Background: The prognostic importance of left atrial (LA) dysfunction is increasingly recognized. Magnetic Resonance Imaging (MRI) can provide excellent visualization of the left atrial wall. We aimed to study the association of LA dysfunction measured using feature-tracking MRI with incident adverse cardiovascular events among subjects with or without HF at baseline. Methods and Results: We prospectively studied 640 adults without HF (n=419), HF with preserved ejection fraction (HFpEF, n=101), or HF with reduced ejection fraction (HFrEF, n=120). We measured phasic LA function by volumetric and feature-tracking methods to derive longitudinal strain. The composite outcome of incident heart failure hospitalization or death was adjudicated over a median follow-up of 37.1 months. Measures of LA phasic function were more prominently impaired in subjects with HFrEF, than among subjects with HFpEF. In unadjusted Cox proportional hazards models, all measures of phasic LA function and volumes (maximum, minimum and diastatic) were associated with the composite outcome. However, in analyses that adjusted for clinical risk factors, heart failure status, maximum LA volume, left ventricular (LV) mass and LV ejection fraction, measures of conduit and reservoir LA function, but not booster-pump function, were associated with the composite outcome. The strongest associations were observed for conduit longitudinal strain (Standardized Hazard ratio=0.66; 95%CI=0.49–0.88, P=0.004), conduit strain rate (Standardized HR=1.59; 95%CI=1.16–2.16, P=0.0035), and reservoir strain (Standardized HR=0.68; 95%CI=0.52–0.89, P=0.0055). Conclusions: Phasic LA function measured using MRI feature-tracking is independently predictive of the risk of incident HF admission or death, even after adjusting for LA volume and LV remodeling.

CKD is associated with increased (inactive) dp-ucMGP, a vitamin K-dependent inhibitor of vascular calcification, which correlates with large artery stiffness. Further studies are needed to assess whether vitamin K2 supplementation represents a suitable therapeutic strategy to prevent or reduce arterial stiffening in CKD.

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Large artery stiffening contributes to the pathophysiology of heart failure (HF) and associated comorbidities. MGP (matrix Gla-protein) is a potent inhibitor of vascular calcification. MGP activation is vitamin K–dependent. We aimed (1) to compare dp-ucMGP (dephospho-uncarboxylated MGP) levels between subjects with HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF) and subjects without HF; (2) to assess the relationship between dp-ucMGP levels and arterial stiffness; and (3) to assess the relationship between warfarin use, dp-ucMGP levels, and arterial stiffness in HF. We enrolled 348 subjects with HFpEF (n=96), HFrEF (n=53), or no HF (n=199). Carotid-femoral pulse wave velocity, a measure of large artery stiffness, was measured with arterial tonometry. Dp-ucMGP was measured with ELISA. Dp-ucMGP levels were greater in both HFrEF (582 pmol/L; 95% CI, 444–721 pmol/L) and HFpEF (549 pmol/L; 95% CI, 455–643 pmol/L) compared with controls (426 pmol/L; 95% CI, 377–475 pmol/L; ANCOVA P =0.0067). Levels of dp-ucMGP were positively associated with carotid-femoral pulse wave velocity (standardized β, 0.31; 95% CI, 0.19–0.42; P <0.0001), which was also true in analyses restricted to patients with HF (standardized β, 0.34; 95% CI, 0.16–0.52; P =0.0002). Warfarin use was significantly associated with carotid-femoral pulse wave velocity (standardized β, 0.13; 95% CI, 0.004–0.26; P =0.043), but this relationship was eliminated after adjustment for dp-ucMGP. In conclusion, levels of dp-ucMGP are increased in HFpEF and HFrEF and are independently associated with arterial stiffness. Future studies should investigate whether vitamin K supplementation represents a suitable therapeutic strategy to prevent or reduce arterial stiffness in HFpEF and HFrEF.

There is controversy regarding the utility of left ventricular (LV) mechanics assessed by featuretracking (FT)-SSFP, a readily implementable technique in clinical practice. In particular, whether LV mechanics assessed by FT-SSFP predicts outcomes in subjects with heart failure (HF) with reduced ejection fraction (HFrEF), with preserved ejection fraction (HFpEF), or without HF is unknown. We aimed to assess whether LV mechanics measured with FT-SSFP cine MRI predicts adverse outcomes. We prospectively enrolled 612 adults without HF (n=402), with HF with reduced ejection fraction (HFrEF; n=113), or HFpEF (n=97) and assessed LV strain using FT-SSFP cine MRI. Over a median follow-up of 39.5 months, 75 participants had a HF admission, and 85 died. In Cox proportional hazards models, lower global longitudinal (Standardized Hazard Ratio: 1.56, 95% CI=1.22 to 2.00, p=0.0004), circumferential (Standardized HR: 1.46, 95% CI=1.08 to 1.95, p=0.0123), and radial strain (Standardized HR: 0.59, 95% CI=0.43-0.83, p=0.0019) were independently associated with the composite endpoint, after adjustment for HF status, LV ejection fraction (LVEF), age, sex, ethnicity, body mass index, systolic and diastolic blood pressure, hypertension, diabetes, coronary artery disease and glomerular filtration rate. Furthermore, global longitudinal strain stratified the risk of adverse outcomes across tertiles better than LVEF. In analyses that included only participants with a preserved LVEF, systolic radial, circumferential and longitudinal strain were independently predictive of adverse outcomes. We conclude that LV longitudinal, circumferential and radial strain measured using FT-SSFP cine

An increased myocardial ECVF, suggesting myocardial fibrosis, is independently associated with poor glycemic control among adults with diabetes. Further research should assess whether tight glycemic control can revert fibrosis to healthy myocardium or ameliorate it and its adverse clinical consequences.

AimsThe arginine vasopressin (AVP) pathway has been extensively studied in heart failure (HF) with reduced ejection fraction (HFrEF), but less is known about AVP in HF with preserved EF (HFpEF). Furthermore, the association between AVP and atrial natriuretic peptide (ANP, a well‐known inhibitor of AVP secretion) in HF is unknown.Methods and resultsWe studied subjects with HFpEF (n = 28) and HFrEF (n = 25) and without HF (n = 71). Left ventricular (LV) mass and left atrial (LA) volumes were measured with cardiac magnetic resonance imaging. Arginine vasopressin and ANP were measured with enzyme‐linked immunosorbent assay. Arginine vasopressin levels were significantly greater in HFpEF [0.96 pg/mL; 95% confidence interval (CI) = 0.83–1.1 pg/mL] compared with subjects without HF (0.69 pg/mL; 95% CI = 0.6–0.77 pg/mL; P = 0.0002). Heart failure with preserved ejection fraction (but not HFrEF) was a significant predictor of higher AVP after adjustment for potential confounders. Arginine vasopressin levels were independently associated with a greater LA volume and also paradoxically, with lower ANP levels. Key independent correlates of higher AVP were the presence of HFpEF (standardized β = 0.32; 95% CI = 0.09–0.56; P = 0.0073) and the ANP/LA volume ratio (standardized β = −0.23; 95% CI = −0.42 to −0.04; P = 0.0196). Arginine vasopressin levels were independently associated with LV mass (β = 0.26; 95% CI = 0.09–0.43; P = 0.003) and with an increased risk of death or HF admissions during follow‐up (hazard ratio = 1.61; 95% CI = 1.13–2.29; P = 0.008).ConclusionsArginine vasopressin is increased in HFpEF and is associated with LV hypertrophy and poor outcomes. Higher AVP is associated with the combination of LA enlargement and paradoxically low ANP levels. These findings may indicate that a relative deficiency of ANP (an inhibitor of AVP secretion) in the setting of chronically increased LA pressure may contribute to AVP excess.

Background: Arterial stiffness as measured by carotid-femoral pulse wave velocity (PWV) has been shown to predict cardiovascular events [1]. However, PWV is blood pressure (BP) dependent [2,3] leading to the development of cardio-ankle vascular index (CAVI) as a more blood pressure-independent index [4] that also shows predictive ability in Asian populations [5]. Recently, CAVI was further refined into CAVI 0 [6], removing residual acute blood pressure dependence [7]. The present study aims to assess risk prediction by CAVI and CAVI 0 in a US population.