VENTRICULAR MURAL THROMBUS IN PATIENT WITH LEFT VENTRICULAR ANEURYSM AFTER MYOCARDIAL INFARCTION

На примере клинического случая впервые диагностированного пристеночного тромба у пациента с развившейся постинфарктной аневризмой после перенесенного инфаркта миокарда с STэлевацией обсудили вероятный риск дальнейших тромбоэмболических осложнений и преимуществ антикоагулянтной терапии. Описаны рекомендации по модификации образа жизни и тактике лечения для предотвращения образования новых пристеночных тромбов.


INTRODUCTION
Left ventricular (LV) thrombus formation is a frequent complication in patients with acute anterior myocardial infarction (MI), occurring in at least 5 % of patients. Left ventricular thrombus is associated with increased risk of embolism. [1]. In the context of STEMI, prolonged ischemia results in subendocardial and endothelial injury and increased concentration of procoagulant factors, whereas akinetic areas of necrotic myocardium lead to blood stasis, especially at the LV apex [2]. Two-dimensional transthoracic echocardiography is the most effective diagnostic technique in this setting and can be quickly performed at the bedside but can lead to misdiagnoses due to difficult echo windows, 110 artifact, or the misinterpretation of LV trabeculations or chordae. [3]. In a recent article by Wada et al [4] was demonstrated the excellent diagnostic power of echo contrast for the diagnosis of LV thrombus in 392 patients with anterior MI. Echo contrast had 100 % sensitivity and specificity compared with left ventriculography and/or multidetector computed tomography used as gold standard [5]. Anticoagulation therapy reduces both risks of thrombus formation and subsequent embolization, but leads to increased risk of bleeding. [6] Therefore, accurate detection and exclusion of LV thrombus in patients with coronary artery disease (CAD) are very important [7]. In observational studies and meta-analyses, anticoagulant therapy is recommended in order to minimize embolization risk. An oral vitamin K antagonist, warfarin, has been being used as an anticoagulant for this purpose for a long period of time. New oral anticoagulants (dabigatran, rivaroxaban, apixaban, etc.) were found to be non-inferior or superior compared to warfarin in prevention of thromboembolism in patients with nonvalvular atrial fibrillation [8].

CLINICAL CASE
A 72-year old man was admitted by ambulance in the emergency department of 25 Kharkiv city clinical multi-field hospital with complains on anxiety, general weakness, trembling inside, palpitation periodically, dyspnea and chest pain after mild physical activity.

ANAMNESIS MORBI
Diagnosis of arterial hypertension (AH) and coronary artery disease were established 20 years ago (in 1993 patient had acute anteriorlateral myocardial infarction). Usual blood pressure levels by patient's words are 170/90-100, he receives constant therapy with angiotensin-converting enzyme inhibitors (ACEIb). Also patients receive constant therapy with aspirin 75 mg/day around 5 years long. This time he felt worse 3 days before hospitalization, when appeared palpitation, trembling inside and anxiety, increased general weakness. Was administered by ambulance in cardiology department of 25 city hospital.

ANAMNESIS VITAE
Childhood infections, injuries, tuberculosis, sexually transmitted diseases were denied by patient. Hereditary diseases are not identified. Allergic history is burdened (penicillin). Smoking -denied, not an alcohol abuser.

RECOMMENDATIONS
Summarizing data from 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with STsegment elevation [9] and 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure [10], the following may be applicable for our patient after discharge from hospital and for prevention of further mural thrombi formation and thromboembolic episodes appearance: 1. For mural thrombi, once diagnosed, oral anticoagulant therapy should be considered for up to 6 months, guided by repeated echocardiography and with consideration of bleeding risk and need for concomitant antiplatelet therapy [11].
2. Secondary mitral valve regurgitation: LV remodeling with lateral and apical displacement of the papillary muscles, leaflet tethering, and annular dilatation are a common cause of secondary (functional) mitral regurgitation. While transthoracic echocardiography is fundamental for the initial diagnosis, transesophageal echocardiography may be needed for better definition of the mechanism and severity of mitral regurgitation. The severity of mitral regurgitation may improve with reperfusion and aggressive medical treatment, including diuretics and arterial vasodilators. In our patients case can be treated symptomatically without surgical correction needed [9]. 3.
ACE-blockers is recommended and should be up-titrated to the maximum tolerated dose, in addition to a beta-blocker, for symptomatic patients with CHF with reduced ejection fraction (HFrEF) to reduce the risk of HF hospitalization and death. A beta-blocker is recommended initially at a low dose with gradually up-titration to the maximum tolerated dose, in addition an ACE-Id or ARB if ACEIb is not tolerated or contraindicated, for patients with stable, symptomatic HFrEF to reduce the risk of HF hospitalization and death. Betablockers are also effective agents for angina control in our patient's case [10].

4.
Mineralocorticoid/aldosterone receptor antagonists are recommended in all symptomatic patients (despite treatment with an ACEI and a beta-blocker) with HFrEF and LVEF ≤ 35 %. Can be avoided in our patient case as EF is 36 %, but used as AH treatment as needed [9,11].

CONCLUSIONS
Left ventricular thrombus is an important complication of acute myocardial infarction that impacts embolic event risk and anticoagulant therapy. Improved understanding of post-MI thrombus in the current era is critical for optimization of diagnostic testing strategies. Advances in MI management, including prompt and effective coronary reperfusion, have yielded improvements in LV function and remodeling. Widespread use of antiplatelet agents may potentiate the benefits of reperfusion, thereby lessening the likelihood of LV thrombus.