Author + information
- William R. Hiatt, MD∗ ()
- ↵∗Reprint requests and correspondence:
Dr. William R. Hiatt, University of Colorado School of Medicine, C/O CPC Clinical Research, 13199 E. Montview Boulevard, Suite 200, Aurora, Colorado 80045.
- ankle-brachial index
- diagnostic testing
- heart failure
- peripheral artery disease
- peripheral vascular disease
In this issue of JACC: Heart Failure, Gupta et al. (1) report on the association of the ankle-brachial index (ABI) with incident heart failure in the ARIC (Atherosclerosis Risk in Communities) study. Although this is not the first report, the association extends our knowledge of the clinical value of the ABI and provides intriguing insights into additional pathophysiologic links between occlusive arterial disease in the peripheral circulation and a variety of cardiovascular disease manifestations.
The ABI has been in use by the vascular community for decades as a noninvasive diagnostic measure of peripheral artery disease (PAD). The measurement is typically performed by obtaining systolic blood pressures with Doppler ultrasound in both arms and the dorsalis pedis and posterior tibial arteries at the ankle (2). Simple ratios are created, with the value in each ankle vessel normalized to the single highest arm pressure. The individual limb ABI is defined by the higher of the 2 ABI ratios in that limb, and the limb with the lowest ABI identifies the presence or absence of PAD as well as the hemodynamic disease severity.
The historical application of the ABI was limited to the initial evaluation of patients with potential PAD, providing objective evidence of hemodynamic compromise in the lower extremity. The typical threshold value to make the diagnosis of PAD is a ratio ≤0.90 (2). However, a number of significant associations have been subsequently described that provide a broader context for this simple measure. For example, a low ABI not only indicates atherosclerotic occlusive disease in the lower extremity but is also highly associated with clinical coronary and carotid disease. Therefore, vascular disease in one territory is associated with disease in another vascular territory. As a consequence, there is a direct inverse correlation between ABI and risk for cardiovascular events and all-cause mortality, even when adjusted for known cardiovascular risk factors (3). Additional associations have been described for lower extremity function. Patients with low ABIs, regardless of limb symptoms, have decreased functional capacity (4). Patients with low ABIs also experience progressive functional decline over time, and therefore both the functional state and the natural history of lower extremity disease is predicted by the ABI (5).
Further characterization of the ABI has been evaluated in numerous epidemiologic studies. In the REACH (Reduction of Atherothrombosis for Continued Health) registry of more than 67,000 subjects who were at risk for or had known clinical evidence of cardiovascular disease, the prevalence of PAD was similar to that of coronary and carotid disease (6). However, what is striking is that the majority of patients with PAD at the time of their diagnosis did not have other clinical evidence of concomitant coronary or carotid disease, despite a high prevalence of cardiovascular risk factors. In many cases, the absence of a clinical history of coronary artery disease or ischemic stroke makes the overall risk assessment of patients with isolated PAD challenging for many clinicians. However, the follow-up of REACH demonstrated that the risk for all-cause mortality and major cardiovascular adverse events was similar in patients with established coronary disease compared with established PAD (7). This indicates that hemodynamic evidence of disease in the lower extremity is highly associated with major adverse cardiovascular outcomes, regardless of an antecedent history of clinical coronary artery disease.
What has been less well studied is the association of the ABI with other cardiovascular disorders, in particular heart failure. In the study by Gupta et al. (1), ABI assessment was performed using limited techniques, including a less validated oscillometric method in the posterior artery of a single leg. Despite these limitations, there was a clear association between a low ABI (defined at a threshold of either ≤1.00 or ≤0.90) and incident heart failure. These associations were robust and remained independent even after accounting other cardiovascular risk factors. The conclusion is that the association may reflect an additional pathophysiology beyond typical atherosclerosis to account for the relationship. What is striking is that only 5.8% of the study population with ABIs ≤0.90 had clinical evidence of coronary heart disease at baseline, whereas almost one-half had imaging evidence of subclinical carotid plaque. Despite controlling for both the clinical and subclinical evidence of atherosclerosis, the associations remained strong.
The study did not further elucidate the exact mechanistic link between a low ABI and incident heart failure, but several mechanisms are proposed. Regardless of the mechanism, the findings appear sound and provide further evidence and extend our knowledge of the relationship between the ABI in the limb and a variety of cardiovascular manifestations and risks of adverse cardiovascular outcomes.
Despite these associations and broadening evidence of the clinical importance of the ABI, the U.S. Preventive Services Task Force provides only an indeterminate recommendation for ABI screening (8). Admittedly, there is a limited number of trials demonstrating the independent contribution of how information on a low ABI would favorably alter patient management to reduce the risk for cardiovascular or limb events. Perhaps added to this list could be early interventions to prevent progression to heart failure. However, given the strong and numerous associations of ABI with cardiovascular disease, continued investment of resources to study the ABI as an early signal of a patient at increased risk for a variety of cardiovascular outcomes is warranted. A particular emphasis should be placed on how ABI screening can favorably affect treatment decisions that, in the absence of ABI information, would be less favorable.
↵∗ Editorials published in JACC: Heart Failure reflect the views of the authors and do not necessarily represent the views of JACC: Heart Failure or the American College of Cardiology.
Dr. Hiatt has reported that he has no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation
- Gupta D.K.,
- Skali H.,
- Claggett B.,
- et al.
- Aboyans V.,
- Criqui M.H.,
- Abraham P.,
- et al.