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A Case Series of Late Myocardial Infarction Following Self-Expanding Transcatheter Aortic Valve Replacement
Muhammad Saad1, Mohammad Hashim Jilani2, Mohsin Munawar2
1Department of Internal Medicine, The Jewish Hospital of Cincinnati, Cincinnati, OH, USA.
Insights
Late heart attacks after transcatheter aortic valve replacement (TAVR) are rare but serious complications. This study highlights three cases of coronary embolism presenting as ST-elevation myocardial infarction (STEMI) months after TAVR, suggesting a non-atherosclerotic cause.
Area of Science:
- Cardiology
- Interventional Cardiology
- Cardiovascular Research
Background:
- Embolic stroke is a known complication following transcatheter aortic valve replacement (TAVR).
- Coronary embolism, particularly late after valve implantation, is infrequently reported.
- ST-segment elevation myocardial infarction (STEMI) is a critical manifestation of coronary embolism.
Abstract:
Embolic stroke is a recognized complication of transcatheter aortic valve replacement (TAVR); however, coronary embolism is rarely reported, particularly when occurring late after valve implantation. We described three patients presenting with ST-segment elevation myocardial infarction (STEMI) between 10 and 50 months after self-expanding TAVR. All patients had angiographically normal coronary arteries prior to TAVR, severe native aortic valve calcification, and well-controlled cardiovascular risk factors, and were maintained on guideline-directed single antiplatelet therapy. At presentation, coronary angiography demonstrated abrupt 100% coronary occlusion without angiographic evidence of underlying atherosclerotic disease. Aspiration thrombectomy was required in all three cases. These cases illustrate a rare presentation of late myocardial infarction following self-expanding TAVR with angiographic features possibly suggestive of a non-atherosclerotic mechanism. Although a definitive embolic source cannot be established, delayed embolization of calcific or thrombotic material may represent a plausible explanation. These observations are hypothesis-generating and underscore the need for clinical vigilance and further mechanistic and imaging-based studies to better characterize potential late thromboembolic pathways after TAVR.
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