Exaggerated blood pressure response and arterial stiffness

Abstract

Exaggerated blood pressure response (EBPR) to exercise stress test is often present in hypertensive patients but the clinical significance in normotensive subjects is unclear and poorly studied. We consider that this group may advance to future cardiovascular (CV) complications such as hypertensive crises and target organ damage for no development of vascular buffer mechanism. Pulse wave velocity (PWV) is nowadays the gold standard and the simplest way to asses arterial stiffness (AS) and has been used as a predictive value of aortic stiffness for cardiovascular events. PWV variation pre and post induced ischemia of brachial artery has been validated for evaluate endothelial dysfunction (ED). The purpose of this study was to examine AS and ED in normotensive subjects with EBPR on a graded treadmill test and compared with healthy people free of CV disease, with normal blood pressure response. We tested 40 normotensive patients (51.4 16.4 years old, 15 males) with EBPR to exercise test and 25 controls. Exercise was performed on a treadmill. For AS we used carotid-femoral PWV (Complior System , Artech, France), and PWV variation for ED. All patients were non smokers and were tested at the same morning times with 4 hours without foods or drinks, with 20 minutes previous rest. Baseline characteristics and biochemistry are shown on table 1. All the patients were studied with ambulatory blood pressure monitoring (ABPM) (Spacelabs Health care USA 90217A) for rule out masked hypertension. We observed a PWVof 8.7 1.8 m/s in EBPR and 7.0 0.9 m/s in control group (p<0,01) and a decrease of 8.2% in PWV post induced ischemia for control subjects versus a paradoxical response in EBPR group with an increase of 4.8% (p<0.001). No major determinants for AS (hypertension, old age, renal insufficiency and diabetes) reach statistical significance. We found AS enhanced and ED in EBPR group (structural and functional vascular impact) and could be, among others, one of the mechanism for increase CV risk in this group.