Left ventricular thrombosis and cerebrovascular accident in acute myocardial infarction.

Johannessen, Karl-Arne; Nordrehaug, Jan Erik; Lippe, G von der

doi:10.1136/hrt.51.5.553

Cited by 104 publications

(23 citation statements)

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“…29) Left ventricular thrombus formation has been frequently correlated to LV wall motion abnormalities. [15][16][17][18][19][20] The documented incidence of LV thrombus varies between 30% and 40% in patients with LV dysfunction, and increases up to 75% in patients with dilated cardiomyopathy. [15][16][17][18][19][20] A limited number of echocardiographic studies suggest that abnormal flow patterns within the LV may also be asscociated with LV thrombus formation.…”

Section: Discussionmentioning

confidence: 99%

“…[15][16][17][18][19][20] The documented incidence of LV thrombus varies between 30% and 40% in patients with LV dysfunction, and increases up to 75% in patients with dilated cardiomyopathy. [15][16][17][18][19][20] A limited number of echocardiographic studies suggest that abnormal flow patterns within the LV may also be asscociated with LV thrombus formation. [19][20][21][22][23][24][25][26][27] The incidence of LV thrombus has been reported to decrease with increasing MR severity in patients with dilated cardiomyopathy, and in patients with ischemic LV dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…[9][10][11][12][13][14] The left ventricle (LV) has been reported to be the primary location of thrombus formation in patients with global or segmentary LV systolic dysfunction in association with endocardial injury, wall motion abnormalities, and coagulation disturbances. [15][16][17][18] The abnormal flow patterns within the left ventricle due to systolic dysfunction have been correlated to LV thrombus formation. [19][20][21][22][23] Recently, some echocardiographic series have reported that the incidence of LV thrombus formation was significantly decreased with increasing MR severity in patients with dilated cardiomyopathy, and in patients with ischemic LV dysfunction.…”

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Severe Mitral Regurgitation May Prevent Mural Thrombus Formation within the Left Ventricle with Systolic Dysfunction.

et al. 2002

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SUMMARYThe protective effect of severe mitral regurgitation (MR) against left atrial thrombus formation has been well documented. It was also proposed that severe MR may prevent thrombus formation within the left ventricle (LV) with systolic dysfunction. Therefore, we investigated whether ischemic MR prevents thrombus formation within the LV in patients with systolic dysfunction. The study population was comprised of 1313 patients (1133 males, 180 females, age 56±18) with ischaemic LV dysfunction documented by coronary angiography and left ventriculography. None of the patients had a history of chronic anticoagulation. Epicardial coronary arteries were normal in 91 patients, and single-vessel, two-vessel, and triple-vessel disease were detected in 328, 330, and 564 patients, respectively. Left ventricular thrombus and severe MR were detected in 191 (14.5%) and 125 (9.5%) patients, respectively. Overall incidence of LV thrombus was lower in patients with severe MR than in patients without severe MR (4% vs 15.6%, OR: 0.2, P<0.001).Severe MR compared with absence of severe MR was associated with a lower incidence of LV thrombus both in patients with ischemic dilated cardiomyopathy (6.8% vs 34.2%, OR: 0.19, P<0.001), and in patients with aneurysm (3% vs 18%, OR: 0.14, P<0.0001) involving anterolateral, septal and/or apical LV segments. A similar trend without statistical significance was also observed in patients with dyskinesia (4.7% vs 16%, OR: 0.26, P=0.1) related to anterolateral, septal and/or apical LV segments. However, MR had no impact on the incidence of LV thrombus in patients with aneurysm or dyskinesia related to posterior and/or inferior segments (3.7% vs 3%, OR: 1.2, P>0.05).In conclusion, severe MR seems to prevent LV mural thrombus formation in patients with ischemic dilated cardiomyopathy, and in patients with aneurysm related to anterolateral, septal, and/or apical LV segments. This relative risk reduction may be associated with diastolic volume overloading due to severe MR which may overcome stagnation and a procoagulant state within the LV with severe systolic dysfunction. (Jpn Heart J 2002; 43: 495-503)

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Section: Discussionmentioning

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Section: Discussionmentioning

confidence: 99%

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Severe Mitral Regurgitation May Prevent Mural Thrombus Formation within the Left Ventricle with Systolic Dysfunction.

et al. 2002

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“…In the setting of acute myocardial infarction, data regarding the embolic risk once a thrombus has formed have varied widely; however, a reasonable estimate based on the largest echocardiographic studies would be 10-20% within the first few months after infarction. 5,[7][8][9][10][11][12]14 In the setting of remote myocardial infarction, the risk of embolization declines; however, a recent echocardiographic study noted an embolic risk of 7% per year, which was sixfold that noted in a control group of patients without thrombi. 13 The increased risk of embolization suggests that antithrombotic therapy should be considered in patients with either acute or long-term ventricular thrombi.…”

Section: Comparison Of Platelet Imaging and Echocardiographymentioning

confidence: 99%

111In platelet imaging of left ventricular thrombi. Predictive value for systemic emboli.

Stratton

Ritchie

1990

Circulation

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To determine whether a positive indium 111 platelet image for a left ventricular thrombus, which indicates ongoing thrombogenic activity, predicts an increased risk of systemic embolization, we compared the embolic rate in 34 patients with positive "'1In platelet images with that in 69 patients with negative images during a mean follow-up of 38±31 (+SD) months after platelet imaging. The positive and negative image groups were similar with respect to age (59± 11 vs. 62± 10 years), prevalence of previous infarction (94% vs. 78%, p<0.05), time from last infarction (28±51 vs. 33±47 months), ejection fraction (29±14 vs. 33+14), long-term or paroxysmal atrial fibrillation (15% vs. 26%), warfarin therapy during follow-up (26% vs. 20%7o), platelet-inhibitory therapy during follow-up (50% vs. 33%), injected "1'In dose (330±+92 vs.344±118 ,uCi), and latest imaging time (.48 hours in all patients). During follow-up, embolic events occurred in 21% (seven of 34) of patients with positive platelet images for left ventricular thrombi as compared with 3% (two of 69) of patients with negative images (p=0.002). By actuarial methods, at 42 months after platelet imaging, only 86% of patients with positive images were embolus free as compared with 98% of patients with negative images (p<0.01). To determine whether platelet imaging, which detects active thrombosis, offered additional predictive value to two-dimensional echocardiography, which is less costly and more widely available, we compared the embolic rates in 30 patients with both a positive echocardiogram and a positive platelet image to the rate in 28 patients with a positive echocardiogram but a negative platelet image. Among patients with both studies positive, embolic events occurred in 23% (seven of 30) versus 4% (one of 28) in patients with a positive echocardiogram but a negative platelet image (p=0.03). The corresponding actuarial rates at 42 months were 85% and 100% (p=O0.07). We conclude that a positive platelet image for a left ventricular thrombus predicts an increased embolic risk and appears more specific for subsequent embolization than a positive echocardiogram. Additionally, in patients with left ventricular thrombus by echocardiography, a negative platelet image predicts a low risk of subsequent embolization. These findings suggest that thrombosis imaging might be useful to assess the risk of thromboembolic complications in patients with arterial thrombosis. (Circulation 1990;81:1182-1189 L eft ventricular thrombi occur in approximately one third of patients with either transmural anterior myocardial infarction or advanced idiopathic congestive cardiomyopathy.1,2 Thrombi that are hematologically active with ongoing platelet deposition can be detected by indium 111 platelet imaging as localized areas of increased labeled plate-

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“…46 Despite treatment with thrombolytic agents, left ventricular thrombus may occur in 28% of patients who have an acute anterior myocardial infarction, with even higher rates in the presence of apical hypokinesis. 47,48 The high risk of subsequent embolic events (OR 5.45,) may be significantly reduced with anticoagulation (OR 0.14, 95% CI 0.04-0.52) 49 and has been suggested for 1-3 months after anterior myocardial infarction 50 especially when complicated by severe left ventricle dysfunction or previous emboli.The presence of aortic atheroma of 4 mm or more in thickness causes a 3-to 9-fold increased risk of stroke. [51][52][53] This risk is further increased if the atheroma is mobile 53,54 or noncalcified.…”

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Current and future concepts in stroke prevention

O’Rourke

Dean

Akhtar

et al. 2004

Canadian Medical Association Journal

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STROKE IS A MAJOR CAUSE OF MORBIDITY and mortality in an aging population. The current understanding of the pathophysiology of atherosclerotic diseases, the most common cause of stroke, and the evidence for existing therapeutic interventions for the prevention of stroke are presented. Specifically, we review the evidence for antiplatelet agents, anticoagulants, antihypertensive medications, lipidlowering agents and carotid endarterectomy for stroke prevention. primary preventive measure, antiplatelet agents do not reduce the risk of ischemic stroke among patients without vascular disease. They are associated with an increased risk of intracranial hemorrhage (odds ratio [OR] 1.35, 95% confidence interval [CI] 0.88-2.10) 23 and major noncerebral hemorrhage (OR 1.73, 95% CI 1.14-2.63 ). 24 The benefits of ASA in the secondary prevention of stroke have been well documented in the period immediately after a stroke 25 (Table 1). Long-term antiplatelet treatment after stroke shows an even more impressive reduction of 25 nonfatal strokes and 36 serious vascular events per 1000 treated over a 29-month follow-up period. 25 There appears to be no difference in efficacy between low (50 mg) and higher doses (up to 1500 mg) of ASA. 29,30 The combination of dipyridamole and ASA has been shown to reduce the relative risk of recurrent stroke compared with ASA alone 26 (Table 1). Dipyridamole inhibits platelet aggregation by increasing levels of cyclic adenosine monophosphate and cyclic guanosine monophosphate. The limiting factor in the use of the ASAdipyridamole combination is the latter's potential effects on coronary perfusion. Dipyridamole can cause coronary vasodilation, which results in increased blood flow to nonstenosed coronary arteries. The result is that myocardial ischemia may be provoked during exercise. As such, the current American College of Cardiology/American Heart Association guidelines recommend that dipyridamole not be used in patients with chronic stable angina. 31 However, this recommendation was based on shortacting dipyridamole, which also reduced myocardial ischemia in a similar number of patients in the study quoted by these guidelines. 32 With the use of sustained-release dipyridamole, no increase in cardiac events was observed in subjects with prior coronary artery disease. 33 Thienopyridines block adenosine-diphosphate-mediated platelet aggregation. Ticlopidine was the first of this class of drug to be studied for stroke prevention. One clinical trial demonstrated that patients treated with ticlopidine had similar rates of stroke as those treated with ASA 28 (Table 1). However, serious granulocytopenia associated with ticlo- Leukocytes localize in the earliest atherosclerotic lesions, binding to vascular cell adhesion molecules (VCAM-1) on the vascular endothelium and migrating into the intima. This initiates and perpetuates a local inflammatory response. Monocytes mature into lipid-scavenging macrophages and subsequently foam cells. T-lymphocytes express inflammatory cytokines, which cont...

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Left ventricular thrombosis and cerebrovascular accident in acute myocardial infarction.

Cited by 104 publications

References 9 publications

Severe Mitral Regurgitation May Prevent Mural Thrombus Formation within the Left Ventricle with Systolic Dysfunction.

Severe Mitral Regurgitation May Prevent Mural Thrombus Formation within the Left Ventricle with Systolic Dysfunction.

111In platelet imaging of left ventricular thrombi. Predictive value for systemic emboli.

Current and future concepts in stroke prevention

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