Search results
4 lip 2023 · Mural thrombi can invade any cardiac chamber. Left ventricular thrombus is a frequent complication of acute myocardial infarction, mostly with the involvement of the cardiac apex. This thrombus can separate from the ventricle and travel through arteries, blocking any blood vessels.[1]
15 wrz 2022 · Studies using echocardiography have historically identified mural LV thrombi to be associated with a lower risk of embolism compared with protuberant or mobile LV thrombi. 23,82 Despite a lack of correlative pathological imaging studies, mural thrombi detected by imaging are often considered organized (and thus with lower thromboembolic ...
Left ventricular (LV) thrombus development following acute myocardial infarction is driven by the elements of Virchow’s triad: endothelial injury, blood stasis, and hypercoagulability. Each of these components further serves as a therapeutic target in the treatment and prevention of left ventricular thrombus following acute myocardial infarction.
A calcified LVT was defined as a persistent left ventricular mural thrombus encapsulated by thickened and calcified endocardium. Left ventricular characteristics including left ventricular ejection fraction (LVEF), left ventricular volume, wall motion, cardiac output, and potential mechanical complications were also collected.
5 mar 2024 · Left ventricular (LV) thrombus may develop after acute myocardial infarction (MI) and occurs most often with a large, anterior ST-elevation MI (STEMI). However, the use of reperfusion therapies, including percutaneous coronary intervention and fibrinolysis, has significantly reduced the risk.
Left ventricular (LV) thrombus is a feared complication of LV dysfunction associated with high rates of systemic embolism, morbidity, and mortality. Traditionally, LV thrombus has been associated with acute myocardial infarction (MI).
15 mar 2022 · Left ventricular (LV) thrombus development following acute myocardial infarction is driven by the elements of Virchow’s triad: endothelial injury, blood stasis, and hypercoagulability. Each of these components further serves as a therapeutic target in the treatment and prevention of left ventricular thrombus following acute myocardial infarction.
