Comorbidities related to cardiovascular disease (CVD) and environmental pollution have emerged as serious concerns. The exposome concept underscores the cumulative impact of environmental factors, including climate change, air pollution, chemicals like PFAS, and heavy metals, on cardiovascular health. Chronic exposure to these pollutants contributes to inflammation, oxidative stress, and endothelial dysfunction, further exacerbating the global burden of CVDs. Specifically, carbon monoxide (CO), ozone, particulate matter (PM_2.5), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), heavy metals, pesticides, and micro- and nanoplastics have been implicated in cardiovascular morbidity and mortality through various mechanisms. PM_2.5 exposure leads to inflammation and metabolic disruptions. Ozone and CO exposure induce oxidative stress and vascular dysfunction. NO₂ exposure contributes to cardiac remodeling and acute cardiovascular events, and sulfur dioxide and heavy metals exacerbate oxidative stress and cellular damage. Pesticides and microplastics pose emerging risks linked to inflammation and cardiovascular tissue damage. Monitoring and risk assessment play a crucial role in identifying vulnerable populations and assessing pollutant impacts, considering factors like age, gender, socioeconomic status, and lifestyle disorders. This review explores the impact of cardiovascular disease, discussing risk-assessment methods, intervention strategies, and the challenges clinicians face in addressing pollutant-induced cardiovascular diseases. It calls for stronger regulatory policies, public health interventions, and green urban planning.

It has been widely accepted for many years that the essential components of the complement cascade (ComC), including C3 and C5 proteins, are produced solely in the liver and released into circulation after synthesis. However, recent evidence shows that complement components are also expressed in other cell types, including human cardiomyocytes. Moreover, a new regulatory loop was identified in lymphocytes that regulates immune responses and metabolism, named the “Complosome.” Following this significant discovery, the Complosome has been shown to play a role in the trafficking and metabolism of hematopoietic stem/progenitor cells (HSPCs) and is expressed in several types of bone marrow (BM) resident stem cells. ComC has been studied in various models of tissue and organ injury and regeneration. However, most of these studies did not distinguish between the role of systemic, liver-derived circulating complement in the blood and the complement expressed as a “Complosome” inside cells. Since Complosome is expressed in several types of stem cells that could influence the clinical outcome of myocardial infarction (MI), this distinction is important because intracellular components of the ComC may have beneficial roles in cell survival, growth, differentiation, and trafficking of stem and progenitor cells. We report herein the systemic activation of the Complosome in the heart and hematopoietic tissues in a murine model of myocardial infarction (MI). Graphical Abstract

Bortezomib is a 26S proteasome inhibitor used to treat multiple myeloma and systemic amyloidosis. While effective in prolonging survival, bortezomib has been increasingly associated with cardiovascular adverse events (CVAEs), including cardiac failure and arrhythmias, yet a comprehensive post-marketing cardiac safety profile remains incompletely defined. We analyzed cardiovascular adverse events reported between May 2003 and May 2025 using the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) via the OpenVigil 2.1 platform. Disproportionality analysis was performed using reporting odds ratios (RORs) with 95% confidence intervals (CIs). Among over 9 million drug-related adverse events in FAERS, 552 cardiac events were linked to bortezomib. Several cardiac outcomes, including atrial flutter, left ventricular dysfunction, cardiac failure, cardiomyopathy, atrial fibrillation, right ventricular failure, myocarditis, and supraventricular tachycardia, demonstrated elevated disproportionality signals. Separately, cardiac amyloidosis exhibited the highest disproportionality signal (ROR: 35.58; 95% CI: 28.16–44.95), a finding that reflects underlying disease severity rather than treatment-emergent cardiotoxicity. Cardiac failure accounted for the greatest number of hospitalizations (301) and deaths (208), followed by atrial fibrillation and cardiac amyloidosis. Older adults (≥65 years) and patients with amyloidosis or multiple myeloma were the most vulnerable populations. Overall, bortezomib was associated with serious cardiac adverse events, particularly cardiac failure and atrial arrhythmias, underscoring the need for routine cardiovascular risk assessment and proactive monitoring in high-risk patients.

Background: Beta-blockers are widely prescribed across cardiovascular indications, yet their real-world cardiovascular adverse-event profiles across drug generations remain incompletely characterized in large pharmacovigilance datasets. Objective: To compare the cardiovascular safety profiles of atenolol, bisoprolol and nebivolol using the FDA Adverse Event Reporting System (FAERS). Methods: Retrospective disproportionality analysis of FAERS reports via OpenVigil 2.1, covering each drug’s available reporting history through January 1st, 2026. Cardiovascular events were identified with Standardized MedDRA Queries; signals were assessed with the Reporting Odds Ratio (ROR, 95% CI) and Information Component (IC) under Evans’ criteria. Individual case safety reports were analysed for demographics, seriousness and outcomes. Results: Atenolol was most strongly associated with bradycardia (ROR = 10.513) and left ventricular hypertrophy (ROR = 6.765). Bisoprolol showed the highest signals for diastolic dysfunction (ROR = 24.875), atrial tachycardia (ROR = 23.283) and chronic cardiac failure (ROR = 23.222), together with the highest bradycardia-associated mortality (14.9%). Nebivolol had the lowest overall reporting burden, though counts are not exposure-adjusted; its strongest signals were bradycardia (ROR = 9.619) and coronary artery stenosis (ROR = 9.351), with lower bradycardia mortality (12.6%). Pediatric reports (0–17 years) occurred for all three agents at similar proportions, none FDA-approved in this group. Reports predominantly involved older adults (60–89 years), with a substantial proportion classified as serious. Conclusion: All three agents generated significant signals across a broad range of cardiovascular events, with nebivolol showing the most favourable profile. Because FAERS disproportionality cannot establish causality, these hypothesis-generating findings may inform beta-blocker selection in older or higher-risk patients, particularly those prone to bradyarrhythmias or diastolic dysfunction, pending prospective confirmation.

Bortezomib is a 26S proteasome inhibitor used to treat multiple myeloma and systemic amyloidosis. While effective in prolonging survival, bortezomib has been increasingly associated with cardiovascular adverse events (CVAEs), such as cardiac failure and arrhythmias. However, a comprehensive post-marketing safety profile has not been fully established. We analyzed cardiovascular adverse events reported between May 2003 and May 2025 using the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) via the Open Vigil 2.1 platform. Disproportionality analysis was conducted using the reporting odds ratio (ROR) with 95% confidence intervals (CI) to detect statistically significant adverse reports. Of over 9 million drug-related adverse events in the FAERS database, 552 Cardiac events were linked to bortezomib. Cardiac amyloidosis showed the strongest association (ROR: 35.58; 95% CI: 28.16–44.95), followed by atrial flutter (ROR: 4.34; 95% CI: 3.41–5.52), left ventricular dysfunction (ROR: 4.25; 95% CI: 3.26–5.55), cardiac failure, acute (ROR: 3.66; 95% CI: 2.75–4.86), congestive cardiomyopathy (ROR: 3.23; 95% CI: 2.33–4.49), hypertrophic cardiomyopathy (ROR: 3.44; 95% CI: 1.95–6.08), cardiac failure (ROR: 3.18; 95% CI: 2.93–3.46), cardiomyopathy (ROR: 2.81; 95% CI: 2.30–3.43), atrial fibrillation (ROR: 2.65; 95% CI: 2.43–2.89), right ventricular failure (ROR: 2.30; 95% CI: 1.63–3.24), myocarditis (ROR: 2.25; 95% CI: 1.73–2.91), and supraventricular tachycardia (ROR: 2.17; 95% CI: 1.61–2.93). cardiac failure led to the highest number of hospitalizations (301) and deaths (208), followed by atrial fibrillation and cardiac amyloidosis. Older adults (≥65 years) and patients with amyloidosis or myeloma were the most vulnerable groups. Bortezomib is associated with a wide spectrum of serious cardiac adverse events, with cardiac amyloidosis and cardiac failure demonstrating particularly high disproportionality and mortality. These findings emphasize the need for routine cardiovascular risk assessment and proactive monitoring in high-risk patient populations receiving bortezomib.