Nicoleta Popa-Fotea

Nicoleta Popa-Fotea

Antithrombotic Therapy in Patients with ST-segment Elevation Myocardial Infarction Undergoing Primary PCI

Ischemic heart disease is one of the most prevalent diseases with a high impact on mortality and morbidity. The main process implicated in acute coronary syndromes (ACS) including its most severe form, the ST elevation myocardial infarction (STEMI), is the development of thrombosis subsequently of plaque erodation or rupture. The thrombus is formed by aggregates of platelets that furthermore drive the process of coagulation, that in this turn stimulates platelet aderation and aggregation, causing a vicious circle. From these physiopathological mechanism derive the indication and role of antiplatelets and anticoagulation in STEMI. Antiplatelets and anticoagulants play a central role in the therapeutic management of STEMI along with the interventional therapy. Correctly conducted by all physicians involved in the management of patients with STEMI, it reduces the area of ischemia, as well as mortality and other major adverse cardiovascular events. The following article will review the antithrombotic treatment adjuvant to the interventional treatment and the evidence based indications for treatment in STEMI.

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Mitral Valve Remodeling after Acute Myocardial Infarction – a Longitudinal Three- Dimensional Echocardiography Study

Background: Recent data suggest that the mechanisms contributing to ischaemic mitral regurgitation (IMR) in the setting of acute myocardial infarction (MI) are different compared to chronic IMR. However, little is known about the dynamic changes over time of mitral valve (MV) geometry after acute MI. Methods and results:Comprehensive three-dimensional (3D) assessment of the MV geometry was performed in 30 patients in the first 7 days after a first ST elevation myocardial infarction (STEMI), and after 4 years of follow-up. The MV annulus diameters and area remained unchanged over time, however the MA became progressively flatter (mean difference of annular height 0.19±0.33 cm, p<0.05), independently of the presence or severity of IMR. The posterior leaflet length and area got smaller over time (1.53±0.51 cm vs 1.27±0.33 cm; p<0.05 and 5.65±1.58 cm2 vs 4.88±1.65 cm2; p<0.05, respectively). The tenting height and area were smaller at follow-up (9.06±2.6 mm vs 7.84±2.61 mm, p<0.05; and 1.88±0.6 cm2 vs 1.57±0.5 cm2; p<0.05, respectively). A larger tenting at follow-up correlated with 3D left atrial (LA) volumes, but not with LV volumes and ejection fraction. Conclusions: MV geometry changes over time even in patients with non-severe IMR. The MV healing process consists in annulus flattening associated with improved tenting.

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