Ventricular–arterial coupling (VAC) plays a major role in the physiology of cardiac and aortic mechanics, as well as in the pathophysiology of cardiac disease. VAC assessment possesses independent diagnostic and prognostic value and may be used to refine riskstratification and monitor therapeutic interventions. Traditionally, VAC is assessed by the non‐invasive measurement of the ratio of arterial (Ea) to ventricular end‐systolic elastance (Ees). With disease progression, both Ea and Ees may become abnormal and the Ea/Ees ratio may approximate its normal values. Therefore, the measurement of each component of this ratio or of novel more sensitive markers of myocardial (e.g. global longitudinal strain) and arterial function (e.g. pulse wave velocity) may better characterize VAC. In valvular heart disease, systemic arterial compliance and valvulo–arterial impedance have an established diagnostic and prognostic value and may monitor the effects of valve replacement on vascular and cardiac function. Treatment guided to improve VAC through improvement of both or each one of its components may delay incidence of heart failure and possibly improve prognosis in heart failure. In this consensus document, we describe the pathophysiology, the methods of assessment as well as the clinical implications of VAC in cardiac diseases and heart failure. Finally, we focus on interventions that may improve VAC and thus modify prognosis.

BackgroundIncretin-based therapies are used in the treatment of type 2 diabetes mellitus (T2DM) and obesity. We investigated the changes in arterial stiffness and left ventricular (LV) myocardial deformation after 6-month treatment with the GLP-1 analogue liraglutide in subjects with newly diagnosed T2DM.MethodsWe randomized 60 patients with newly diagnosed and treatment-naive T2DM to receive either liraglutide (n = 30) or metformin (n = 30) for 6 months. We measured at baseline and after 6-month treatment: (a) carotid-femoral pulse wave velocity (PWV) (b) LV longitudinal strain (GLS), and strain rate (GLSR), peak twisting (pTw), peak twisting velocity (pTwVel) and peak untwisting velocity (pUtwVel) using speckle tracking echocardiography. LV untwisting was calculated as the percentage difference between peak twisting and untwisting at MVO (%dpTw–UtwMVO), at peak (%dpTw–UtwPEF) and end of early LV diastolic filling (%dpTw–UtwEDF) (c) Flow mediated dilatation (FMD) of the brachial artery and percentage difference of FMD (FMD%) (d) malondialdehyde (MDA), protein carbonyls (PCs) and NT-proBNP.ResultsAfter 6-months treatment, subjects that received liraglutide presented with a reduced PWV (11.8 ± 2.5 vs. 10.3 ± 3.3 m/s), MDA (0.92 [0.45–2.45] vs. 0.68 [0.43–2.08] nM/L) and NT-proBNP (p < 0.05) in parallel with an increase in GLS (− 15.4 ± 3 vs. − 16.6 ± 2.7), GLSR (0.77 ± 0.2 vs. 0.89 ± 0.2), pUtwVel (− 97 ± 49 vs. − 112 ± 52°, p < 0.05), %dpTw–UtwMVO (31 ± 10 vs. 40 ± 14), %dpTw–UtwPEF (43 ± 19 vs. 53 ± 22) and FMD% (8.9 ± 3 vs. 13.2 ± 6, p < 0.01). There were no statistically significant differences of the measured markers in subjects that received metformin except for an improvement in FMD. In all subjects, PCs levels at baseline were negatively related to the difference of GLS (r = − 0.53) post-treatment and the difference of MDA was associated with the difference of PWV (r = 0.52) (p < 0.05 for all associations) after 6-month treatment.ConclusionsSix-month treatment with liraglutide improves arterial stiffness, LV myocardial strain, LV twisting and untwisting and NT-proBNP by reducing oxidative stress in subjects with newly diagnosed T2DM.ClinicalTrials.gov Identifier NCT03010683

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We investigated the association of endothelial glycocalyx damage with arterial stiffness, impairment of coronary microcirculatory function, and LV myocardial deformation in 320 untreated hypertensives and 160 controls. We measured perfused boundary region (PBR) of the sublingual microvessels, a marker inversely related with glycocalyx thickness, coronary flow reserve (CFR), and Global Longitudinal strain (GLS) by echocardiography, pulse wave velocity (PWV), and central systolic blood pressure (cSBP). Hypertensives had higher PBR, PWV cSBP, and lower CFR and GLS than controls (P < .05). In hypertensives, increased PBR was associated with increased cSBP, PWV, and decreased CFR and GLS after adjustment for age, sex, BMI, smoking LV mass, heart rate, hyperlipidemia, and office SBP (P < .05). PBR had an additive value to PWV, CFR, and office SBP for the prediction of abnormal GLS (x 2 = 2.4-3.8, P for change = .03). Endothelial glycocalyx is impaired in untreated hypertensives and is related to arterial stiffness, coronary, and myocardial dysfunction. | 673IKONOMIDIS et al.reserve (CFR), a marker of coronary microcirculatory function, is related to arterial stiffness and is impaired in hypertensive heart disease. 22 The effect of endothelial glycocalyx damage on arterial wall properties, coronary flow reserve, and LV myocardial deformation has not been clarified.We hypothesized that endothelial glycocalyx is impaired in newly diagnosed untreated hypertensives, leading to impaired arterial elasticity, coronary flow reserve, and consequently, abnormal myocardial deformation. Therefore, we investigated the association of endothelial glycocalyx damage with pulse wave velocity, coronary flow reserve, and LV myocardial deformation in untreated hypertensives. | MATERIAL S AND ME THODS | Study populationOut of 348 consecutive patients with new onset essential hypertension who attended our outpatient hypertension clinic, 320 patients (mean age: 51 ± 11 years, 67% males) with normal ejection fraction (>60%) had adequate 2-dimensional echocardiography images for the analysis of speckle parameters (feasibility of the method 92%). The diagnosis of essential hypertension was defined as One-hundred and sixty normotensive individuals (age:48 ± 13 years, 66% males) who visited our outpatient clinic for a routine check-up were selected using a ratio of 1 control to 2 hypertensive patients as controls.Exclusion criteria were history of diabetes, familiar hyperlipidemia, coronary artery disease (CAD), cardiomyopathy, and chronic pulmonary disease. All patients and controls had no history of CAD, normal resting electrocardiogram, and underwent a non-invasive test (thallium scintigraphy after a treadmill exercise test or dobutamine stress echocardiography) to exclude myocardial ischemia. None of the female patients were on hormone replacement treatment. None of the patients or controls were on any kind of medication, including statins. All patients and controls had a glomerular filtration rate (GFR) > 60 mL/min/1.732 (MDRD formula) at enr...

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Background Arterial elastance to left ventricular elastance ratio assessed by echocardiography is widely used as a marker of ventricular‐arterial coupling. Materials and methods We investigated whether the ratio of carotid‐femoral pulse wave velocity, as a marker of arterial stiffness, to global longitudinal strain, as a marker of left ventricular performance, could be better associated with vascular and cardiac damage than the established arterial elastance/left ventricular elastance index. In 299 newly‐diagnosed untreated hypertensives we measured, carotid‐femoral pulse wave velocity, and carotid intima‐media thickness, coronary‐flow reserve, arterial elastance/left ventricular elastance, global longitudinal strain, and markers of left ventricular diastolic function (E/A and E’) by echocardiography. Results Pulse wave velocity‐to‐global longitudinal strain ratio (PWV/GLS) was lower in hypertensives than controls (−0.61 ± 0.21 vs −0.45 ± 0.11 m/sec%, P < 0.001). Low PWV/GLS values were associated with carotid‐intima media thickness > 0.9 mm (P = 0.003), E/A ≤ 0.8 (P = 0.019) and E’ ≤ 9 cm/sec (P = 0.002) and coronary‐flow reserve < 2.5 (P = 0.017), after adjustment for age, sex and mean arterial pressure. Low PWV/GLS was also associated with increased left ventricular mass and left atrial volume in the univariate (P = 0.003 and 0.038) but not in the multivariate model. In hypertensives, there was no significant association of arterial elastance‐to‐left ventricular elastance index with carotid intima media thickness, coronary flow reserve, E/A, E’, or left atrial volume with the exception of an inverse association with left ventricular mass (P = 0.027). Conclusions Pulse wave velocity‐to‐global longitudinal strain ratio but not the echocardiography‐derived arterial elastance‐to left ventricular elastance index is related to impaired carotid‐intima media thickness, coronary‐flow reserve and diastolic function in hypertensives.

Background and Purpose Cardioembolism is a postulated mechanism of embolic stroke of undetermined source (ESUS). We investigated endothelial glycocalyx, aortic elastic properties, oxidative stress, and their association with left atrial (LA) function in ESUS and healthy individuals. Methods In 90 ESUS patients (age 50.4 ± 13.2) and 90 controls with similar risk factors, we measured: (1) perfused boundary region (PBR) of the sublingual arterial microvessels (range 5–25 µm), a marker inversely related with glycocalyx thickness, (2) pulse wave velocity (PWV), central systolic blood pressure (cSBP), and augmentation index (AIx), (3) LA volume and strain using speckle-tracking imaging, and (4) malondialdehyde (MDA) and protein carbonyls (PCs), as oxidative stress markers. Results Compared with controls, ESUS had higher PWV, PBR, MDA, and PC levels as well as higher LA volume and reduced reservoir LA strain (p < 0.05). PBR > 1.2 μm of microvessel ranging from 5 to 9 μm and PWV > 10.2 m/s were associated with ESUS on multivariable analysis (odds ratio: 2.374 and 5.429, p < 0.05, respectively) and increased the c-statistic of the initial model from 0.54 to 0.71. In ESUS, glycocalyx damage (increased PBR) was related with increased PWV (p < 0.01) which was linked with LA reservoir strain after controlling for age, sex, and risk factors (p = 0.03). Increased MDA and PC were related with glycocalyx damage, increased PWV (r = 0.67 and r = 0.52), AIx, cSBP, and aortic atheroma (p < 0.01). Conclusion Arterial function and endothelial glycocalyx are severely impaired in ESUS and are linked to LA dysfunction suggesting their contribution to ESUS pathogenesis. Clinical Trial Registration URL-http://www.clinicaltrials.gov. Unique identifier: NCT03609437.