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Published on: November 4, 2021
Noncompaction and embolic myocardial infarction: the importance of oral anticoagulation
Giovanni Pulignano1, Maria Denitza Tinti1, Stefano Tolone1
1Cardiology 1/CCU, S. Camillo Hospital, Rome, Italy.
Insights
Left ventricular noncompaction (LVNC) can lead to serious heart issues. Discontinuing anticoagulation in an LVNC patient caused extensive left ventricular thrombosis, resulting in myocardial infarction due to coronary thromboembolism.
Area of Science:
- Cardiology
- Internal Medicine
- Pathology
Background:
- Left ventricular noncompaction (LVNC) is a rare cardiomyopathy defined by excessive left ventricular (LV) trabeculations.
- LVNC is associated with increased risks of heart failure, arrhythmias, and embolic events.
Observation:
- A 67-year-old patient with LVNC, previously on oral anticoagulation (OAC) for apical thrombosis, discontinued OAC therapy.
- Following OAC cessation, the patient developed extensive left ventricular thrombosis, worsening cardiac function, and requiring hospitalization.
Findings:
- Despite heparin treatment, the patient suffered a myocardial infarction (MI) attributed to embolic occlusion of the left anterior descending artery.
- This case suggests coronary thromboembolism from dislodged LV thrombus as a cause of MI in LVNC, distinct from typical microvascular dysfunction.
Implications:
- This case highlights the critical role of anticoagulation in managing LVNC patients with thrombosis.
- It underscores the potential for LVNC-associated thrombosis to cause significant embolic complications, including myocardial infarction.
- Further research into optimal anticoagulation strategies for LVNC patients is warranted.
Abstract:
Left ventricular noncompaction (LVNC) is characterized by left ventricular (LV) hypertrabeculations and is associated with heart failure, arrhythmias and embolism. We report the case of a 67-year-old LVNC patient, under oral anticoagulation (OAC) therapy for apical thrombosis. After she discontinued OAC, the thrombus involved almost the whole of the left ventricle; in a few months her condition worsened, requiring hospitalization, and despite heparin infusion she experienced myocardial infarction (MI), caused by embolic occlusion of the left anterior descending artery. Although infrequent as a complication of LVNC, and usually attributable to microvascular dysfunction, in this case MI seems due to coronary thromboembolism from dislodged thrombotic material in the left ventricle.
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