Empagliflozin reduces the risk of cardiovascular mortality in subjects with type 2 diabetes. We demonstrated that empagliflozin increases blood viscosity and carotid shear stress and decreases carotid wall thickness. Shear stress is the force acting on the endothelial surface and modulates arterial function. The current study evaluates the influence of empagliflozin on brachial artery shear stress and endothelial function compared to incretin-based therapy. The study is a nonrandomized, open, prospective cohort study including 35 subjects with type 2 diabetes administered empagliflozin or incretin-based therapy. Shear stress was calculated with a validated formula, and endothelial function was evaluated using the flow-mediated dilation technique. Both treatments resulted in comparable reductions in blood glucose and glycated haemoglobin. Brachial artery shear stress significantly increased exclusively in the empagliflozin group (61 ± 20 vs 68 ± 25 dynes/cm2, p = 0.04), whereas no significant difference was detected in the incretin-based therapy group (60 ± 20 vs 55 ± 12 dynes/cm2, p = not significant). Flow-mediated dilation significantly increased in the empagliflozin group (4.8 ± 4.5% vs 8.5 ± 5.6%, p = 0.03). Again, no change was detected in the incretin-based therapy group (5.1 ± 4.5% vs 4.7 ± 4.7%, p = not significant). The present findings demonstrate the beneficial effect of empagliflozin on shear stress and endothelial function in subjects with type 2 diabetes independent of the hypoglycaemic effect.
Subjects with Neurofibromatosis 1 (NF1) develop vascular complications. The protein product of the gene affected in NF1, neurofibromin, physiologically modulates endothelial function and preserves vascular and myocardial structure. Our study aimed to verify whether subjects with NF1 have early, preclinical abnormalities of carotid artery structure, brachial artery function, and cardiac function. We recruited 22 NF1 subjects without previous cardiovascular events and 22 healthy control subjects. All subjects underwent measurement of carotid artery intima-media thickness (IMT), evaluation of brachial artery endothelial function after ischemia and exercise, and cardiac function. Mean IMT was 543 ± 115 μ in NF1 subjects and 487 ± 70 μ in Controls (p < 0.01). Endothelial function was significantly dumped in NF1 subjects. The dilation after ischemia and exercise was respectively 7.5(± 4.8)% and 6.7(± 3.0)% in NF1 versus 10.5(± 1.2)% and 10.5(± 2.1)% in control subjects (p < 0.02; p < 0.002). Left ventricular systolic function assessed by Global Longitudinal Strain was significantly different between NF1 subjects and Controls: − 19.3(± 1.7)% versus − 21.5(± 2.7)% (p < 0.008). These findings demonstrate that NF1 patients have early morphological and functional abnormalities of peripheral arteries and systolic cardiac impairment and suggest the need for a tight cardiovascular risk evaluation and primary prevention in subjects with NF1. Neurofibromatosis 1 (NF1) is a common genetic disease, affecting approximately 1 in 3,500 subjects. It has an autosomal dominant inheritance with complete penetrance, variable expression, and a high rate of new mutations. The disease is characterized by cafe-au-lait spots, dermal neurofibromas, skeletal dysplasia, Lish nodules, and optic glioma 1. Neurofibromin (encoded by the NF1 gene) is a modulator of cell growth, downregulates ras signaling, and its loss of function promotes cellular proliferation 2. For these reasons, subjects with NF1 have increased risk for malignancies like peripheral nerve sheath tumor, leukemia, and rhabdomyosarcoma. Furthermore, they may develop vascular complications as renal artery stenosis with secondary hypertension, aneurysm, arterial stenosis/occlusion, myocardial infarction, and cerebral or visceral infarcts arteriovenous fistulae 3. The vascular involvement does not seem directly linked to the proliferation and malignant transformation of neural-crest derivatives 2. Though pathogenesis of vascular lesions in NF1 remains unclear, previous studies in murine models and humans demonstrated that neurofibromin is expressed in the endothelial cells and vascular smooth muscle cells as well 2,4. Therefore NF1 vasculopathy might be the consequence of a direct involvement in vascular layers 5. Cardiac alterations have also been under the spotlight in NF1. The neurofibromin protein is physiologically involved in cardiac development 6. Besides, microdeletions of the NF1 gene often involve the nearby SUZ12 and CENTA2 genes, whose haploinsufficiency may also influence c...
Introduction The Watchman‐FLX left atrial appendage closure (LAAC) device presents innovative features: higher conformability, reduced length, closed distal "flex‐ball" during deployment, and flattened surface. We report our real‐world experience with the Watchman‐FLX device in two centers with consolidated LAAC expertise. Methods We enrolled 200 consecutive Watchman‐FLX patients (2019–2021) in a nonrandomized double‐center registry; procedural data and follow‐up for midterm clinical outcomes were collected. A control group of 100 patients treated with first‐generation Watchman (2.5) was included. Results According to mean CHAD2DS2‐VASc (5 ± 1.40) and HAS‐BLED (3.8 ± 1.01) scores, the population included in this study was at high risk: 29% had a previous stroke and 56.5% a bleeding event. Main LAAC indications were symptomatic hemorrhage (39.5%), need for triple antithrombotic therapy (39%), gastrointestinal bleeding (32%), and oral anticoagulation intolerance (18%). Transesophageal echocardiography guidance was followed in 93% of cases (48% in general anesthesia and 45% under conscious sedation). Repositioning an FLX device was required in 20% of cases and no complication occurred. In 96% of patients, the first selected device was delivered, while in 4% a device size change was required after the first choice (7% with Watchman 2.5). Peridevice leaks (<5 mm) were found postimplant in two cases (1%). Overall, the procedural success rate was 99.5%. One patient's procedure was unsuccessful (0.5%), due to left atrial appendage (LAA) anatomy; differently, the mean failure rate with Watchman 2.5 was 2%. No device embolization was reported. Complications (8.5%) were mainly related to the access site (3%); major bleedings (1%), and in‐hospital death (0.5%) rarely occurred. After a follow‐up of 272 ± 173 days, 2.3% of cases experienced a non‐device‐related stroke and 0.6% fatal bleeding. Conclusion Our registry showed a high procedural success rate of the Watchman‐FLX in a high‐risk population. According to our experience, the main advantages include easy implanting and repositioning, absence of embolization, good LAA sealing, and low rate of complications in the follow‐up period.
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