Case presentation

The patient is a 65-year-old man with a past medical history significant for ischemic cardiomyopathy with LV apical aneurysm, chronic heart failure with reduced ejection fraction (HFrEF) with left ventricular ejection fraction (LVEF) of 30%-35% diagnosed in 2022, atrial flutter status post flutter line, and stage II chronic kidney disease (baseline creatinine: 1.7 mg/dL). He started treatment for heart failure, and he had improvement in LV systolic function from an initial LVEF of 30%-35% to 40%-45% on transthoracic echocardiogram (TTE) done in October 2024, although an apical aneurysm remained present, with no LV apical thrombus reported.

The patient had regular follow-up in the outpatient cardiology clinic at the VA NY Harbor Healthcare System-Brooklyn for his chronic cardiovascular conditions. His medications included carvedilol 6.25 mg twice daily, sacubitril/valsartan 49/51 mg twice daily, empagliflozin 10 mg daily, atorvastatin 40 mg daily, apixaban 5 mg twice a day, and aspirin 81 mg daily.

He denied chest pain, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, palpitations, syncope, focal neurologic deficits, constitutional symptoms, or recent hospitalizations. Functionally, he was classified as New York Heart Association (NYHA) class I. Review of systems was otherwise negative, and physical examination was unremarkable.

A TTE performed one year later, in October 2025, reported borderline decreased systolic function with an aneurysmal LV apex that was not well visualized (Figure 1), which led to a recommendation for a repeat limited echocardiogram using ultrasound contrast agent Definity (perflutren lipid microsphere). A contrast-enhanced transthoracic echocardiogram (TTE) using perflutren lipid microsphere (Definity) performed days later demonstrated mildly to moderately reduced left ventricular systolic function with an estimated LVEF of 40%-45% and confirmed an apical left ventricular thrombus with improved delineation of the left ventricular endocardial borders (Figure 2). The patient was subsequently started on therapeutic anticoagulation with apixaban.

Figure 1: TTE in October 2025 (without ultrasound contrast agent) (A4C view)LV apex not well-visualized, suspected apical thrombusTTE: transthoracic echocardiography, A4C: apical four-chamber, LV: left ventricle

Figure 2: TTE in October 2025 with contrast (Definity) (A4C view)Left ventricle: mild to moderately decreased systolic function. Ejection fraction is mild to moderately decreased. The estimated ejection fraction is 40%-45%. Apex and apical segments are akinetic. Mild basal infero-septal severely hypokinetic. With contrast injection, an echolucency approximately 0.7 x 2 cm is visualized in the LV apex.TTE: transthoracic echocardiography, A4C: apical four-chamber, LV: left ventricle

A follow-up TTE approximately six months later, performed in April 2026 (Figure 3 and Figure 4), demonstrated persistent mildly to moderately reduced left ventricular systolic function with an estimated LVEF of 40%-45% and a persistent left ventricular apical thrombus despite anticoagulation.

Figure 3: Repeat TTE in April 2026 without ultrasound contrast agent (A4C view)Apical thrombus still presentTTE: transthoracic echocardiography, A4C: apical four-chamber, LV: left ventricle

Figure 4: Repeat TTE in April 2026 with contrast agent (Definity) (A4C view)Apical thrombus still presentTTE: transthoracic echocardiogram, A4C: apical four-chamber, LV: left ventricle

The patient remained asymptomatic despite persistent thrombus on full-dose apixaban, although he acknowledged inconsistent medication adherence during the initial three months after diagnosis of LV apical thrombus. Cardiac magnetic resonance imaging (CMR) was planned to further characterize thrombus morphology, evaluate the apical aneurysm, and guide subsequent management decisions. Cardiothoracic surgery consultation was obtained to assess potential therapeutic options should high-risk features be identified.

The development of LVT in this patient raised several clinically relevant questions. Although suboptimal adherence to apixaban likely contributed to thrombus persistence, this case also highlights broader uncertainties frequently encountered in clinical practice regarding the identification of patients at increased risk for thrombus persistence, recurrence, and future thromboembolic complications.

Unlike the classic presentation of LVT following an acute anterior ST-segment elevation myocardial infarction (STEMI), this patient developed thrombus in the setting of chronic HFrEF with persistent systolic dysfunction, with thrombus remaining present after six months of prescribed therapeutic anticoagulation. The case illustrates the limitations of current generalized treatment recommendations and emphasizes the importance of incorporating patient-specific clinical characteristics, thrombus morphology, ventricular remodeling, adherence to prescribed medical therapy, and anticoagulation-related factors into decisions regarding the optimal duration of anticoagulation and follow-up imaging.