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[Figure: see text].

Arterial load is composed of resistive and various pulsatile components, but their relative contributions to left ventricular (LV) remodeling in the general population are unknown. We studied 4145 participants enrolled in the Multi-Ethnic Study of Atherosclerosis, who underwent cardiac MRI and radial arterial tonometry. We computed systemic vascular resistance (SVR=mean arterial pressure/cardiac output) and indices of pulsatile load including total arterial compliance (TAC, approximated as stroke volume/central pulse pressure), forward wave amplitude (Pf), and reflected wave amplitude (Pb). TAC and SVR were adjusted for body surface area to allow for appropriate sex comparisons. We performed allometric adjustment of LV mass for body size and sex and computed standardized regression coefficients (β) for each measure of arterial load. In multivariable regression models that adjusted for multiple confounders, SVR (β=0.08; P<0.001), TAC (β=0.44; P<0.001), Pb (β=0.73; P<0.001), and Pf (β=-0.23; P=0.001) were significant independent predictors of LV mass. Conversely, TAC (β=-0.43; P<0.001), SVR (β=0.22; P<0.001), and Pf (β=-0.18; P=0.004) were independently associated with the LV wall/LV cavity volume ratio. Women demonstrated greater pulsatile load than men, as evidenced by a lower indexed TAC (0.89 versus 1.04 mL/mm Hg per square meter; P<0.0001), whereas men demonstrated a higher indexed SVR (34.0 versus 32.8 Wood Units×m2; P<0.0001). In conclusion, various components of arterial load differentially associate with LV hypertrophy and concentric remodeling. Women demonstrated greater pulsatile load than men. For both LV mass and the LV wall/LV cavity volume ratio, the loading sequence (ie, early load versus late load) is an important determinant of LV response to arterial load., (© 2014 American Heart Association, Inc.)

Arterial wave reflections have been associated with mortality in an ethnically homogenous Asian population. It is unknown whether this association is present in a multiethnic population or whether it is independent of subclinical atherosclerosis. We hypothesized that reflection magnitude (defined as the ratio of the amplitude of the backward wave [Pb] to that of the forward wave [Pf]) is associated with all-cause mortality in a large multiethnic adult community-based sample. We studied 5984 participants enrolled in the Multi-Ethnic Study of Atherosclerosis who had analyzable arterial tonometry waveforms. During 9.8±1.7 years of follow-up, 617 deaths occurred, of which 134 (22%) were adjudicated cardiovascular deaths. In Cox proportional hazards models, each 10% increase in reflection magnitude was associated with a 31% increased risk for all-cause mortality (hazard ratio [HR]=1.31; 95% confidence interval [CI]=1.11-1.55; P=0.001). This relationship persisted after adjustment for various confounders and for markers of subclinical atherosclerosis (HR=1.23; 95% CI=1.01-1.51; P=0.04), including the coronary calcium score, ankle-brachial index, common carotid intima-media thickness, and ascending thoracic aortic Agatston score. Pb was independently associated with all-cause mortality in a similarly adjusted model (HR per 10 mm Hg increase in P(b)=2.18; 95% CI=1.21-3.92; P=0.009). Reflection magnitude (HR=1.71; 95% CI=1.06-2.77; P=0.03) and P(b) (HR=5.02; 95% CI=1.29-19.42; P=0.02) were mainly associated with cardiovascular mortality. In conclusion, reflection magnitude is independently associated with all-cause mortality in a multiethnic population initially free of clinically evident cardiovascular disease. This relationship persists after adjustment for a comprehensive set of markers of subclinical atherosclerosis., (© 2014 American Heart Association, Inc.)

A parallel physiological pathway for elastic changes is hypothesized for declines in arterial elasticity and lung function. Endothelial dysfunction and inflammation could potentially decrease elasticity of both vasculature and lung tissue. We examined biomarkers, large arterial elasticity and small arterial elasticity (SAE), and forced vital capacity (FVC) in a period cross-sectional design in the multiethnic study of atherosclerosis, which recruited 1823 women and 1803 men, age range 45 to 84 years, black, white, Hispanic, and Chinese, free of clinically recognized cardiovascular disease. Radial artery tonometric pulse waveform registration was performed and large arterial elasticity and SAE were derived from diastole. Spirometric data and markers of endothelial dysfunction and inflammation (soluble intracellular adhesion molecule-1, fibrinogen, hs-C-reactive protein, and interleukin-6) were obtained. Mean large arterial elasticity was 13.7 ± 5.5 mL/mm Hg × 10 and SAE was 4.6 ± 2.6 mL/mm Hg × 100. Mean FVC was 3192 ± 956.0 mL and forced expiratory volume in 1 second was 2386 ± 734.5 mL. FVC was about 40 ± 5 mL higher per SD of SAE, stronger in men than women. The association was slightly weaker with large arterial elasticity, with no sex interaction. After regression adjustment for demographic, anthropometric, and cardiovascular risk factors, the biomarkers tended to be related to reduced SAE and FVC, particularly in men. These biomarker associations suggest important cardiovascular disease risk alterations that occur concurrently with lower arterial elasticity and lung function. The observed positive association of SAE with FVC and with forced expiratory volume in 1 second in middle-aged to older free-living people is consistent with the hypothesis of parallel physiological pathways for elastic changes in the vasculature and in lung parenchymal tissue.

Lung function studies in middle-aged subjects predict cardiovascular disease mortality. We studied whether greater loss of forced vital capacity (FVC) early in life predicted incident hypertension. The sample was 3205 black and white men and women in the Coronary Artery Risk Development in Young Adults Study examined between 1985 and 1986 (Coronary Artery Risk Development in Young Adults year 0, ages 18-30 years) and 2005-2006 and who were not hypertensive by year 10. FVC was assessed at years 0, 2, 5, 10, and 20. Proportional hazard ratios and linear regression models predicted incident hypertension at years 15 or 20 (n=508) from the change in FVC (FVC at year 10 - peak FVC, where peak FVC was estimated as the maximum across years 0, 2, 5, and 10). Covariates included demographics, center, systolic blood pressure, FVC maximum, smoking, physical activity, asthma, and body mass index. Unadjusted cumulative incident hypertension was 25% in the lowest FVC loss quartile (Q1; median loss: 370 mL) compared with 12% cumulative incident hypertension in those who achieved peak FVC at year 10 (Q4). Minimally adjusted hazard ratio for Q1 versus Q4 was 2.21 (95% CI: 1.73-2.83), and this association remained significant in the fully adjusted model (1.37; 95% CI: 1.05-1.80). Decline in FVC from average age at peak (29.4 years) to 35 years old predicted incident hypertension between average ages 35 and 45 years. The findings may represent a common pathway that may link low normal FVC to cardiovascular disease morbidity and mortality.

Early cardiovascular disease can be identified in asymptomatic individuals by noninvasive evaluation of functional and structural abnormalities of the vasculature and heart. These abnomalities are usually a consequence of endothelial dysfunction. A panel of 10 tests, including small and large artery elasticity, has been used as the basis for a screening system that provides a score of 0 to 20 as a guide to the severity of disease. Using that Rasmussen score allows for stratification of patients into low, intermediate, or high risk for progression to cardiovascular morbid events. This comprehensive screening can be performed efficiently in a single room with a single technician. The sensitivity and specificity of this screening system in predicting future cardiovascular events, its superiority to traditional risk factor assessment, and its potential to track the response to therapeutic interventions must be validated in long-term follow-up studies.

Several methodologically independent measures of arterial stiffness derived from either the systolic or diastolic segments of the arterial pulse have been proposed. The exact nature of the large and small artery elasticity indices (C1 and C2, respectively) derived from diastolic pulse contour analysis remains largely unexplored, although C2 has controversially been termed to be "oscillatory" and "reflective." We investigated the relation between C2 and, respectively, a prototype of arterial reflectivity (ie, the augmentation index, AIx) and a covariate of arterial reflectivity (body height). A validated transfer function is used to transform a tonometrically obtained radial pressure wave into an ascending aortic pressure wave, from which AIx is derived using systolic pulse contour analysis. Diastolic pulse contour analysis using a modified Windkessel model is used to derive C1 and C2. One hundred subjects, who were free from atherothrombotic disease and 19 to 77 years of age, with a wide pressure range (97 to 186/52 to 104 mm Hg) were studied. Mean values of C1, C2, AIx, and body height were, respectively, 13.8+/-4.3 mL/mm Hgx10, 5.9+/-3.1 mL/mm Hgx100, 128.5+/-24.9%, and 169+/-9 cm. Coefficients of variation were 32.8% for C1, 33.3% for C2, and 6.7% for AIx. C2 was significantly and inversely correlated to AIx (r=-0.707, P<0.001). Both AIx and C2 were correlated to body height (r=-0.487, P<0.001, and r=0.514, P<0.001). In conclusion, the results of this study provide the first clinical evidence that validates a probable biophysical equivalent of the C2 element of a third-order, 4-element modified Windkessel model. We suggest that C2 is, at least in part, a measure of arterial wave reflectance. However, although short-term reproducibility of AIx is excellent, C2 showed markedly increased variability with the devices used.