Category: 8. Health

Air pollution exposure can be a key contributing factor to increasingly diffuse myocardial fibrosis, according to cardiac magnetic resonance imaging (MRI) findings from a new study.

For the retrospective study, recently published in Radiology, researchers reviewed cardiac MRI data for 694 patients (mean age of 47), including 493 people with dilated cardiomyopathy (DCM) and 201 people with normal cardiac MRI.

In a multivariable analysis, the study authors found that for patients with DCM, each 1 µg/m³ increase in one-year mean exposure to ambient fine particulate matter with 2.5-µm or smaller aerodynamic diameter (PM_2.5) corresponded to a 30 percent higher native T1 z score.

The researchers also noted that each 1 µg/m³ increase in one-year mean exposure to PM_2.5 was associated with a 27 percent higher native T1 z score in people with normal cardiac MRI findings.

“In line with other studies, our results indicate that adverse effects of fine particulate air pollution on the heart are observed at exposures below current air quality guidelines, reinforcing that there are no safe exposure limits. Our results bolster evidence that air pollution is a modifiable risk factor for cardiovascular disease,” noted study co-author Kate Hanneman, M.D., MPH, FRCPC, an associate professor and vice chair of research with the Department of Medical Imaging at the University of Toronto, and colleagues.

Late gadolinium enhancement (LGE) was 25 percent more likely for each 1 µg/m³ increase in one-year mean exposure to PM_2. in patients with DCM, according to the study authors.

The researchers also found that the association between ambient PM_2.5 exposure and native T1 z scores was particularly prevalent among women (β coefficient of 49 percent), people with hypertension (β coefficient of 48 percent) and smokers (β coefficient of 43 percent).

“Myocardial fibrosis is irreversible; therefore, it is imperative to implement measures to reduce exposure to long-term air pollution, especially in the most vulnerable patients,” emphasized Hanneman and colleagues.

In an accompanying editorial, Davis M. Vigneault, M.D., D.Phil, said the study builds upon previous biochemical and epidemiological studies demonstrating elevated cardiovascular risks with air pollution exposure.

“… This study provides new and compelling evidence for a potential pathologic mechanism by which fine particulate matter pollution increases cardiovascular risk, tying together biochemical evidence implicating PM2.5 in the induction of myocardial fibrosis with epidemiologic evidence associating PM2.5 with morphologic changes and increased cardiovascular morbidity and mortality,” wrote Dr. Vigneault, who is affiliated with the Department of Radiology at the Stanford University School of Medicine in Stanford, Ca.

(Editor’s note: For related content, see “Could Cardiac MRI Improve Risk Stratification in Patients with Dilated Cardiomyopathy?,” “Stress Cardiovascular MRI: What a New Meta-Analysis Reveals” and “Multimodal AI with CCTA and MRI Data Shows Promise in Predicting MACE in Patients with Obstructive CAD.”)

Beyond the inherent limitations of a single-center retrospective study, the study authors conceded possible differences with respect to the timing of exposure to PM_2.5, and potentially unknown confounding factors that may have affected the results. The researchers acknowledged that indoor PM_2.5, ozone and nitrogen dioxide exposures were not assessed. They also noted that the COVID-19 pandemic occurred within the study period.

A study involving 76 primary care practices in Colorado explored two different approaches to initiating continuous glucose monitor (CGM) use with their diabetic patients.

The study from the University of Colorado Anschutz Medical Campus was published in BMC Primary Care. Some practices chose a self-guided option using educational tools developed by the American Academy of Family Physicians. Others referred patients to a virtual CGM initiation service run by a team of primary care-based healthcare professionals who were part of the research team.

Practices with in-house diabetes care and education specialists, formerly known as diabetes educators, were more likely to choose the self-guided route, while those without specialists preferred the study’s virtual service. Other than this difference, the practices were largely similar.

The researchers found that practices had success with both models in boosting use of CGM. 
“This is great news for people with diabetes, especially those who don’t have easy access to a diabetes specialist,” said Kimberly Wiggins, M.A., M.Ed, the lead author on the study, in a statement. “It shows that novel approaches can be developed to share resources, including diabetes care and education specialists, to start patients on CGM and then transition them back to their primary care practice.”

Despite their potential benefits, fewer than half of primary care doctors in the United States have ever prescribed a CGM.

“Our goal was to find practical approaches to help primary care clinics offer CGMs to their patients,” said Tamara Oser, M.D., senior author of the study and professor, in a statement. Oser is director of the Primary Care Diabetes Lab in the Department of Family Medicine at the University of Colorado School of Medicine. “We found that both methods worked. Even clinics without in-house diabetes experts were able to successfully offer CGM by using the remote option.”

Oser noted that this is now the standard of care for many people with type 1 or type 2 diabetes, no matter where they live or what kind of clinic they go to. “This is another huge step in better treatment for the 38 million people living with diabetes in the U.S.,” she added. 

Imperceptible electrical signals delivered to the brain can improve college students’ mathematics skills, a new study has found.

The researchers say that the technology is not far from being ready for at-home use — though one expert emphasized that more research is needed.

In a new study published in Science Signaling titled, “Restoration of striatal neuroprotective pathways by kinase inhibitor treatment of Parkinson’s linked-LRRK2 mutant mice,” researchers from Stanford University and University of Dundee have shown that inhibition of a specific enzyme may rescue neurons that are dying due to a type of Parkinson’s disease that is caused by a single genetic mutation in a mouse model. 

About 25% of Parkinson’s disease cases are caused by genetic mutations. Activating mutations in leucine-rich repeat kinase 2 (LRRK2) is one of the most common Parkinson’s associated mutations. Overactive LRRK2 leads to the loss of primary cilia in neurons which disrupts crucial communication that makes the neurotransmitter dopamine.  

Overactive LRRK2 can be mitigated using MLi-2 LRRK2 kinase inhibitor. Given that the genetic mutation is not the only mechanism of overactive LRRK2, the inhibitor treatment might help with other types of neurodegenerative diseases. 

“Findings from this study suggest that inhibiting the LRRK2 enzyme could stabilize the progression of symptoms if patients can be identified early enough,” said Suzanne Pfeffer, PhD, professor of biochemistry at Stanford and corresponding author of the study. 

In a healthy brain, many messages are sent between dopamine neurons in the substantia nigra and the striatum. This signaling is possible because dopamine neuron axons reach the striatum to communicate with neurons and glia. 

Dopamine neurons release Sonic Hedgehog (Shh), a signaling protein critical for brain development and function, which plays a key role in cell growth, differentiation, and the formation of neural circuits. In a healthy brain, Shh causes certain neurons and astrocytes in the striatum to produce proteins called neuroprotective factors. Overactivation of LRRK2 disrupts Shh signaling and lowers neuroprotective factor production. 

Results showed that three month-dietary administration of MLi-2 LRRK2 kinase inhibitor to mice restored primary cilia and Shh responsive production of neuroprotective factors. In addition, indicators of the density of dopamine nerve endings within the striatum doubled, suggesting an initial recovery for neurons that had been in the process of dying. The findings potentially offer an avenue to improve, not just stabilize, the condition of patients with Parkinson’s disease. 

“Many kinds of processes necessary for cells to survive are regulated through cilia sending and receiving signals,” Pfeffer explained. “We think that when cells have lost their cilia, they are also on the pathway to death because they need cilia to receive signals that keep them alive.” 

The earliest symptoms of Parkinson’s disease begin about 15 years before a patient notices a tremor. Pfeffer said the hope is that people who have the LRRK2 genetic mutation can start a treatment that inhibits the enzyme as early as possible. 

Looking ahead, the research team will test whether other forms of Parkinson’s disease not associated with the LRRK2 genetic mutation could benefit from this type of treatment. 

“We are so excited about these findings. They suggest this approach has great promise to help patients in terms of restoring neuronal activity in this brain circuit,” Pfeffer said. “There are multiple LRRK2 inhibitor clinical trials underway, and our hope is that these findings in mice will hold true for patients in the future.” 

A scientific team from the University of Liège has just developed an innovative polymer, PHOx, which could significantly improve the safety of implantable medical devices, while being more environmentally friendly. This invention is the subject of an international patent application.

Every year, millions of patients receive medical devices inserted or implanted in the cardiovascular system: arterial and venous catheters, cardiac devices, pacemaker leads, artificial hearts, vascular prostheses, etc. These devices, often made from polyurethane (PU), perform vital functions, but are not without defects. PU production relies on toxic chemicals called isocyanates, and PU is also partly responsible for serious complications in patients, such as blood clots and infections.

Faced with these limitations, a team of chemists and cardiologists at the University of Liège has come up with a promising alternative: PHOx, a thermoplastic elastomer without isocyanate PU (NIPU), which is therefore less toxic to produce and much better tolerated by the human body.

“PHOx (Poly Hydroxy-Oxazolidone) is a flexible, transformable plastic that can be moulded, pressed, spun into fibres or 3D printed,” explain Anna Pierrard and Christine Jérôme, chemists. It can thus be used to produce a variety of personalised medical devices. Better still, its manufacture is based on ‘greener’ raw materials, derived in particular from carbon dioxide, reducing the environmental impact of the process.

Extensive laboratory tests have shown that PHOx outperforms PU in several key respects,” enthuse Sofia Melo, bioengineer, and Cécile Oury, Head of the Cardiology Laboratory at ULiège.” PHOx is more compatible with blood. In particular, it reduces the adhesion of platelets (essential cells in the formation of blood clots) and the activation of coagulation, limiting the risks of clot formation. It is also thought to inhibit the adhesion of bacteria such as staphylococcus aureus, which is often implicated in implant infections. No toxicity was observed, either for human cells or during implantation, and the material did not cause excessive inflammation, degradation or rejection.

3D printable implants

Another major advantage of PHOx is that it can be easily 3D printed. “This means that we could eventually produce custom-made devices for each patient, reducing waste and at lower cost,” explains Patrizio Lancellotti, Head of Cardiology at Liège University Hospital.” Tailor-made implants, heart valves adapted to the anatomy of each individual: the applications are numerous.

Thanks to its mechanical (flexibility, strength) and biological (biocompatibility, compatibility with blood, stability) properties, PHOx could well replace PUs in many medical applications. This is a major step towards medical devices that are safer for patients, more environmentally friendly, and potentially more economical thanks to customised manufacturing and reduced healthcare costs associated with fewer complications.

The researchers stress that this is the first time that a NIPU (non-isocyanate polyurethane) material has demonstrated such performance in critical medical applications. An international patent application (WO2025082761) has already been filed.