During the meeting, there were hundred of poster presentations. Hypertension-specific posters are profiled here.
Researchers: Syrseloudis D, Tsioufis K, Andrikou E, et al.
Purpose: “Both blood pressure (BP) non-dipping and nocturnal hypertension have been associated with accelerated target organ damage (TOD) in subjects with hypertension,” explains Syrseloudis; “However the combination of a nocturnal BP reduction within the range of the dipping profile with increased absolute nocturnal BP values has never been investigated as regards TOD.” Therefore, he and his colleagues “investigated the relationships of nocturnal BP with indices of vascular and kidney damage and inflammatory activation in dipper hypertensive subjects.”
Results: Syrseloudis states that the research team concluded that nighttime blood pressure is associated more closely with carotid-femoral pulse wave velocity (c-f PWV) and albumin-to-creatinine ratio than daytime and 24-hour BP. “Moreover, dipper nocturnal hypertensives compared to dipper nocturnal normotensives exhibit a worse profile regarding c-f PWV, ACR and” high-sensitivity C-reactive protein.
Pulsatile Versus Steady Components of Blood Pressure and Their Relations With Aortic Stiffness: A Bone to Pick?
Researchers: Xaplanteris P, Vlachopoulos C, Vyssoulis G, et al.
Purpose: To explore associations of “pulsatility, and mean blood pressure (MBP) (the steady component of BP) with aortic stiffness,” as the “pulsatile component of blood pressure (BP) is implicated in atherosclerosis,” and aortic stiffness, “measured by pulse wave velocity (PWV), reflects changes in aortic structure and predicts outcomes.
Results: Xaplanteris concludes that the “pulsatile component of BP correlates with PWV,” adding that “cyclic strain on aortic wall that promotes arteriosclerosis and subsequent stiffening may be implicated as a pathophysiological mechanism.” He also notes that MBP, however, correlates more strongly with “PWV in never-treated hypertensives, indicating that elevated levels of BP per se, rather than relative changes in BP from diastole to systole, drive aortic stiffening.”
Arterial and Venous Endothelial Dysfunction in Resistant Hypertensive Patients
Researchers: Yugar-Toledo J, Souza L, Girioli S, et al.
Purpose: “The aim of our study,” says Yugar-Toledo “was to evaluate endothelial-dependent and -independent venous and arterial vasodilation in optimized resistant hypertensive [RH] patients compared to well-controlled hypertensive [CH] patients and normotensive individuals.” The research team conducted the study because arterial hypertension is known to cause “endothelial-dependent and -independent dysfunction as measured by flow-mediated dilation [FMD] and nitroglycerine administration [NTG], respectively,” and evidence exists that “venous compliance is reduced in primary hypertension.”
Results: Although a significant difference was seen in regards to endothelial-dependent venous vasodilation between the RH and NT groups, no difference was seen in regards to endothelial-independent venous vasodilation induced by sodium nitroprusside. Yugar-Toledo sums up the results by saying “RH patients present with venous and arterial endothelium-dependent vascular dysfunction. Additionally, a decrease in nitroglycerin-induced arterial vasodilatation was observed in this group.”
The Adverse Effects of Nocturnal Hypertension on Arterial Stiffness and Urinary Albumin Excretion in Hypertension