Semaglutide Has Found Its STRIDE
A Common Comorbidity
T2D and PAD are not strangers to one another; patients with T2D are twice as likely to develop PAD compared with the general population. PAD has been shown to be the most common initial manifestation of cardiovascular disease in T2D. Moreover, patients with diabetes foot complications fear amputation and infection more than death.
However, PAD is underrecognized in T2D; only around 20% of patients present with the classical symptoms of intermittent claudication (IC). PAD also has insidious onset: Patients experience slow functional decline and leg discomfort, which is often not recognized as PAD by healthcare professionals or patients.
T2D and PAD are growing in incidence and share many risk factors, including obesity. A recent systematic literature review exploring the epidemiology and burden of PAD in T2D found that 12.5%-22% of patients with T2D had comorbid PAD. Furthermore, patients with T2D and PAD have a very high risk for major lower-limb complications and major adverse cardiovascular events, including all-cause and cardiovascular mortality. Unsurprisingly, PAD was associated with poor quality of life and significant healthcare use and costs.
Notably, the ADA 2025 Standards of Medical Care in Diabetes now recommends screening for PAD using ankle-brachial index (ABI) testing in asymptomatic patients with diabetes aged > 65 years, microvascular disease in any location, or foot complications or any end-organ damage from diabetes if a PAD diagnosis would change management. PAD screening should also be considered in patients with diabetes duration > 10 years and high cardiovascular risk.
PAD in T2D is often recalcitrant to surgical intervention because it tends to affect the distal vasculature (that is, the infrapopliteal vessels). These lesions are less amenable to traditional revascularization procedures such as femoropopliteal bypass and stenting. Unfortunately, this circumstance often leaves patients with T2D and PAD with persistent debilitating symptoms and few surgical options.
Many international medical guidelines have class I recommendations to consider SGLT2 inhibitors and GLP-1 RAs for patients with T2D and atherosclerotic cardiovascular disease, though not specifically PAD. The only class I recommendation in PAD is for cilostazol for improving claudication symptoms. Cilostazol is a phosphodiesterase 3 inhibitor that promotes vasodilation and increased blood flow, which can improve symptoms of IC (but not cardiovascular outcomes). A recent Cochrane review found that cilostazol resulted in only a 40 m improvement in absolute claudication distance. From my clinical experience, cilostazol is often poorly tolerated (headache and diarrhea are common). It is contraindicated in heart failure, which frequently occurs with PAD.
STRIDE Results
The randomized controlled STRIDE trial was published in the Lancet in May 2025 and explored the impact of subcutaneous semaglutide (1 mg weekly) plus standard of care, compared with placebo, on walking capacity in patients with symptomatic PAD and T2D. In essence, STRIDE has laid the foundation for a paradigm shift in how we use GLP-1 RAs for symptomatic PAD.
The trial recruited 792 patients with T2D and Fontaine stage IIa PAD. Fontaine stage IIa is early-stage symptomatic PAD, in which patients experience symptoms of IC after walking more than 200 m. Mean ABI was ≤ 0.9 in all participants; a normal ABI is typically 0.90-1.30 and indicates normal blood flow to the lower limbs. One-quarter of participants were female, and median age was 68 years. Obesity was not a criterion for study enrollment; 35% of participants had a BMI < 27. The primary outcome of the study was maximum walking distance after 52 weeks compared with baseline.
STRIDE achieved its primary outcome. Subcutaneous semaglutide was associated with a significantly increased maximum walking distance (40 m improvement on a 12% incline, which is equivalent to 80 m improvement on a flat surface). This improvement is double that associated with cilostazol and, importantly, was confirmed to be clinically meaningful. The researchers also observed significantly improved symptoms and quality of life, as evidenced by improvements in the VascuQoL questionnaire. Notably, the reported improvements in ABI and disease progression confirm the vascular benefits of semaglutide. Encouragingly, clinical benefits persisted even 5 weeks after stopping semaglutide therapy. The treatment's safety profile was consistent with previous semaglutide trials, and no unexpected safety findings emerged.
New data presented and simultaneously published in Diabetes Care confirmed that the effect of semaglutide on maximum walking distance was consistent, irrespective of T2D characteristics; benefits were independent of baseline diabetes duration, BMI, HbA1c, or concomitant use of sodium/glucose cotransporter 2 inhibitors or insulin. Functional benefits did not appear to correlate with weight loss or glycemic improvement, again highlighting the vascular benefits of semaglutide in reducing atherosclerosis, possibly through an anti-inflammatory effect.
In conclusion, STRIDE increases the suite of recognized cardiometabolic and renal benefits of semaglutide by adding improved walking capacity, quality of life, and disease progression for patients with T2D and PAD. During my resident year as a junior doctor, my vascular consultant always reminded me of the core management of PAD in five words: 'stop smoking and keep walking.' While this remains the cornerstone of management 25 years later, semaglutide is now well positioned as a foundational therapy to improve quality and quantity of life in patients with T2D and PAD.
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