Supervisors: professor Jaan Eha (TÜ kardioloogia kliinik), professor Mihkel Zilmer (TÜ biokeemia instituut)
ja vanemteadur Priit Kampus (TÜ kardioloogia kliinik, TÜ biokeemia instituut).
Oponent: professor Jan Filipovsky, PhD (Pilseni Ülikool, Tšehhi Vabariik)
Summary:
Arterial hypertension is a major cardiovascular risk factor which is poorly controlled despite available treatment. Assessment of novel risk factors, early subclinical organ damage, and haemodynamic profile, as well as treatment based on these findings have become a mainstay in the management of hypertension. Endothelial dysfunction is the earliest process of vascular impairment. Asymmetric dimethylarginine is a new marker of endothelial dysfunction. Vascular damage is also related to increased levels of oxidative stress which additionally increases total cardiovascular risk in hypertensive patients. Due to pulse pressure amplification blood pressure is increased when moving from the aorta (central blood pressure) to the periphery. Central blood pressure is more important than brachial blood pressure in the development of subclinical organ damage (e.g. left ventricular hypertrophy) and assessment of total cardiovascular risk. Hypertension is characterised by altered haemodynamic profile. Treatment strategy based on haemodynamic profile could improve blood pressure control in these patients. We found that asymmetric dimethylarginine was independently associated with endothelial dysfunction. Beta-blockers metoprolol and nebivolol equally reduced brachial blood pressure during a 1-year therapy. However, only nebivolol reduced central blood pressure and left ventricular wall thickness. The reduction in left ventricular wall thickness correlated more significantly with the decrease in central than brachial blood pressure. Nebivolol and metoprolol both reduced oxidative stress markers. However, the effect of only nebivolol on these factors was independent of the reduction in blood pressure. Haemodynamic profiling by baseline augmentation index and pulse pressure amplification predicted blood pressure reduction with antihypertensive therapy.