Cardiopulmonary exercise testing and its relation to oxidative stress in patients with hypertension

Abstract

An increase in reactive oxygen species has been implicated in the pathologies of hypertension. This study was designed to evaluate antioxidant activity in hypertensive patients and to assess the relationship between oxidative stress and exercise tolerance in hypertensive patients with mild left ventricular diastolic dysfunction (LVDD). A total of 42 patients, aged 51 ± 9 years, with a long history of hypertension and mild LVDD (mitral flow velocities-E/A o1, deceleration time of E 4220 ms, and preserved ejection fraction-EF 450%), and 30 controls without cardiovascular disease, aged 50 ± 7 years, underwent cardiopulmonary exercise testing (CPET). Peak oxygen uptake (peak VO 2 ), oxygen pulse (VO 2 /heart rate (HR)) and ventilatory anaerobic threshold (VAT) were obtained during CPET. Antioxidant activity of superoxide dismutase (SOD) and glutathione peroxidase in the blood was measured before and after exercise. Reduced peak VO 2 (1715 ± 426 vs. 2083±465 ml min À1 , Po0.001), VO 2 /HR (12.0±2.8 vs. 14.6±3.3 ml per beat, Po0.001) and percentage of peak VO 2 at VAT (55.5 ± 15.8% vs. 64.5 ± 14.7%, P ¼ 0.007) were observed in hypertensive patients, compared with controls. Antioxidant protection was significantly attenuated in hypertensive patients, compared with controls, before (945 vs. 1006, P ¼ 0.012) and after exercise (954 vs. 1051, Po0.001). The level of SOD before and after exercise was significantly associated with LVDD in hypertensive patients (P ¼ 0.012 and 0.02, respectively). In addition, the degree of LVDD before exercise (E/A) influenced the degree of exercise capability (peak VO 2 ) (P ¼ 0.016). Asymptomatic hypertensive patients with mild LVDD had reduced cardiopulmonary capacity, accurately identified by CPET. The redox state in hypertensive patients was significantly related to LVDD and exercise tolerance. Attenuated antioxidant protection was associated with long-term hypertension.

Is there a relationship between right-ventricular and right atrial mechanics and functional capacity in hypertensive patients?

“…Previous studies found that functional capacity in hypertensive patients is decreased [25][26][27]. Our results agree with these findings, and furthermore reveal the difference between the well treated, the untreated and the unsatisfactory treated hypertensive patients.…”

“…Additionally, the interaction between LV and RV could be an important mechanism which explains the association between the right heart and functional capacity. Namely, investigators have already demonstrated the relationship between left-ventricular structure and function with functional capacity [25][26][27]35,36], as well as the strong correlation between left-ventricular and right-ventricular function achieved mostly through IVS [37], which could further connect the right heart function and peak oxygen consumption. The strength of the present study lies in the fact that we succeeded to show that right-ventricular function and right-ventricular myocardial deformation are associated with functional capacity independently of leftventricular remodeling.…”

Why is functional capacity decreased in hypertensive patients? From mechanisms to clinical studies

“…Namely, Bruning et al 26 and Cockcroft et al 27 found no difference in endothelium-dependent vasodilator microvasculature responses between arterial hypertensive patients and normotensive individuals, whereas other studies revealed impaired endothelium-dependent relaxation in microcirculation in arterial hypertensive patients due to oxidative stress. 3,4,18,28 The impairment of endothelium-dependent relaxation in arterial hypertensive patients could be the reason of increased peripheral resistance and the cause of significantly greater exercise-induced blood pressure elevation in arterial hypertensive patients. Furthermore, increased systemic resistance leads to a reduction in cardiac output, which could be an additional cause of decreased oxygen uptake and reduced functional capacity in the hypertensive population.…”

“…3,4,20,33,36 The cornerstone of the relationship between the left ventricle and functional capacity is myocardial perfusion reserve, which is significantly reduced in arterial hypertension patients. 29 On the other hand, some authors have claimed that myocardial oxygen consumption is even increased in arterial hypertension patients without left ventricular hypertrophy, but normal in arterial hypertension patients with hypertrophy.…”

“…Studies also showed that exercise capacity is significantly decreased in patients with arterial hypertension, [1][2][3][4][5][6] and even in individuals with high-normal blood pressure. 7,8 Furthermore, Faselis et al 9 found an inverse relationship between exercise capacity and the rate of progression from prehypertension to hypertension in middle-aged male veterans.…”