Left atrial appendage closure with AMPLATZER cardiac plug for stroke prevention in atrial fibrillation: initial Asia-Pacific experience.

BACKGROUND: Left atrial appendage (LAA) is the main source of left atrial thrombus that causes stroke in patients with non-valvular atrial fibrillation (NVAF). This study reported the initial safety, feasibility, and 1-yr clinical outcomes following AMPLATZER cardiac plug (ACP) implantation in Asia-Pacific region. METHODS: Twenty NVAF patients (16 males, age 68 ± 9 yr) with high risk for developing cardioembolic stroke (CHADS(2) score: 2.3 ± 1.3) and contraindications to warfarin received ACP implants from June 2009 to May 2010. Patients received general anesthesia (n = 9) or controlled propofol sedation (n = 11) and the procedures were guided by fluoroscopy and transesophageal echocardiography (TEE). Clinical follow-up was arranged at 1 month and then every 3 months after implantation, whereas, a TEE was scheduled at 1 month upon completion of dual anti-platelet therapy. RESULTS: The LAA was successfully occluded in 19/20 patients (95%) at two Asian centers. One procedure was abandoned because of catheter-related thrombus formation. Other complications included coronary artery air embolism (n = 1) and TEE-attributed esophageal injury (n = 1). The median procedural and fluoroscopic times were 79 (IQR: 59-100) and 18 (IQR 12-27) minutes, respectively. The mean size of implant was 23.6 ± 3.1 mm. The average hospital stay was 1.8 ± 1.1 days. Follow-up TEE showed all the LAA orifices were sealed without device-related thrombus formation. No stroke or death occurred at a mean follow-up of 12.7 ± 3.1 months. CONCLUSIONS: Our preliminary data suggested LAA closure with ACP is safe, feasible with encouraging 1-yr clinical outcomes. Further large-scaled trials are needed to confirm the efficacy of this device.

The relationship between coronary stenosis severity and compression type coronary artery movement in acute myocardial infarction.

BACKGROUND: Acute myocardial infarction is thought to occur at sites of minor coronary stenosis. Recent data challenge this and also propose a role for coronary artery movement (CAM) in plaque instability. We examined the relationship between coronary stenosis severity, CAM pattern, and infarct-related lesions (IRLs) in acute myocardial infarction. METHODS: We investigated 203 consecutive patients with ST-segment elevation myocardial infarction after successful fibrinolysis. Quantitative coronary angiography, CAM pattern, and extent score (atheroma burden) analysis was performed for each coronary artery segment. RESULTS: The IRL stenosis was at least moderate (>50%) and severe (>70%) in 78% and 31% of patients, respectively. Culprit arteries were associated with higher atheroma extent scores (25.2 vs 21.6, P < .001). Analysis of 2,228 coronary segments showed that stenosis severity and IRLs were highly correlated, such that the likelihood of being a culprit segment progressively increased with worsening stenosis (odds ratio [OR] 30.0, 95% confidence interval [CI] 19.0-47.6, P < .001, for >70% vs <30% stenosis). Compression CAM was also strongly associated with culprit segments (OR 3.4, 95% CI 2.6-4.5, P < .001). In addition, compression CAM and stenosis severity were strongly correlated, with the likelihood of a coronary segment having compression CAM progressively increasing with worsening stenosis (OR 56.4, 95% CI 37.9-83.8, P < .001, for >70% vs <30% stenosis). CONCLUSIONS: In patients with ST-segment elevation myocardial infarction, there is a strong relationship between stenosis severity and IRLs. Our study also raises the hypothesis that compression CAM may accelerate atherosclerosis and predispose to plaque vulnerability.