The association between impaired lung function (reduction in FEV1 or FEV1) and cardiovascular morbidity and mortality is well established.1–2 In the last decade, similar associations have been shown between FEV1 and stroke incidence and mortality.,2–4 The predominant risk factors for stroke are hypertension and preexisting vascular disease or atherosclerosis (and the risk factors leading to atherosclerosis, such as age, cigarette smoking, or diabetes). In a large 20-year follow-up study, Hart and colleagues4 showed a significant association between stroke mortality and BP (systolic and diastolic), smoking, blood glucose level, cardiothoracic ratio, height, preexisting coronary heart disease, and FEV1. The British Regional Heart Study,,3 a large prospective cardiovascular risk assessment study, showed that stroke is inversely related to FEV1 in older hypertensive men with preexisting ischemic heart disease who are nonsmokers or ex-smokers. Several other studies have supported this inverse relationship between FEV1 and stroke, independent of other risk factors, including smoking,,3–5 suggesting that impaired lung function is an independent risk factor for stroke mortality. In this issue of CHEST (see page 1642), Hozawa and colleagues,6 using data from the Atherosclerotic Risk in Communities study, showed an inverse relationship between FEV1 (and FVC) and ischemic stroke incidence in never-smokers, which is a novel finding that underlines the importance of impaired lung function as a independent risk factor for stroke. The biological mechanisms responsible for the association between reduced lung function and the incidence of ischemic stroke are still unclear.