Cardiovascular disease is a significant cause of on-duty death among firefighters and a primary source of morbidity in law enforcement officers. The American Heart Association’s Life’s Essential 8 (LE8) offers a standardized cardiovascular health phenotype across diet, physical activity, nicotine exposure, sleep, body mass index, blood lipids, blood glucose, and blood pressure. Published first-responder studies generally report individual LE8 components rather than composite scores. This narrative review synthesizes evidence for the eight components across both professions and evaluates five domains not directly measured by LE8: structural and occupational conditions, psychological health, sex-specific and reproductive context, functional reserve and occupational readiness, and occupational cardiovascular toxicity. Evidence is strongest for obesity, hypertension, fitness, sleep disruption, and psychological distress. Firefighter studies also document subclinical atherosclerosis and acute vascular effects of fire suppression, whereas law enforcement studies identify substantial cardiometabolic risk, frequent sleep disorders, and stress-related vulnerability. Evidence in women remains limited, so sex-specific conclusions should be treated as assessment and research priorities rather than established occupation-specific causal pathways. LE8 provides a useful starting point for assessing cardiovascular health in first responders, but occupational factors should also be considered. Prospective studies are needed to determine whether adding these occupational factors improves risk assessment or prevention beyond LE8 alone.
Background Elevated lipoprotein(a) is a well-established cardiovascular risk factor with limited therapeutic options. Both PCSK9 inhibitors and GLP-1 receptor agonists are used in patients with elevated Lp(a), yet any observational comparison between these two drug classes is highly vulnerable to confounding by indication. Methods We used the TriNetX U.S. Collaborative Network to identify adults with elevated Lp(a) (>125 nmol/L or >50 mg/dL) initiated on either a PCSK9 inhibitor (evolocumab, alirocumab, or inclisiran) or a GLP-1 receptor agonist within one year of diagnosis. After 1:1 propensity score matching, 1,594 patients were included in each cohort. One-year cardiovascular outcomes were compared using Cox proportional hazards regression. Results After matching, MACE-3 occurred in 11.3% versus 9.1% of patients (HR 1.25, 95% CI 1.01–1.56). Numerically higher rates of MACE-4, incident ASCVD, and peripheral artery disease were also observed in the PCSK9 inhibitor arm. These associations ran opposite to randomized-trial evidence and occurred in the presence of residual imbalance on body-mass index (standardized difference 0.647), HbA1c, and total cholesterol. Conclusions A naïve reading of these results would suggest GLP-1 receptor agonists outperform PCSK9 inhibitors. This interpretation is almost certainly an artifact of confounding by indication. Residual imbalance in body-mass index, the coherent excess of all atherosclerotic endpoints in the PCSK9 inhibitor arm, and lower statin initiation in that arm indicate that matching failed to equalize baseline cardiovascular severity. This analysis serves as a cautionary case: propensity-score matching on measured covariates cannot support causal comparison between drug classes with such divergent prescribing indications.
Subclinical thyroid disease, defined by abnormal thyroid-stimulating hormone (TSH) with normal thyroid hormone levels, is common and may be an underrecognized contributor to atrial fibrillation (AF). This narrative review summarizes current evidence on how mild thyroid dysfunction influences AF risk and highlights practical implications for clinical management, drawing on mechanistic studies, observational epidemiology, and major guideline recommendations addressing subclinical hyperthyroidism, subclinical hypothyroidism, and cardiac rhythm outcomes. Subclinical hyperthyroidism shows a consistent association with increased AF risk. Proposed mechanisms include thyroid hormone–mediated changes in cardiac electrophysiology, increased adrenergic sensitivity, and atrial structural and electrical remodeling. Current American Thyroid Association and European Thyroid Association guidance supports treating higher-risk patients, particularly those older than 65 years or with cardiovascular comorbidities, when TSH is below 0.1 mIU/L. In contrast, evidence linking subclinical hypothyroidism to AF is weak. Although it has traditionally been associated with bradyarrhythmias, newer studies suggest a possible modest increase in AF risk. Treatment decisions for subclinical hypothyroidism are more nuanced, with the strongest consensus favoring therapy when TSH exceeds 10.0 mIU/L, while lower-level elevations generally require individualized assessment. Overall, subclinical thyroid dysfunction, especially subclinical hyperthyroidism, appears meaningfully related to AF risk, but important evidence gaps remain, including limited large-scale trial data showing that treatment prevents AF. Because subclinical thyroid disease and AF both increase with age, management should be individualized according to age, TSH severity, cardiovascular risk, and comorbidities.
Background Cardiovascular-kidney-metabolic (CKM) syndrome describes the overlapping burden of metabolic dysfunction, chronic kidney disease, and cardiovascular disease. Tirzepatide and semaglutide are both recommended for patients with type 2 diabetes and obesity, yet no randomized trial has directly compared their effect on hard cardiovascular and renal outcomes. Methods We conducted a retrospective, propensity score matched cohort study using the TriNetX Research Network (115 healthcare organizations queried). Adults with Stage 2 CKM syndrome and no established atherosclerotic, cerebrovascular, or heart failure disease were grouped by receipt of tirzepatide or semaglutide. Efficacy, safety, and exploratory outcomes were assessed over 1-year and 3-year windows. Cohorts were matched 1:1 (caliper 0.2 SD) on demographics, comorbidities, medications, and laboratory values, with a separate match performed for each analysis. Risk differences, risk ratios, odds ratios, hazard ratios (HR), and Kaplan–Meier survival analyses were calculated, and prespecified negative-control outcomes were used to test for residual confounding. Results After matching, cohorts ranged from 198,753 to 238,370 patients per group. Median observed follow-up was 163 days (tirzepatide) and 172 days (semaglutide) in the 3-year efficacy analysis. Compared with semaglutide, tirzepatide was associated with lower rates of major adverse cardiovascular events (1-year HR 0.83, 95% CI 0.77–0.90; 3-year HR 0.84, 0.78–0.91; 3-year risk difference −1.09 per 1,000 patients), all-cause mortality (1-year HR 0.75; 3-year HR 0.78), the cardiorenal composite, major adverse kidney events, end-stage kidney disease, and heart failure exacerbation at both time points. New atherosclerotic heart disease, acute kidney injury, and macroalbuminuria did not differ significantly. No prespecified safety outcome was more frequent with tirzepatide, and negative-control outcomes were null, although coronary artery calcium testing and HbA1c measurement were more frequent with tirzepatide, suggesting differential surveillance. Mean HbA1c was modestly lower with tirzepatide. Conclusion In this large real-world analysis with predominantly short observed follow-up, tirzepatide was associated with lower cardiovascular and renal event rates than semaglutide, with comparable safety. These findings are hypothesis-generating, may be affected by residual confounding, and require confirmation in randomized controlled trials.
