Spontaneous calcific cerebral embolus from a calcific aortic stenosis in a middle cerebral artery infarct.

Rancurel, G; Marelle, L.; Vincent, D; Catala, Martin; Arzimanoglou, Alexis; Vacheron, A

doi:10.1161/01.str.20.5.691

Cited by 46 publications

(24 citation statements)

References 8 publications

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“…In spite of these findings, we found 5 published cases of documented cerebral SCE from the aortic valve [1, 7, 8, 9, 10]. One could argue that most of these strokes were not due to real SCE, but to microthrombi originating from a calcified valve; alternatively, it has been suggested that CAS could be a marker of a generalized atherosclerotic process in patients with concomitant multiple risk factors [6].…”

Section: Discussionmentioning

confidence: 96%

Stroke as the First Manifestation of Calcific Aortic Stenosis

et al. 2000

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Heart valve calcifications are rarely recognized as a potential source for cerebral embolism. Previous studies have identified mitral, but not aortic, valve calcifications to be risk factors for stroke. Based on these studies, heart surgery is unlikely to be indicated in patients who present with a stroke and an ‘incidental’ aortic valve calcification. We report a case of a 46-year-old man presenting with acute onset of left-sided weakness and numbness. A previous smoking history was the only cardiovascular risk factor found. Head CT scan revealed a right middle cerebral artery territory infarct and an adjacent high-density lesion. CT angiography demonstrated the presence of calcific embolic material in the middle cerebral artery. A search for embolic sources revealed a calcific aortic stenosis (CAS). Initially placed on coumadin, the patient developed silent myocardial infarction 2 months later, presumed to be also embolic in origin from the CAS. After aortic valve replacement, the patient has been symptom-free during a 2-year follow-up. In conclusion, CT angiography may be the method of choice for detecting calcific cerebral emboli, and demonstration of a causal relationship between CAS and an embolic stroke by CT angiography may be an important adjunct in surgical decision-making.

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Section: Discussionmentioning

confidence: 96%

Stroke as the First Manifestation of Calcific Aortic Stenosis

et al. 2000

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“…- 82 Calcium deposition in the aortic valve may be visible by fluoroscopy or chest roentgenogram. The electrocardiogram may show left bundle branch block or advanced atrioventricular block with extensive aortic calcification.…”

mentioning

confidence: 99%

Cardiac evaluation of the patient with stroke.

Sirna

Biller

Skorton

et al. 1990

Stroke

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Coronary artery disease and ischemic cerebrovascular disease are leading causes of morbidity and mortality in the United States. Coronary artery disease often coexists with asymptomatic carotid artery atherosclerosis, transient ischemic attacks, or ischemic stroke. Numerous studies have shown that mortality from all forms of ischemic cerebrovascular disease is primarily due to coronary artery disease. Thus, there is increasing interest in identifying coronary artery disease in patients with cerebrovascular disease, including those without clinical manifestations of heart disease. We review the use of current noninvasive techniques to detect coronary artery disease and present practical approaches to screen for ischemic heart disease. Current diagnostic imaging methods for potential cardioembolic sources of cerebral infarction are also discussed.

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“…These risk factors are similar to those of ischemic stroke [14,15,16]. Case reports separately provide evidence of brain infarction due to calcific emboli from aortic valves [17,18,19,20,21,22,23]. However, several previous studies have suggested that there is no association between aortic VaT and cerebrovascular events [24, 25].…”

Section: Discussionmentioning

confidence: 85%

Impact of Valvular Thickness on Stroke Recurrence in Medically Treated Patients with Stroke

Okajima¹,

Abe²,

Suzuki³

et al. 2007

Cerebrovasc Dis

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Background: It remains controversial whether left-sided valvular thickening (VaT) is a risk factor for ischemic stroke. Little is known about the relationship between VaT and the recurrent adverse event rate in medically treated patients with stroke. Methods: We examined the outcomes of 627 noncardioembolic stroke patients who were double-blindly assigned to either warfarin or aspirin therapy and assessed VaT using transesophageal echocardiography. Endpoints were recurrent ischemic stroke or death from any cause. The Cox proportional hazards model was used to adjust for covariates. Results: VaT was present in 57.3% of the patients (359/627), 34.6% (271/627) involving the aortic valve and 46.4% (291/627) involving the mitral valve. There was no difference in the time to primary endpoints between those with and without VaT of the aortic valve (p = 0.49; hazard ratio, HR: 1.17; 95% CI: 0.74–1.85; 2-year event rates: 18.9 vs. 13.2%) or mitral valve (p = 0.66; HR: 0.91; 95% CI: 0.60–1.38; 2-year event rates: 16.9 vs. 14.7%). Among the patients with VaT, there was no significant difference in the time to primary endpoints between those treated with warfarin and those with aspirin (p = 0.13, HR: 0.65, 95% CI: 0.37–1.14, 2-year event rates: 15.2 vs. 22.7% for the aortic valve; p = 0.22, HR: 0.70, 95% CI: 0.40–1.23, 2-year event rates: 14.2 vs. 19.6% for the mitral valve). Conclusions: VaT does not appear to increase recurrent adverse event rates in medically treated patients with ischemic stroke, regardless of warfarin or aspirin therapy.

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Spontaneous calcific cerebral embolus from a calcific aortic stenosis in a middle cerebral artery infarct.

Cited by 46 publications

References 8 publications

Stroke as the First Manifestation of Calcific Aortic Stenosis

Stroke as the First Manifestation of Calcific Aortic Stenosis

Cardiac evaluation of the patient with stroke.

Impact of Valvular Thickness on Stroke Recurrence in Medically Treated Patients with Stroke

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