ABSTRACT: The objective of this study was to compare the incidence of cerebral embolism (CE) as evaluated by diffusion-weighted magnetic resonance imaging (DW-MRI) following transapical (TA) transcatheter aortic valve implantation (TAVI) versus transfemoral (TF) TAVI.
The TA-TAVI approach avoids both the manipulation of large catheters in the aortic arch/ascending aorta and the retrograde crossing of the aortic valve, and this avoidance might lead to a lower rate of CE.
This was a prospective multicenter study including 60 patients who underwent cerebral DW-MRI the day before and within the 6 days following TAVI (TF approach: 29 patients; TA approach: 31 patients). Neurologic and cognitive function assessments were performed at DW-MRI time points.
The TAVI procedure was performed with the Edwards valve and was successful in all cases but one (98%). A total of 41 patients (68%) had 251 new cerebral ischemic lesions at the DW-MRI performed 4 ± 1 days after the procedure, 19 patients in the TF group (66%) and 22 patients in the TA group (71%; p = 0.78). Most patients (76%) with new ischemic lesions had multiple lesions (median number of lesions per patient: 3, range 1 to 31). There were no differences in lesion number and size between the TF and TA groups. No baseline or procedural factors were found to be predictors of new ischemic lesions. The occurrence of CE was not associated with a measurable impairment in cognitive function, but 2 patients (3.3%) had a clinically apparent stroke within the 24 h following the procedure (1 patient in each group).
TAVI is associated with a high rate of silent cerebral ischemic lesions as evaluated by DW-MRI, with no differences between the TF and TA approaches. These results provide important novel insight into the mechanisms of CE associated with TAVI and support the need for further research to both reduce the incidence of CE during these procedures and better determine their clinical relevance.
Journal of the American College of Cardiology 12/2010; 57(1):18-28. · 14.16 Impact Factor
ABSTRACT: To further determine the mechanisms of cryptogenic stroke or transient ischemic attack in young patients, we evaluated indices of atherosclerosis in patients <or=55 years old diagnosed with cryptogenic cerebrovascular event comparing those with patent foramen ovale (PFO) with those without PFO.
This was a prospective study including 100 consecutive patients <or=55 years old (mean age, 45+/-8 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.
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 (P<0.0001) in patients without PFO (1.03+/-0.31 mm) compared with those with PFO (0.75+/-0.20 mm) and control subjects (0.79+/-0.17 mm). The absence of PFO was also associated with lower brachial flow-mediated vasodilation (without PFO: 5.04+/-3.39%; with PFO: 7.16+/-4.09%; control subjects: 7.33+/-4.07%; P=0.02). 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 (P<0.0001) and increased flow-mediated vasodilation (P=0.019).
In patients <or=55 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.
Stroke 01/2009; 40(2):419-25. · 5.73 Impact Factor
ABSTRACT: The objectives of this study were to evaluate the incidence, predictive factors, and duration of migraine headache attack (MHA) after transcatheter atrial septal defect (ASD) or patent foramen ovale (PFO) closure. A total of 260 consecutive patients who underwent ASD or PFO closure in our center answered a structured headache questionnaire focused in 3 period times, including (1) at baseline (just before closure), (2) within the 3 months after ASD-PFO closure, and (3) at the last (median 27 months, range 6 to 80 months) follow-up. All questionnaires were evaluated by a neurologist who established the diagnosis of MHA with or without aura, according to International Headache Society criteria. The Amplatzer ASD or PFO device was used in 95% of the patients, and aspirin, for at least 6 months, was the antithrombotic treatment in 91% of the cases. A total of 185 patients (71%) had no history of MHA before ASD-PFO closure, and these constituted the study population (mean age 39 +/- 21 years). MHA occurred in 13 patients (7%) after ASD-PFO closure, with aura in 9 of them. MHA appeared after a median of 10 days (range 0.3 to 30 days) after the procedure and were still present at the last follow-up (23 +/- 17 months) in 9 patients (69%). The median number of MHA within the 3 months after the procedure was 4 per month (interquartile range 1 to 23), and decreased to 1 per month (interquartile range 0.3 to 1) at the latest follow-up (p = 0.03). Compared with the patients who did not develop MHA, patients with MHA after ASD-PFO closure were younger (26 +/- 16 vs 39 +/- 21 years; p = 0.02) and were more likely to have undergone ASD closure (100% vs 58%; p = 0.001). In the multivariate analysis, ASD closure was the only predictor of MHA occurrence after the procedure (odds ratio 7.7; 95% confidence interval 1.5 to 22; p = 0.01). In conclusion, MHA, mostly with aura, occurred in 7% of patients after transcatheter ASD-PFO closure and persisted in most of them after a mean follow-up of 2 years. ASD closure was the only independent predictor of MHA occurrence after the procedure. These results suggest that mechanisms other than device composition are involved in the occurrence of MHA in these cases.
The American Journal of Cardiology 04/2008; 101(5):688-92. · 3.37 Impact Factor
ABSTRACT: No studies have yet determined whether antiplatelet or anticoagulant therapy is the more appropriate treatment after transcatheter closure of patent foramen ovale (PFO) in patients with cryptogenic stroke. The objective of this study was to prospectively evaluate the presence, degree, and timing of activation of the platelet and coagulation systems after transcatheter closure of PFO in patients with cryptogenic stroke.
Twenty-four consecutive patients (mean age, 44+/-10 years; 11 men) with previous cryptogenic stroke who had undergone successful transcatheter closure of PFO were included in the study. Prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin III (TAT) were used as markers of coagulation activation, and soluble P-selectin and soluble CD40 ligand were used as markers of platelet activation. Measurements of all hemostatic markers were taken at baseline just before the procedure and at 7, 30, and 90 days after device implantation.
F1+2 and TAT levels increased from 0.41+/-0.16 nmol/L and 2.34+/-1.81 ng/mL, respectively, at baseline to a maximal value of 0.61+/-0.16 nmol/L and 4.34+/-1.83 ng/mL, respectively, at 7 days, gradually returning to baseline levels at 90 days (P<0.001 for both markers). F1+2 and TAT levels at 7 days after PFO closure were higher than those obtained in a group of 25 healthy controls (P<0.001 for both markers). Levels of soluble P-selectin and soluble CD40 ligand did not change at any time after PFO closure.
Transcatheter closure of PFO is associated with significant activation of the coagulation system, with no increase in platelet activation markers. These findings raise the question of whether optimal antithrombotic treatment after PFO closure should be short-term anticoagulant rather than antiplatelet therapy.
Stroke 02/2007; 38(1):100-4. · 5.73 Impact Factor