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Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Dr Georgiopoulos was supported by the Onassis Foundation under the special grant & support program for scholars" association members Introduction – Black Afro-Caribbean hypertensives (BAHs) are exposed to a higher risk of heart failure (HF) than white hypertensives (WHs). Arterial afterload is higher in BAHs due to increased arterial stiffness and vascular volume; BAHs develop more often left ventricular (LV) hypertrophy, dilatation and systolic dysfunction than WHs. However, it is unclear whether other racial differences concur to the more pronounced LV remodelling in BAHs. Methods – This cross-sectional study included hypertensive patients undergoing cardiovascular magnetic resonance for their clinical work-up (1.5T Aera Siemens-Healthcare). Clinical history and haemodynamic parameters were collected in all participants; a subset of patients had complete bio-humoral assay of the renin-angiotensin-aldosterone system (RAAs). Arm cuff pressure was measured during CMR. The CMR protocol included: i) Arterial afterload / LV arterial-coupling - pulse-wave-velocity (PWV), aortic (Ea) and LV elastance (Ees) by aorta anatomic and phase-contrast velocity-encoding imaging; ii) ventricular remodelling and function - LV and right ventricular (RV) volumes, mass, EF, LV peak-filling rate by short-axis cine images; global circumferential and longitudinal strains by cine feature tracking; iii) left atrial (LA) remodelling volumes and reservoir, conduit and booster functions by long-axis cine images; iv) tissue characterisation: T2 and pre/post-contrast T1 relaxation times, extracellular volume (ECV) by single mid-ventricular short-axis T1/T2-mapping. Results – 34 BAHs and 35 WHs (52 ± 12 vs 45 ± 14 years, P Conclusion – BAHs have heightened LV remodelling than WHs because of racial predisposition to develop hypertrophy which also encompasses derangements in RAAs. Altogether, these findings may account for the greater risk for HF in BAHs than WHs.

Alzheimer’s disease (AD) is the most common cause of dementia. Several haemodynamic risk factors for AD have been identified, including high systolic blood pressure (BP), brain hypoperfusion and arterial stiffness, as well as ageing. We propose a novel approach for assessing haemodynamic risk factors by analysing arterial pulse waves (PWs). The aim of this feasibility study was to determine whether features extracted from PWs might have utility for stratifying patients at risk of AD. A numerical model of PW propagation was used to simulate arterial PWs at a range of potential measurement sites, for virtual subjects of each age decade from 25 to 75 years, with subjects at each age exhibiting normal variation in BP and arterial stiffness. Several PW features were extracted, and their relationships with AD risk factors were investigated. PWs closer to the brain (at carotid and temporal arteries) were found to be suitable for detecting haemodynamic changes associated with AD. Several candidate PW features were identified for future clinical testing. These included features extracted from both BP and photoplethysmogram (PPG) PWs. This study demonstrates the potential feasibility of using non-invasive PWs to assess haemodynamic risk factors for AD. Not only could these factors be assessed from the BP PW, which is usually measured by a skilled operator, but also from the PPG, which can be acquired by smart watches and phones. If the findings are replicated in clinical studies, then this may provide opportunity for patients to assess their own risk and make lifestyle changes accordingly.

Aortic pulse pressure and other pulsatile components of the aortic pressure pulse are important predictors of cardiovascular outcomes, however the properties of the arterial tree that determine the aortic pulse are still poorly understood. We used numerical modelling to predict aortic pulse morphology and the characteristics of the arterial tree that determine pulse wave morphology when modulated by pharmacological agents with differential actions on the myocardium and arterial tree. Healthy volunteers aged 35 to 63 received cumulative doses of nitroglycerin (NTG, n=8), dobutamine (DB, n=10) and nor-epinephrine (NE, n=9). Aortic pressure was measured by carotid tonometry. Aortic dimensions, pulse wave velocity (PWV), blood velocity and flow were measured by echocardiography. These parameters were used to calculate the input data of a single-vessel, nonlinear one-dimensional model of pulse wave propagation in the human aorta coupled to a three-element Windkessel model of the downstream vasculature. The simulated pressure waveforms relative to the clinical data were reproduced with a averaged normalised root-mean-square-error < 10%, 7% and 6% for DB, NE and NTG groups respectively. By systematically and uniquely changing the parameters of the model by the amount measured clinically whilst keeping all other parameters at baseline conditions we identified the most significant determinant of the final pressure waveform to be total compliance and PWV for DB and peripheral vascular resistance for NTG and NE. Thus the majority of the change in aortic pulse morphology can be explained without invoking a change in the distributed characteristics of the arterial tree.

Left ventricular (LV) dysfunction is often seen in acute coronary syndromes (ACS) and high–risk percutaneous coronary intervention (PCI). Wave intensity analysis (WIA) quantifies energy flux within the circulation. We used WIA to examine the hemodynamic perturbations following ACS and PCI with

Summary It has been recognised for nearly 200 years that the human pressure waveform changes in shape with ageing and disease. The shape of the pressure waveform has been explained in terms of two fundamental models: the Windkessel (reservoir) and wave theory. In its simplest form the Windkessel model satisfactorily explains the pressure waveform in diastole but cannot model pressure changes in systole. Wave theory satisfactorily models the pressure waveform but predicts the existence of ‘self-cancelling’ forward and backward waves in diastole which are difficult to explain in biological terms. We propose that a hybrid reservoire wave model better describes the pressure waveform and may enable assessment of aortic function from pressure measurements made at any large systemic artery. a 2007 Published by Elsevier B.V. on behalf of Association for Research into Arterial Structure and Physiology.