) therapy showed no evidence of coronary thrombosis.

19 be associated with the development of acute coronary thrombosis.

20 Of the three types of coronary thrombosis, a precursor lesion for acute ruptur

21 rapeutic strategy in the prevention of acute coronary thrombosis after plaque disruption.

22 flow reductions (CFRs) in a canine model of coronary thrombosis after thrombolysis.

23 (NO) in a canine model of platelet-mediated coronary thrombosis after thrombolysis.

24 Plaque disruption is the inciting event for coronary thrombosis and acute coronary syndromes.

25 tivation and likely plays important roles in coronary thrombosis and arteriosclerosis.

26 can lead to vascular events including acute coronary thrombosis and may be associated with an increa

27 clerotic plaque rupture is the main cause of coronary thrombosis and myocardial infarcts.

28 nto the pathophysiologic mechanisms of acute coronary thrombosis and reperfusion.

29 t-mediated contributions to atherosclerosis, coronary thrombosis and restenosis after angioplasty.

30 ized that circulating S. sanguis might cause coronary thrombosis and signs of myocardial infarction (

31 ivity could be a novel target for therapy in coronary thrombosis and stroke and after angioplasty.

32 ced platelet function and increased risk for coronary thrombosis and stroke, although these findings

33 mal cholesterol values may precipitate acute coronary thrombosis and sudden death resulting from eith

34 artery disease, both with and without acute coronary thrombosis, and correlates with immunohistochem

35 , chronic inflammatory conditions, diabetes, coronary thrombosis, and stroke.

36 hism of the glycoprotein IIIa gene and acute coronary thrombosis, and this association was strongest

37 cans/hyaluronan, in the development of acute coronary thrombosis associated with erosion.

38 cidence and morphological characteristics of coronary thrombosis associated with plaque rupture versu

39 Seventeen had documented coronary thrombosis by cardiac catheterization.

40 g aspirin-independent pathways through which coronary thrombosis can be precipitated.

41 coronary syndromes are caused by obstructive coronary thrombosis complicating myocardial ischaemic di

42 is a frequent finding in sudden death due to coronary thrombosis, comprising 44% of cases in the pres

43 ow reductions occurring in a canine model of coronary thrombosis despite aspirin therapy.

44 hat underlie superficial erosion, a cause of coronary thrombosis distinct from plaque rupture, have g

45 Coronary thrombosis has been reported to occur most freq

46 batide) to Minimize Platelet Aggregation and Coronary Thrombosis-II (trial) (IMPACT-II), a trial of t

47 egrilin to Minimize Platelet Aggregation and Coronary Thrombosis (IMPACT) II trial, which studied ang

48 nodule has been suggested as a rare cause of coronary thrombosis in highly calcified and tortious art

49 ences suggest an increased vulnerability for coronary thrombosis in patients with diabetes mellitus.

50 further insight into the pathophysiology of coronary thrombosis in the absence of rupture.

51 lar level and protected against experimental coronary thrombosis in vivo in dogs suggests a potential

52 ion ex vivo and protect against experimental coronary thrombosis in vivo in dogs.

53 Experimental coronary thrombosis in vivo was studied in an open-chest

54 Concomitant acute myocarditis and acute coronary thrombosis is a rare presentation of acute ches

55 The most common cause of coronary thrombosis is plaque rupture followed by plaque

56 gs cardiovascular disease, coronary disease, coronary thrombosis, myocardial ischemia, coronary steno

57 ease, including myocardial infarction due to coronary thrombosis, myocarditis, and new onset arrhythm

58 fibrous cap rupture is the primary cause of coronary thrombosis, plaque erosion is responsible for 3

59 plaques may suddenly cause life-threatening coronary thrombosis presenting as an acute coronary synd

60 plaque rupture is the most frequent cause of coronary thrombosis, studies with optical coherence tomo

61 The cyclic flow model of experimental coronary thrombosis suggests that elevations of plasma c

62 This is the first study of a murine model of coronary thrombosis that occurs in the absence of severe

63 -risk, vulnerable plaques is responsible for coronary thrombosis, the main cause of unstable angina,

64 hypothesized to be the predisposing event in coronary thrombosis, the possibility cannot be excluded

65 ardial infarctions, three instances of fresh coronary thrombosis, three cases of obstructive coronary

66 atecholamine inotropic agents may potentiate coronary thrombosis via a platelet alpha2-adrenergic mec

67 After successful demonstration, in-stent coronary thrombosis was induced by x-ray-guided placemen

68 Using a canine model of coronary thrombosis, we aimed to (1) reproduce these cli

69 was designed to determine in a dog model of coronary thrombosis whether short-term eptifibatide (Ep)