Risk of Stroke and Thrombus Formation From Delay Incontinence of a PLAATO‐Device in Friedreich Ataxia

Abstract

We present the case of a 76-year-old female with suspected Friedreich ataxia, in whom leakage and thrombosis of a percutaneously implanted left atrial appendage occluder (PLAATO) was observed 2 years after implantation. Because of late developing leakages and thrombi, regular transesophageal echocardiographic examinations should be carried out in patients with occluded left atrial appendagaes. In view of these complications and the potential important hemodynamic role of the left atrial appendage, the benefit of its occlusion is questionable, and the indications of PLAATO should be strongly reconsidered.The percutaneous left atrial appendage transcatheter occlusion device (PLAATO) is considered a safe and feasible alternative to oral anticoagulation (OAC) in atrial fibrillation (AF) patients with contraindications to OAC. 1 In March 2005, a 74-year-old female with paroxysmal AF, arterial hypertension, and two ischemic strokes with left hemiparesis (in 1989 and 1990), underwent left atrial appendage (LAA) occlusion by a PLAATO system. This procedure had to be performed since the patient did not tolerate OAC, which resulted in hair loss as well as her risk for stroke/embolism being considered as high. LAA occlusion was successful, as documented by transesophageal echocardiography (TEE) and dye injection into the left atrium during the procedure. Postprocedural cranial computed tomography showed no signs of recent ischemia. The patient was released with a therapy of 100 mg aspirin, 75 mg clopidogrel, 20 mg pantoprazole, 4 mg tizanidine, 5 mg bisoprolol, and 10 mg enalapril. After 2 months, TEE showed complete sealing of the LAA without any thrombus on the device. Clopidogrel was discontinued and aspirin 100 mg/day continued.In March 2007, the patient was readmitted because of chest pain. ECG showed AF but no signs of ischemia. Neither blood tests nor perfusion scintigraphy showed signs of myocardial ischemia, why her chest pain was assumed to be musculoskeletal. There were no signs of infection as per the patient's history, clinically, or through laboratory investigations. Chest pain decreased after analgetic drugs and physiotherapy. AF converted spontaneously to sinus rhythm. Clinical neurologic investigation showed postural tremor, intention tremor, dysdiadochokinesia, weakness for hip flexion (M5-) and foot extension (M4-), bilateral foot deformity (Friedreich foot), reduced Achilles tendon reflexes, and atactic stance. Cerebral magnetic resonance imaging (MRI) showed spotted small hyperintense lesions subcortically and in the frontal and parietal, lobes, referring to microangiopathy. Friedreich ataxia and polyneuropathy were suspected.TEE showed a structure measuring 6 × 2 mm in the niche between the LAA wall and the PLAATO device, highly suggestive of a thrombus (Figure 1). Additionally, by color-Doppler, a small jet between the LAA wall and the PLAATO device was detected (Figure 2). Cardiac MRI failed to visualize the jet and the suspected thrombus, due to artifacts deriving from the PLAATO device and the sma...

Intraprocedural and Long‐Term Incomplete Occlusion of the Left Atrial Appendage Following Placement of the WATCHMAN Device: A Single Center Experience

“…Theoretically a small communication between the LA and the LAA may (1) result in higher blood velocity at the LAA os, which might actually increase the risk of stroke 15 ; and (2) produce stagnation of low velocity blood flow within the LAA that would then be a milieu of thrombus formation and continue to serve as a potential source of embolization because a port of entry into the systemic circulation still exists. 11 In one of our patients who had a stroke 4.7 months after the WATCHMAN device implantation, the intraprocedural gap persisted and became slightly larger at the 45-day TEE. Warfarin therapy was discontinued because the gap size still remained in the "safe limits" suggested by previous publications.…”

“…What is happening after WATCHMAN implantation is a complex process that may include 1 or more of the following changes in the same patient: (1) The LAA might shrink and become more tightly anchored with the device if the LAA ostium was completely blocked by the device; (2) Progressive LA/LAA remodeling occurs over time in persistent AF, which might be associated with a dilation or deformation of these structures. Because the LAA myocardium has a higher distensibility than the LA myocardium, the disconcordance may lead to splitting of the device struts from the LAA wall 11 ; (3) Under a fluid‐dynamical effect of blood flow antegradely or/and retrogradely passing through the gap, the size of gap may become larger over time; (4) With the force of LA and LAA contraction, the relative position of the device inside LAA may slightly change, which generates a mechanical stretch to the LAA wall; and (5) During the period time of endothelialization, the endothelial proliferation, organization of microthrombus and fibrotic tissue may fill up a gap, partially or fully. These could explain the different situations we found in our patients after WATCHMAN device implantation.…”

“…It has been reported that in patients with incomplete surgical ligation, 50% had spontaneous echo smoke or thrombus in the LAA, whereas 22% developed thromboembolic events 12,13 . In fact, thrombus formation after implantation has been associated with both PLAATO (ev3 Inc., Plymouth, MN, USA) and AMPLATZER (AGA Medical Corp., Minneapolis, MN, USA) device, 11,14 another 2 transcatheter LAA closure systems in addition to the WATCHMAN device. Theoretically a small communication between the LA and the LAA may (1) result in higher blood velocity at the LAA os, which might actually increase the risk of stroke 15 ; and (2) produce stagnation of low velocity blood flow within the LAA that would then be a milieu of thrombus formation and continue to serve as a potential source of embolization because a port of entry into the systemic circulation still exists 11 .…”

“…In fact, thrombus formation after implantation has been associated with both PLAATO (ev3 Inc., Plymouth, MN, USA) and AMPLATZER (AGA Medical Corp., Minneapolis, MN, USA) device, 11,14 another 2 transcatheter LAA closure systems in addition to the WATCHMAN device. Theoretically a small communication between the LA and the LAA may (1) result in higher blood velocity at the LAA os, which might actually increase the risk of stroke 15 ; and (2) produce stagnation of low velocity blood flow within the LAA that would then be a milieu of thrombus formation and continue to serve as a potential source of embolization because a port of entry into the systemic circulation still exists 11 . In one of our patients who had a stroke 4.7 months after the WATCHMAN device implantation, the intraprocedural gap persisted and became slightly larger at the 45‐day TEE.…”