Journal of the American College of Cardiology

1996

DOI: 10.1016/0735-1097(95)00526-9

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Aortic atherosclerotic plaques as a source of systemic embolism

Mehran Khatibzadeh

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et al.

Abstract: Complicated atherosclerotic plaques in the aortic arch represent an independent risk factor for systemic embolism similar to atrial fibrillation and severe atherosclerosis of the carotid arteries.

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Cited by 133 publications

(86 citation statements)

References 42 publications

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“…The presence of thrombi on aortic plaques was further documented on autopsy in a more recent study, 46 which found aortic thrombi in 17 of 120 cases, as well as a significant association of complex plaque with previous emboli. In addition, mobile lesions in the aorta seen on TEE in 6 patients were seen to be thrombi on surgical pathology.…”

Section: Pathological Correlationsmentioning

confidence: 99%

Aortic Atherosclerotic Disease and Stroke

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2006

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“…The presence of thrombi on aortic plaques was further documented on autopsy in a more recent study, 46 which found aortic thrombi in 17 of 120 cases, as well as a significant association of complex plaque with previous emboli. In addition, mobile lesions in the aorta seen on TEE in 6 patients were seen to be thrombi on surgical pathology.…”

Section: Pathological Correlationsmentioning

confidence: 99%

Aortic Atherosclerotic Disease and Stroke

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2006

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“…[1][2][3][4][5][6] Aortic atheroma is recognized as an important marker of stroke and peripheral embolism in patients with AF. [7][8][9] The SPAF-III investigators reported that complex aortic plaque emerged as a risk factor of thromboembolism in patients with nonrheumatic AF, and warfarin was effective in reducing stroke in patients with AF and complex aortic plaque. 10 Complex aortic plaques with ulcerated or mobile plaques and superimposed thrombi would activate hemostatic markers.…”

mentioning

confidence: 99%

Thoracic Aortic Plaque Enhances Hypercoagulability in Patients With Nonrheumatic Atrial Fibrillation

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et al. 2007

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trial fibrillation (AF) is associated with higher thromboembolic risk, possibly because of the hypercoagulable state. 1,2 Elevated levels of hemostatic markers have been shown in patients with nonrheumatic AF. [2][3][4][5][6] During AF, stagnation of blood flow in the left atrial appendage (LAA) could contribute to the hypercoagulable state and clot formation in the fibrillating atria. Hemostatic markers could be therefore used for stratification of patients at high risk vs low risk for thromboembolism as demonstrated in previous studies. [1][2][3][4][5][6] Aortic atheroma is recognized as an important marker of stroke and peripheral embolism in patients with AF. 7-9 The SPAF-III investigators reported that complex aortic plaque emerged as a risk factor of thromboembolism in patients with nonrheumatic AF, and warfarin was effective in reducing stroke in patients with AF and complex aortic plaque. 10 Complex aortic plaques with ulcerated or mobile plaques and superimposed thrombi would activate hemostatic markers. The Framingham Offspring Study raised the possibility that the increases in hemostatic factors in patients with AF were mainly caused by the confounding effect of traditional risk factors and coexistent cardiovascular diseases rather than by AF itself. 2 We recently reported that patients with nonrheumatic AF had elevated levels of D-dimer when complicated with spontaneous echocardiographic contrast (SEC) in the descending thoracic aorta. 11Because AF and aortic atherosclerosis might contribute synergistically to increased levels of hemostatic markers, and could be associated with increased risk of thromboembolism, we determined the relationship between plasma levels of hemostatic markers and atherosclerosis in the descending thoracic aorta assessed by transesophageal echocardiography (TEE) in patients with nonrheumatic AF and in those in sinus rhythm (SR). Methods Study PatientsEchocardiographic and hematologic studies were performed in 106 consecutive patients (79 men, 27 women; mean age of 67±11 years) referred to a university hospital for cardiovascular assessment for stroke risk or identification of the cardiogenic source of recent embolism. Patients who received anticoagulant therapy were not included in the present study. Of these 106 patients, AF was documented electrocardiographically in 60 patients (AF group) but not in the remaining 46 patients (SR group). The study protocol was approved by the institutional ethics committee and written informed consent was given by all patients. Underlying heart diseases included the following: ischemic heart disease (n=8), hypertrophic cardiomyopathy (n=4), dilated cardiomyopathy (n=5), sick sinus syndrome (n=3), atrial septal defect (n=5), post pericarditis (n=6), and miscellaneous diseases (n=20). No apparent underlying diseases were identified in 55 patients. Baseline clinical characteristics, including body mass index, diabetes mellitus, hyperlipidemia, smoking, previous cerebral or peripheral embolic event and the use of oral antiplatelet medication at...

“…Because cardioembolism in our series and in others is the main cause of systemic embolization, 2,11,19 the discovery of SDVI associated with cryptogenic stroke should be taken into account in the diagnosis of probable cardiac embolism and therefore may assist in making decisions for anticoagulant therapy. Earlier studies 20,21 described the association between complex atherosclerotic plaques in the thoracic aorta and peripheral embolic events. We did not find any association between SDVI and ulcerated plaques in the abdominal or thoracic aorta among patients with brain infarction, but we could not exclude that this association was overlooked as a result of the lack of statistical power.…”

Section: Discussionmentioning

confidence: 99%

Prevalence and Determinants of Subdiaphragmatic Visceral Infarction in Patients With Fatal Stroke

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Gongora-Riverra

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et al. 2007

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Background and Purpose-Arterial thromboembolism is a common cause of both visceral and brain infarctions. Because the cause of brain infarction is unknown in up to 39% of patients, the discovery of subdiaphragmatic visceral infarction (SDVI) in this context is important, but its frequency is unknown. We therefore investigated the prevalence of SDVI in subjects who died from stroke. We also evaluated the yield of SDVI diagnosis for stroke subtyping. Methods-We performed a case-control study using a series of 815 consecutive autopsies of patients who had died from a neurological disease, including 350 with stroke (260 infarcts and 90 hemorrhages). We systematically assessed the presence of renal, splenic, and mesenteric infarction (no case of spinal cord was recorded) and analyzed their determinants in patients with stroke. Patients with other neurological diseases served as the control group. Results-Renal infarction was the most frequent SDVI (10.2%), whereas mesenteric infarction was rare (1.1%). At least one SDVI was found in 16.9% of patients with stroke (38.7% of patients with a cardioembolic stroke) and in 5.1% of patients with other neurological diseases (adjusted ORϭ2.12; 95% CIϭ1.08 to 4.16). Among patients with stroke, a significant heterogeneity in the prevalence of SDVI was found across etiological stroke subgroups with only three patients (3.3%) with hemorrhagic stroke having an SDVI (2 mesenteric and one renal infarction) compared with 56 patients (21.5%) with ischemic stroke (PϽ0.0001). Among patients with brain infarction and a SDVI, 76.8% had a definite cardiac source of embolism. Conclusions-In patients with fatal brain infarction, the prevalence of SDVI is higher than previously thought, especially in those with stroke attributed to cardiac emboli. Seeking SDVI may assist in the etiologic diagnosis of brain infarction

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