LAUSR

The term peripheral arterial disease (PAD) refers to a broad spectrum of atherosclerotic manifestations that can affect several vascular beds, including lower extremity arteries, the carotid and vertebral, upper extremities, and renal arteries. In recent decades, there has been a great interest in the evaluation of PAD in patients with coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI) with evidence indicating that patients with both CAD and PAD are at an increased risk for adverse events. However, many of these studies have focused on examining a single vascular bed at a time, whereas the assessment of PAD, intended as a family with its components, has been less thoroughly investigated. In this issue of the Journal, Bashar et al. leveraged the National Inpatient Sample database, which is derived from all the states participating in the Healthcare Cost and Utilization Project (HCUP) and covers more than 97% of the US population. In this analysis, they included about 1.4 million patients undergoing PCI and evaluated in‐ hospital outcomes in relation to the type of PAD as well as the number of vascular beds involved. The overall prevalence of PAD amounted to 14% and PAD was associated with an increased risk of mortality, ischemic stroke, and bleeding. However, the strength of this association varied, with lower extremity artery disease having the greatest impact on mortality, followed by cerebrovascular disease. In contrast, the risk of stroke was highest among patients with cerebrovascular disease, indicating that certain recurrent atherosclerotic manifestations tend to affect again the same vascular bed. In addition, the odds of in‐hospital mortality associated with multisite atherosclerosis increased progressively from 1.20 to 1.38 and 2.38 when one, two, or three vascular territories were affected, respectively. How should we then interpret the findings of this study? First, the authors should be congratulated for providing new data on the association between CAD and PAD subtypes based on a large sample size. Regretfully, with the exception of cerebrovascular disease, the other forms of PAD continue to be frequently neglected, undertreated, and underdiagnosed with treatments frequently extrapolated from the CAD field. Second, when treating CAD patients with PCI, we should not overlook the fact that atherosclerosis is a systemic disease; this should prompt screening of other vascular beds. On the other hand, when we know that a PCI patient has a history of PAD, we must remember that the risk of in‐hospital mortality is increased and proportional to the number of vascular sites involved. This is a simple information that can be easily added to our algorithm of risk prediction in clinical practice. Some caveats deserve mention and need to be considered for the interpretation of this study. When considering the association between risk factors and health outcomes, it is always necessary to differentiate between association and causation. Concurrent PAD in the setting of PCI should be interpreted as larger burden of atherosclerosis and elevated risk profile (all tested baseline characteristics were different between study groups) rather than a modifiable risk factor. Hence, we should not assume that treating PAD will necessarily improve PCI outcomes. As acknowledged by the authors, the National Inpatient Sample database is based on ICD‐10 coding system, which is limited by insufficient data entry, missing information, and incorrect coding. However, this tradeoff between quantity and data granularity must be anticipated when querying extremely large datasets. In summary, the study by Bashar and colleagues is an important contribution of the field of multisite atherosclerosis. The presence of PAD