Clin Res Cardiol DOI 10.1007/s00392-017-1169-z
LETTER TO THE EDITORS
Lack of silent cerebral ischemic events: a case series of patients after left atrial appendage closure Christian Fastner1 · Michael Behnes1 · Thomas Henzler2 · Martin Borggrefe1 · Ibrahim Akin1
Received: 2 August 2017 / Accepted: 26 September 2017 © Springer-Verlag GmbH Germany 2017
Sirs: Thromboembolic prophylaxis is crucial for the prognosis of atrial fibrillation (AF) patients. Catheter-based left atrial appendage closure (LAAC) has evolved as the therapy of choice for those non-valvular AF patients being unable or unwilling to take a lifelong oral anticoagulation (OAC) [1]. It has been reported that less than 1% of treated patients suffer from procedure-related overt strokes [2]; however, the number of patients affected by silent cerebral embolic events during transseptal cardiac procedures appears to be higher [3]. Most recently, two studies reported peri-procedural and short-term follow-up subclinical event rates of 4.8 and 35.7%, respectively [4, 5]. In general, the rate of thrombus formation on LAAC devices detected by follow-up imaging procedures is low (i.e., around 4%) [2]. In fact, there is a lack of data on long-term occurrence of silent cerebral embolic events after LAAC. We report on a case series of nine consecutive patients (mean age 77 ± 6.8 years, 78% males) derived from a subset of our in-house LAAC registry. The WATCHMAN™ device (Boston Scientific, Natick, MA, USA) was implanted in six patients (67%); the Amplatzer™ Amulet™ (St. Jude Medical, St. Paul, MN, USA) was used for the remaining three patients (33%). Following device implantation, patients * Christian Fastner [email protected] 1
First Department of Medicine, University Medical Center Mannheim, Medical Faculty Mannheim, University of Heidelberg, Theodor‑Kutzer‑Ufer 1‑3, 68167 Mannheim, Germany
Institute of Clinical Radiology and Nuclear Medicine, University Medical Center Mannheim, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
2
received acetylsalicylic acid lifelong and clopidogrel for 6 months, except for one patient who had recently suffered from a non-ST elevation myocardial infarction and was, therefore, 11 months on clopidogrel after the intervention. The patients underwent cerebral magnetic resonance imaging (cMRI) prior to (T0) and 12 months after the LAAC procedure (T1). At follow-up, all patients were thoroughly examined and interrogated for clinical presentations of stroke. The mean CHA2DS2–VASc score was 5 ± 1.9 and mean HAS-BLED score was 4 ± 0.7, reflecting a collective at risk for both, thromboembolic events as well as bleeding complications with OAC. As routinely practiced, a pre-existing LAA thrombus was ruled out by trans-esophageal echocardiography immediately prior to the transseptal puncture. 3 of 9 patients (33%) revealed pre-existing post-hemorrhagic lesions in the cMRI conducted before the procedure, which were unchanged at T1 in these three patients (Fig. 1). These were most probably caused by intracerebral hemorrhages, presumptively serving as the indication for a LAAC. It is interesting to note that none of the nine patients showed signs of acute cerebral microembolism in diffusion-weighted imaging (DWI) or signs of gliotic lesions as a surrogate for post-embolic remodeling processes in T2-fluid attenuated inversion recovery (FLAIR) sequences, 1 year after the index procedure. Furthermore, an in-depth analysis of the medical history of each patient suggested no striking features of transient or on-going symptoms of stroke. There are two plausible explanations for the absence of any acute or post-embolic cerebral lesions: first, there was no cerebral embolism in any of the nine patients peri-procedurally, and during follow-up, a statement clearly limited by the small number of patients included in this case series. Second, in the study of Majunke et al., short-term follow-up already showed a relevant reduction of demarcated lesions in cMRI (only 33% of initially detectable
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Vol.:(0123456789)
Clin Res Cardiol
Fig. 1 Pre- (left) and postinterventional (right) cerebral MRI (FLAIR) with residual leak (arrow) after intracerebral hemorrhage in the left thalamic region without any modification within 12 months of follow-up
DWI alterations led to signals in FLAIR sequences after 45 days) [4]. This was explained by a relevant proportion of small initial lesions
LETTER TO THE EDITORS
Lack of silent cerebral ischemic events: a case series of patients after left atrial appendage closure Christian Fastner1 · Michael Behnes1 · Thomas Henzler2 · Martin Borggrefe1 · Ibrahim Akin1
Received: 2 August 2017 / Accepted: 26 September 2017 © Springer-Verlag GmbH Germany 2017
Sirs: Thromboembolic prophylaxis is crucial for the prognosis of atrial fibrillation (AF) patients. Catheter-based left atrial appendage closure (LAAC) has evolved as the therapy of choice for those non-valvular AF patients being unable or unwilling to take a lifelong oral anticoagulation (OAC) [1]. It has been reported that less than 1% of treated patients suffer from procedure-related overt strokes [2]; however, the number of patients affected by silent cerebral embolic events during transseptal cardiac procedures appears to be higher [3]. Most recently, two studies reported peri-procedural and short-term follow-up subclinical event rates of 4.8 and 35.7%, respectively [4, 5]. In general, the rate of thrombus formation on LAAC devices detected by follow-up imaging procedures is low (i.e., around 4%) [2]. In fact, there is a lack of data on long-term occurrence of silent cerebral embolic events after LAAC. We report on a case series of nine consecutive patients (mean age 77 ± 6.8 years, 78% males) derived from a subset of our in-house LAAC registry. The WATCHMAN™ device (Boston Scientific, Natick, MA, USA) was implanted in six patients (67%); the Amplatzer™ Amulet™ (St. Jude Medical, St. Paul, MN, USA) was used for the remaining three patients (33%). Following device implantation, patients * Christian Fastner [email protected] 1
First Department of Medicine, University Medical Center Mannheim, Medical Faculty Mannheim, University of Heidelberg, Theodor‑Kutzer‑Ufer 1‑3, 68167 Mannheim, Germany
Institute of Clinical Radiology and Nuclear Medicine, University Medical Center Mannheim, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany
2
received acetylsalicylic acid lifelong and clopidogrel for 6 months, except for one patient who had recently suffered from a non-ST elevation myocardial infarction and was, therefore, 11 months on clopidogrel after the intervention. The patients underwent cerebral magnetic resonance imaging (cMRI) prior to (T0) and 12 months after the LAAC procedure (T1). At follow-up, all patients were thoroughly examined and interrogated for clinical presentations of stroke. The mean CHA2DS2–VASc score was 5 ± 1.9 and mean HAS-BLED score was 4 ± 0.7, reflecting a collective at risk for both, thromboembolic events as well as bleeding complications with OAC. As routinely practiced, a pre-existing LAA thrombus was ruled out by trans-esophageal echocardiography immediately prior to the transseptal puncture. 3 of 9 patients (33%) revealed pre-existing post-hemorrhagic lesions in the cMRI conducted before the procedure, which were unchanged at T1 in these three patients (Fig. 1). These were most probably caused by intracerebral hemorrhages, presumptively serving as the indication for a LAAC. It is interesting to note that none of the nine patients showed signs of acute cerebral microembolism in diffusion-weighted imaging (DWI) or signs of gliotic lesions as a surrogate for post-embolic remodeling processes in T2-fluid attenuated inversion recovery (FLAIR) sequences, 1 year after the index procedure. Furthermore, an in-depth analysis of the medical history of each patient suggested no striking features of transient or on-going symptoms of stroke. There are two plausible explanations for the absence of any acute or post-embolic cerebral lesions: first, there was no cerebral embolism in any of the nine patients peri-procedurally, and during follow-up, a statement clearly limited by the small number of patients included in this case series. Second, in the study of Majunke et al., short-term follow-up already showed a relevant reduction of demarcated lesions in cMRI (only 33% of initially detectable
13
Vol.:(0123456789)
Clin Res Cardiol
Fig. 1 Pre- (left) and postinterventional (right) cerebral MRI (FLAIR) with residual leak (arrow) after intracerebral hemorrhage in the left thalamic region without any modification within 12 months of follow-up
DWI alterations led to signals in FLAIR sequences after 45 days) [4]. This was explained by a relevant proportion of small initial lesions
