Providing independent clinical excellence since 2005
Posted on Friday December 19, 2025 in Metabolic Health
An article written by Dr Edward Leatham, Consultant Cardiologist © 2025 E.Leatham
Tags: VAT, Metabolic Health, Stent search website using Tags to find related stories.
When a coronary stent is implanted, the immediate problem—an obstructed artery—is treated. Blood flow improves, symptoms often settle, and the procedure is labelled a success. But a stent treats a local narrowing, not the systemic biology that caused it. For some patients, that biology increases the risk of the artery narrowing again—a process known as in-stent restenosis (ISR).
One of the most important and overlooked contributors to ISR is metabolic health, particularly insulin resistance driven by visceral fat.
ISR is not simply scar tissue. It represents an exaggerated vascular healing response to arterial injury, characterised by:
Despite major advances in drug-eluting stent (DES) technology, ISR still occurs—especially in certain biological states¹².
One group has consistently higher risk across all stent eras: patients with diabetes³,⁴.
Large registries and pathological studies show that patients with diabetes have:
Classic intravascular ultrasound studies demonstrated that the excess restenosis seen in diabetes is due to exaggerated intimal growth, rather than stent under-expansion or recoil⁵.
Importantly, this increased risk persists even with modern DES, indicating that diabetes reflects an underlying biological driver rather than a stent-related issue⁶.
Diabetes is the visible end-stage. The process usually begins years earlier with insulin resistance and compensatory hyperinsulinaemia.
This matters because insulin is not just a glucose-lowering hormone—it is also a growth and repair signal within the vascular wall.
Clinical studies have shown that:
These findings suggest that the artery is responding to injury in a pro-proliferative metabolic environment.
ISR is driven largely by vascular smooth muscle cell (VSMC) behaviour. Insulin resistance and hyperinsulinaemia amplify this process by:
Experimental work supports causality: animal models lacking insulin receptors on vascular smooth muscle cells develop less intimal hyperplasia after vascular injury, directly implicating insulin signalling in restenosis biology⁹.
Many patients with insulin resistance do not appear “obese” by BMI standards. The key issue is where fat is stored.
Visceral adipose tissue (VAT)—fat stored deep around the organs—is:
A simple screening tool is waist-to-height ratio:
Waist circumference ÷ height
A ratio >0.5 suggests excess visceral fat¹¹
For patients with a history of stenting, this measurement provides critical information that cholesterol and glucose tests may miss.
When imaging (CT, DEXA, MRI) or consistent anthropometric data confirm high VAT, several things become likely:
This helps explain why some patients experience ISR or progressive coronary disease despite optimal procedural results and guideline-based therapy.
GLP-1 receptor agonists are often discussed as weight-loss drugs. In cardiovascular medicine, that framing is incomplete.
GLP-1 mimetics:
Although trials have not been designed specifically with ISR as a primary endpoint, the biological rationale is strong: reducing visceral fat and insulin resistance addresses the upstream drivers of restenosis.
This mirrors earlier preventive strategies—such as statins—where mechanistic benefit preceded formal ISR-specific trial endpoints.
If you have had a coronary stent:
If visceral fat is confirmed, management should extend beyond antiplatelets and cholesterol lowering. Alongside lifestyle change, targeting insulin resistance and VAT—including consideration of GLP-1 therapy—may reduce future risk.
If you’ve had a stent, checking your waist may be one of the most important follow-up steps you take.
In cardiometabolic medicine, muscle is not a cosmetic tissue but a metabolic organ. Evidence consistently shows that strength, not muscle mass, predicts insulin resistance, cardiovascular risk, and survival. Many older adults are not losing muscle tissue — they are losing muscle function, and that is the pathology that matters.
The hallmark feature of OSA is the repetitive cycle of breathing cessation followed by gasping or choking as the body attempts to restore airflow. These disruptions can occur multiple times throughout the night, impacting the individual's overall sleep quality and daytime functioning.
Carbohydrate Sensitive Phenotype (CSP) is not a diagnosis of diabetes or obesity. Rather, it’s a biologically driven pattern of visceral fat accumulation and carbohydrate intolerance which is highly prevalent in those with a raised waist-to-height ratio (WHtR > 0.5), triggered by aging, Western-style diet and lifestyle. More importantly, CSP gives individuals a name for their experience—one that invites support instead of judgement, and allows them to engage with food and health choices free from social shame.
I feel passionately that medicine has to change due to rising costs, complexity and manpower issues. Doctors and influencers need to get patients to take charge of their own health. My job has morphed from 'fixing broken hearts' to, quite literally, preventing them from getting broken in the first place.