No abstract

Aneurysm of the left atrial appendage is extremely rare, and afflicted patients most commonly present with atrial tachyarrhythmia or thromboembolism. For these patients, resection of the aneurysm is the recommended and preferred therapy. We present the case of a 57-year-old woman who was found incidentally to have a large aneurysm of the left atrial appendage presenting as atrial fibrillation. After surgical intervention with resection of the aneurysm and a Cox maze III procedure, the patient recovered and was discharged in sinus rhythm.

Severe hyper-catecholaminergic states likely cause heart failure and cardiac fibrosis. While previous studies demonstrated the effects of beta-blockade in experimental models of single-catecholamine excess states, the detailed benefits of beta-blockade in more realistic models of hyper-adrenergic states are less clearly understood. In this study, we examined different therapeutic dosages and the effects of propranolol in rats with hyper-acute catecholamine-induced heart failure, and subsequent cardiopulmonary changes. Rats (n = 41) underwent a 6 h infusion of epinephrine and norepinephrine alone, with additional low-dose (1 mg/kg) or high-dose propranolol (10 mg/kg) at hour 1. Cardiac and pulmonary tissues were examined after 6 h. Catecholamine-only groups had the lowest survival rate. Higher doses of propranolol (15 mg/kg) caused similarly low survival rates and were not further analyzed. All low-dose propranolol rats survived, with a modest survival improvement in the high-dose propranolol groups. Left ventricular (LV) systolic pressure and LV end-diastolic pressure improved maximally with low-dose propranolol. Cardiac immunohistochemistry revealed an LV upregulation of FGF−23 in the catecholamine groups, and this improved in low-dose propranolol groups. These results suggest catecholamine-induced heart failure initiates early pre-fibrotic pathways through FGF−23 upregulation. Low-dose propranolol exerted cardio-preventative effects through FGF−23 downregulation and hemodynamic-parameter improvement in our model of hyper-acute catecholamine-induced heart failure.

BackgroundVaricose veins (VVs), a common vascular disease is associated with a huge medical burden. The prevalence in women surpasses that in men. The role of vegetarian diets in the pathogenesis of the disease remains inconclusive. In this study, we examined the risk of VVs in vegetarian and non-vegetarian men and women.MethodsThe study involved 9905 adults whose data were obtained from Taiwan Biobank between 2008 and 2020. Information on VVs, sex, and vegetarian diets was obtained from participants’ self-responses to the Taiwan Biobank questionnaires.ResultsThe study subjects consisted of 4,142 men and 5,763 women. About 12% of men and 35% of women had VVs. Study participants were predominantly non-vegetarians (91.84% were men and 88.24% were women). Women had a higher risk of VVs than men. The odds ratio (OR); 95% confidence interval (CI) was 3.414; 2.995–3.891. There was a significant interaction between sex and vegetarian diets (p = 0.0034). Women were at higher risk of VVs than men both in the vegetarian (OR = 1.877, 95% CI = 1.270–2.774) and non-vegetarian (OR = 3.674, 95% CI = 3.197–4.223) groups. Based on vegetarian diets, only vegetarian men had a higher risk of VVs (OR = 1.453, 95% CI = 1.069 to 1.976). Based on the sex-stratified model, the risk of VVs was significantly higher in vegetarian men (OR = 1.457, 95% CI = 1.072–1.979), and in vegetarian and non-vegetarian women with corresponding ORs (95% CI) of 3.101 (2.528–3.803) and 3.599 (3.140–4.124), respectively.ConclusionWomen were more susceptible to varicose veins compared to men, regardless of diet. However, in terms of diet, only men who followed a vegetarian diet were at greater risk for developing VVs.