Shopping carts are the next frontier in cardiac health and stroke prevention

[July 10, 2023: Staff Writer, The Brighter Side of News]

In a novel approach to preventative healthcare, grocery shopping might soon be accompanied by heart health checks. An innovative device, seamlessly incorporated into the handle of a supermarket cart, could revolutionize the way we monitor for atrial fibrillation, a pervasive heart arrhythmia associated with an increased risk of stroke.

Atrial fibrillation (AF), the most common heart disorder worldwide, is characterized by chaotic, irregular beating in the heart's upper chambers (the atria), disrupting their synchronization with the lower chambers (the ventricles).

Notably, the disorder can manifest episodically or exist permanently. In many cases, affected individuals remain unaware of their condition, compounding the risks involved. AF's core issue lies in its propensity to instigate blood clot formation within the heart, escalating the risk of stroke by five times.

The breakthrough device, dubbed MyDiagnostick, emerges from Liverpool John Moores University in the UK. Its design is deceptively simple - a cylindrical tool capable of recording a single-lead electrocardiogram (ECG) tracing when a shopper's hands engage with the metallic electrodes.

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MyDiagnostick utilizes internal software to analyze the ECG over a one-minute period while the contact is preserved. The inventors' intention to integrate the device discreetly into the everyday lives of potential users led them to embed it into supermarket cart handles, making heart checks part and parcel of routine grocery shopping.

The research team put the device to test through the SHOPS-AF study, in which 2,155 participants agreed to use the modified cart. The study's procedure involved the participant holding the handle for at least 60 seconds, after which a green light would indicate no detection of an irregular heartbeat.

As a fail-safe, researchers manually checked the individual's pulse in tandem. In instances where the device detected an irregular heartbeat, a red light would flash, and an in-store pharmacist would conduct manual and additional device checks. Cardiologists reviewed any ECGs associated with a red-light indication.

Participants received prompt feedback - either a clean bill of health, an invitation to repeat unclear ECG results, or, if AF was detected, a scheduled cardiologist appointment within a fortnight.

Out of the 220 ECG readings that triggered a red light, AF was ruled out in 115 cases upon review by a cardiologist, 46 results were unclear, and AF was diagnosed in 59 participants. Interestingly, 39 of these were previously undiagnosed cases.

The study's lead author, Ian Jones, spoke of the vast potential of such a device in preventative healthcare. "This study shows the potential of taking health checks to the masses without disrupting daily routines," Jones said. "Over the course of two months, we identified 39 patients who were unaware that they had atrial fibrillation. That's 39 people at greater risk of stroke who received a cardiologist appointment."

The current version of MyDiagnostick boasts a sensitivity level exceeding 94%, although its accuracy necessitates further refinement. The study noted a high frequency of false positives, with only a quarter to a half of red-light indicators actually being AF cases.

Additionally, the current algorithm missed around half of actual AF cases, signaling a significant number of false negatives. While the researchers plan to address these issues, they remain pleased with the willingness of the study participants to engage with the device.

"Nearly two-thirds of the shoppers we approached were happy to use a trolley, and the vast majority of those who declined were in a rush rather than wary of being monitored," Jones reported. "This shows that the concept is acceptable to most people and worth testing in a larger study. Before we conduct SHOPS-AF II, some adjustments are needed to make the system more accurate."

The research team maintains that having immediate access to a healthcare professional is crucial to MyDiagnostick's success. "Checking for atrial fibrillation while people do their regular shopping holds promise for preventing strokes and saving lives," Jones stated. "A crucial aspect is providing immediate access to a health professional who can explain the findings and refer patients on for confirmatory tests and medication if needed."

The team presented their groundbreaking findings at the Annual Congress of the Association of Cardiovascular Nursing and Allied Professionals (ACNAP) 2023, held in Edinburgh, Scotland. This innovative approach could soon become a cornerstone of proactive heart health management, taking preventative medicine directly to the masses, embedded in their everyday routines.

The study was published in the Journal of Personalized Medicine.

As humans, our bodies have a remarkable knack for self-repair and self-maintenance. But in the case of certain vascular diseases, this ability gets commandeered into a self-sustaining cycle of damage and inflammation.

The mechanism responsible for this damaging transformation is known as endothelial-to-mesenchymal transition (EndMT). In the process of EndMT, the cells lining the insides of our blood vessels—known as endothelial cells—undergo a radical phenotype change and begin expressing genes that lead to chronic inflammation.

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This scientific breakthrough was led by Michael Simons, MD, a professor of medicine specializing in cardiology at Yale University. Simons and his team identified an enzyme called ACSS2 as the key player in EndMT, which can perpetuate the long-standing tissue inflammation that drives vasculature disease.

Their findings, published in the prestigious journal Cell Metabolism, show that by selectively neutralizing this enzyme, the progression of atherosclerosis—a disease driven by EndMT—was dramatically reduced in mice.

"Through our research, we've unearthed the underlying driver that makes these diseases stimulus-independent. If we eliminate this driver, we have the potential to reverse diseases once deemed intractable, offering treatment alternatives that do not currently exist," said Michael Simons.

Michael Simons co-led this groundbreaking study with Zoltan Arany, MD, PhD, the Samuel Bellet Professor of Cardiology at the University of Pennsylvania’s Perelman School of Medicine. Simons explained the pervasive and relentless nature of such diseases, stating, “We have a group of diseases that once started, continue to advance even if you eliminate the offending stimulus.”

Every organ in the human body relies on the vascular system for oxygen, nutrients, and physiological maintenance. Consequently, abnormalities in the vasculature often translate into a myriad of chronic diseases. Simons' lab focuses on elucidating the relationship between vascular abnormalities, diseases, and aging.

This study was the result of their relentless investigation into EndMT, a process they were among the first to discover and whose involvement they identified in conditions such as atherosclerosis, peripheral vascular disease, heart attacks, and pulmonary hypertension.

EndMT instigates abnormalities in endothelial cells that lure in inflammatory stimuli like white blood cells. Simons describes this phenomenon, saying, "Under normal conditions, these cells would just pass by, but now they halt, infiltrate the tissues, and begin secreting inflammatory cytokines." Unfortunately, once initiated, this process has proven to be irreversible. "Every endeavor to cure diseases with this underlying chronic inflammatory process has met with failure," laments Simons.

But the journey to unraveling the secrets of EndMT is a complex one, due in part to the role of TGF-β signaling. This signaling mechanism, which regulates many cellular functions, has an unusual dual nature—it promotes inflammation in endothelial cells while suppressing it in virtually all other cell types. This stark contrast in behavior makes it dangerous to use systemic agents to block the process, as they could end up causing more harm than good.

During the team's intensive research, they uncovered intriguing metabolic peculiarities about endothelial cells. Unlike most other cells that use fat as a primary energy source, endothelial cells heavily depend on sugar. Additionally, they undergo considerable gene expression changes during EndMT, which likely have metabolic roots. This led the team to question whether a unique metabolic underpinning could be linked to EndMT, which could in turn provide a new therapeutic target.

They began their exploration by studying the metabolic alterations that TGF-β signaling initiated in endothelial cells. To their surprise, the signaling led to the cells producing an abundance of a molecule known as acetyl-CoA (Ac-CoA). Intrigued, the team traced the source of this sudden influx of Ac-CoA and stumbled upon another unexpected discovery. "A large part of the Ac-CoA came from acetate—a small metabolite typically produced by gut bacteria and rarely used to create Ac-CoA," recounts Arany.

The plot thickened when the team discovered that acetate was not produced by gut bacteria in this instance. Instead, it was being synthesized from sugar by the endothelial cells themselves, which then used it to manufacture a significant part of their Ac-CoA. While Ac-CoA is typically known as a major source of energy, it played a different role in the context of EndMT. Instead of providing energy, it served as a source of acetyl-groups that stabilized the expression of TGF-β signaling molecules.

In a normal scenario, endothelial cells remain unresponsive to the surrounding TGF-β in the blood and tissues due to the low expression of the TGF-b receptor. However, when excessive acetyl-groups originating from Ac-CoA bind to the TGF-β receptor, a dramatic increase in its expression ensues. This, in turn, exposes the now abundant receptors on the endothelial cells to the harmful TGF-β stimulus. The team also discovered that the enzyme ACSS2 was essential for the synthesis of Ac-CoA in endothelial cells.

The final challenge lay in applying these findings to a real-world scenario. The team experimented on mice with atherosclerosis, and upon deleting the ACSS2 gene, they noticed a drastic reduction in the progression of the disease. This significant finding positions ACSS2 as a promising target for therapeutics aimed at EndMT.

"We aim to utilize this discovery to develop new therapies and translate those therapies in vivo," says Simons with a glimmer of hope. This research represents a significant stride towards understanding and potentially reversing vascular diseases that were previously deemed incurable. As we move forward in scientific progress, it's these moments of breakthrough and perseverance that bring us closer to overcoming our greatest health challenges.

Note: Materials provided above by The Brighter Side of News. Content may be edited for style and length.

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