Author + information
- Received November 25, 2003
- Revision received December 17, 2003
- Accepted December 23, 2003
- Published online May 19, 2004.
- Ibrahim R. Hanna, MD*,
- Paul Kolm, PhD*,
- Randolph Martin, MD, FACC*,
- Mark Reisman, MD, FACC†,
- William Gray, MD, FACC† and
- Peter C. Block, MD, FACC*,* ()
- ↵*Reprint requests and correspondence:
Dr. Peter C. Block, Division of Cardiology, Emory University Hospital, 1634 Clifton Road, Suite F606, Atlanta, Georgia 30322, USA.
Objectives This study was designed to evaluate the effects of percutaneous left atrial appendage transcatheter occlusion (PLAATO) on the anatomic and hemodynamic properties of the mitral valve (MV) and left upper pulmonary vein (LUPV).
Background PLAATO is a device designed to seal the neck of the left atrial (LA) appendage and reduce embolization in patients with atrial fibrillation intolerant of warfarin. The impact of deployment of this device on adjacent structures has not been reported.
Methods Patients with atrial fibrillation participating in the ongoing study for evaluation of PLAATO were enrolled. Transesophageal echocardiographies at baseline, one, and six months were reviewed to measure LA and LUPV dimensions, degree of mitral regurgitation, stability of the device, peak MV E-wave velocity, and peak systolic and diastolic flow velocities in the LUPV. Data were analyzed by a linear mixed model for repeated measures.
Results Eleven patients (mean age of 72 ± 7 years) completed six months of follow-up. Left upper pulmonary vein diameter (mean: 1.55, 1.61, 1.54 cm, p = 0.13) and peak systolic (mean: 0.38, 0.34, 0.31 m/s, p = 0.72) and diastolic flow velocities (mean: 0.39, 0.40, 0.42 m/s, p = 0.46) did not differ over the follow-up period. Left atrial size, mitral regurgitation severity, and MV peak E-wave velocities (mean: 0.94, 0.94, 0.82 m/s, p = 0.58) showed no significant change from baseline. The devices remained stable at their sites of deployment with minimal residual flow around them.
Conclusions PLAATO achieved an adequate seal of the neck of the left atrial appendage without significant effect on the structure or function of the LA and LUPV.
Atrial fibrillation (AF) is a major determinant of mortality and stroke, especially in older patients and those with left ventricular dysfunction, hypertension, diabetes, or prior stroke(s) (1,2). Over the past decade researchers have evaluated a variety of pharmacologic therapies aimed at reducing this risk. Oral anticoagulation with warfarin targeting an international normalized ratio (INR) of 2 to 3 has emerged as preferred therapy, providing an acceptable compromise between stroke prevention and bleeding risk (3–9). Despite evidence supporting its use, warfarin is approached with caution for real or perceived contraindications (10). Recently, a novel mechanical approach for the prevention of cardioembolic strokes in high-risk patients with AF has been introduced: the percutaneous left atrial appendage (LAA) transcatheter occlusion (PLAATO) device seals the communication between the left atrium (LA) and its appendage. Initial animal testing (11), and more recently human feasibility data (12), have suggested successful occlusion and stroke prevention. However, the anatomic and hemodynamic effects of PLAATO on the LA and its adjacent structures have not been reported. We studied six months' echocardiographic follow-up of patients enrolled in the PLAATO feasibility trial, with particular attention to the impact of the device on the structure and function of the mitral valve (MV) and the left upper pulmonary vein (LUPV).
The study population is part of the cohort of patients enrolled in the ongoing multicenter feasibility trial evaluating PLAATO for prevention of thromboembolism in AF. Patients with contraindication to warfarin use, including cerebral or gastrointestinal bleeding, chronic severe liver disease, unstable INR, or reluctance to take oral anticoagulation, were recruited if they had two or more of the following risk factors for stroke: age >65 years, diabetes mellitus, hypertension, prior transient ischemic attack or stroke, congestive heart failure, or spontaneous echocardiographic contrast in the LA by transesophageal echocardiography (TEE). Patients with TEE evidence of LAA thrombus or atrial septal abnormalities (patent foramen ovale, atrial septal defect) were excluded. The PLAATO device was positioned transseptally in the neck of the LAA under TEE and fluoroscopic guidance. Implant size was chosen to achieve complete sealing of the appendage from the LA cavity as judged by the operator.
Twelve of 45 U.S. patients had completed their six months' echocardiographic follow-up as of May 2003 and were included in the study. These patients were enrolled at Emory University Hospital and the Swedish Hospital. Eleven of 12 patients were included in this analysis. One patient was excluded because of limited echocardiographic images precluding accurate measurements.
Baseline parameters were obtained before device implantation. The size of the LA was measured in the antero-posterior and cranio-caudal planes with the TEE probe at 0° and 120°, respectively, with the largest dimension reported. The diameter of the LUPV was measured at or near its site of insertion into the LA opposite the largest diameter of the device. Flow across the MV was assessed by color Doppler to grade the degree of mitral regurgitation (1+ to 4+ by a single observer) and by pulse-wave Doppler to determine peak mitral E-wave velocity. Peak systolic and diastolic flows in the LUPV were measured using pulse-wave Doppler. After successful deployment of the device these parameters were remeasured. Patients were prescribed aspirin (325 mg daily) indefinitely and clopidogrel (75 mg daily) for four to six weeks.
All patients were scheduled for repeat TEE at one and six months to assess stability of the device and healing of the LAA and to remeasure LUPV diameter and flow parameters, as well as MV anatomy and flow parameters. In view of underlying AF, each measured parameter at any of the follow-up time points was reported as the average of measurements made over four to six cardiac cycles.
The data were analyzed by a linear mixed model for repeated measures. Heart rate, MV peak E-wave velocity, LUPV peak systolic wave (S-wave), and peak diastolic wave (D-wave) velocities were modeled as a function of follow-up time from baseline to six months, where follow-up time was included in the model as a fixed factor.
Occlusion of the LAA was successful in the 11 patients studied (Table 1), with follow-up data available for most study parameters at one and six months. The average age of the patients was 72 ± 7 years. Seven of the 11 patients were men. Ten patients had chronic AF of more than one year's duration, whereas one patient had been diagnosed with AF less than a year before PLAATO insertion. This patient was in normal sinus rhythm at baseline and at six months. One patient had a single-lead permanent pacemaker for complete atrioventricular node block and had a ventricular paced rhythm at all study time points. Mitral regurgitation (MR) was estimated by color Doppler as moderate in two patients, mild in four, and trace in five. Minimal residual flow around the device as determined by color Doppler was noted in all patients in the absence of fluoroscopically detectable leak, and these findings were considered to represent satisfactory placement of the device. Baseline and immediate postimplantation measurements were identical for all study parameters (data not shown), and only the baseline values were used for statistical analysis (Table 2).
Follow-up (Tables 3 and 4)
At ⇑⇓one month the device was stable in all but one patient, whose device appeared to have tilted slightly into the LA. The seal around the neck of the LAA was not compromised. In all patients there was minimal residual flow around PLAATO by color Doppler in a pattern similar to that observed immediately after device placement. No masses or thrombi were noted on the atrial surface of the implanted devices (Fig. 1). The severity of MR was unchanged. At six months, no further changes in implant position were noted. The LA surface of the device appeared smooth, with no irregular trailing edges, and the LAA distal to the device was thrombosed without evidence of detectable flow distal to the device (Fig. 1). The degree of MR and the amount of flow around PLAATO were also unchanged from baseline (Fig. 1).
Importantly, there was no significant difference from baseline to six months for any of the variables measured (Table 5).
Warfarin has been shown to reduce the risk of thromboembolism in patients with AF at the expense of an increased incidence of bleeding. Bleeding, falls, difficult-to-control INR levels, and personal preference preclude the use of oral anticoagulation in some patients. Because the LAA is the source of cardiac emboli in 90% of patients with nonrheumatic AF in whom an intracardiac thrombus has been visualized (13), exclusion of the LAA from the circulation is an alternative for the prevention of strokes in high-risk patients with AF and contraindication for long-term anticoagulation. Recently published data evaluating the PLAATO device have demonstrated the feasibility of this approach, and the successful prevention of thromboemboli in the 15 patients studied (12). One concern, however, is that the deployment of a foreign body in the neck of the LAA and the resulting thrombosis/fibrosis of the appendage might deleteriously affect LA structure and function. Close proximity of the device to the LUPV and the MV could result in pulmonary vein stenosis or impairment of mitral leaflet excursion. Our study shows that PLAATO has little if any impact on the structural and functional integrity of the LUPV and the MV. At six months, none of the measured parameters showed significant changes from baseline. Given the stability of the device and the complete healing of the LAA over that time period, the data analyzed at six months are likely to represent long-term behavior of the device. Furthermore, PLAATO was incorporated in the LA without thrombosis on the atrial surface, likely the result of successful neoendocardial formation. Interestingly, all patients had minimal flow around PLAATO immediately after implantation and at follow-up, but this communication between LA and LAA did not preclude thrombosis/fibrosis of the distal LAA. Even in the patient in whom the device tilted slightly into the body of the LA during the first month after implantation, the displacement did not progress and the seal of the LAA remained preserved. This study was not designed to evaluate the effect of PLAATO on stroke risk, precluding an assessment of the impact of the residual flow seen by color Doppler on clinical end points.
In conclusion, these data show that the implantation of the PLAATO device in the neck of the LAA does not result in any detrimental anatomic or physiologic changes to adjacent structures over six months of follow-up. The device is stable without thrombus formation on its atrial surface.
The authors gratefully acknowledge the help of Jill Moland and Kristine Zurowski.
☆ Dr. Reisman is a consultant for ev3.
- atrial fibrillation
- international normalized ratio
- left atrium
- left atrial appendage
- left upper pulmonary vein
- mitral regurgitation
- mitral valve
- percutaneous left atrial appendage transcatheter occlusion
- transesophageal echocardiography
- Received November 25, 2003.
- Revision received December 17, 2003.
- Accepted December 23, 2003.
- American College of Cardiology Foundation
- Stafford R.S.,
- Singer D.E.
- Nakai T.,
- Lesh M.D.,
- Gerstenfeld E.P.,
- Virmani R.,
- Jones R.,
- Lee R.J.
- Sievert H.,
- Lesh M.D.,
- Trepels T.,
- et al.