BackgroundCentral artery dilation and remodeling are associated with higher heart failure and cardiovascular risks. However, data regarding carotid artery diameter from hypertension to heart failure have remained elusive. We sought to investigate this issue by examining the association between carotid artery diameter and surrogates of ventricular dysfunction.Methods and ResultsTwo hundred thirteen consecutive patients including 49 with heart failure and preserved ejection fraction (HFpEF), 116 with hypertension, and an additional 48 healthy participants underwent comprehensive echocardiography and tissue Doppler imaging. Ultrasonography of the common carotid arteries was performed for measurement of intima‐media thickness and diameter (CCAD). Cardiac mechanics, including LV twist, were assessed by novel speckle‐tracking software. A substantial graded enlargement of CCAD was observed across all 3 groups (6.8±0.6, 7.7±0.73, and 8.7±0.95 mm for normal, hypertension, and HFpEF groups, respectively; ANOVA P<0.001) and correlated with serum brain natriuretic peptide level (R2=0.31, P<0.001). Multivariable models showed that CCAD was associated with increased LV mass, LV mass‐to‐volume ratio (β‐coefficient=10.9 and 0.11, both P<0.001), reduced LV longitudinal and radial strain (β‐coeffficient=0.81 and −3.1, both P<0.05), and twist (β‐coefficient=−0.84, P<0.05). CCAD set at 8.07 mm as a cut‐off had a 77.6% sensitivity, 82.3% specificity, and area under the receiver operating characteristic curves (AUROC) of 0.86 (95% CI 0.80 to 0.92) in discriminating HFpEF. In addition, CCAD superimposed on myocardial deformation significantly expanded AUROC (for longitudinal strain, from 0.84 to 0.90, P of ΔAUROC=0.02) in heart failure discrimination models.ConclusionsIncreased carotid artery diameter is associated with worse LV geometry, higher brain natriuretic peptide level, and reduced contractile mechanics in individuals with HFpEF.

The incidence of symptomatic newly developed large pleural effusions first diagnosed at more than 30 days post CABG was 3.1%. Those who were diagnosed between 30 and 90 days post CABG tended to have exudative effusions, whereas those diagnosed more than 90 days post CABG often had left ventricular impairment and transudative effusions. Most of these effusions settled with conservative management and did not recur.

s u m m a r y Background: Age has been shown to be related with increased vascular stiffness, cardiac structural alterations, and geometric remodeling. Data regarding the relationship between clinical heart failure (HF) symptoms and aging-related alterations of ventricular geometries are scarce. We therefore investigated this issue. Methods: We subsequently studied 1,577 participants without cardiovascular or chronic lung disorders. Echocardiography-defined cardiac structures and left ventricular (LV) geometries, including LV mass, relative wall thickness, and mass-to-volume ratio were all determined. Baseline clinical variables, medical histories, and functional impairment in terms of HF symptoms during exercise were all obtained. Multivariate bootstrapping derived odds ratio from various models were used to represent the independent predictors for HF. Results: Of all, 1,459 participants (age: 49.3 AE 10.8; 36% female) with normal ejection fraction (66.8 AE 4.7%) were enrolled in our study. Cardiac structural alterations, ventricular geometric remodeling, and diastolic dysfunction were significantly related to aging process, along with increasing cardiovascular morbidities and risk factors. After adjusting for confounders and LV mass, change in ventricular geometries in terms of mass-to-volume ratio remained an independent risk, whereas relative wall thickness had a borderline significance for HF symptoms (odds ratio: 2.79 and 1.04, p ¼ 0.047 and 0.08, respectively). Conclusion: Cardiac structure, function, and various ventricular remodeling patterns were age-related. Such remodeling process is not only associated with a higher incidence of cardiovascular morbidities but also more likely to develop HF symptoms, which are independent of clinical variables and LV mass.

The authors consecutively assessed various arterial pulse-wave velocity (PWV) indices and ankle-brachial index (ABI) by an automatic device (VP2000, OMRON Health Care Co. Ltd., Kyota, Japan) in outpatients with ≥ 1 cardiovascular risk. PAD was defined as ABI ≤ 0.9. Among 2309 outpatients (mean age 62.4 years), worse renal function was associated with higher brachial-ankle PWV, heart-carotid PWV, heart-femoral PWV (hf-PWV), and lower ABI (all P < .001). Multivariate regression models showed independent associations between lower eGFR, lower ABI (Coef: 0.42 & 0.41 for right and left), higher hf-PWV (Coef: -11.4 [95% CI: -15.4, -7.3]) and greater PAD risk (adjusted OR: 0.83 [95% CI: 0.76, 0.91], all P < .05). eGFR set at 77 mL/min/1.73m was observed to be useful clinical cutoff (c-statistics: 0.67) for identifying PAD (P for ΔAUROC: .009; likelihood X : 93.82 to 137.43, P < .001) when superimposed on clinical risks. This study suggested early renal insufficiency is tightly linked to region-specific vascular stiffness and PAD.