Risk Of Arterial Embolism Research Articles

Genetic evidence for a causal link between gut microbiota and arterial embolism and thrombosis: a two-sample Mendelian randomization study.

Previous research has hinted at a crucial link between gut microbiota and arterial embolism and thrombosis, yet the causal relationship remains enigmatic. To gain a deeper understanding, we aimed to comprehensively explore the causal relationship and elucidate the impact of the gut microbiota on the risk through a two-sample Mendelian randomization (MR) study. Genetic instrumental variables for gut microbiota were identified from a genome-wide association study (GWAS) of 18,340 participants. Summary statistics for IBS were drawn from a GWAS including 1,076 cases and 381,997 controls. We used the inverse-variance weighted (IVW) method as the primary analysis. To test the robustness of our results, we further performed the weighted median method, MR-Egger regression, and MR pleiotropy residual sum and outlier test. We identified three bacterial traits that were associated with the risk of arterial embolism and thrombosis: odds ratio (OR): 1.58, 95% confidence interval (CI): 1.08-2.31, p = 0.017 for genus Catenibacterium; OR: 0.64, 95% CI: 0.42-0.96, p = 0.031 for genus Dialister; and OR: 2.08, 95% CI: 1.25-3.47, p = 0.005 for genus Odoribacter. The results of sensitivity analyses for these bacterial traits were consistent (P<0.05). Our systematic analyses provided evidence to support a potential causal relationship between several gut microbiota taxa and the risk of arterial embolism and thrombosis. More studies are required to show how the gut microbiota affects the development of arterial embolism and thrombosis.

Diving-Induced Venous Gas Emboli Do not Increase Pulmonary Artery Pressure

Venous gas emboli are frequently observed in divers even if proper decompression procedures are followed. This study was initiated to determine if pulmonary artery pressure increases in asymptomatic divers, which could increase the risk of arterial embolization due to passage of venous gas emboli from the right to the left side of the heart. Recordings of venous gas emboli and estimation of pulmonary artery pressure by non-invasive transthoracic echocardiography were applied in 10 recreational scuba diving volunteers before and 20, 40, 60, and 80 min after simulated dives to 18 m (80 min bottom time) in a hyperbaric chamber. The ratio between pulmonary artery acceleration time and right ventricular ejection time was used as an estimate of pulmonary artery pressure. None of investigated divers had signs of decompression sickness. Despite the post-dive presence of the venous gas emboli, measured in the region of the pulmonary valve annulus (mean=1.71 bubbles.cm-2, 40 min after dive), the ratio between pulmonary artery acceleration time and right ventricular ejection time did not decrease, but actually increased (from 0.43+/-0.06 to 0.49+/-0.06, 40 min after dive; p<0.05), suggesting a decrease in pulmonary artery pressure after the dive. We conclude that diving-induced venous gas bubbles do not cause significant changes in the central circulation which could increase the risk of arterial embolization.

Left atrial thrombi despite anticoagulant and antiplatelet therapy

To investigate risk factors for embolization in patients with echocardiographically detected left atrial thrombi and to evaluate thrombus development, we examined 29 patients with transesophageal and transthoracic echocardiography at two points during a follow-up of 18 months. We compared patients with a history of possible arterial embolization (n = 13) with those without (n = 16) in regard to age, gender, left atrial dilatation, localization of the thrombus in the left atrial cavity, spontaneous echo contrast, and atrial fibrillation. Eight patients were treated with aspirin, 20 with phenprocoumon. Only left atrial spontaneous contrast was associated with thromboembolism (10/15 patients with spontaneous contrast experienced arterial embolism; p = 0.038). In six patients arterial embolism occurred after thrombus detection (14% per patient per year). Four of these patients were treated with phenprocoumon, two with aspirin. At reexamination, one thrombus was detected in the patient without anticoagulant treatment and one thrombus was detected in the 8 patients treated with aspirin (13%), compared with ten thrombi detected in the 20 patients (50%) treated with phenprocoumon (p = NS). In 17 patients no thrombus was seen at reexamination. Since only 2 patients had undergone thrombectomy and 3 experienced arterial embolism during follow-up, thrombi disappeared under medical therapy in 12 patients. Patients with left atrial thrombi have a high risk of arterial embolization despite proper anticoagulative or antiplatelet treatment. Embolization occurs significantly more often if spontaneous echo contrast can be visualized. Left atrial thrombi can be reduced in size by the administration of antiplatelet and anticoagulative agents.(ABSTRACT TRUNCATED AT 250 WORDS)