Cryptogenic Stroke, Aortic Arch Atheroma and Patent Foramen Ovale

Molina, Carlos A.; Santamarina, Estevo; Álvarez-Sabín, José

doi:10.1159/000107382

Cited by 14 publications

(8 citation statements)

References 47 publications

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“…Established risk factors for stroke, such as previous stroke or transient ischemic attack (TIA), atrial septal aneurysm, aortic arch atheroma, atrial fibrillation, and left atrial dilation, were included along with other comorbidities as potential confounders in propensity analyses. 14,[23][24][25][26][27][28][29][30][31][32][33]…”

Section: Outcome Measures and Risk Factorsmentioning

confidence: 99%

Prevalence and Repair of Intraoperatively Diagnosed Patent Foramen Ovale and Association With Perioperative Outcomes and Long-term Survival

Krasuski

Hart

Allen

et al. 2009

JAMA

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Context A recent survey suggested that cardiothoracic surgeons may alter planned procedures to repair incidentally discovered patent foramen ovale (PFO). How frequently this occurs and the impact on outcomes remain unknown. Objective To measure the frequency of incidentally discovered PFO closure during cardiothoracic surgery and determine its perioperative and long-term impact. Design, Setting, and Patients We reviewed the intraoperative transesophageal echocardiograms of 13 092 patients without prior diagnosis of PFO or atrial septal defect undergoing surgery at the Cleveland Clinic, Cleveland, Ohio, from 1995 through 2006. Postoperative outcomes were prospectively collected until discharge. Main Outcome Measures All-cause hospital mortality and stroke were predetermined primary outcomes; length of hospital stay, length of intensive care unit stay, and time on cardiopulmonary bypass were secondary outcomes. Results Intraoperative PFO was diagnosed in 2277 patients in the study population (17%), and risk factors for stroke were similar in patients with and without PFO. After propensity matching was performed with the comparator groups, patients with PFO demonstrated similar rates of in-hospital death (3.4% vs 2.6%, P=.11) and postoperative stroke (2.3% vs 2.3%, P=.84). Surgical closure was performed in 639 PFO patients (28%), and surgeons were more likely to close defects in patients who were younger (mean [SD] age, 61.1 [14] vs 64.4 [13] years; PϽ.001), were undergoing mitral or tricuspid valve surgery (51% vs 32%, PϽ.001), or had history of transient ischemic attack or stroke (16% vs 10%, PϽ.001). Patients with repaired PFO demonstrated a 2.47-times greater odds (95% confidence interval, 1.02-6.00) of having a postoperative stroke compared with those with unrepaired PFO (2.8% vs 1.2%, P=.04). Long-term analysis demonstrated that PFO repair was associated with no survival difference (P=.12). Conclusions Incidental PFO is common in patients undergoing cardiothoracic surgery but is not associated with increased perioperative morbidity or mortality. Surgical closure appears unrelated to long-term survival and may increase postoperative stroke risk.

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Section: Outcome Measures and Risk Factorsmentioning

confidence: 99%

Prevalence and Repair of Intraoperatively Diagnosed Patent Foramen Ovale and Association With Perioperative Outcomes and Long-term Survival

Krasuski

Hart

Allen

et al. 2009

JAMA

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“…Some studies have evaluated the presence of significant atheromatosis of the aortic arch in patients with cryptogenic stroke, but the association between aortic arch atheroma and cryptogenic stroke has been limited to patients Ͼ60 years old. 1,2 In fact, the role of atherosclerosis in young adults with cryptogenic stroke has been mostly limited to the evaluation of the prevalence of cardiovascular risk factors in these patients. [3][4][5] Also, a role for patent foramen ovale (PFO) in the pathogenesis of cryptogenic stroke in patients Յ55 years old has been suggested on the basis of case-control studies that have shown a higher prevalence of PFO among these patients compared with stroke-free control subjects, 6 but no studies have determined whether or not the atherosclerotic burden in young patients with cryptogenic stroke might vary depending on the presence of a PFO.…”

mentioning

confidence: 99%

Atherosclerotic Burden Findings in Young Cryptogenic Stroke Patients With and Without a Patent Foramen Ovale

Rodés‐Cabau

Noël

Marrero

et al. 2009

Stroke

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Background and Purpose-To further determine the mechanisms of cryptogenic stroke or transient ischemic attack in young patients, we evaluated indices of atherosclerosis in patients Յ55 years old diagnosed with cryptogenic cerebrovascular event comparing those with patent foramen ovale (PFO) with those without PFO. Methods-This was a prospective study including 100 consecutive patients Յ55 years old (mean age, 45Ϯ8 years; 56 males) diagnosed with cryptogenic stroke/transient ischemic attack. PFO was identified in 59 of these patients with the use of transesophageal echocardiography with contrast study. The following surrogate markers of atherosclerosis were evaluated in all patients: carotid intima media thickness as measured by carotid ultrasonography and endothelial function as determined by brachial flow-mediated vasodilation. The same measurements were obtained in a control group of 50 age-and sex-matched control subjects. Results-Patients without PFO were more likely to be current smokers and obese and more frequently had a history of hypertension and dyslipidemia. Carotid intima media thickness measurements were higher (PϽ0.0001) in patients without PFO (1.03Ϯ0.31 mm) compared with those with PFO (0.75Ϯ0.20 mm) and control subjects (0.79Ϯ0.17 mm). The absence of PFO was also associated with lower brachial flow-mediated vasodilation (without PFO: 5.04Ϯ3.39%; with PFO: 7.16Ϯ4.09%; control subjects: 7.33Ϯ4.07%; Pϭ0.02). There were no differences in carotid intima media thickness and flow-mediated vasodilation between patients with stroke/transient ischemic attack with PFO and control subjects. The presence of PFO was independently associated with reduced carotid intima media thickness (PϽ0.0001) and increased flow-mediated vasodilation (Pϭ0.019). Conclusions-In patients Յ55 years old diagnosed with cryptogenic stroke/transient ischemic attack, the presence of PFO was associated with a lower atherosclerotic burden as measured by carotid intima media thickness and endothelial function with no differences compared with a control group without cerebrovascular event. These results suggest that an atherosclerotic-mediated mechanism may be involved in cryptogenic stroke/transient ischemic attack in patients without PFO, whereas a nonatherosclerotic mechanism may mediate the cerebrovascular event in the presence of PFO.

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“…Of TEE-identified aortic arch lesions showing an association with LSCA plaque, large arch plaque (≥4.0 mm) and ulcer are typical findings of advanced atherosclerosis and indicators for stroke and systemic atherosclerotic disease [1,2,3,4,5,6,7,8,20,21,22,23,24,25]. A spontaneous echo contrast is a pulsatile, swirling echo pattern that is associated with the rouleau phenomenon due to erythrocyte aggregation, increased plasma fibrinogen levels, and plasma viscosity.…”

Section: Discussionmentioning

confidence: 99%

Atheromatous Plaques at the Origin of the Left Subclavian Artery in Patients with Ischemic Stroke

et al. 2010

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Background: Atheromatous plaques of the aortic arch that extend to the origin of its branches may cause stroke. The frequency and clinical implications of plaque at the origin of the left subclavian artery (LSCA) in patients with recent ischemic stroke were investigated. Methods: We studied 347 consecutive patients (223 men, 69 ± 12 years) who developed symptomatic ischemic stroke and underwent transesophageal echocardiography (TEE). Results: The origin of the LSCA was identified in 303 of 347 patients (87.3%). Plaque ≧1.0 mm was detected in 108 of the 303 patients (35.6%), ranging between 1.0 and 6.1 mm (median, 2.5 mm). Patients having thicker plaque (≧2.5 mm) were older (p = 0.012) and more commonly took antiplatelets prior to stroke (p = 0.038) than patients with no plaque and those with thinner plaque (<2.5 mm). Of the aortic arch findings detected on TEE, maximum intima-media thickness (IMT) was the highest (p < 0.001) in patients with thicker plaque, and large plaque (≧4.0 mm) (p = 0.017), ulcerative plaques (p < 0.001), and spontaneous echo contrasts (p = 0.001) were identified most commonly in patients with thicker plaque. The frequency of infarcts involving the posterior circulation was similar among the three groups. After multivariate adjustment, maximum IMT of the aortic arch was independently related to thicker plaque at the LSCA origin (OR = 1.24, 95% CI = 1.03–1.51, p = 0.024, per 1-mm increase). Conclusions: Atheromatous plaque at the origin of the LSCA was present in approximately one third of patients with a recent ischemic stroke. High IMT at the aortic arch was independently related to the presence of thick plaque at the LSCA origin. The present study does not support the concept that plaque at the LSCA origin may be associated with posterior circulation infarction.

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Cryptogenic Stroke, Aortic Arch Atheroma and Patent Foramen Ovale

Cited by 14 publications

References 47 publications

Prevalence and Repair of Intraoperatively Diagnosed Patent Foramen Ovale and Association With Perioperative Outcomes and Long-term Survival

Prevalence and Repair of Intraoperatively Diagnosed Patent Foramen Ovale and Association With Perioperative Outcomes and Long-term Survival

Atherosclerotic Burden Findings in Young Cryptogenic Stroke Patients With and Without a Patent Foramen Ovale

Atheromatous Plaques at the Origin of the Left Subclavian Artery in Patients with Ischemic Stroke

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