Background: Sodium‐glucose cotransporter‐2 inhibitors (SGLT2is) and glucagon‐like peptide‐1 receptor agonists (GLP‐1RAs) mitigate cardiovascular risk in individuals with type 2 diabetes, but most eligible patients do not receive them. We characterized temporal trends in SGLT2i and GLP‐1RA use by cardiologists compared with other groups of clinicians. Methods and Results: We conducted a descriptive analysis of serial, cross‐sectional data derived from IQVIA’s National Prescription Audit, a comprehensive audit capturing ≈90% of US retail prescription dispensing and projected to population‐level data, to estimate monthly SGLT2is and GLP‐1RAs dispensed from January 2015 to December 2020, stratified by prescriber specialty and molecule. We also used the American Medical Association’s Physician Masterfile to calculate average annual SGLT2is and GLP‐1RAs dispensed per physician. Between January 2015 and December 2020, a total of 63.2 million SGLT2i and 63.4 million GLP‐1RA prescriptions were dispensed in the United States. Monthly prescriptions from cardiologists increased 12‐fold for SGLT2is (from 2228 to 25 815) and 4‐fold for GLP‐1RAs (from 1927 to 6981). Nonetheless, cardiologists represented only 1.5% of SGLT2i prescriptions and 0.4% of GLP‐1RA prescriptions in 2020, while total use was predominated by primary care physicians/internists (57% of 2020 SGLT2is and 52% of GLP‐1RAs). Endocrinologists led in terms of prescriptions dispensed per physician in 2020 (272 SGLT2is and 405 GLP‐1RAs). Cardiologists, but not noncardiologists, increasingly used SGLT2is over GLP‐1RAs, with accelerated uptake of empagliflozin and dapagliflozin coinciding with their landmark cardiovascular outcomes trials and subsequent US Food and Drug Administration label expansions. Conclusions: While use of SGLT2is and GLP‐1RAs by cardiologists in the United States increased substantially over a 6‐year period, cardiologists still account for a very small proportion of all use, contributing to marked undertreatment of individuals with type 2 diabetes at high cardiovascular risk.

Introduction: Depression is one of the under-recognized health problems in adolescents. Emotional instability resulted from childhood to adulthood transition makes adolescents vulnerable to depression. Aims: The aim of the study was to explore the prevalence of depression and its associated sociodemographic factors among school-going adolescents. Materials and Methods: This cross-sectional study was undertaken from January 2016 to June 2016 in adolescents studying in 9–12^th standard from forty schools located in an urban area of Patna, Bihar. The self-administered questionnaire of Beck's Depression Inventory II was utilized to assess the prevalence of depression. Statistical analysis was done with Pearson's Chi-square test using SPSS software version 21.0. Results: Among the 1412 selected students, the prevalence of depression was found to be 49.2%, wherein the prevalence of severe depression was 7.7%. The overall prevalence of depression was significantly (P < 0.001) higher among girls (55.1%) than boys (45.8%). The prevalence of depression was found to be higher among students belonging to minorities (Buddhism, Jainism, etc.) (63.3%, P < 0.001). Elder students were found to be more depressed than younger students. Depression was found to be statistically significantly associated with gender and religion (P < 0.005). Guilty feeling (69.48%) was one of the most prominent clinical factors associated with depression followed by pessimism (58.14%), sadness (56.52%), and past failure (55.81%). Conclusions: Mental health is one of the most neglected aspects of our society. There is a need to increase awareness about depression among teachers and parents to identify and help depressed adolescents in the school.

Background: Uncertainties persist regarding the precise shape of the smoking-outcome curves across various cardiovascular and mortality endpoints. This study aims to elucidate the relationships among smoking burden, intensity, and cessation duration across multiple cardiovascular outcomes. Methods and findings: Cox proportional hazard models were constructed to evaluate the association between pack-years, cigarettes per day (CPD), and years since cessation with cardiovascular outcomes in participants from 22 prospective cohort studies within the Cross-Cohort Collaboration Tobacco Working Group. We evaluated myocardial infarction (MI), stroke, coronary heart disease (CHD; MI, coronary revascularization, or coronary death), cardiovascular disease (CVD; stroke or cardiovascular death), heart failure (HF), atrial fibrillation (AFib), CHD mortality, CVD mortality, and all-cause mortality. Median follow-up varied across outcomes, with 14.4 years for MI (17,570 events), 19.3 years for CHD (30,625 events), 18.6 years for CVD (54,078 events), and approximately 19.4–19.9 years for mortality outcomes (CHD mortality: 17,429 events; CVD mortality: 33,120 events; all-cause mortality: 125,044 events). Spline terms were used to investigate the nonlinear association of continuous smoking/cessation measures with the examined outcomes. Models were adjusted for demographic, socioeconomic, and other cardiovascular risk factors. The study included 323,826 adults (148,635 non-mortality and 176,396 mortality outcomes with 25 and 16 million person-years at risk, respectively). Compared to never-smokers, current smokers had significantly increased risks for CVD (hazard ratio (HR) 1.74, 95% confidence intervals (CIs) [1.66,1.83] in men; HR 2.07, 95% CI [2.00,2.14] in women) and all-cause mortality (HR 2.17, 95% CI [2.09,2.25] in men; HR 2.43, 95% CI [2.38,2.48] in women; all p < 0.001). Compared with never-smokers, participants with 2–5 CPD demonstrated substantially elevated cardiovascular risks, with HR ranging from 1.26 (95% CI [1.09,1.45], p = 0.002) for AFib to 1.57 (95% CI [1.39,1.78], p < 0.001) for HF. Smoking 2–5 CPD was associated with increased CVD mortality (HR 1.57, 95% CI [1.41,1.75]), and all-cause mortality (HR 1.60, 95% CI [1.52,1.69]; both p < 0.001). Smoking 11–15 CPD conferred a higher risk of CVD (HR 1.87, 95% CI [1.69,2.06]) and all-cause mortality (HR 2.30, 95% CI [2.14,2.47]; both p < 0.001). The increased risk associated with the evaluated outcomes was steeper for the initial 20 pack-years and 20 CPD, respectively, compared to further smoking exposure. The most substantial reduction in risk across all outcomes was observed within the first 10 years after smoking cessation. However, the progressive risk reduction continues over extended time periods, with former smokers demonstrating over 80% lower relative risk than those of current smokers within 20 years of cessation. Limitations include potential exposure misclassification due to reliance on single baseline self-reported smoking measurements with extended follow-up periods, which may underestimate true risk associations, and lack of data on other tobacco products and electronic nicotine delivery systems, preventing analysis of dual- and poly-use patterns. Conclusion: Lower-intensity smoking is associated with cardiovascular risk and the primary public health message for current smokers should be early cessation, rather than reducing the amount of smoking. Cessation provides substantial immediate risk reduction, although risk continues to decrease significantly for the following two decades.

A man aged 30 years presented to the emergency department (ED) with ataxia, areflexia, facial weakness, ophthalmoplegia, extremity weakness and back pain for 4 days. 4 days prior to attending the ED, the patient had suffered from diarrhoea for 2 weeks. The diagnosis of Miller Fisher syndrome was performed on the dual basis of clinical features in addition to an investigations report. Nerve conduction studies and anti-GQ1b IgG antibody analysis were requested. Once IgA deficiency was ruled out, the patient was started on intravenous immunoglobulin (400 mg/kg/day).

BACKGROUND: Understanding the associations of tobacco product use with subclinical markers is essential in evaluating health effects to inform regulatory policy. This is particularly relevant for noncigarette products (eg, cigars, pipes, and smokeless tobacco), which have been understudied because of their low prevalence in individual cohorts. METHODS: This cross-sectional study included 98 450 participants from the Cross-Cohort Collaboration–Tobacco data set. Associations between the use of tobacco products and subclinical markers (high-sensitivity C-reactive protein, interleukin-6, fibrinogen, D-dimer, coronary artery calcium, carotid intima-media thickness, carotid plaque, and ankle-brachial index) were evaluated. The analyses used multivariable linear and logistic regression models to examine current use status for each product, with additional analyses of “sole” and “exclusive” noncigarette use (versus never use of either cigarettes or specific noncigarette tobacco). Sole use was defined as the current use of a given noncigarette tobacco without concurrent combustible cigarette use, whereas exclusive use was defined as current noncigarette tobacco use without any history of combustible cigarette use. RESULTS: A total of 20.0%, 3.0%, 0.8%, and 1.5% of participants were current cigarette, cigar, pipe, or smokeless tobacco users, respectively. Current cigarette use was linked to higher levels of all markers compared with never cigarette use. Compared with respective reference groups, current, sole, and exclusive cigar use was associated with 10% (95% CI, 1–20), 19% (95% CI, 12–26), and 11% (95% CI, 2–21) higher high-sensitivity C-reactive protein levels on the geometric mean scale. Similar associations were noted for pipe and smokeless tobacco use. For interleukin-6, we observed that sole cigar use was associated with a 15% (95% CI, 6–24) higher level, whereas current, sole, and exclusive pipe use were associated with 22% to 32% (all P values <0.05) higher levels compared with their respective reference groups. Fibrinogen levels were 2% to 6% higher (all P values <0.05) among sole users of cigars, pipes, and smokeless tobacco, compared with their respective reference groups. Additionally, noncigarette tobacco use was moderately associated with carotid plaque and carotid intima-media thickness. CONCLUSIONS: Use of noncigarette tobacco products is linked to subclinical markers related to cardiovascular harm. Inflammatory markers, such as high-sensitivity C-reactive protein and interleukin-6, have the potential for assessing early cardiovascular harm from using these products and aiding regulatory authorities in evaluating their associated risks.

BACKGROUND: Aortic valve calcification (AVC), Lp(a) [lipoprotein(a)], and low-density lipoprotein cholesterol (LDL-C) are associated with severe aortic stenosis (AS). We aimed to determine which of these risk factors were most strongly associated with the risk of incident severe AS. METHODS: A total of 6792 participants from the MESA study (Multi-Ethnic Study of Atherosclerosis) had computed tomography-quantified AVC, Lp(a), and LDL-C values at MESA visit 1 (2000–2002). We calculated the absolute event rate of incident adjudicated severe AS per 1000 person-years and performed multivariable adjusted Cox proportional hazards regression. RESULTS: The mean age was 62 years old, and 47% were women. Over a median 16.7-year follow-up, the rate of incident severe AS increased exponentially with higher AVC, regardless of Lp(a) or LDL-C values. Participants with AVC=0 had a very low rate of severe AS even with elevated Lp(a) ≥50 mg/dL (0 was strongly associated with severe AS when Lp(a) <50 mg/dL hazard ratio (HR) of 33.8 (95% CI, 16.4–70.0) or ≥50 mg/dL HR of 61.5 (95% CI, 7.7–494.2) and when LDL-C <130 mg/dL HR of 31.1 (95% CI, 14.4–67.1) or ≥130 mg/dL HR of 50.2 (95% CI, 13.2–191.9). CONCLUSIONS: AVC better identifies people at high risk for severe AS compared with Lp(a) or LDL-C, and people with AVC=0 have a very low long-term rate of severe AS regardless of Lp(a) or LDL-C level. These results suggest AVC should be the preferred prognostic risk marker to identify patients at high risk for severe AS, which may help inform participant selection for future trials testing novel strategies to prevent severe AS.