Antonio Orlando

The global spread of micro- and nanoplastics (MNPs) has emerged as an environmental and medical concern, with growing evidence of their role in cardiovascular disease (CVD). These particles, originating from the degradation of larger plastics and consumer products, can be ingested or inhaled, cross biological barriers, and accumulate in human tissues, including blood, myocardium, and atherosclerotic plaques. Experimental and clinical studies suggest that MNPs contribute to CVD through multiple mechanisms: activation of systemic inflammation and inflammasomes, oxidative stress, endothelial dysfunction, prothrombotic activity, and direct myocardial injury, ultimately promoting fibrosis and impaired contractility. Epidemiological data further indicate that populations exposed to higher plastic pollution or with pre-existing cardiovascular risk factors may be particularly vulnerable. Taken together, these findings identify MNPs as a potential novel environmental cardiovascular risk factor. Advancing detection methods, mechanistic research, and public health strategies will be essential to mitigate their impact and reduce plastic-related cardiovascular burden.

Background: In systemic sclerosis (SSc), cardiac involvement is frequent, heterogeneous, and related to a poor prognosis. Due to a longer life expectancy, the development of degenerative aortic stenosis (AS) is not uncommon. The aim of this article is to report the characteristics of AS in SSc, analyzing the rate of progression, the management, and the outcome. Methods: This is a case series conducted at the Department of Cardiology of Monaldi Hospital, Naples, Italy. Results: From January 2007 to December 2022, we analyzed 234 patients with SSc. Ten/234 patients (4.3%) showed severe AS and were included in the analysis (age 75.5 years [IQR 58–84], nine females). Nine had limited and one diffuse SSc. Two patients were in NHYA/WHO II and eight in NYHA/WHO III. All had degenerative three-leaflet AS. Two patients showed severe AS at the first evaluation, and eight developed severe AS during the follow-up, with a time progression from moderate to severe AS of 3.2 ± 1.1 years (progression rate −0.190 ± 0.012 cm²/year for aortic valve area, 8.6 ± 6.1 mmHg/year for mean aortic gradient, 16 ± 7 mmHg/year for peak aortic gradient, and 0.5 ± 0.3 m/s/year for aortic peak velocity). Seven out of 10 patients underwent transcatheter aortic valve implantation (TAVI), one underwent surgical aortic valve replacement (SAVR), one was left untreated, and one was on a waiting list for TAVI. No major complications after TAVI or SAVR occurred. At a mean follow-up of 5.9 ± 3.9 years, eight patients are alive and two died. Conclusion: Severe AS is a relevant cardiac complication of SSc and must be considered in the screening and during the follow-up. Its rapid progression rate may tentatively be due to autoimmunity, degenerative burden, and chronic inflammation.