Treatment of peripheral artery disease (PAD) is difficult on its own, particularly in more severe cases, but becomes exceedingly costly and complex in patients in risk groups and affected with comorbid conditions. Good examples of those are diabetes mellitus and chronic kidney disease (CKD). There is a certain overlap between the two since diabetes is a significant risk factor for CKD and many patients have both diseases. However, even on its own, CKD is associated with challenges in accurately and timely detecting PAD, leading to greater cardiovascular and all-cause mortality.
In this blog you will learn:
- Differences/similarities between ABI and TBI
- Correlation between ABI and TBI scores and mortality in patients CKD
What are the differences/similarities between ABI and TBI?
There are several methods for diagnosing PAD currently in use, from various questionnaires of questionable accuracy and reliability to MRI angiography. Ankle-Brachial Index (ABI) measurement is somewhere in between and is generally regarded as the go-to method for screening for PAD in general practice. Its main advantages are low cost, convenience, and speed, if performed with an oscillometric-plethysmographic device. However, it does have certain drawbacks.
ABI has limited diagnostic value in patients with incompressible arteries. Medial arterial calcification is most often found in individuals with diabetes, rheumatoid arthritis, and of course, renal insufficiency. In practice, this translates to an unusually high ABI score (generally in the ≥1.30 or 1.40 range) due to the need for higher cuff pressures to achieve compression of the measured artery. Fortunately, calcification rarely affects toe arteries, which makes them suitable for measuring blood pressure, although with different equipment than the one used for ABI.
This new diagnostic method is, therefore, named the Toe-Brachial Index (TBI). Briefly, it shares some similarities with the ABI method. However, it uses considerably smaller pressure cuffs for measuring blood pressure at the toe, and the calculated numerical values are lower than those in ABI (normal TBI is generally ≥0.7). However, like ABI, it has diagnostic value beyond diagnosing PAD. Low TBI is, for example, associated with increased risk of recurrent cardiovascular disease (CVD) in patients with type 2 diabetes and progression of diabetic nephropathy in type 2 diabetics. Combined with ABI, it may even have better diagnostic value than by itself, particularly in patients with CKD.
What is the correlation between ABI and TBI scores and mortality in patients CKD?
The TBI is generally recommended for use only in patients with very high ABI (>1.4); those with definite incompressible arteries. However, this utilisation of TBI fails to address the problem of coexisting PAD and medial artery calcification and normal ABI values. Of course, such patients are not given a TBI or other non-ABI assessment, resulting in non- or late diagnosis with obvious adverse outcomes. Some have noted that these individuals may have a relatively wide difference between ABI and TBI and that the difference between the two values may be a clinically significant diagnostic value.
A prospective cohort study aimed to prove this hypothesis. It enrolled 471 patients with clinical suspicion for PAD who were given a TBI and ABI assessment between 1990 and 1994 and were followed up through 2001 to ascertain the outcome for each of them. All participants were given both an ABI and TBI assessment, had their creatinine levels measured (for calculation of kidney function) and had at least one CVD risk factor (diabetes, hypertension, smoking, and high body mass index).
It should be noted that the researchers’ hypothesis was multidimensional. They hypothesised that high ABI-TBI rather than low ABI-TBI values would be associated with higher all-cause mortality, particularly in patients with an ABI lower than 0.9. Additionally, they suspected the presence of CKD would have a negative effect on this association in the light of the fact that individuals with CKD are especially at risk for high and low values of ABI. Moreover, in formulating their hypothesis, they drew from their experience in another study that demonstrated that low TBI was associated with increased mortality risk in patients undergoing dialysis.
It should, therefore, come as no surprise that the results of the study generated statistically significant differences in mortality rates between patients with CKD and those without. Diagnosis of CKD and higher than median ABI-TBI value was associated with a 79% increased risk in all-cause mortality (unadjusted model). Even when adjusted for age, demographic and clinical characteristics, researchers noted a nearly 40% increase in risk.
Researchers have also noted that greater than median values of ABI-TBI (and mortality) were, in general, identified in significantly older patients, and those with diabetes and poor kidney function. Further study of ABI-TBI is still needed, on a broader scale and encompassing a more diverse demographic range, to validate its clinical utility. However, the preliminary findings are promising and may even lead to the inclusion of ABI-TBI in vascular laboratory reports as another important variable.
Since patients with CKD are more likely to have both PAD and incompressible arteries, they should be given both an ABI and TBI assessment regardless of whether their ABI score is in the normal range. Additionally, a high ABI-TBI value is likely associated with higher all-cause mortality in patients with CKD.