• heart failure
• hypertension

Hypertension represents a leading risk factor for the development of symptomatic heart failure and is now considered the factor who carries the highest attributable risk for heart failure in the general population. In terms of prevalence, according to the data from the Olmsted County cohort, 73.6% of patients with Heart Failure with reduced Ejection Fraction had hypertension compared with 89.3% of patients with Heart Failure with preserved Ejection Fraction. Cardiopulmonary exercise test (CPET) combined with exercise stress echocardiography (ESE) offers a feasible, non-invasive evaluation of different cardiac conditions, with the possibility of simultaneously exploring the peripheral and central components of oxygen consumption (VO2). Therefore, we assessed with CPET-ESE the hemodynamic and metabolic characteristics of HT subjects with and without HFpEF, including a cohort of healthy controls in order to understand the differences in exercise physiology and their relation with both hypertension related organ damage and transition to failure.
We prospectively enrolled HT subjects between September 2017 and May 2019. All patients were clinically stable; we excluded from the study patients presenting with more than moderate primary valvular disease, hypertrophic cardiomyopathy, active ischemia, atrial fibrillation, unable to complete exercise (respiratory exchange ratio [RER] <1.0), diabetes mellitus or with inadequate acoustic windows. The overall population (n=145) consisted of HT individuals (n=63) and patients with HT and HFpEF (HFpEF-HT, n=50), including a control group (n=32) of healthy subjects who demonstrated a normal exercise capacity and ultrasound scan. A symptom-limited graded ramp bicycle exercise test was performed in the semi-supine position on a tilting, dedicated, microprocessor-controlled stress echocardiography cycle ergometer. We estimated the expected peak oxygen consumption (VO2) based on patient age, height, weight and clinical history. Then, we calculated the work rate increment necessary to reach the patient’s estimated peak VO2 in 8 to 12 min. The protocol included 2 min of unloaded pedalling and 4 min of recovery after peak effort. Breath-by-breath minute ventilation, carbon dioxide production (VCO2), and VO2 were measured using a dedicated cardiopulmonary diagnostic software. A comprehensive echocardiographic examination was performed concurrently with breath-by-breath gas exchange measurements at different stages of effort: rest, within the first 4 min of exercise (low-load effort), after reaching a stable RER ≥1.00, and at peak effort. A post-processing speckle tracking analysis (GE healthcare EchoPAC BT 12) to measure global longitudinal strain (GLS) was performed from the apical long-axis view and 2- and 4-chamber views, after ensuring a frame rate >50 Hz. We reported the average values from the three apical views at rest and low-load effort, while AT and peak images were excluded due to algorithm undersampling at high HR and breathing-induced through-plane motion artifacts. The acquisition protocol included B-lines evaluation at rest at the end of the exercise, after peak-effort image acquisition.
HT subjects had a peak VO2 lower than controls but higher than HFpEF-HT. The reduced peak VO2 in HT may be related to an early peripheral dysfunction, expressed by the decreased peak AVO2diff. Indeed AVO2diff (peripheral component of VO2) at rest and low-load effort was similar between groups, but it was significantly reduced in HT and HFpEF-HT in comparison to controls at peak exercise. Moreover, it is possible to identify a mild cardiovascular dysfunction associated with HT. Despite a preseerved cardiac output and LVEF increase throughout the exercise, The HT patients during effort reached E/e’ values higher than controls but lower than HT-HFpEF, conversely LV compliance resulted lower than controls but higher than HT-HFpEF, outlining an intermediate profile of HT patients between healthy subjects and HFpEF.