The healing response of LAMax LAAC™ left atrial appendage occluder in a canine model: the potential influence of the implantation technique on the healing response.

BACKGROUND: Device-associated thrombus are potential causes for thromboembolic events post left atrial appendage closure (LAAC), and correlated with the complete endothelialization of the device surface. Our aim was to evaluate the endothelialization of LAMax LAAC™ occluder surface and analyze the potential influence of the implantation technique on the healing response. METHODS: A total of 29 healthy dogs (28.0 ± 3.7 kg) were implanted with the devices successfully after ensuring COVER signs was met (Concavity of the disc, Oversizing by 20-50%, Verifying position, Ensuring stability, Residual flow < 5 mm by transesophageal echocardiographic (TEE) examination), and sacrificed at < 24 h, 1-, 2-, 3-, and 6-months. Gross examinations were conducted to evaluate healing response. RESULTS: The mean diameters of LAA orifice measured by angiography and TEE were 19.0 ± 2.9 mm and 16.6 ± 2.9 mm (P < 0.05), respectively. TEE found that the discs in 18 dogs (62.1%) were completely pulled into the LAA with concavity and in 11 dogs incompletely pulled into the LAA with suboptimally concavity, while 5 of them had residual flow. Gross examinations showed that the complete endothelialization on the device surface with concaved disc was found at 1-month after LAAC. Microscopic examinations confirmed complete healing on the device with optimal closure effect. CONCLUSIONS: The good healing response and the optimal closure effect were observed using the LAMax device in a canine model by following the COVER implantation technique.

Contrast-enhanced transesophageal echocardiography predicts neo-intimal coverage of device post-left atrial appendage closure.

BACKGROUND: Left atrial appendage (LAA) closure (LAAC) is a viable alternative to anticoagulation for stroke prevention in non-valvular atrial fibrillation. However, device-associated thrombosis (DAT) is known as a complication of LAAC as observed within the first few weeks after implantation. A noninvasive method is needed to predict the progress for endothelialization surveillance. The aim of the study was to develop a noninvasive visual contrast-enhanced transesophageal echocardiography (cTEE) method for monitoring the communication between left atrium (LA) and LAA post-LAAC by cTEE-score evaluating the contrast enhancement in LAA. METHODS: A total of 29 healthy dogs were studied by LAAC at < 24 h and 1, 2, 3 and 6-months. The LAAC procedure was assessed by TEE with color Doppler flow imaging (CDFI) and contrast imaging. The cTEE score was calculated based on the differential contrast opacification of LA and LAA cavities, the CDFI on the width of peri-device color flow, and that of histology on the level of occluder surface endothelialization in postmortem histological examination. Spearman's correlation analysis was used to correlate these scores. RESULTS: The correlation between cTEE and histology scores was superior to that between CDFI and histology scores. The trend of average cTEE score was tracked with that of histology, while that of CDFI was far from that of histology. The correlation coefficient of CDFI and histology scores was not significant (p > 0.05). CONCLUSIONS: The noninvasive visual cTEE is feasible and reliable to monitor communication between the LA and LAA post-LAAC. cTEE is superior to CDFI as a tool in predicting the progress for endothelialization surveillance.

Monocyte to HDL cholesterol ratio as a marker of the presence and severity of obstructive sleep apnea in hypertensive patients.

This study aimed to investigate the correlation between monocyte to high-density lipoprotein cholesterol ratio (MHR) and obstructive sleep apnea (OSA) in patients with hypertension. A total of 246 hypertensive patients (67 controls, 65 mild, 51 moderate, and 63 severe OSA) were included. The relationship between MHR and OSA was analyzed. MHR correlated positively with apnea-hypopnea index (AHI), while negatively with mean SpO2 (P < 0.01). MHR was higher in OSA group than the control group (9.2 ± 2.6 vs. 10.8 ± 3.6, P < 0.001). Moreover, MHR in severe OSA group was the highest among all groups (9.2 ± 2.6, 10.2 ± 3.2, 10.4 ± 4.0, and 11.8 ± 3.4 in control, mild, moderate, and severe OSA group, respectively, P < 0.001). Logistic regression analysis demonstrated that MHR was an independent predictor of the presence of OSA (OR = 1.152, P < 0.01) and severe OSA (OR = 1.142, P < 0.01). Area under the curve of MHR was 0.634 (P < 0.05) and 0.660 (P < 0.05) for predicting OSA and severe OSA respectively in the ROC analysis. In conclusion, MHR increased with the severity of OSA. As a practical and cost-effective test, MHR was expected to be an available marker in evaluating OSA risk and severity in hypertensive patients.