Current European guidelines for the management of arterial hypertension introduce the assessment of arterial stiffness by pulse wave velocity (PWV) as an index of hypertension-related cardiovascular target organ damage. An increase in arterial stiffness is related to haemodynamic modifications at the level of the aorta, leading to a rise in cardiac afterload, a reduction in coronary perfusion and an overstretch of the aortic walls. An increasing number of studies have demonstrated the accuracy of PWV as an independent predictor of cardiovascular events and cardiovascular mortality in patients with different co-morbidities and cardiovascular risk. Many strategies have demonstrated their efficacy in preventing arterial stiffening; therapy of arterial hypertension is the mainstay in the management of patients with increased PWV and altered pulse wave reflection. Literature has clearly shown the specific efficacy of drugs interfering with the renin-angiotensin-aldosterone system and calcium-channel blockers in the control of central haemodynamics, particularly when compared with β-blockers (β-adrenoceptor antagonists). The same action has not yet been demonstrated on PWV. Further studies are needed to assess the real relative efficacy of different drug classes on the management of arterial stiffness and the clinical and prognostic relevance of these therapies.

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Mitral valve repair is the preferred treatment for patients with severe degenerative mitral valve regurgitation resulting from prolapsed mitral leaflets with or without chordal rupture. The NeoChord procedure is an innovative microinvasive, transventricular, beating-heart chordal replacement technique that is designed to replace ruptured or elongated chordae tendinae on the prolapsing segment of a mitral valve leaflet with artificial chordae made of expanded polytetrafluoroethylene (ePTFE). 1-3 The artificial chordae or neochordae are placed on the mitral leaflet, while the heart is beating using the DS1000 System (NeoChord, Inc St. Louis Park, MN). The DS1000 system is introduced via a transventricular approach through the distal, posterolateral wall of left ventricle. Preprocedure, use of three-dimensional (3D) transoesophageal (TOE) imaging is crucial for optimal patient selection. In addition, 3D TOE is critical for procedural navigation of the device and to confirm ePTFE chordal placement and positioning on the mitral leaflet. Awareness of the morphological details of the prolapsed mitral leaflet segment is an important consideration when assessing patient selection. However, understanding the change in morphological characteristics of the mitral leaflet segments during the procedure is also a key driver for successful outcomes. Use of real time 3D, with single beat acquisition, allows for visualization of the valvular anatomy and any related structural dysfunction with near-instantaneous volume-rendered reconstructions.Additionally, this 3D rendering technique avoids spatial motion artifacts by acquiring 3D volumetric datasets without requiring the need of cardiac or respiratory gating, single beat acquisition of datasets, that is, possible thanks to matrix phased-array transducer technology that includes the use of thousands of transmit-receive elements to generate the image volume. As such, real time 3D TOE

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Aim: Obesity is associated with an increased cardiovascular risk. This study aimed to assess the role of echocardiography in the early detection of subclinical cardiac abnormalities in a cohort of obese patients with a preserved ejection fraction (EF) undergoing bariatric surgery. Methods and Results: Forty consecutive severely obese patients (body mass index≥35 kg/m2) referring to our center for bariatric surgery were enrolled in this prospective cohort study. Despite a baseline EF of 61% ± 3%, almost half patients (43%) had a systolic dysfunction (SD) defined as global longitudinal strain (GLS)>−18%, and most of them (60%) had left ventricular hypertrophy (LVH) or concentric remodeling (CR). At 10-months after surgery, body weight decreased from 120 ± 15 kg to 83 ± 12 kg, body mass index from 44 ± 5 kg/m 2 to 31 ± 5 kg/m 2 (both P < 0.001). Septal and left ventricular posterior wall thickness decreased respectively from 10 ± 1 mm to 9 ± 1 mm ( P = 0.004) and from 10 ± 1 mm to 9 ± 1 mm ( P = 0.007). All systolic parameters improved: EF from 61% ± 3% to 64% ± 3% ( P = 0.002) and GLS from −17% ± 2% to −20% ± 1% ( P < 0.001). Epicardial fat thickness reduction (from 4.7 ± 1 mm to 3.5 ± 0.7 mm, P < 0.001) correlated with the reduction of left atrial area ( P < 0.001 R = 0.35) and volume ( P = 0.02 R = 0.25). Following bariatric surgery, we observed a reduced prevalence of LVH/CR (before 60%, after 22%, P = 0.001) and a complete resolution of preclinical SD (before 43%, after 0%, P < 0.001). Moreover, a postoperative reduction of at least 30 kg correlated with regression of septal hypertrophy ( P < 0.001). Conclusions: Obese patients candidate to bariatric surgery have an high prevalence of preclinical SD and LVH/CR, early detectable with echocardiography. Bariatric surgery is associated with reverse cardiac remodeling; it might also have a preventive effect on atrial fibrillation occurrence by reducing its substrate.

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Introduction: Acute and chronic aortic syndromes are associated with substantial morbidity and mortality. Silent risk factors such as arterial hypertension and aortic root dilatation can increase the likelihood of aortic dissection or rupture. The relationship between arterial hypertension and the dimensions of the aortic root dimension is a topic of active debate. Materials and methods: We reviewed the literature on the physiopathology, diagnosis, natural history, and management of thoracic aortic aneurysms. Results: Biological variables influencing the size of the aorta include age, sex, body surface area, pressure values, and stroke volume. Pathologic enlargement of the thoracic aorta can be caused by genetic, degenerative, inflammatory, traumatic, or toxic factors. Studies investigating the correlation between aortic dimensions and arterial pressures (diastolic, systolic, or pulse) have produced discordant results. Discussion: Classically, emphasis has been placed on the importance of hypertension-related degeneration of the medial layer of the aortic wall, which leads to dilatation of the thoracic aorta, reduced aortic wall compliance, and increased pulse pressures. However, there are no published data that demonstrate unequivocally the existence of a pathogenetic correlation between arterial hypertension and aortic root dilatation. Furthermore, there is no evidence that antihypertensive therapy is effective in the management of nonsyndromic forms of aortic root dilatation. An interesting branch of research focuses on the importance of genetic predisposition in the pathogenesis of thoracic aortic aneurysms. Different genetic backgrounds could explain differences in the behaviour of aortic walls exposed to the same hemodynamic stress. Further study is needed to evaluate these focal physiopathological aspects.