Systemic Embolism in Chronic Left Ventricular Aneurysm: Incidence and the Role of Anticoagulation

Abstract

The incidence and prevention of systemic embolism in patients with chronic left ventricular aneurysm have been controversial. This retrospective study investigated the incidence of clinically evident embolic events and the effect of oral anticoagulation in patients with unequivocal angiographically defined left ventricular aneurysm. Between 1971 and 1979, 76 patients met the ventriculographic criteria and received initial medical management. The median interval from myocardial infarction to ventriculography was 11 months (range 1 month to 16 years) and subsequent median follow-up time was 5 years. Twenty patients receiving anticoagulant therapy were followed up for a total of 40 patient-years and 69 patients not on anticoagulant therapy were followed up for a total of 288 patient-years; 13 patients were included in both subsets. Twenty-eight patients died during follow-up and the 3 and 5 year survival rates were 75 and 61%, respectively. Only one patient not receiving anticoagulant therapy had a clinical embolic event, resulting in an incidence of 0.35 per 100 patient-years. Therefore, in the absence of other predisposing conditions, the extremely low incidence of systemic emboli in these patients with chronic (first documented at least 1 month after myocardial infarction) left ventricular aneurysm does not justify the use of long-term oral anticoagulant therapy.

Current approaches to antithrombotic therapy in patients with cardioembolic stroke

“…После образования тромба взаимодействие гидрав-лических сил потока крови и адгезивных сил тромба опре-деляет риск последующей эмболизации. Так, левожелу-дочковые тромбы при остром ИМ, которые по данным ЭхоКГ выступают в полость желудочка и являются мо-бильными, имеют высокую склонность к системной эм-болизации [17], тогда как хронические левожелудочковые аневризмы содержат тромбы, которые редко эмболизиру-ют [18]. Таким образом, свежие тромбы более эмбологен-ны вследствие их рыхлости и мобильности, а тромбы вну-три хронических желудочковых аневризм менее склонны к эмболизации по трем причинам: во-первых, тромб име-ет широкое прикрепление к стенке желудочка; во-вторых, отсутствие контрактильных волокон внутри аневризмы предупреждает движение тромба в просвет желудочка и нарушение его прикрепления; в-третьих, тромб вследст-вие его расположения внутри аневризмы изолирован от гидравлических сил внутри просвета желудочка [19].…”

Antithrombotic therapy in cardiac disease. An emerging approach based on pathogenesis and risk.

“…In contrast to the prevalence of thromboembolism in acute myocardial infarction, the incidence of embolism in chronic left ventricular aneurysm is significantly lower (0.35% per year). 83 The reason for this difference is probably twofold. First, thrombi formed after acute infarction are usually mobile, friable, and protrude into the ventricular cavity, whereas thrombi in chronic aneurysms are laminated and more adherent to the endocardium.11'79 Second, thrombi located within an aneurysmal sac, which is devoid of contractile fibers, are less prone to propulsion into the ventricular outflow tract.…”

Antithrombotic and interventional treatment options in cardioembolic transient ischaemic attack and ischaemic stroke

“…79 Patients with idiopathic dilated cardiomyopathy seem to have a higher risk of cardiogenic embolism than patients with a left ventricular aneurysm after a myocardial infarction. 78 This may in part be secondary to the fact that a left ventricular thrombus in patients with cardiomyopathy is more likely to protrude into the lumen of the ventricle and embolise, 78 rather than undergo organisation in a left ventricular aneurysmal cavity.…”

“…The risk of thrombus formation is related to the site and extent of the myocardial injury 77 and is more common in the acute than convalescent phase after symptom onset 78 ; 1 in 3 anterior Q wave myocardial infarcts, but ,1 in 20 inferior Q wave infarcts or non-Q wave infarcts are associated with left ventricular thrombus formation. 77 Chronic mural thrombi are also commonly identified in patients with chronic left ventricular aneurysm after myocardial infarction, but most of these patients do not subsequently develop cardioembolic TIA or stroke.…”

“…79 High-risk factors for embolisation include a fresh mobile thrombus protruding into the ventricular cavity and acute anterior infarction associated with apical dykinesia or akinesia. 78 Left ventricular thrombus formation also occurs in idiopathic dilated cardiomyopathy (ie, in the absence of coronary artery disease), and is usually confined to the left ventricular apex because of relative stasis of blood in this region. 79 Patients with idiopathic dilated cardiomyopathy seem to have a higher risk of cardiogenic embolism than patients with a left ventricular aneurysm after a myocardial infarction.…”