Abstract-Brachial-ankle elasticity index (baEI; also known as brachial-ankle pulse wave velocity) has been proposed as a surrogate end point for cardiovascular disease. We performed a meta-analysis of longitudinal cohort studies for determining the ability of baEI to predict risk of cardiovascular events and all-cause mortality and dissecting factors influencing this predictive ability. Multiple online databases, reference lists from retrieved articles, and abstracts from international cardiovascular conventions were searched until April 2012. Longitudinal cohort studies that reported associations of baEI with clinical risk were included. Of the 18 studies included (8169 participants; mean follow-up, 3.6 years), 15 reported results on total cardiovascular events (5544 individuals), 7 on cardiovascular mortality (2274 individuals), and 9 on all-cause mortality (5097 individuals). The pooled relative risks for total cardiovascular events, cardiovascular mortality, and all-cause mortality were 2.95 (95% CI, 1.63-5.33), 5.36 (95% CI, 2.17-13.27), and 2.45 (95% CI, 1.56 -3.86), respectively, for subjects with high versus low baEI (all PϽ0.001). An increase in baEI by 1 m/s corresponded with an increase of 12%, 13%, and 6% in total cardiovascular events, cardiovascular mortality, and all-cause mortality, respectively. We conclude that baEI is associated with increased risk of total cardiovascular events and all-cause mortality. Issues such as expansion of data to non-Asian populations, validation of path length estimation, determination of reference values, and prospective comparison with carotid-femoral pulse wave velocity remain to be resolved. (Hypertension. 2012;60:556-562.) • Online Data Supplement Key Words: brachial-ankle pulse wave velocity Ⅲ cardiovascular risk Ⅲ cardiovascular disease Ⅲ mortality Ⅲ prediction Ⅲ meta-analysis Ⅲ arterial stiffness A rterial stiffness is increasingly recognized as a surrogate end point for cardiovascular (CV) disease and is associated with presence of CV risk factors and atherosclerotic disease.1 Arterial stiffness can be measured with noninvasive, reproducible, and relatively inexpensive techniques, and, thus, it is suitable for large-scale studies. Carotid-femoral pulse wave velocity (PWV; cfPWV) is considered the goldstandard method for assessing aortic stiffness 2 and predicts future CV events and all-cause mortality in a strong and independent manner. Brachial-ankle PWV, calculated as the ratio of the distance between the brachial and the tibial artery divided by the transit time between these 2 arteries, has been proposed as an additional arterial biomarker of CV risk. PWV is classically referred to "segmental stiffness." Because of the complexity of the anatomic course of the brachial-ankle arterial system, it is unclear whether the term brachial-ankle PWV is appropriate to define any particular segmental stiffness or whether it is just the ratio of a virtual brachial-ankle distance and the measurement of the brachial-ankle transit time. For this reason, this index will ...

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A significant fall in wave reflections was observed after marathon race, whereas aortic stiffness was not altered. Moreover, marathon runners have increased aortic stiffness and pressures, whereas wave reflections indexes do not differ compared to controls.

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Key PointsQuestionDo estimated markers of aortic stiffness, such as estimated pulse wave velocity and their change with time, predict cardiovascular events in individuals with hypertension?FindingsThe results of this post hoc analysis of the randomized Systolic Blood Pressure Intervention Trial (SPRINT) support an incremental predictive role of estimated pulse wave velocity with outcomes beyond Framingham Risk Score. Individuals whose estimated pulse wave velocity responded to 1 year of antihypertensive treatment demonstrated a 42% lower risk of death compared with nonresponders independent of systolic blood pressure reduction in the standard treatment group of the Systolic Blood Pressure Intervention Trial.MeaningAortic stiffness could be used in individuals with hypertension to assess risk; it could be used also as a therapeutic target to assist patient management and improve prognosis.

Endothelial dysfunction is an important process in the development of atherosclerotic cardiovascular disease, while it is also a major pathophysiological mechanism underlying vasculogenic erectile dysfunction (ED). Expectedly, these two prevalent disorders are linked also at the clinical level: ED is common in patients with overt and silent coronary artery disease, while ED is increasingly being regarded as the early clinical manifestation of a generalized vascular disease and carries an independent risk for future cardiovascular events. The emerging awareness of ED as a barometer for cardiovascular disease offers a unique opportunity to enhance preventive vascular health in men. Lifestyle and risk factor modification, as well as pharmacologic therapy (both phosphodiesterase type-5 inhibitors and non-ED-targeting drugs), appear to confer additional benefit both in terms of ED treatment and overall cardiovascular risk; this benefit may be related, at least partly, to the improvement of endothelial function and anti-inflammatory effects. The present review identifies pathophysiologic links between endothelial dysfunction, ED and coronary artery disease, presents methodological aspects regarding penile and systemic endothelial function, and discusses the clinical implications in terms of diagnosis of ED, assessment of patient risk, and treatment.

Immediate assessment of coronary microcirculation during treatment of ST elevation myocardial infarction (STEMI) may facilitate patient stratification for targeted treatment algorithms. Use of pressure-wire to measure the index of microcirculatory resistance (IMR) is possible but has inevitable practical restrictions. We aimed to develop and validate angiographyderived index of microcirculatory resistance (IMR angio) as a novel and pressure-wire-free index to facilitate assessment of the coronary microcirculation. 45 STEMI patients treated with primary percutaneous coronary intervention (pPCI) were enrolled. Immediately before stenting and at completion of pPCI, IMR was measured within the infarct related artery (IRA). At the same time points, 2 angiographic views were acquired during hyperaemia to measure quantitative flow ratio (QFR) from which IMR angio was derived. In a subset of 15 patients both IMR and IMR angio were also measured in the non-IRA. Patients underwent cardiovascular magnetic resonance imaging (CMR) at 48 h for assessment of microvascular obstruction (MVO). IMR angio and IMR were significantly correlated (ρ: 0.85, p < 0.001). Both IMR and IMR angio were higher in the IRA rather than in the non-IRA (p = 0.01 and p = 0.006, respectively) and were higher in patients with evidence of clinically significant MVO (> 1.55% of left ventricular mass) (p = 0.03 and p = 0.005, respectively). Post-pPCI IMR angio presented and area under the curve (AUC) of 0.96 (CI95% 0.92-1.00, p < 0.001) for prediction of post-pPCI IMR > 40U and of 0.81 (CI95% 0.65-0.97, p < 0.001) for MVO > 1.55%. IMR angio is a promising tool for the assessment of coronary microcirculation. Assessment of IMR without the use of a pressure-wire may enable more rapid, convenient and cost-effective assessment of coronary microvascular function.

ED is associated with increased risk of CV events and all-cause mortality. RR is higher at younger ages, in intermediate-risk groups, and when a questionnaire is used instead of a single question.