Severity of Coronary Artery Disease by Friesinger Score Among Women With Acute Coronary Syndrome in a Tertiary Care Hospital in Bangladesh.

BACKGROUND: The chance of coronary artery disease (CAD) is much higher in women who have gone through menopause than in those who have not, owing to hormonal defense against atherosclerosis. More advanced CAD and several comorbidities were observed in postmenopausal women. Nevertheless, there is a paucity of information comparing the angiographic severity of acute coronary syndrome (ACS) in premenopausal and postmenopausal women of different ages. This research sought to determine the Friesinger score's use in evaluating the degree of CAD in premenopausal and postmenopausal women with ACS. METHODS: A total of 145 female patients with ACS were included in this cross-sectional observational research. Depending on the stage of menopause, they were categorized into two groups: group I (premenopausal) and group II (postmenopausal). The study examined the differences in clinical data and the severity of coronary angiographic features based on the Friesinger score between the premenopausal and postmenopausal ACS groups. RESULTS: A statistically significant difference (p = 0.001) was found in the mean age of premenopausal ACS patients, which was 41.53 ± 5.45 years, and postmenopausal ACS patients, which was 57.23 ± 7.45 years. Between the premenopausal group (31.4% vs. 17.1%; p = 0.04 and 31.4% vs. 15.7%; p = 0.002) and postmenopausal group (48.6% vs. 20%; p = 0.001), there was a greater prevalence of normal coronary angiography, single-vessel disease, and triple-vessel disease. Comparing the postmenopausal group to the premenopausal group, the high to intermediate Friesinger score (11-15) was found to be considerably higher (2.9% vs. 1.4%; 72.9% vs. 50%; p = 0.003). CONCLUSION: Prior to menopause, single-vessel disease and normal coronary angiography were more common, whereas postmenopausal individuals had triple-vessel disease. The postmenopausal group's CAD was found to be more severe than the premenopausal group's according to the Friesinger score used for severity evaluation.

The α7 nicotinic receptor silent agonist R-47 prevents and reverses paclitaxel-induced peripheral neuropathy in mice without tolerance or altering nicotine reward and withdrawal.

Various antitumor drugs, including paclitaxel, frequently cause chemotherapy-induced peripheral neuropathy (CIPN) that can be sustained even after therapy has been completed. The current work was designed to evaluate R-47, an α7 nAChR silent agonist, in our mouse model of CIPN. R-47 was administered to male C57BL/6J mice prior to and during paclitaxel treatment. Additionally, we tested if R-47 would alter nicotine's reward and withdrawal effects. The H460 and A549 non-small cell lung cancer (NSCLC) cell lines were exposed to R-47 for 24-72 h, and tumor-bearing NSG mice received R-47 prior to and during paclitaxel treatment. R-47 prevents and reverses paclitaxel-induced mechanical hypersensitivity in mice in an α7 nAChR-dependent manner. No tolerance develops following repeated administration of R-47, and the drug lacks intrinsic rewarding effects. Additionally, R-47 neither changes the rewarding effect of nicotine in the Conditioned Place Preference test nor enhances mecamylamine-precipitated withdrawal. Furthermore, R-47 prevents paclitaxel-mediated loss of intraepidermal nerve fibers and morphological alterations of microglia in the spinal cord. Moreover, R-47 does not increase NSCLC cell viability, colony formation, or proliferation, and does not interfere with paclitaxel-induced growth arrest, DNA fragmentation, or apoptosis. Most importantly, R-47 does not increase the growth of A549 tumors or interfere with the antitumor activity of paclitaxel in tumor-bearing mice. These studies suggest that R-47 could be a viable and efficacious approach for the prevention and treatment of CIPN that would not interfere with the antitumor activity of paclitaxel or promote lung tumor growth.