Damping is the conversion of mechanical energy of a structure into thermal energy, and it is related to the material viscous behavior. To evaluate the role of damping in the common carotid artery (CCA) wall in human hypertension and the possible improvement of angiotensin-converting enzyme (ACE) inhibition, we used noninvasive CCA pressure (tonometry) and diameter (B-mode echography) waveforms in normotensive subjects (NT group; n=12) and in hypertensive patients (HT group; n=22) single-blind randomized into HT-placebo (n=10) or HT-treated (ramipril, 5 to 10 mg/d during 3 months; n=12). Vascular smooth muscle (VSM) null tonus condition was achieved from in vitro pressure and diameter waveforms (Konigsberg microtransducer and sonomicrometry) measured in explanted human CCA (n=14). Arterial wall dynamics was described by viscous (eta), inertial (M), and compliance (C) parameters, mean circumferential wall stress, viscous energy dissipation (WD), peak strain energy (WSt), damping ratio (xi=WD/WSt), and modeling isobaric indexes CIso and WSt(Iso). The lack of VSM tonus isobarically increased wall stress and reduced eta, CIso, and damping (P<0.01). Wall stress, eta, and WD were greater in HT than in NT (P<0.015) and arrived near normal in HT-treated (P<0.032 respect to HT), with no changes in HT-placebo. Whereas CIso increased in HT-treated (P<0.01) approaching the NT level, xi did not vary among groups. During hypertension, because of the WSt increase, the arterial wall reacts increasing WD to maintain xi. ACE inhibition modulates VSM activation and vessel wall remodeling, significantly improving wall energetics and wall stress. This protective vascular action reduces extra load to the heart and maintains enhanced arterial wall damping.

Wall inertia increase was associated with a higher IMT, suggesting that the intima-media thickening might be partially related to vascular hypertrophy manifested as increase of inertial behaviour.

No abstract

In 2008, the American Heart Association published resistant hypertension (RH) guidelines.1 Since that year, there has been a lot of research regarding the relevance of making a proper diagnosis and choosing the best treatment. In recent years, there has been an increasing interest in RH because uncontrolled RH is a pathological condition with a poor prognosis.In this regard, it is important to follow steps with the purpose of ruling out pseudoresistant hypertension and then excluding secondary causes. Suboptimal drug therapy, poor adherence to medications, white-coat effect, and inaccurate BP measurement are the most prev- It is difficult to establish the actual prevalence of true RH. Some series have reported a variable prevalence from 2% to 40%, depending on the criteria and the accuracy of the diagnostic procedures. 9,10All guidelines advise the use of three kinds of drugs for treatment:antagonists of the renin-angiotensin system (angiotensin-converting enzyme inhibitors or angiotensin II antagonists), calcium channel blockers, and diuretics, preferably long-lasting agents such as chlorthalidone. All agents must be prescribed at the best doses tolerated and at the optimal regimen of administration. Furthermore, if blood pressure is not under control, a fourth drug should be added. There are some controversies about whether the choice of this fourth drug should be empirically guided or guided by renin profile.To answer these questions, we must consider the paradigmatic tri- In addition, the registries of real-world patients treated with RD, which, taken together, support the safety and efficacy of RD.However, this conclusion must be reached through randomized controlled trials. [16][17][18][19] RH is characterized by an overexpression of humoral and hormonal factors that are involved in the development and maintenance of target organ damage (TOD). In this regard, mineralocorticoid receptor blockade has been proven effective and safe in the treatment of hypertension. Renin-angiotensin system blockade alone is not enough