Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 148

LV thrombus is most common in patients with anteroapical MI, with a 30–40% incidence in the pre-reperfusion era, down to 10% in the thrombolytic era and 5–10% in the PCI era.^167,168 It usually forms 3-6 days after MI, with at least 25% of thrombi forming in the first 24 hours;^168,169 however, a few thrombi form 1–3 months later. In addition to akinesis, the hypercoagulable state of STEMI promotes the formation of LV thrombi, particularly early LV thrombi. Severe global LV dysfunction is not a prerequisite for LV thrombus formation. LV thrombus may rarely form over a large inferoposterior MI.

In the absence of anticoagulation, LV thrombus is associated with a ~10–15% embolization risk (contrast this risk with the 1% stroke risk in STEMI patients without AF or LV thrombus).¹⁷⁰ In 2 old landmark analyses, nearly all embolic events occurred within 3 months of MI. Beyond this period, as LV aneurysm becomes chronic, the thrombus becomes organized and unlikely to embolize.¹⁷¹ Some studies suggest that a mobile or a pedunculated thrombus bulging in the LV has a higher risk of embolization than a laminated, mural thrombus.¹⁷¹ More importantly than the pedunculated morphology, AF, severe HF, severe LV dysfunction, and older age are associated with higher embolization rates.¹⁶⁷ Interestingly, the risk of late embolization beyond 3 months from a LV thrombus seemed greater with dilated cardiomyopathy than segmental apical aneurysm, likely because in the latter the segment adjacent to the thrombus is static and unlikely to dislodge the thrombus.

Echo is usually used for diagnosis. However, echo may give a false positive diagnosis because of side lobe artifacts or reverberations from the ribs. On the other hand, MRI studies have shown that echo frequently misses apical thrombi, in up to 50% of the cases, particularly when the thrombus is laminated/flat or when the echo plane does not cut through the true apex. Delayed-enhancement MRI allows an accurate diagnosis and allows the distinction between thrombus and the underlying myocardial scar.¹⁷²

Treatment – Warfarin anticoagulation almost abolishes the embolization risk.^168,170,172 In addition, warfarin allows intrinsic lysis of the thrombus or, at least, organization and endothelialization. In fact, ~60-70% of LV thrombi resolve within 6–12 months of anticoagulation, while the rest organize and become laminated. It is believed that an organized thrombus actually has beneficial effects, as it adheres to the dyskinetic apex preventing further infarct expansion and reducing the paradoxical myocardial motion by a plugging effect.

Thus, ACC guidelines recommend the use of warfarin for at least 3 months in patients with LV thrombus (class IIa), as most emboli occur within 3 months of MI.¹⁷¹ Warfarin may be beneficial beyond 3 months in patients who continue to have a low bleeding risk and a high embolic risk, such as: (i) history of embolization; (ii) severe HF or LV dilatation with EF<35%, ischemic or not. One study of patients with LV thrombus, most of whom had ischemic cardiomyopathy with apical akinesis, suggested a benefit of prolonged anticoagulant therapy >3 months, particularly if EF<35%.¹⁷³ It is unclear whether dual antiplatelet therapy has any effect on LV thrombus, and thus, anticoagulation seems warranted on top of antiplatelet therapy, particularly for the first 3 months. NOACs have been used and found to be comparable to warfarin in one retrospective study,¹⁷³ but significantly inferior in a larger study.¹⁷⁴