1 Introduction
2 Patients and methods
2.1 Patient enrollment
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Ipsilateral carotid atherosclerotic stenosis >70%, vertebral or carotid dissection with cervical Doppler-echography or angio-MR.
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Documented atrial fibrillation, with a 12-lead electrocardiogram and 24-h Holter monitoring.
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Intracardiac thrombus or any other cause of cardiac embolism, with transthoracic (n = 24/24) and transesophageal echocardiography (n = 22/24).
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Vascular malformation, by means of cerebral CT, MRI or angio-MRI if necessary.
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Hypercoagulable states, hematological disorders, and inflammatory diseases, with biological tests carried out at least 2 months after stroke: prothrombin ratio, activated partial thromboplastin time, C and S proteins, antithrombin, mutation in Factor V Leiden gene, circulating anticoagulants, antiphospholipid and anti-ß2gp1 antibodies, homocysteinemia, erythrocyte sedimentation rate, and C-reactive protein.
2.2 Study of atrial vulnerability
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Measurement of basic conduction intervals and determination of the Wenckebach point of the atrioventricular node.
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Determination of the right atrium refractory periods (RP) and the duration of the atrial electrogram. RPs were determined by means of an extrastimulus (S2) delivered at three different constant pacing rates 100, 120, 150 bpm. Effective RP was defined as the longest attainable S1–S2 interval that did not produce an atrial electrogram. Finally, we measured the duration of the atrial electrogram (A2) following S2 at a pacing rate of 100 bpm. Latent vulnerability index (LVI) was defined as the ratio between high right atrium effective refractory period (ERP) and A2 duration at a pacing rate of 100 bpm [7, 14].
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Assessment of the inducibility of atrial arrhythmia was performed by programmed atrial stimulation with up to three extrastimuli (S2, S3, S4) at constant pacing rates of 100, 120, and 150 bpm at two different stimulation sites: HRA and LRA.
2.3 Implantation of Holter monitor
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Semi-automatic activation mode.
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Recording of 13 automatic events and 1 event by patient activation. Patients were provided with an activator at the time of device implantation.
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The criteria for automatic recording were bradycardia <30 bpm or pause >3 s, tachycardia >165 bpm for more than 32 complexes.
2.4 Treatment
2.5 Patient follow-up
3 Results
Male n (%) | 15 (62.5) |
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Age (years) (mean ± SD) | 49 ± 13.6 |
<50 years n (%) | 14 (58.3) |
Diabetes mellitus | 0 |
Hypertension n (%) | 7 (29.2) |
Dyslipidemia n (%) | 8 (33.3) |
Active tobacco use n (%) | 10 (41.7) |
Overweight (BMI > 27.5) n (%) | 4 (16.7) |
Vascular ischemic hereditary n (%) | 5 (20.8) |
3.1 Neurological features
Topography of infarcts | Number | Percentage |
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Middle cerebral artery (MCA) territory | 20 | 83.3 |
Superficial MCA | 14 | 58.3 |
Deep MCA | 3 | 12.5 |
Global MCA | 3 | 12.5 |
Vertebrobasilar territory | 7 | 29.2 |
Posterior cerebral artery territory | 3 | 12.5 |
Cerebellum | 4 | 16.7 |
Multiple lesions | 8 | 33.3 |
Bilateral | 5 | 20.8 |
3.2 Electrophysiological study
Mean ± SD | Min | Max | Number (%) | |
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AH interval (ms) | 83 ± 22.4 | 15 | 125 | |
HV interval (ms) | 43 ± 9.38 | 30 | 65 | |
Wenckebach point of AV node (bpm) | 162 ± 35.2 | 110 | 230 | |
HRA ERP (ms) | 234 ± 37.1 | 180 | 290 | |
A2 duration (ms) | 85 ± 26.4 | 50 | 140 | |
LVI (n = 20) | 2.9 ± 1.02 | 1.5 | 5.6 | |
LVI < 2.5 | 9 (37.5) | |||
Inducibility of atrial arrhythmia (including AF, flutter, and other atrial tachycardias) | 18 (75.0) | |||
0–30 s | 8 (33.3) | |||
30–59 s | 2 (8.3) | |||
1–5 min | 5 (20.8) | |||
>5 min | 3 (12.5) |